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other provinces and regions in Vietnam and other country.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Address\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Headquarters of Can Tho Journal of Medicine and Pharmacy, located Scientific Research and International Cooperation Office: 179 Nguyen Van Cu Street, An Khanh Ward, Ninh Kieu District, Can Tho City, Vietnam.\u003C\u002Fspan>\u003C\u002Fp>","\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Ngày 16\u002F7\u002F2015, Tạp chí Y Dược học Cần Thơ được cấp chỉ số quốc tế: ISSN 2354-1210.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 4\u002F2016, Tạp chí đã được Hội đồng Giáo sư ngành Y đưa vào danh sách các tạp chí khoa học Y học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Năm 2020 Tạp chí Y Dược học Cần Thơ đã được phê duyệt vào danh mục của các Hội đồng Giáo sư ngành Dược học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ ra 12 số\u002Fnăm, 180-200 trang\u002Fsố.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 12\u002F2022 Tạp chí Y Dược học Cần Thơ là thành viên của hệ thống Crossref và từ tháng 01\u002F2023 tạp chí thực hiện bình duyệt online kín 2 chiều nhằm tăng tính minh bạch, tin cậy của các công trình nghiên cứu khoa học và đảm bảo tốt nhất chất lượng khoa học của bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ, mục đích và phạm vi của tạp chí\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ và mục đích hoạt động của tạp chí: xuất bản nhằm mục đích phổ biến kết quả từ các đề tài nghiên cứu khoa học; giao lưu trao đổi khoa học, chia sẻ kinh nghiệm, học tập, đồng thời cập nhật thông tin khoa học mới trong các lĩnh vực y, sinh, dược học trong và ngoài nước.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phạm vi của tạp chí: Tạp chí xuất bản được chia thành 3 chuyên mục: (i) Bài báo nghiên cứu khoa học là kết quả công trình nghiên cứu khoa học có giá trị đã được triển khai nghiên cứu, (ii) Bài tổng quan y, sinh, dược học: phục vụ mục tiêu đào tạo liên tục trong lĩnh vực y, sinh, dược học; nhằm hệ thống hóa những kiến thức kinh điển và hiện đại; (iii) Thông tin cập nhật kiến thức mới về y, sinh, dược học trong nước và trên thế giới.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Chính sách truy cập mở\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ áp dụng chính sách truy cập mở đối với các bài báo đã xuất bản đến với độc giả, nhằm mở rộng cơ hội tiếp cận các kết quả nghiên cứu chất lượng cao và tăng cường trao đổi kiến thức. Tạp chí đăng tải trực tuyến (miễn phí) toàn văn các bài báo được công bố trên website của Tạp chí (https:\u002F\u002Ftapchi.ctump.edu.vn).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đạo đức xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ cam kết tuân thủ đạo đức xuất bản phù hợp với các hướng dẫn và tiêu chuẩn của the Committee on Publication Ethics (COPE), tuân thủ các nguyên tắc của COPE’s Core Practices, Best Practices Guidelines for Journal Editors và Guidelines on Good Publication Practices.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Bản thảo bài báo chỉ được chấp nhận khi được tác giả chịu trách nhiệm chính cam kết các nội dung sau: Các nội dung của bản thảo chưa được đăng tải toàn bộ hoặc một phần ở các tạp chí khác; Tất cả các tác giả đều có đóng góp một cách đáng kể vào quá trình nghiên cứu hoặc chuẩn bị bản thảo và cùng chịu trách nhiệm về các nội dung của bản thảo; Tuân thủ các biện pháp đảm bảo đạo đức nghiên cứu (ví dụ thỏa thuận đồng ý tham gia nghiên cứu).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Cam kết bảo mật\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí cam kết thực hiện và tuân thủ các quy định của luật và các văn bản hướng dẫn liên quan đến bảo mật thông tin cá nhân trên không gian mạng. Các thông tin mà người dùng (tác giả, độc giả, biên tập viên, người phản biện) nhập vào các biểu mẫu trên Hệ thống Quản lý xuất bản trực tuyến của tạp chí chỉ được sử dụng vào các mục đích đã được tuyên bố rõ ràng và sẽ không được cung cấp cho bất kỳ bên thứ ba nào khác, hay dùng vào bất kỳ mục đích nào khác.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phí gửi bài\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng bài: 1.000.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng nhanh: 1.500.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với tác giả là cán bộ viên chức thuộc Trường Đại học Y Dược Cần Thơ thì được hỗ trợ 50% lệ phí gửi đăng bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với sinh viên thực hiện đề tài nghiên cứu khoa học cấp trường được hỗ trợ 100% lệ phí đăng bài ( Tác giả gửi đính kèm “ Quyết định về việc giao tổ chức thực hiện đề tài nghiên cứu khoa học cấp Trường của sinh viên”).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Hình thức nộp lệ phí:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Tiền mặt:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Nộp trực tiếp tại Phòng Tài chính - Kế toán, Trường Đại học Y Dược Cần Thơ, số 179 Nguyễn Văn Cừ, P. An Khánh, Q. Ninh Kiều, thành phố Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Chuyển khoản:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tên Tài khoản: Trường ĐHYD Cần Thơ, Số TK: 0111000115668, tại ngân hàng Vietcombank chi nhánh Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Thời gian: Áp dụng từ ngày 01\u002F02\u002F2023.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">* Phí gửi bài không được hoàn trả khi bài viết bị từ chối hoặc tác giả xin rút bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Quy trình phản biện bài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ thực hiện quy trình phản biện kín hai chiều nghiêm ngặt. Danh tính của những người phản biện không được tiết lộ cho các tác giả và ngược lại. Quy trình thẩm định bài báo đăng gồm các bước sau:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tiếp nhận bản thảo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tác giả liên hệ gửi bản thảo đến Tạp chí qua hệ thống trực tuyến tại website: https:\u002F\u002Ftapchi.ctump.edu.vn. Hướng dẫn về cách đăng ký, gửi bài và chuẩn bị bản thảo được cung cấp trên website của Tạp chí.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sàng lọc sơ bộ\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sau khi Tòa soạn nhận được bài báo của tác giả, Ban Thư ký sẽ tiến hành kiểm tra sơ bộ bài báo (các yêu cầu về nội dung và hình thức). Những bài báo không đúng quy cách hoặc có nội dung không phù hợp hoặc vi phạm bản quyền sẽ bị từ chối (Ban Thư ký thông báo phản hồi đến tác giả trong vòng 1 tuần). Những bài báo đủ điều kiện, được Ban Thư ký tòa soạn chuyển đến Ban Biên tập có cùng chuyên môn với nội dung bài báo để đề xuất người phản biện. Thời gian kể từ khi Ban Biên tập nhận bài báo đến khi đề xuất người phản biện bài báo chậm nhất là 5 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Vòng phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký gửi bài và yêu cầu phản biện đến 02 phản biện độc lập.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Các phản biện gởi nhận xét cho Ban Thư ký. Thời gian từ khi gửi bài cho phản biện đến khi nhận ý kiến của phản biện tối đa là 20 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xử ký kết quả phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Nếu ý kiến đồng ý cho đăng và không cần chỉnh sửa, Ban Thư ký tiếp tục đăng bài theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Nếu ý kiến đồng ý đăng và cần chỉnh sửa, Ban Thư ký sẽ thông tin đến tác giả chỉnh sửa theo yêu cầu của người phản biện. Thời gian chỉnh sửa và gửi lại kéo dài không quá 2 tuần, từ khi tác giả bài báo nhận được thông tin (Quá trình này có thể lặp lại tối đa 2 lần\u002F1 bài báo). Khi có sự thống nhất, đồng ý của người phản biện; bài báo được tiếp tục đăng theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Những bài báo có chất lượng không đạt yêu cầu, cả 2 phản biện không đồng ý cho đăng sẽ bị Tòa soạn từ chối đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký tổng hợp các bản thảo đã được tác giả hoàn thiện sau thẩm định trình Ban Biên tập xem xét, Tổng Biên tập phê duyệt, quyết định bài đăng theo các tiêu chí: sự phù hợp nội dung với tôn chỉ và mục đích, thể loại bài viết (ưu tiên các bài có bài có nghiên cứu chuyên sâu, hàm lượng khoa học cao), đóng góp mới bài báo, bài báo được ưu tiên đăng trong số gần nhất của Tạp chí theo thứ tự: tính thời sự, chất lượng bài báo và thời gian gửi bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Ban Biên tập và Ban Thư ký biên tập bản thảo, chế bản, đọc rà soát lỗi. Thời gian hoàn thành từ 10-15 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Ban Thư ký có trách nhiệm thông báo cho tác giả bài báo (bằng e-mail) về tình hình phê duyệt bài báo, thời gian, số kỳ, tập xuất bản bài báo theo qui định.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">4. 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Assessing progress, advancing change. 2005–2006 Annual report",{},false,{"id":1075,"createTime":1076,"updateTime":1077,"relativeEntities":1078,"slug":1079,"properties":1080,"entityType":826,"verifyStatus":25,"verifyTime":1076,"verifyNote":827,"syncStatus":28,"languages":1096,"translateLanguages":1097,"viewCount":36,"primaryUrl":1098,"fullTextUrl":26,"authors":1099,"publicationType":902,"publisherRelationship":1226,"citationCount":1263,"citationInfo":1264,"publishDate":1267,"publishYear":945,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":1268,"isForceReanalyzing":1073},"14b8dfd8-9988-49fa-a273-08989340618e","2024-09-04T10:48:36.584+00:00","2025-02-06T08:04:26.372+00:00",[],"Cancer-Related-Fatigue-The-Scale-of-the-Problem",{"mag":1081,"keywords":1083,"openalex":1084,"abstract":1086,"title":1089,"pm":1092,"doi":1094},{"VOID":1082},"2150471053",{"VI":813},{"VOID":1085},"W2150471053",{"EN":1087,"VI":1088},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n               \u003Cjats:p>Fatigue is one of the most common and debilitating symptoms experienced by patients with cancer. Cancer-related fatigue (CRF) is characterized by feelings of tiredness, weakness, and lack of energy, and is distinct from the “normal” drowsiness experienced by healthy individuals in that it is not relieved by rest or sleep. It occurs both as a consequence of the cancer itself and as a side effect of cancer treatment, although the precise underlying pathophysiology is largely unknown. CRF may be an early symptom of malignant disease and is reported by as many as 40% of patients at diagnosis. Virtually all patients expect fatigue from cancer therapy. Up to 90% of patients treated with radiation and up to 80% of those treated with chemotherapy experience fatigue. CRF continues for months and even years ollowing completion of treatment in approximately one third of the patients with cancer. The impact of CRF on a patient's quality of life (QoL), particularly in relation to physical functioning and the ability to perform activities of daily living, is both profound and pervasive. In addition, CRF is associated with considerable psychological distress and can impose a significant financial burden by limiting a patient's ability to work. These effects can extend to caregivers and family members, who may also have to reduce their working capacity in order to provide additional care for a patient with CRF. This paper examines the prevalence of CRF and explores the impact of this distressing symptom on patients' functioning and QoL.\u003C\u002Fjats:p>\n               \u003Cjats:p>Disclosure of potential conflicts of interest is found at the end of this article.\u003C\u002Fjats:p>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n               \u003Cjats:p>Mệt mỏi là một trong những triệu chứng phổ biến và ảnh hưởng nghiêm trọng nhất mà bệnh nhân ung thư gặp phải. Mệt mỏi liên quan đến ung thư (CRF) được đặc trưng bởi cảm giác mệt mỏi, yếu ớt và thiếu năng lượng, và khác biệt với tình trạng buồn ngủ “bình thường” mà người khỏe mạnh trải qua ở chỗ nó không được cải thiện bằng nghỉ ngơi hay ngủ. CRF xảy ra như một hệ quả của chính căn bệnh ung thư và cũng là tác dụng phụ của các phương pháp điều trị ung thư, mặc dù cơ chế sinh bệnh chính xác vẫn chưa được hiểu rõ. CRF có thể là triệu chứng sớm của bệnh ác tính và được báo cáo bởi tới 40% bệnh nhân tại thời điểm chẩn đoán. Hầu hết bệnh nhân đều dự đoán sẽ cảm thấy mệt mỏi từ liệu pháp điều trị ung thư. Lên đến 90% bệnh nhân điều trị bức xạ và 80% bệnh nhân điều trị hóa trị đều trải qua hiện tượng mệt mỏi. CRF có thể kéo dài trong nhiều tháng và thậm chí nhiều năm sau khi hoàn thành điều trị, ảnh hưởng đến khoảng một phần ba bệnh nhân ung thư. Ảnh hưởng của CRF đến chất lượng cuộc sống (QoL) của bệnh nhân, đặc biệt liên quan đến khả năng hoạt động thể chất và khả năng thực hiện các hoạt động hàng ngày, thực sự sâu sắc và lan tỏa. Hơn nữa, CRF còn liên quan đến sự căng thẳng tâm lý đáng kể và có thể tạo ra gánh nặng tài chính lớn bằng cách giới hạn khả năng làm việc của bệnh nhân. Những tác động này cũng có thể lan rộng đến những người chăm sóc và thành viên trong gia đình, những người cũng có thể phải giảm khả năng làm việc để cung cấp sự chăm sóc thêm cho bệnh nhân mắc CRF. Bài báo này xem xét tỷ lệ mắc CRF và khám phá ảnh hưởng của triệu chứng khó chịu này đến khả năng hoạt động và chất lượng cuộc sống của bệnh nhân.\u003C\u002Fjats:p>\n               \u003Cjats:p>Các thông tin về những xung đột lợi ích tiềm năng được công bố ở cuối bài viết này.\u003C\u002Fjats:p>",{"EN":1090,"VI":1091},"Cancer-Related Fatigue: The Scale of the Problem","Mệt mỏi liên quan đến ung thư: Quy mô của vấn đề",{"VOID":1093},"17573451",{"VOID":1095},"10.1634\u002Ftheoncologist.12-s1-4",[102],[101],"https:\u002F\u002Facademic.oup.com\u002Foncolo\u002Farticle\u002F12\u002FS1\u002F4\u002F6395717",[1100,1120,1147,1174,1199],{"id":1101,"sortIndex":36,"researcher":26,"roles":1102,"affiliations":1103,"properties":1115},"569e53ba-7c4a-4175-8588-473ede394524",[],[1104],{"id":1105,"sortIndex":36,"affiliation":1106,"properties":26},"36e1d773-7b5b-48c6-9192-c164120c2fc4",{"id":1107,"createTime":1108,"updateTime":1109,"relativeEntities":1110,"slug":1111,"properties":1112,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"18d3222f-c8b8-4bfe-8951-dac62c82c19e","2024-09-04T10:48:36.596+00:00","2024-12-25T08:53:30.137+00:00",[],"aDepartment-of-Radiation-Oncology-James-P-Wilmot-Cancer-Center-Rochester-New-York-USA",{"title":1113},{"EN":1114},"aDepartment of Radiation Oncology, James P. 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Results of a multi-centre patient survey. Cancer Fatigue Forum, Ann Oncol, 11, 971, 10.1023\u002FA:1008318932641",{"doi":1420},"10.1023\u002FA:1008318932641",{"id":26,"text":1422,"url":26,"identifiers":1423},"Vogelzang, 1997, Patient, caregiver, and oncologist perceptions of cancer-related fatigue: Results of a tripart assessment survey. The Fatigue Coalition., Semin Hematol, 34, 4",{},{"id":26,"text":1425,"url":26,"identifiers":1426},"Crawford, 2000, Therapeutic Options for Anemia and Fatigue, Medscape Oncology",{},{"id":26,"text":1428,"url":26,"identifiers":1429},"Brown, 2005, The correlation between fatigue, physical function, the systemic inflammatory response, and psychological distress in patients with advanced lung cancer, Cancer, 103, 377, 10.1002\u002Fcncr.20777",{"doi":1430},"10.1002\u002Fcncr.20777",{"id":26,"text":1432,"url":26,"identifiers":1433},"Mallinson, 2006, Giving meaning to measure: Linking self-reported fatigue and function to performance of everyday activities, J Pain Symptom Manage, 31, 229, 10.1016\u002Fj.jpainsymman.2005.07.012",{"doi":1434},"10.1016\u002Fj.jpainsymman.2005.07.012",{"id":26,"text":1436,"url":26,"identifiers":1437},"Ahlberg, 2004, Fatigue, psychological distress, coping and quality of life in patients with uterine cancer, J Adv Nurs, 45, 205, 10.1046\u002Fj.1365-2648.2003.02882.x",{"doi":1438},"10.1046\u002Fj.1365-2648.2003.02882.x",{"id":26,"text":1440,"url":26,"identifiers":1441},"Flechtner, 1998, Quality of life assessment in Hodgkin's disease: A new comprehensive approach. First experience from the EORTC\u002FGELA and GHSG trials, Ann Oncol, 9, 147, 10.1093\u002Fannonc\u002F9.suppl_5.S147",{"doi":1442},"10.1093\u002Fannonc\u002F9.suppl_5.S147",{"id":26,"text":1444,"url":26,"identifiers":1445},"Holzner, 2003, Fatigue in ovarian carcinoma patients: A neglected issue?, Cancer, 97, 1564, 10.1002\u002Fcncr.11253",{"doi":1446},"10.1002\u002Fcncr.11253",{"id":26,"text":1448,"url":26,"identifiers":1449},"Monga, 2005, Longitudinal study of quality of life in patients with localized prostate cancer undergoing radiotherapy, J Rehabil Res Dev, 42, 391, 10.1682\u002FJRRD.2004.06.0071",{"doi":1450},"10.1682\u002FJRRD.2004.06.0071",{"id":26,"text":1452,"url":26,"identifiers":1453},"Dimeo, 1999, Effects of physical activity on the fatigue and psychologic status of cancer patients during chemo-therapy, Cancer, 85, 2273, 10.1002\u002F(SICI)1097-0142(19990515)85:10\u003C2273::AID-CNCR24>3.0.CO;2-B",{"doi":1454},"10.1002\u002F(SICI)1097-0142(19990515)85:10\u003C2273::AID-CNCR24>3.0.CO;2-B",{"id":26,"text":1456,"url":26,"identifiers":1457},"Stone, 2000, A study to investigate the prevalence, severity and correlates of fatigue among patients with cancer in comparison with a control group of volunteers without cancer, Ann Oncol, 11, 561, 10.1023\u002FA:1008331230608",{"doi":1458},"10.1023\u002FA:1008331230608",{"id":26,"text":1460,"url":26,"identifiers":1461},"McDaniel, 1995, Depression in patients with cancer: Diagnosis, biology, and treatment, Arch Gen Psychiatry, 52, 89, 10.1001\u002Farchpsyc.1995.03950140007002",{"doi":1462},"10.1001\u002Farchpsyc.1995.03950140007002",{"id":26,"text":1464,"url":26,"identifiers":1465},"Irvine, 1998, Fatigue in women with breast cancer receiving radiation therapy, Cancer Nurs, 21, 127, 10.1097\u002F00002820-199804000-00006",{"doi":1466},"10.1097\u002F00002820-199804000-00006",{"id":26,"text":1468,"url":26,"identifiers":1469},"Tchekmedyian, 2003, The relationship between psychologic distress and cancer-related fatigue, Cancer, 98, 198, 10.1002\u002Fcncr.11463",{"doi":1470},"10.1002\u002Fcncr.11463",{"id":26,"text":1472,"url":26,"identifiers":1473},"Berndt, 2005, Reductions in anaemia and fatigue are associated with improvements in productivity in cancer patients receiving chemotherapy, Pharmacoeconomics, 23, 505, 10.2165\u002F00019053-200523050-00009",{"doi":1474},"10.2165\u002F00019053-200523050-00009",{"id":26,"text":1476,"url":26,"identifiers":1477},"Mormont, 2000, Marked 24-h rest\u002Factivity rhythms are associated with better quality of life, better response, and longer survival in patients with metastatic colorectal cancer and good performance status, Clin Cancer Res, 6, 3038",{},{"id":1479,"createTime":1480,"updateTime":1481,"relativeEntities":1482,"slug":1483,"properties":1484,"entityType":826,"verifyStatus":25,"verifyTime":1480,"verifyNote":827,"syncStatus":28,"languages":1501,"translateLanguages":1502,"viewCount":36,"primaryUrl":1503,"fullTextUrl":26,"authors":1504,"publicationType":902,"publisherRelationship":1546,"citationCount":1584,"citationInfo":1585,"publishDate":1587,"publishYear":1588,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":1589,"isForceReanalyzing":1073},"7c0a729f-1335-41b1-9b8a-ed884b8bdeba","2024-07-19T02:56:02.561+00:00","2025-02-06T08:05:27.071+00:00",[],"Tumor-Hypoxia-Causative-Factors-Compensatory-Mechanisms-and-Cellular-Response",{"mag":1485,"keywords":1487,"openalex":1489,"abstract":1491,"title":1494,"pm":1497,"doi":1499},{"VOID":1486},"2123894943",{"VI":1488},"thiếu oxy trong khối u, khả năng điều trị, xạ trị, tế bào ác tính, thiếu máu",{"VOID":1490},"W2123894943",{"EN":1492,"VI":1493},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n               \u003Cjats:sec>\n                  \u003Cjats:title>Learning Objectives\u003C\u002Fjats:title>\n                  \u003Cjats:p>After completing this course, the reader will be able to:\u003C\u002Fjats:p>\n                  \u003Cjats:p>Explain the effect of hypoxia on resistance to treatment. Describe the causes of tumor hypoxia. Characterize cellular response to hypoxia.\u003C\u002Fjats:p>\n                  \u003Cjats:p>Access and take the CME test online and receive 1 hour of AMA PRA category 1 credit at CME.TheOncologist.com\u003C\u002Fjats:p>\n                  \u003Cjats:p>Hypoxia is a characteristic feature of locally advanced solid tumors resulting from an imbalance between oxygen (O2) supply and consumption. Major causative factors of tumor hypoxia are abnormal structure and function of the microvessels supplying the tumor, increased diffusion distances between the nutritive blood vessels and the tumor cells, and reduced O2 transport capacity of the blood due to the presence of disease- or treatment-related anemia. Tumor hypoxia is a therapeutic concern since it can reduce the effectiveness of radiotherapy, some O2-dependent cytotoxic agents, and photodynamic therapy. Tumor hypoxia can also negatively impact therapeutic outcome by inducing changes in the proteome and genome of neoplastic cells that further survival and malignant progression by enabling the cells to overcome nutritive deprivation or to escape their hostile environment. The selection and clonal expansion of these favorably altered cells further aggravate tumor hypoxia and support a vicious circle of increasing hypoxia and malignant progression while concurrently promoting the development of more treatment-resistant disease. This pattern of malignant progression, coupled with the demonstration of a relationship between falling hemoglobin level and worsening tumor oxygenation, highlights the need for effective treatment of anemia as one approach for correcting anemic hypoxia in tumors, and in so doing, possibly improving therapeutic response.\u003C\u002Fjats:p>\n               \u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n               \u003Cjats:sec>\n                  \u003Cjats:title>Mục tiêu học tập\u003C\u002Fjats:title>\n                  \u003Cjats:p>Sau khi hoàn thành khóa học này, người đọc sẽ có khả năng:\u003C\u002Fjats:p>\n                  \u003Cjats:p>Giải thích tác động của tình trạng thiếu oxy đối với khả năng điều trị. Mô tả nguyên nhân của tình trạng thiếu oxy trong khối u. Đặc trưng phản ứng của tế bào với tình trạng thiếu oxy.\u003C\u002Fjats:p>\n                  \u003Cjats:p>Truy cập và làm bài kiểm tra CME trực tuyến và nhận 1 giờ tín chỉ AMA PRA loại 1 tại CME.TheOncologist.com\u003C\u002Fjats:p>\n                  \u003Cjats:p>Tình trạng thiếu oxy là một đặc điểm nổi bật của các khối u rắn tiên tiến tại chỗ do sự mất cân bằng giữa cung cấp và tiêu thụ oxy (O2). Các yếu tố nguyên nhân chính của tình trạng thiếu oxy trong khối u bao gồm cấu trúc và chức năng bất thường của các mạch vi cung cấp cho khối u, khoảng cách khuếch tán gia tăng giữa các mạch máu dinh dưỡng và tế bào khối u, và khả năng vận chuyển O2 của máu giảm do sự hiện diện của thiếu máu liên quan đến bệnh hoặc điều trị. Tình trạng thiếu oxy trong khối u là một mối quan tâm trong điều trị vì nó có thể làm giảm hiệu quả của xạ trị, một số tác nhân độc tính phụ thuộc oxy và liệu pháp quang động học. Tình trạng thiếu oxy trong khối u cũng có thể ảnh hưởng tiêu cực đến kết quả điều trị bằng cách gây ra những thay đổi trong proteome và genome của các tế bào ác tính, điều này hỗ trợ sự sống sót và tiến triển ác tính bằng cách cho phép các tế bào vượt qua tình trạng thiếu dinh dưỡng hoặc thoát khỏi môi trường khó khăn. Việc chọn lọc và mở rộng clon của những tế bào được thay đổi theo chiều hướng thuận lợi further làm trầm trọng thêm tình trạng thiếu oxy trong khối u và hỗ trợ một vòng tròn ác tính của tình trạng thiếu oxy ngày càng tăng và tiến triển ác tính, trong khi đồng thời thúc đẩy sự phát triển của bệnh kháng điều trị nhiều hơn. Mô hình tiến triển ác tính này, kết hợp với việc chứng minh mối quan hệ giữa mức hemoglobin giảm và tình trạng oxy hóa khối u xấu đi, nhấn mạnh sự cần thiết của việc điều trị hiệu quả tình trạng thiếu máu như một phương pháp để khắc phục tình trạng thiếu oxy do thiếu máu trong khối u, và từ đó, có thể cải thiện phản ứng điều trị.",{"EN":1495,"VI":1496},"Tumor Hypoxia: Causative Factors, Compensatory Mechanisms, and Cellular Response","Thiếu oxy trong khối u: Các yếu tố nguyên nhân, cơ chế bù trừ và phản ứng của tế bào",{"VOID":1498},"15591417",{"VOID":1500},"10.1634\u002Ftheoncologist.9-90005-4",[102],[101],"https:\u002F\u002Facademic.oup.com\u002Foncolo\u002Farticle\u002F9\u002FS5\u002F4\u002F6388136",[1505,1524],{"id":1506,"sortIndex":115,"researcher":26,"roles":1507,"affiliations":1508,"properties":1519},"47d7302e-0208-4b52-bb1d-40b86abff19e",[],[1509],{"id":1510,"sortIndex":36,"affiliation":1511,"properties":26},"3847605a-701b-4529-b1cb-4be6827d1466",{"id":1512,"createTime":1513,"updateTime":1513,"relativeEntities":1514,"slug":1515,"properties":1516,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"c485a553-0507-4d87-aafe-f5c998a1b0bf","2024-07-19T02:56:02.583+00:00",[],"Beth-Israel-Medical-Center-New-York-City-New-York-USA",{"title":1517},{"EN":1518},"Beth Israel Medical Center, New York City, New York, USA",{"openalex":1520,"title":1522},{"VOID":1521},"A5046046756",{"EN":1523},"Louis B. Harrison",{"id":1525,"sortIndex":36,"researcher":26,"roles":1526,"affiliations":1527,"properties":1539},"7b718eb6-c636-48e1-90a1-ad4f9e8228d4",[],[1528],{"id":1529,"sortIndex":36,"affiliation":1530,"properties":26},"488c0a75-513e-4365-83b2-7c7959b06a3d",{"id":1531,"createTime":1532,"updateTime":1533,"relativeEntities":1534,"slug":1535,"properties":1536,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"e8a10eab-783d-400b-9e68-a7c8713e6aab","2023-12-19T07:03:26.384+00:00","2024-07-19T02:56:02.573+00:00",[],"Institute-of-Physiology-and-Pathophysiology-University-of-Mainz-Mainz-Germany-",{"title":1537},{"VI":1538},"Institute of Physiology and Pathophysiology, University of Mainz, Mainz, Germany.",{"openalex":1540,"orcid":1542,"title":1544},{"VOID":1541},"A5078928066",{"VOID":1543},"https:\u002F\u002Forcid.org\u002F0000-0003-4238-3188",{"EN":1545},"Peter Vaupel",{"url":26,"publisher":1547,"properties":1577},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":1548,"slug":663,"properties":1549,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":1555,"manageAffiliations":1556,"indexDatabases":1557,"url":761,"thumbnailPath":26,"statistic":1572,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":1550,"issn":1551,"introduce":1552,"eissn":1553,"title":1554},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":663},[],[],[1558,1565],{"id":743,"indexDatabase":1559,"url":758,"indexYears":26,"academicFieldIds":1564,"indexDatabaseRanking":26},{"id":745,"createTime":746,"updateTime":747,"relativeEntities":1560,"label":1561,"description":1562,"key":754,"publicationTags":1563,"standard":26},[],{"EN":750,"VI":750},{"VI":752,"EN":753},[756,757],[760],{"id":722,"indexDatabase":1566,"url":735,"indexYears":736,"academicFieldIds":1571,"indexDatabaseRanking":741},{"id":724,"createTime":725,"updateTime":726,"relativeEntities":1567,"label":1568,"description":1569,"key":732,"publicationTags":1570,"standard":26},[],{"EN":729,"VI":729},{"EN":729,"VI":731},[734],[738,739,740],{"impactFactor":36,"impactFactorByYear":1573,"i10Index":252,"i10IndexLast5Year":59,"totalPublication":257,"totalPublicationByYear":1574,"totalCitation":770,"totalCitationByYear":1575,"totalCitationPerPublication":785,"totalCitationPerPublicationByYear":1576,"hindexLast5Year":159,"hindex":159},{"2012":764,"2013":59,"2014":114,"2015":50,"2017":125,"2018":765,"2019":766,"2020":517,"2021":767,"2022":768,"2023":59},{"1997":115,"2000":114,"2001":114,"2002":59,"2004":162,"2005":59,"2006":114,"2007":114,"2008":135,"2009":114,"2010":114,"2011":115,"2013":115,"2016":115,"2017":114,"2019":115,"2020":114,"2022":115},{"1997":772,"2000":773,"2001":143,"2002":774,"2004":775,"2005":776,"2006":777,"2007":778,"2008":779,"2009":780,"2010":781,"2011":652,"2013":142,"2016":782,"2017":783,"2019":784,"2020":258,"2022":135},{"1997":772,"2000":787,"2001":788,"2002":789,"2004":790,"2005":791,"2006":792,"2007":793,"2008":794,"2009":795,"2010":796,"2011":652,"2013":142,"2016":782,"2017":797,"2019":784,"2020":798,"2022":135},{"volume":1578,"pages":1580,"issue":1582},{"VOID":1579},"9",{"VOID":1581},"4-9",{"VOID":1583},"S5",676,{"total":1584,"publishYear":26,"statisticByYear":1586},{"2012":125,"2013":241,"2014":257,"2015":517,"2016":159,"2017":517,"2018":125,"2019":398,"2020":45,"2021":286,"2022":257,"2023":517,"2024":356},"2004-11-01",2004,[1590,1593,1597,1601,1604,1608,1611,1614,1618,1622,1626,1630,1634,1637,1640,1644,1648,1652,1656,1660,1663,1667,1671,1675,1679,1682,1686,1690,1694],{"id":26,"text":1591,"url":26,"identifiers":1592},"Schwarz, 1909, Über Desensibilisierung gegen Röntgen- und Radiumstrahlen, Münchener Med Wochenschr, 24, 1",{},{"id":26,"text":1594,"url":26,"identifiers":1595},"Mottram, 1931, A factor of importance in the radio-sensitivity of tumours, Br J Radiol, 9, 606, 10.1259\u002F0007-1285-9-105-606",{"doi":1596},"10.1259\u002F0007-1285-9-105-606",{"id":26,"text":1598,"url":26,"identifiers":1599},"Gray, 1953, The concentration of oxygen dissolved in tissues at the time of irradiation as a factor in radiotherapy, Br J Radiol, 26, 638, 10.1259\u002F0007-1285-26-312-638",{"doi":1600},"10.1259\u002F0007-1285-26-312-638",{"id":26,"text":1602,"url":26,"identifiers":1603},"Teicher, 1990, Classification of antineoplastic treatments by their differential toxicity toward putative oxygenated and hypoxic tumor subpopulations in vivo in the FSaIIC murine fibrosarcoma, Cancer Res, 50, 3339",{},{"id":26,"text":1605,"url":26,"identifiers":1606},"Littlewood, 2001, The impact of hemoglobin levels on treatment outcomes in patients with cancer, Semin Oncol, 28, 49, 10.1016\u002FS0093-7754(01)90213-1",{"doi":1607},"10.1016\u002FS0093-7754(01)90213-1",{"id":26,"text":1609,"url":26,"identifiers":1610},"Höckel, 1991, Oxygenation of carcinomas of the uterine cervix: evaluation by computerized O2 tension measurements, Cancer Res, 51, 6098",{},{"id":26,"text":1612,"url":26,"identifiers":1613},"Vaupel, 1991, Oxygenation of human tumors: evaluation of tissue oxygen distribution in breast cancers by computerized O2 tension measurements, Cancer Res, 51, 3316",{},{"id":26,"text":1615,"url":26,"identifiers":1616},"Vaupel, 2001, Treatment resistance of solid tumors: role of hypoxia and anemia, Med Oncol, 18, 243, 10.1385\u002FMO:18:4:243",{"doi":1617},"10.1385\u002FMO:18:4:243",{"id":26,"text":1619,"url":26,"identifiers":1620},"Vaupel, 2001, Oxygen status of malignant tumors: pathogenesis of hypoxia and significance for tumor therapy, Semin Oncol, 28, 29, 10.1016\u002FS0093-7754(01)90210-6",{"doi":1621},"10.1016\u002FS0093-7754(01)90210-6",{"id":26,"text":1623,"url":26,"identifiers":1624},"Vaupel, 2002, Hypoxia in breast cancer: pathogenesis, characterization and biological\u002Ftherapeutic implications, Wien Med Wochenschr, 152, 334, 10.1046\u002Fj.1563-258X.2002.02032.x",{"doi":1625},"10.1046\u002Fj.1563-258X.2002.02032.x",{"id":26,"text":1627,"url":26,"identifiers":1628},"Höckel, 2001, Tumor hypoxia: definitions and current clinical, biologic, and molecular aspects, J Natl Cancer Inst, 93, 266, 10.1093\u002Fjnci\u002F93.4.266",{"doi":1629},"10.1093\u002Fjnci\u002F93.4.266",{"id":26,"text":1631,"url":26,"identifiers":1632},"Vaupel, 2002, Oxygenation status of gynecologic tumors: what is the optimal hemoglobin level?, Strahlenther Onkol, 178, 727, 10.1007\u002Fs00066-002-1081-x",{"doi":1633},"10.1007\u002Fs00066-002-1081-x",{"id":26,"text":1635,"url":26,"identifiers":1636},"Vaupel, 2003, Oxygenation gain factor: a novel parameter characterizing the association between hemoglobin level and the oxygenation status of breast cancers, Cancer Res, 63, 7634",{},{"id":26,"text":1638,"url":26,"identifiers":1639},"Zander, 1996, [Oxygen supply and acid-base status in extreme anemia.] Anaesthesiol Intensivmed Notfallmed Schmerzther, 31, 492",{},{"id":26,"text":1641,"url":26,"identifiers":1642},"Becker, 2000, Severe anemia is associated with poor tumor oxygenation in head and neck squamous cell carcinomas, Int J Radiat Oncol Biol Phys, 46, 459, 10.1016\u002FS0360-3016(99)00384-3",{"doi":1643},"10.1016\u002FS0360-3016(99)00384-3",{"id":26,"text":1645,"url":26,"identifiers":1646},"Höckel, 2001, Biological consequences of tumor hypoxia, Semin Oncol, 28, 36, 10.1016\u002FS0093-7754(01)90211-8",{"doi":1647},"10.1016\u002FS0093-7754(01)90211-8",{"id":26,"text":1649,"url":26,"identifiers":1650},"Moulder, 1987, Tumor hypoxia: its impact on cancer therapy, Cancer Metastasis Rev, 5, 313, 10.1007\u002FBF00055376",{"doi":1651},"10.1007\u002FBF00055376",{"id":26,"text":1653,"url":26,"identifiers":1654},"Durand, 1991, Keynote address: the influence of microenvironmental factors on the activity of radiation and drugs, Int J Radiat Oncol Biol Phys, 20, 253, 10.1016\u002F0360-3016(91)90100-I",{"doi":1655},"10.1016\u002F0360-3016(91)90100-I",{"id":26,"text":1657,"url":26,"identifiers":1658},"Giaccia, 1996, Hypoxic stress proteins: survival of the fittest, Semin Radiat Oncol, 6, 46, 10.1016\u002FS1053-4296(96)80035-X",{"doi":1659},"10.1016\u002FS1053-4296(96)80035-X",{"id":26,"text":1661,"url":26,"identifiers":1662},"Riva, 1998, Cellular physiology and molecular events in hypoxia-induced apoptosis, Anticancer Res, 18, 4729",{},{"id":26,"text":1664,"url":26,"identifiers":1665},"Haroon, 2000, Early wound healing exhibits cytokine surge without evidence of hypoxia, Ann Surg, 231, 137, 10.1097\u002F00000658-200001000-00020",{"doi":1666},"10.1097\u002F00000658-200001000-00020",{"id":26,"text":1668,"url":26,"identifiers":1669},"Goda, 2003, Hypoxia-inducible factor 1 alpha is essential for cell cycle arrest during hypoxia, Mol Cell Biol, 23, 359, 10.1128\u002FMCB.23.1.359-369.2003",{"doi":1670},"10.1128\u002FMCB.23.1.359-369.2003",{"id":26,"text":1672,"url":26,"identifiers":1673},"Koumenis, 2001, Regulation of p53 by hypoxia: dissociation of transcriptional repression and apoptosis from p53-dependent transactivation, Mol Cell Biol, 21, 1297, 10.1128\u002FMCB.21.4.1297-1310.2001",{"doi":1674},"10.1128\u002FMCB.21.4.1297-1310.2001",{"id":26,"text":1676,"url":26,"identifiers":1677},"Soengas, 1999, Apaf-1 and caspase-9 in p53-dependent apoptosis and tumor inhibition, Science, 284, 156, 10.1126\u002Fscience.284.5411.156",{"doi":1678},"10.1126\u002Fscience.284.5411.156",{"id":26,"text":1680,"url":26,"identifiers":1681},"Prehn, 1991, The inhibition of tumor growth by tumor mass, Cancer Res, 51, 2",{},{"id":26,"text":1683,"url":26,"identifiers":1684},"Demicheli, 1994, Local recurrences following mastectomy: support for the concept of tumor dormancy, J Natl Cancer Inst, 86, 45, 10.1093\u002Fjnci\u002F86.1.45",{"doi":1685},"10.1093\u002Fjnci\u002F86.1.45",{"id":26,"text":1687,"url":26,"identifiers":1688},"Holmgren, 1995, Dormancy of micrometastases: balanced proliferation and apoptosis in the presence of angiogenesis suppression, Nat Med, 1, 149, 10.1038\u002Fnm0295-149",{"doi":1689},"10.1038\u002Fnm0295-149",{"id":26,"text":1691,"url":26,"identifiers":1692},"Folkman, 1995, Clinical applications of research on angiogenesis, N Engl J Med, 333, 1757, 10.1056\u002FNEJM199512283332608",{"doi":1693},"10.1056\u002FNEJM199512283332608",{"id":26,"text":1695,"url":26,"identifiers":1696},"Vaupel, 2004, The role of hypoxia-induced factors in tumor progression, The Oncologist, 9, 10, 10.1634\u002Ftheoncologist.9-90005-10",{"doi":1697},"10.1634\u002Ftheoncologist.9-90005-10",{"id":1699,"createTime":1700,"updateTime":1701,"relativeEntities":1702,"slug":1703,"properties":1704,"entityType":826,"verifyStatus":25,"verifyTime":1700,"verifyNote":827,"syncStatus":28,"languages":1720,"translateLanguages":1721,"viewCount":36,"primaryUrl":1722,"fullTextUrl":26,"authors":1723,"publicationType":902,"publisherRelationship":1745,"citationCount":1783,"citationInfo":1784,"publishDate":1787,"publishYear":1788,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":1789,"isForceReanalyzing":1073},"98042e61-0fcb-4348-a1ba-9060c24911b4","2024-09-05T17:54:10.301+00:00","2025-02-06T08:06:24.311+00:00",[],"Extending-Survival-with-Chemotherapy-in-Metastatic-Breast-Cancer",{"mag":1705,"keywords":1707,"openalex":1708,"abstract":1710,"title":1713,"pm":1716,"doi":1718},{"VOID":1706},"2102118972",{"VI":813},{"VOID":1709},"W2102118972",{"EN":1711,"VI":1712},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n               \u003Cjats:sec>\n                  \u003Cjats:title>Learning Objectives\u003C\u002Fjats:title>\n                  \u003Cjats:p>After completing this course, the reader will be able to: Identify trials that have demonstrated a survival benefit with a modern chemotherapeutic agent or regimen in MBC.Summarize recent findings of randomized trials showing survival benefits with targeted therapy–chemotherapy combinations in MBC.Discuss quality-of-life findings and their implications in clinical practice.\u003C\u002Fjats:p>\n                  \u003Cjats:p>Access and take the CME test online and receive 1 AMA PRA category 1 credit at CME.TheOncologist.com\u003C\u002Fjats:p>\n                  \u003Cjats:p>Metastatic breast cancer (MBC) remains essentially incurable, and goals of therapy include the palliation of symptoms, delay of disease progression, and prolongation of overall survival time without negatively impacting quality of life. Anthracycline and taxane-based therapies have traditionally shown the highest degree of activity in MBC. Though numerous randomized clinical trials have shown improvements in overall response rates, few have found clear survival benefits. In recent years, however, there has been a small but growing series of clinical trials demonstrating modest, but meaningful survival advantages in metastatic disease. A common feature in many of these trials has been the use of a taxane, and more recently, a taxane combined with an antimetabolite. In addition, the development of targeted biologic agents active against MBC, such as trastuzumab and bevacizumab, has demonstrated great potential for enhancing the effects of chemotherapy and producing meaningful survival improvements. The role of the taxanes, antimetabolites, and biologics in extending survival in MBC is discussed.\u003C\u002Fjats:p>\n               \u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n               \u003Cjats:sec>\n                  \u003Cjats:title>Mục Tiêu Học Tập\u003C\u002Fjats:title>\n                  \u003Cjats:p>Sau khi hoàn thành khóa học này, người đọc sẽ có khả năng: Nhận diện các thử nghiệm đã chứng minh lợi ích sống sót với một tác nhân hoặc phác đồ hóa trị hiện đại trong ung thư vú di căn (MBC). Tóm tắt các phát hiện gần đây từ các thử nghiệm ngẫu nhiên cho thấy lợi ích sống sót với các sự kết hợp giữa liệu pháp nhắm mục tiêu – hóa trị trong MBC. Thảo luận về các phát hiện liên quan đến chất lượng cuộc sống và ý nghĩa của chúng trong thực hành lâm sàng.\u003C\u002Fjats:p>\n                  \u003Cjats:p>Truy cập và tham gia bài kiểm tra CME trực tuyến và nhận 1 tín chỉ vào loại 1 AMA PRA tại CME.TheOncologist.com\u003C\u002Fjats:p>\n                  \u003Cjats:p>Ung thư vú di căn (MBC) vẫn chủ yếu là không thể chữa khỏi, và các mục tiêu điều trị bao gồm giảm triệu chứng, trì hoãn tiến triển bệnh và kéo dài thời gian sống tổng thể mà không làm tổn hại đến chất lượng cuộc sống. Các liệu pháp dựa trên anthracycline và taxane truyền thống đã cho thấy hoạt động cao nhất trong MBC. Mặc dù nhiều thử nghiệm lâm sàng ngẫu nhiên đã cho thấy cải thiện tỷ lệ đáp ứng tổng thể, nhưng rất ít thử nghiệm tìm thấy lợi ích sống sót rõ ràng. Tuy nhiên, trong những năm gần đây, đã có một loạt thử nghiệm lâm sàng nhỏ nhưng đang phát triển chứng minh những lợi thế sống sót khiêm tốn nhưng có ý nghĩa trong bệnh di căn. Một đặc điểm chung trong nhiều thử nghiệm này là việc sử dụng taxane, và gần đây hơn là taxane kết hợp với một antimetabolite. Ngoài ra, sự phát triển của các tác nhân sinh học nhắm mục tiêu có hoạt động chống lại MBC, chẳng hạn như trastuzumab và bevacizumab, đã cho thấy tiềm năng lớn trong việc tăng cường hiệu quả hóa trị và tạo ra những cải thiện về sống còn có ý nghĩa. Vai trò của taxanes, antimetabolites, và sinh học trong việc kéo dài thời gian sống ở MBC được thảo luận.",{"EN":1714,"VI":1715},"Extending Survival with Chemotherapy in Metastatic Breast Cancer","Kéo Dài Thời Gian Sống Với Hóa Trị Trong Ung Thư Vú Di 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Cancer Society, 2005, Cancer Facts and Figures 2005, 9",{},{"id":26,"text":1794,"url":26,"identifiers":1795},"Surveillance, Epidemiology, and End Results (SEER) Program",{},{"id":26,"text":1797,"url":26,"identifiers":1798},"Gralow, 2005, Optimizing the treatment of metastatic breast cancer, Breast Cancer Res Treat, 89, S9, 10.1007\u002Fs10549-005-0143-z",{"doi":1799},"10.1007\u002Fs10549-005-0143-z",{"id":26,"text":1801,"url":26,"identifiers":1802},"Blum, 1999, Multicenter phase II study of capecitabine in paclitaxel-refractory metastatic breast cancer, J Clin Oncol, 17, 485, 10.1200\u002FJCO.1999.17.2.485",{"doi":1803},"10.1200\u002FJCO.1999.17.2.485",{"id":26,"text":1805,"url":26,"identifiers":1806},"Blum, 2001, Capecitabine (Xeloda) in 162 patients with paclitaxel-pretreated MBC: updated results and analysis of dose modification, Eur J Cancer, 37, S190a, 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Mature results of a large multicenter phase II trail, Eur J Cancer, 37, S191a, 10.1016\u002FS0959-8049(01)81191-6",{"doi":1815},"10.1016\u002FS0959-8049(01)81191-6",{"id":26,"text":1817,"url":26,"identifiers":1818},"Fumoleau, 2001, Phase II study of capecitabine (Xeloda®) in patients with advanced breast cancer (ABC), previously treated with anthracyclines and taxanes, Breast Cancer Res Treat, 69, 285a",{},{"id":26,"text":1820,"url":26,"identifiers":1821},"Miles, 2002, Combination versus sequential single-agent therapy in metastatic breast cancer, The Oncologist, 7, 13, 10.1634\u002Ftheoncologist.2002-0013",{"doi":1822},"10.1634\u002Ftheoncologist.2002-0013",{"id":26,"text":1824,"url":26,"identifiers":1825},"Sledge, 2003, Phase III trial of doxorubicin, paclitaxel, and the combination of doxorubicin and paclitaxel as front-line chemotherapy for metastatic breast cancer: an intergroup trial (E1193), J Clin Oncol, 21, 588, 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10.1023\u002FA:1008330527188",{"doi":1861},"10.1023\u002FA:1008330527188",{"id":26,"text":1863,"url":26,"identifiers":1864},"Bruzzi, 2005, Objective response to chemotherapy as a potential surrogate end point of survival in metastatic breast cancer patients, J Clin Oncol, 23, 5117, 10.1200\u002FJCO.2005.02.106",{"doi":1865},"10.1200\u002FJCO.2005.02.106",{"id":26,"text":1867,"url":26,"identifiers":1868},"Chia, 2003, The impact of new chemotherapeutic and hormonal agents on the survival of women with metastatic breast cancer in a population based cohort, Proc Am Soc Clin Oncol, 22, 6",{},{"id":26,"text":1870,"url":26,"identifiers":1871},"Nabholtz, 1999, Prospective randomized trial of docetaxel versus mitomycin plus vinblastine in patients with meta-static breast cancer progressing despite previous anthracycline-containing chemotherapy. 304 Study Group, J Clin Oncol, 17, 1413, 10.1200\u002FJCO.1999.17.5.1413",{"doi":1872},"10.1200\u002FJCO.1999.17.5.1413",{"id":26,"text":1874,"url":26,"identifiers":1875},"Jones, 2005, Randomized phase III study of docetaxel compared with paclitaxel in metastatic breast cancer, J Clin Oncol, 23, 5542, 10.1200\u002FJCO.2005.02.027",{"doi":1876},"10.1200\u002FJCO.2005.02.027",{"id":26,"text":1878,"url":26,"identifiers":1879},"O'shaughnessy, 2002, Superior survival with capecitabine plus docetaxel combination therapy in anthracycline-pre-treated patients with advanced breast cancer: phase III trial results, J Clin Oncol, 20, 2812, 10.1200\u002FJCO.2002.09.002",{"doi":1880},"10.1200\u002FJCO.2002.09.002",{"id":26,"text":1882,"url":26,"identifiers":1883},"Albain, 2004, Global phase III study of gemcitabine plus paclitaxel (T) as frontline therapy for metastatic breast cancer (MBC): first report of overall survival, J Clin Oncol, 22, 5s, 10.1200\u002Fjco.2004.22.90140.510",{"doi":1884},"10.1200\u002Fjco.2004.22.90140.510",{"id":26,"text":1886,"url":26,"identifiers":1887},"O'shaughnessy, 2003, Gemcitabine plus paclitaxel (GT) versus paclitaxel (T) as first-line treatment for anthracycline pre-treated metastatic breast cancer (MBC): interim results of a global phase III study, Proc Am Soc Clin Oncol, 22, 7",{},{"id":26,"text":1889,"url":26,"identifiers":1890},"Bishop, 1999, Initial paclitaxel improves outcome compared with CMFP combination chemotherapy as front-line therapy in untreated metastatic breast cancer, J Clin Oncol, 17, 2355, 10.1200\u002FJCO.1999.17.8.2355",{"doi":1891},"10.1200\u002FJCO.1999.17.8.2355",{"id":26,"text":1893,"url":26,"identifiers":1894},"Bontenbal, 2003, Phase II study comparing AT to FAC as first line chemotherapy in patients with MBC, Eur J Cancer, 1, S201, 10.1016\u002FS1359-6349(03)90702-6",{"doi":1895},"10.1016\u002FS1359-6349(03)90702-6",{"id":26,"text":1897,"url":26,"identifiers":1898},"Jassem, 2001, Doxorubicin and paclitaxel versus fluorouracil, doxorubicin, and cyclophosphamide as first-line therapy for women with metastatic breast cancer: final results of a randomized phase III multicenter trial, J Clin Oncol, 19, 1707, 10.1200\u002FJCO.2001.19.6.1707",{"doi":1899},"10.1200\u002FJCO.2001.19.6.1707",{"id":26,"text":1901,"url":26,"identifiers":1902},"Feher, 2005, First-line gemcitabine versus epirubicin in postmenopausal women aged 60 or older with metastatic breast cancer: a multicenter, randomized, phase III study, Ann Oncol, 16, 899, 10.1093\u002Fannonc\u002Fmdi181",{"doi":1903},"10.1093\u002Fannonc\u002Fmdi181",{"id":26,"text":1905,"url":26,"identifiers":1906},"Perez, 1998, Paclitaxel in breast cancer, The Oncologist, 3, 373, 10.1634\u002Ftheoncologist.3-6-373",{"doi":1907},"10.1634\u002Ftheoncologist.3-6-373",{"id":26,"text":1909,"url":26,"identifiers":1910},"Figgitt, 2000, Docetaxel: an update of its use in advanced breast cancer, Drugs, 59, 621, 10.2165\u002F00003495-200059030-00015",{"doi":1911},"10.2165\u002F00003495-200059030-00015",{"id":26,"text":1913,"url":26,"identifiers":1914},"Sjöström, 1999, Docetaxel compared with sequential methotrexate and 5-fluorouracil in patients with advanced breast cancer after anthracycline failure: a randomised phase III study with crossover on progression by the Scandinavian Breast Group, Eur J Cancer, 35, 1194, 10.1016\u002FS0959-8049(99)00122-7",{"doi":1915},"10.1016\u002FS0959-8049(99)00122-7",{"id":26,"text":1917,"url":26,"identifiers":1918},"Bonneterre, 2002, Docetaxel vs 5-fluorouracil plus vinorelbine in metastatic breast cancer after anthracycline therapy failure, Br J Cancer, 87, 1210, 10.1038\u002Fsj.bjc.6600645",{"doi":1919},"10.1038\u002Fsj.bjc.6600645",{"id":26,"text":1921,"url":26,"identifiers":1922},"Gradishar, 2005, Superior efficacy of albumin-bound paclitaxel, ABI-007, compared with polyethylated castor oil-based paclitaxel in women with metastatic breast cancer: results of a phase III trial, J Clin Oncol, 23, 10.1200\u002FJCO.2005.04.937",{"doi":1923},"10.1200\u002FJCO.2005.04.937",{"id":26,"text":1925,"url":26,"identifiers":1926},"Miles, 2004, Survival benefit with capecitabine\u002Fdocetaxel versus docetaxel alone: analysis of therapy in a randomized phase III trial, Clin Breast Cancer, 5, 273, 10.3816\u002FCBC.2004.n.030",{"doi":1927},"10.3816\u002FCBC.2004.n.030",{"id":26,"text":1929,"url":26,"identifiers":1930},"Moinpour, 2004, Gemcitabine plus paclitaxel (GT) versus paclitaxel (T) as first-line treatment for anthracycline pre-treated metastatic breast cancer (MBC): quality of life (QoL) and pain palliation results from the global phase III study, J Clin Oncol, 2222, 621, 10.1200\u002Fjco.2004.22.90140.621",{"doi":1931},"10.1200\u002Fjco.2004.22.90140.621",{"id":26,"text":1933,"url":26,"identifiers":1934},"Chan, 1999, Prospective randomized trial of docetaxel versus doxorubicin in patients with metastatic breast cancer, J Clin Oncol, 8, 2341, 10.1200\u002FJCO.1999.17.8.2341",{"doi":1935},"10.1200\u002FJCO.1999.17.8.2341",{"id":26,"text":1937,"url":26,"identifiers":1938},"Paridaens, 2000, Paclitaxel versus doxorubicin as first-line single-agent chemotherapy for metastatic breast cancer: a European Organization for Research and Treatment of Cancer randomized study with cross-over, J Clin Oncol, 18, 724, 10.1200\u002FJCO.2000.18.4.724",{"doi":1939},"10.1200\u002FJCO.2000.18.4.724",{"id":26,"text":1941,"url":26,"identifiers":1942},"Nabholtz, 2003, Docetaxel and doxorubicin compared with doxorubicin and cyclophosphamide as first-line chemotherapy for metastatic breast cancer: results of a randomized, multicenter phase III trial, J Clin Oncol, 21, 968, 10.1200\u002FJCO.2003.04.040",{"doi":1943},"10.1200\u002FJCO.2003.04.040",{"id":26,"text":1945,"url":26,"identifiers":1946},"Mackey, 2002, Final results of the phase III randomized trial comparing docetaxel (T) doxorubicin (A) and cyclophosphamide (C) to FAC as first line chemotherapy (CT) for patients (pts) with metastatic breast cancer (MBC), Proc Am Soc Clin Oncol, 21, 35a",{},{"id":26,"text":1948,"url":26,"identifiers":1949},"Biganzoli, 2002, Doxorubicin and paclitaxel versus doxorubicin and cyclophosphamide as first-line chemotherapy in metastatic breast cancer: the European Organization for Research and Treatment of Cancer 10961 multicenter phase III trial, J Clin Oncol, 20, 3114, 10.1200\u002FJCO.2002.11.005",{"doi":1950},"10.1200\u002FJCO.2002.11.005",{"id":26,"text":1952,"url":26,"identifiers":1953},"Carmichael, 2001, UKCCCR trial of epirubicin and cyclophosphamide (EC) versus epirubicin and Taxol (ET) in the first-line treatment of women with metastatic breast cancer (MBC), Proc Am Soc Clin Oncol, 20, 22",{},{"id":26,"text":1955,"url":26,"identifiers":1956},"Lück, 2000, Multicentric phase III study in first line treatment of advanced metastatic breast cancer (ABC). Epirubicin\u002Fpaclitaxel (ET) vs epirubicin\u002Fcyclophosphamide (EC). A study of the AGO Breast Cancer Group, Proc Am Soc Clin Oncol, 19, 73a",{},{"id":26,"text":1958,"url":26,"identifiers":1959},"Pegram, 2004, Rational combinations of trastuzumab with chemotherapeutic drugs used in the treatment of breast cancer, J Natl Cancer Inst, 96, 739, 10.1093\u002Fjnci\u002Fdjh131",{"doi":1960},"10.1093\u002Fjnci\u002Fdjh131",{"id":26,"text":1962,"url":26,"identifiers":1963},"Osoba, 2002, Effects on quality of life of combined trastuzumab and chemotherapy in women with metastatic breast cancer, J Clin Oncol, 20, 3106, 10.1200\u002FJCO.2002.03.090",{"doi":1964},"10.1200\u002FJCO.2002.03.090",{"id":26,"text":1966,"url":26,"identifiers":1967},"Jain, 2005, Antiangiogenic therapy of cancer: current and emerging concepts, Oncology, 19, 7",{},{"id":26,"text":1969,"url":26,"identifiers":1970},"Kim, 1993, Inhibition of vascular endothelial growth factor-induced angiogenesis suppresses tumour growth in vivo, Nature, 362, 841, 10.1038\u002F362841a0",{"doi":1971},"10.1038\u002F362841a0",{"id":26,"text":1973,"url":26,"identifiers":1974},"Cobleigh, 2003, A phase II dose-escalation trial of bevacizumab in previously treated metastatic breast cancer, Semin Oncol, 30, 117, 10.1053\u002Fj.seminoncol.2003.08.013",{"doi":1975},"10.1053\u002Fj.seminoncol.2003.08.013",{"id":26,"text":1977,"url":26,"identifiers":1978},"Miller, 2005, Randomized phase III trial of capecitabine compared with bevacizumab plus capecitabine in patients with previously treated metastatic breast cancer patients, J Clin Oncol, 23, 792, 10.1200\u002FJCO.2005.05.098",{"doi":1979},"10.1200\u002FJCO.2005.05.098",{"id":1981,"createTime":1982,"updateTime":1983,"relativeEntities":1984,"slug":1985,"properties":1986,"entityType":826,"verifyStatus":25,"verifyTime":2004,"verifyNote":827,"syncStatus":28,"languages":2005,"translateLanguages":2006,"viewCount":36,"primaryUrl":2007,"fullTextUrl":26,"authors":2008,"publicationType":902,"publisherRelationship":2079,"citationCount":2117,"citationInfo":2118,"publishDate":2121,"publishYear":2122,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":2123,"isForceReanalyzing":1073},"7b29529c-55c4-4fa7-b387-bf76090ac104","2024-09-21T15:21:26.842+00:00","2025-02-06T08:07:24.002+00:00",[],"FDA-Drug-Approval-Summary-Bevacizumab-Avastin-as-Treatment-of-Recurrent-Glioblastoma-Multiforme",{"mag":1987,"keywords":1989,"pmc":1990,"openalex":1992,"abstract":1994,"title":1997,"pm":2000,"doi":2002},{"VOID":1988},"2163458899",{"VI":813},{"VOID":1991},"3500371",{"VOID":1993},"W2163458899",{"EN":1995,"VI":1996},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n               \u003Cjats:sec>\n                  \u003Cjats:title>Learning Objectives\u003C\u002Fjats:title>\n                  \u003Cjats:p>After completing this course, the reader will be able to: Discuss and compare currently approved drugs for treatment of glioblastoma multiforme (GBM) and explain the advantages of bevacizumab for GBM treatment.Debate the use of response rate as an endpoint for GBM treatment with bevacizumab.Differentiate between accelerated and regular drug approval by the Food and Drug Administration.\u003C\u002Fjats:p>\n                  \u003Cjats:p>This article is available for continuing medical education credit at CME.TheOncologist.com.\u003C\u002Fjats:p>\n                  \u003Cjats:p>On May 5, 2009, the U.S. Food and Drug Administration granted accelerated approval to bevacizumab injection (Avastin®; Genentech, Inc., South San Francisco, CA) as a single agent for patients with glioblastoma multiforme (GBM) with progressive disease following prior therapy. The approval was based on durable objective responses (independent radiologic review with stable or decreasing corticosteroid use). Two trials evaluating bevacizumab, 10 mg\u002Fkg by i.v. infusion every 2 weeks, were submitted. One trial also randomized patients to bevacizumab plus irinotecan treatment. All patients had received prior surgery, radiotherapy, and temozolomide. Patients with active brain hemorrhage were excluded. One trial enrolled 78 independently confirmed GBM patients. Partial responses were observed in 25.9% (95% confidence interval [CI], 17.0%–36.1%) of the patients. The median response duration was 4.2 months (95% CI, 3.0–5.7 months). The second trial enrolled 56 GBM patients. Partial responses were observed in 19.6% (95% CI, 10.9%–31.3%) of the patients. The median response duration was 3.9 months (95% CI, 2.4–17.4 months). Safety data were provided for the first study. The most frequently reported bevacizumab adverse events of any grade were infection, fatigue, headache, hypertension, epistaxis, and diarrhea. Grade 3–5 bevacizumab-related adverse events included bleeding\u002Fhemorrhage, central nervous system (CNS) hemorrhage, hypertension, venous and arterial thromboembolic events, wound-healing complications, proteinuria, gastrointestinal perforation, and reversible posterior leukoencephalopathy. The attribution of certain adverse events (e.g., CNS hemorrhage, wound-healing complications, and thromboembolic events) to either bevacizumab, underlying disease, or both could not be determined because of the single-arm, noncomparative study design.\u003C\u002Fjats:p>\n               \u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n               \u003Cjats:sec>\n                  \u003Cjats:title>Mục tiêu học tập\u003C\u002Fjats:title>\n                  \u003Cjats:p>Sau khi hoàn thành khóa học này, người đọc sẽ có thể: Thảo luận và so sánh các loại thuốc hiện đang được phê duyệt để điều trị glioblastoma multiforme (GBM) và giải thích những lợi thế của bevacizumab trong điều trị GBM. Tranh luận về việc sử dụng tỷ lệ phản ứng như một chỉ tiêu cho việc điều trị GBM bằng bevacizumab. Phân biệt giữa việc phê duyệt thuốc nhanh và phê duyệt thuốc thông thường bởi Cục Quản lý Thực phẩm và Dược phẩm Hoa Kỳ.\u003C\u002Fjats:p>\n                  \u003Cjats:p>Bài viết này có sẵn để nhận tín chỉ giáo dục y tế liên tục tại CME.TheOncologist.com.\u003C\u002Fjats:p>\n                  \u003Cjats:p>Vào ngày 5 tháng 5 năm 2009, Cục Quản lý Thực phẩm và Dược phẩm Hoa Kỳ đã cấp phép phê duyệt nhanh cho thuốc tiêm bevacizumab (Avastin®; Genentech, Inc., South San Francisco, CA) như một tác nhân đơn lẻ cho các bệnh nhân mắc glioblastoma multiforme (GBM) có bệnh tiến triển sau điều trị trước đó. Quyết định phê duyệt dựa trên các phản ứng khách quan bền vững (đánh giá hình ảnh độc lập với việc sử dụng corticosteroid ổn định hoặc giảm). Hai thử nghiệm đánh giá bevacizumab, 10 mg\u002Fkg qua truyền tĩnh mạch cách hai tuần một lần, đã được trình lên. Một thử nghiệm cũng ngẫu nhiên bệnh nhân vào điều trị kết hợp bevacizumab và irinotecan. Tất cả bệnh nhân đã nhận các phương pháp điều trị trước đó như phẫu thuật, xạ trị và temozolomide. Những bệnh nhân có hemorrhage não hoạt động đã bị loại trừ. Một thử nghiệm đã tuyển 78 bệnh nhân GBM được xác nhận độc lập. Phản ứng một phần đã được quan sát thấy ở 25.9% (KTC 95%, 17.0%–36.1%) trong số các bệnh nhân. Thời gian đáp ứng trung vị là 4.2 tháng (KTC 95%, 3.0–5.7 tháng). Thử nghiệm thứ hai tuyển 56 bệnh nhân GBM. Phản ứng một phần đã được quan sát thấy ở 19.6% (KTC 95%, 10.9%–31.3%) trong số các bệnh nhân. Thời gian đáp ứng trung vị là 3.9 tháng (KTC 95%, 2.4–17.4 tháng). Dữ liệu an toàn đã được cung cấp cho nghiên cứu đầu tiên. Các sự kiện bất lợi thường gặp nhất liên quan đến bevacizumab ở bất kỳ mức độ nào là nhiễm trùng, mệt mỏi, đau đầu, cao huyết áp, chảy máu cam và tiêu chảy. Các sự kiện bất lợi liên quan đến bevacizumab từ cấp độ 3-5 bao gồm chảy máu, hemorrhage hệ thần kinh trung ương (CNS), cao huyết áp, các sự kiện huyết khối tĩnh mạch và động mạch, biến chứng lành vết thương, protein niệu, thủng đường tiêu hóa, và leukoencephalopathy có thể hồi phục ở vùng sau. Việc quy kết một số sự kiện bất lợi (ví dụ, hemorrhage CNS, biến chứng lành vết thương và các sự kiện huyết khối) cho bevacizumab, bệnh lý cơ bản, hay cả hai không thể xác định do thiết kế nghiên cứu một nhánh, không có đối chứng. \n               \u003C\u002Fjats:sec>",{"EN":1998,"VI":1999},"FDA Drug Approval Summary: Bevacizumab (Avastin®) as Treatment of Recurrent Glioblastoma Multiforme","Tóm tắt phê duyệt thuốc của FDA: Bevacizumab (Avastin®) trong điều trị glioblastoma multiforme tái phát",{"VOID":2001},"19897538",{"VOID":2003},"10.1634\u002Ftheoncologist.2009-0121","2024-09-21T15:21:26.841+00:00",[102],[101],"https:\u002F\u002Facademic.oup.com\u002Foncolo\u002Farticle\u002F14\u002F11\u002F1131\u002F6398783",[2009,2030,2047,2062],{"id":2010,"sortIndex":59,"researcher":26,"roles":2011,"affiliations":2012,"properties":2023},"821713e1-fe96-46e7-8b9f-4eedacf2eadd",[],[2013],{"id":2014,"sortIndex":36,"affiliation":2015,"properties":26},"71410bbb-c305-4187-a532-7eeb586f6616",{"id":2016,"createTime":2017,"updateTime":2017,"relativeEntities":2018,"slug":2019,"properties":2020,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"f9609585-990f-4752-99b9-0534020b8c64","2024-09-21T15:21:26.856+00:00",[],"Division-of-Biological-Oncology-Products-Office-of-Oncology-Drug-Products-Center-for-Drug-Evaluation-and-Research-U-S-Food-and-Drug-Administration-Silver-Spring-Maryland-USA",{"title":2021},{"EN":2022},"Division of Biological Oncology Products, Office of Oncology Drug Products, Center for Drug Evaluation and Research, U.S. Food and Drug Administration, Silver Spring, Maryland, USA",{"openalex":2024,"orcid":2026,"title":2028},{"VOID":2025},"A5051520990",{"VOID":2027},"https:\u002F\u002Forcid.org\u002F0000-0002-4771-9923",{"EN":2029},"Richard Pazdur",{"id":2031,"sortIndex":115,"researcher":26,"roles":2032,"affiliations":2033,"properties":2040},"aa27f751-bdb8-4146-9dd5-aadd47ffac28",[],[2034],{"id":2035,"sortIndex":36,"affiliation":2036,"properties":26},"7cdfefa8-3709-4a7e-8367-aba587d8e221",{"id":2016,"createTime":2017,"updateTime":2017,"relativeEntities":2037,"slug":2019,"properties":2038,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":2039},{"EN":2022},{"openalex":2041,"orcid":2043,"title":2045},{"VOID":2042},"A5013196129",{"VOID":2044},"https:\u002F\u002Forcid.org\u002F0000-0002-7345-2521",{"EN":2046},"Yuan Li Shen",{"id":2048,"sortIndex":36,"researcher":26,"roles":2049,"affiliations":2050,"properties":2057},"aa724141-da99-4f47-a6f1-35f75c0a5882",[],[2051],{"id":2052,"sortIndex":36,"affiliation":2053,"properties":26},"99141147-08b3-4543-a35e-c3f97ab0d9a9",{"id":2016,"createTime":2017,"updateTime":2017,"relativeEntities":2054,"slug":2019,"properties":2055,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":2056},{"EN":2022},{"openalex":2058,"title":2060},{"VOID":2059},"A5057752378",{"EN":2061},"Martin H. Cohen",{"id":2063,"sortIndex":114,"researcher":26,"roles":2064,"affiliations":2065,"properties":2072},"8f455b8f-ee97-46be-b6a3-b584b6326ffe",[],[2066],{"id":2067,"sortIndex":36,"affiliation":2068,"properties":26},"3bbec656-d866-4c4b-9047-e90367c6b7e3",{"id":2016,"createTime":2017,"updateTime":2017,"relativeEntities":2069,"slug":2019,"properties":2070,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":2071},{"EN":2022},{"openalex":2073,"orcid":2075,"title":2077},{"VOID":2074},"A5077268765",{"VOID":2076},"https:\u002F\u002Forcid.org\u002F0000-0002-7266-395X",{"EN":2078},"Patricia Keegan",{"url":26,"publisher":2080,"properties":2110},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":2081,"slug":663,"properties":2082,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":2088,"manageAffiliations":2089,"indexDatabases":2090,"url":761,"thumbnailPath":26,"statistic":2105,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":2083,"issn":2084,"introduce":2085,"eissn":2086,"title":2087},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":663},[],[],[2091,2098],{"id":743,"indexDatabase":2092,"url":758,"indexYears":26,"academicFieldIds":2097,"indexDatabaseRanking":26},{"id":745,"createTime":746,"updateTime":747,"relativeEntities":2093,"label":2094,"description":2095,"key":754,"publicationTags":2096,"standard":26},[],{"EN":750,"VI":750},{"VI":752,"EN":753},[756,757],[760],{"id":722,"indexDatabase":2099,"url":735,"indexYears":736,"academicFieldIds":2104,"indexDatabaseRanking":741},{"id":724,"createTime":725,"updateTime":726,"relativeEntities":2100,"label":2101,"description":2102,"key":732,"publicationTags":2103,"standard":26},[],{"EN":729,"VI":729},{"EN":729,"VI":731},[734],[738,739,740],{"impactFactor":36,"impactFactorByYear":2106,"i10Index":252,"i10IndexLast5Year":59,"totalPublication":257,"totalPublicationByYear":2107,"totalCitation":770,"totalCitationByYear":2108,"totalCitationPerPublication":785,"totalCitationPerPublicationByYear":2109,"hindexLast5Year":159,"hindex":159},{"2012":764,"2013":59,"2014":114,"2015":50,"2017":125,"2018":765,"2019":766,"2020":517,"2021":767,"2022":768,"2023":59},{"1997":115,"2000":114,"2001":114,"2002":59,"2004":162,"2005":59,"2006":114,"2007":114,"2008":135,"2009":114,"2010":114,"2011":115,"2013":115,"2016":115,"2017":114,"2019":115,"2020":114,"2022":115},{"1997":772,"2000":773,"2001":143,"2002":774,"2004":775,"2005":776,"2006":777,"2007":778,"2008":779,"2009":780,"2010":781,"2011":652,"2013":142,"2016":782,"2017":783,"2019":784,"2020":258,"2022":135},{"1997":772,"2000":787,"2001":788,"2002":789,"2004":790,"2005":791,"2006":792,"2007":793,"2008":794,"2009":795,"2010":796,"2011":652,"2013":142,"2016":782,"2017":797,"2019":784,"2020":798,"2022":135},{"volume":2111,"pages":2113,"issue":2115},{"VOID":2112},"14",{"VOID":2114},"1131-1138",{"VOID":2116},"11",570,{"total":2117,"publishYear":26,"statisticByYear":2119},{"2012":29,"2013":517,"2014":2120,"2015":517,"2016":252,"2017":257,"2018":397,"2019":159,"2020":238,"2021":168,"2022":257,"2023":539,"2024":238},62,"2009-11-01",2009,[2124,2128,2132,2136,2140,2144,2148,2152,2156,2160,2164,2167,2171,2175,2179,2183,2187,2191,2195,2199,2203,2207,2210,2213,2217,2221,2225,2229,2233,2237],{"id":26,"text":2125,"url":26,"identifiers":2126},"Stupp, 2005, Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma, N Engl J Med, 352, 987, 10.1056\u002FNEJMoa043330",{"doi":2127},"10.1056\u002FNEJMoa043330",{"id":26,"text":2129,"url":26,"identifiers":2130},"Grossman, 2003, Phase III study comparing three cycles of infusional carmustine and cisplatin followed by radiation therapy with radiation therapy and concurrent carmustine in patients with newly diagnosed supratentorial glioblastoma multiforme: Eastern Cooperative Oncology Group Trial 2394, J Clin Oncol, 21, 1485, 10.1200\u002FJCO.2003.10.035",{"doi":2131},"10.1200\u002FJCO.2003.10.035",{"id":26,"text":2133,"url":26,"identifiers":2134},"Yung, 2000, A phase II study of temozolomide vs. procarbazine in patients with glioblastoma multiforme at first relapse, Br J Cancer, 83, 588, 10.1054\u002Fbjoc.2000.1316",{"doi":2135},"10.1054\u002Fbjoc.2000.1316",{"id":26,"text":2137,"url":26,"identifiers":2138},"Wong, 1999, Outcomes and prognostic factors in recurrent glioma patients enrolled onto phase II clinical trials, J Clin Oncol, 17, 2572, 10.1200\u002FJCO.1999.17.8.2572",{"doi":2139},"10.1200\u002FJCO.1999.17.8.2572",{"id":26,"text":2141,"url":26,"identifiers":2142},"Parney, 2003, Current chemotherapy for glioblastoma, Cancer J, 9, 149, 10.1097\u002F00130404-200305000-00003",{"doi":2143},"10.1097\u002F00130404-200305000-00003",{"id":26,"text":2145,"url":26,"identifiers":2146},"Walker, 1978, Evaluation of BCNU and\u002For radiotherapy in the treatment of anaplastic gliomas. A cooperative clinical trial, J Neurosurg, 49, 333, 10.3171\u002Fjns.1978.49.3.0333",{"doi":2147},"10.3171\u002Fjns.1978.49.3.0333",{"id":26,"text":2149,"url":26,"identifiers":2150},"Brem, 1995, Placebo-controlled trial of safety and efficacy of intraoperative controlled delivery by biodegradable polymers of chemotherapy for recurrent gliomas. The Polymer-brain Tumor Treatment Group, Lancet, 345, 1008, 10.1016\u002FS0140-6736(95)90755-6",{"doi":2151},"10.1016\u002FS0140-6736(95)90755-6",{"id":26,"text":2153,"url":26,"identifiers":2154},"Valtonen, 1997, Interstitial chemotherapy with carmustine- loaded polymers for high-grade gliomas: A randomized double-blind study, Neurosurgery, 41, 44, 10.1097\u002F00006123-199707000-00011",{"doi":2155},"10.1097\u002F00006123-199707000-00011",{"id":26,"text":2157,"url":26,"identifiers":2158},"Westphal, 2003, A phase 3 trial of local chemotherapy with biodegradable carmustine (BCNU) wafers (Gliadel wafers) in patients with primary malignant glioma, Neuro Oncol, 5, 79, 10.1093\u002Fneuonc\u002F5.2.79",{"doi":2159},"10.1093\u002Fneuonc\u002F5.2.79",{"id":26,"text":2161,"url":26,"identifiers":2162},"Newlands, 1997, Temozolomide: A review of its discovery, chemical properties, pre-clinical development and clinical trials, Cancer Treat Rev, 23, 35, 10.1016\u002FS0305-7372(97)90019-0",{"doi":2163},"10.1016\u002FS0305-7372(97)90019-0",{"id":26,"text":2165,"url":26,"identifiers":2166},"Brem, 1972, Tumor angiogenesis: A quantitative method for histologic grading, J Natl Cancer Inst, 48, 347",{},{"id":26,"text":2168,"url":26,"identifiers":2169},"Salmaggi, 2003, Intracavitary VEGF, bFGF, IL-8, IL-12 levels in primary and recurrent malignant glioma, J Neurooncol, 62, 297, 10.1023\u002FA:1023367223575",{"doi":2170},"10.1023\u002FA:1023367223575",{"id":26,"text":2172,"url":26,"identifiers":2173},"Vredenburgh, 2007, Bevacizumab plus irinotecan in recurrent glioblastoma multiforme, J Clin Oncol, 25, 4722, 10.1200\u002FJCO.2007.12.2440",{"doi":2174},"10.1200\u002FJCO.2007.12.2440",{"id":26,"text":2176,"url":26,"identifiers":2177},"Bokstein, 2008, Treatment with bevacizumab and irinotecan for recurrent high-grade glial tumors, Cancer, 112, 2267, 10.1002\u002Fcncr.23401",{"doi":2178},"10.1002\u002Fcncr.23401",{"id":26,"text":2180,"url":26,"identifiers":2181},"Buie, 2008, Bevacizumab: A treatment option for recurrent glioblastoma multiforme, Ann Pharmacother, 42, 1486, 10.1345\u002Faph.1L030",{"doi":2182},"10.1345\u002Faph.1L030",{"id":26,"text":2184,"url":26,"identifiers":2185},"Kang, 2008, Irinotecan and bevacizumab in progressive primary brain tumors, an evaluation of efficacy and safety, J Neurooncol, 89, 113, 10.1007\u002Fs11060-008-9599-0",{"doi":2186},"10.1007\u002Fs11060-008-9599-0",{"id":26,"text":2188,"url":26,"identifiers":2189},"Wong, 2007, Taming glioblastoma: Targeting angiogenesis, J Clin Oncol, 25, 4705, 10.1200\u002FJCO.2007.13.1037",{"doi":2190},"10.1200\u002FJCO.2007.13.1037",{"id":26,"text":2192,"url":26,"identifiers":2193},"Ananthnarayan, 2008, Time course of imaging changes of GBM during extended bevacizumab treatment, J Neurooncol, 88, 339, 10.1007\u002Fs11060-008-9573-x",{"doi":2194},"10.1007\u002Fs11060-008-9573-x",{"id":26,"text":2196,"url":26,"identifiers":2197},"Macdonald, 1990, Response criteria for phase II studies of supratentorial malignant glioma, J Clin Oncol, 8, 1277, 10.1200\u002FJCO.1990.8.7.1277",{"doi":2198},"10.1200\u002FJCO.1990.8.7.1277",{"id":26,"text":2200,"url":26,"identifiers":2201},"Pope, 2006, MRI in patients with high-grade gliomas treated with bevacizumab and chemotherapy, Neurology, 66, 1258, 10.1212\u002F01.wnl.0000208958.29600.87",{"doi":2202},"10.1212\u002F01.wnl.0000208958.29600.87",{"id":26,"text":2204,"url":26,"identifiers":2205},"Henson, 2005, MRI in treatment of adult gliomas, Lancet Oncol, 6, 167, 10.1016\u002FS1470-2045(05)01767-5",{"doi":2206},"10.1016\u002FS1470-2045(05)01767-5",{"id":26,"text":2208,"url":26,"identifiers":2209},"U.S. Food and Drug Administration., FDA Oncology Drug Advisory Committee (ODAC) January 12, 1999 Meeting Minutes",{},{"id":26,"text":2211,"url":26,"identifiers":2212},"U.S. Food and Drug Administration, FDA Workshop Brain Cancer Endpoints January 16, 2006",{},{"id":26,"text":2214,"url":26,"identifiers":2215},"Vos, 2003, Interobserver variability in the radiological assessment of response to chemotherapy in glioma, Neurology, 60, 826, 10.1212\u002F01.WNL.0000049467.54667.92",{"doi":2216},"10.1212\u002F01.WNL.0000049467.54667.92",{"id":26,"text":2218,"url":26,"identifiers":2219},"Kreisl, 2009, Phase II trial of single-agent bevacizumab followed by bevacizumab plus irinotecan at tumor progression in recurrent glioblastoma, J Clin Oncol, 27, 740, 10.1200\u002FJCO.2008.16.3055",{"doi":2220},"10.1200\u002FJCO.2008.16.3055",{"id":26,"text":2222,"url":26,"identifiers":2223},"Schiff, 2008, Bevacizumab in combination with irinotecan for patients with recurrent glioblastoma multiforme, Nat Clin Pract Oncol, 5, 186, 10.1038\u002Fncponc1077",{"doi":2224},"10.1038\u002Fncponc1077",{"id":26,"text":2226,"url":26,"identifiers":2227},"Wong, 2008, Bevacizumab reverses cerebral radiation necrosis, J Clin Oncol, 26, 5649, 10.1200\u002FJCO.2008.19.1866",{"doi":2228},"10.1200\u002FJCO.2008.19.1866",{"id":26,"text":2230,"url":26,"identifiers":2231},"Gonzalez, 2007, Effect of bevacizumab on radiation necrosis of the brain, Int J Radiat Oncol Biol Phys, 67, 323, 10.1016\u002Fj.ijrobp.2006.10.010",{"doi":2232},"10.1016\u002Fj.ijrobp.2006.10.010",{"id":26,"text":2234,"url":26,"identifiers":2235},"Norden, 2008, Bevacizumab for recurrent malignant gliomas: Efficacy, toxicity, and patterns of recurrence, Neurology, 70, 779, 10.1212\u002F01.wnl.0000304121.57857.38",{"doi":2236},"10.1212\u002F01.wnl.0000304121.57857.38",{"id":26,"text":2238,"url":26,"identifiers":2239},"Federal Register, 21 CFR 314.500 and 601.40",{},{"id":2241,"createTime":2242,"updateTime":2243,"relativeEntities":2244,"slug":2245,"properties":2246,"entityType":826,"verifyStatus":25,"verifyTime":2265,"verifyNote":827,"syncStatus":28,"languages":2266,"translateLanguages":2267,"viewCount":36,"primaryUrl":2268,"fullTextUrl":26,"authors":2269,"publicationType":902,"publisherRelationship":2371,"citationCount":2408,"citationInfo":2409,"publishDate":2411,"publishYear":2412,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":2413,"isForceReanalyzing":1073},"850a78c4-9919-4a66-a002-340dfe9554eb","2024-10-08T15:08:20.134+00:00","2025-02-06T08:09:20.646+00:00",[],"Systematic-Review-of-Medical-Treatment-in-Melanoma-Current-Status-and-Future-Prospects",{"mag":2247,"keywords":2249,"pmc":2251,"openalex":2253,"abstract":2255,"title":2258,"pm":2261,"doi":2263},{"VOID":2248},"2155104279",{"VI":2250},"hắc sắc tố, điều trị, liệu pháp hỗ trợ, interferon-α, vaccine ung thư, cytokine, IL-2, di căn, giai đoạn cao",{"VOID":2252},"3228046",{"VOID":2254},"W2155104279",{"EN":2256,"VI":2257},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>The incidence of melanoma is increasing worldwide, and the prognosis for patients with high-risk or advanced metastatic melanoma remains poor despite advances in the field. Standard treatment for patients with thick (≥2.0 mm) primary melanoma with or without regional metastases to lymph nodes is surgery followed by adjuvant therapy or clinical trial enrollment. Adjuvant therapy with interferon-α and cancer vaccines is discussed in detail. Patients who progress to stage IV metastatic melanoma have a median survival of ≤1 year. Standard treatment with chemotherapy yields low response rates, of which few are durable. Cytokine therapy with IL-2 achieves durable benefits in a greater fraction, but it is accompanied by severe toxicities that require the patient to be hospitalized for support during treatment. A systematic literature review of treatments for advanced, metastatic disease was conducted to present the success of current treatments and the promise of those still in clinical development that may yield incremental improvements in the treatment of advanced, metastatic melanoma.\u003C\u002Fjats:p>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\u003Cjats:p>Tỷ lệ mắc bệnh hắc sắc tố đang gia tăng trên toàn cầu, và tiên lượng cho bệnh nhân mắc bệnh hắc sắc tố di căn giai đoạn cao hoặc có nguy cơ cao vẫn kém mặc dù đã có nhiều tiến bộ trong lĩnh vực này. Phương pháp điều trị chuẩn cho bệnh nhân có hắc sắc tố nguyên phát dày (≥2.0 mm) có hoặc không có di căn khu vực đến hạch bạch huyết là phẫu thuật, sau đó là liệu pháp hỗ trợ hoặc tham gia vào các thử nghiệm lâm sàng. Liệu pháp hỗ trợ bằng interferon-α và vaccine ung thư được bàn luận chi tiết. Bệnh nhân tiến triển đến giai đoạn IV hắc sắc tố di căn có thời gian sống trung bình ≤1 năm. Phương pháp điều trị chuẩn bằng hóa trị suất ít hiệu quả và chỉ một số ít có thời gian sống bền vững. Liệu pháp cytokine với IL-2 đạt được lợi ích bền vững ở một phần lớn bệnh nhân hơn, nhưng kèm theo đó là độc tính nặng nề yêu cầu bệnh nhân phải nhập viện để hỗ trợ trong suốt quá trình điều trị. Một cuộc tổng quan tài liệu có hệ thống về các phương pháp điều trị cho bệnh tiến triển, di căn đã được thực hiện nhằm trình bày thành công của các phương pháp điều trị hiện tại và những hứa hẹn của những phương pháp vẫn đang trong giai đoạn phát triển lâm sàng có thể mang lại những cải tiến nhỏ trong điều trị hắc sắc tố di căn giai đoạn cao.",{"EN":2259,"VI":2260},"Systematic Review of Medical Treatment in Melanoma: Current Status and Future Prospects","Xem xét hệ thống về điều trị y tế trong bệnh hắc sắc tố: Tình trạng hiện tại và Triển vọng tương lai",{"VOID":2262},"21212434",{"VOID":2264},"10.1634\u002Ftheoncologist.2010-0190","2024-10-08T15:08:20.133+00:00",[102],[101],"https:\u002F\u002Facademic.oup.com\u002Foncolo\u002Farticle\u002F16\u002F1\u002F5\u002F6400684",[2270,2291,2312,2329,2350],{"id":2271,"sortIndex":36,"researcher":26,"roles":2272,"affiliations":2273,"properties":2284},"ec63508e-a6b8-4c23-97a7-7ecc8c14279c",[],[2274],{"id":2275,"sortIndex":36,"affiliation":2276,"properties":26},"e8e5d648-6eba-4ef2-aa55-9c7ff7082b0e",{"id":2277,"createTime":2278,"updateTime":2278,"relativeEntities":2279,"slug":2280,"properties":2281,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"aecb2b3a-5d67-4403-85c4-ed3fa263b6bf","2024-10-08T15:08:20.156+00:00",[],"a-Department-of-Dermatology-University-Hospital-T%C3%BCbingen-T%C3%BCbingen-Germany-",{"title":2282},{"EN":2283},"a Department of Dermatology, University Hospital Tübingen, Tübingen, Germany;",{"openalex":2285,"orcid":2287,"title":2289},{"VOID":2286},"A5001548963",{"VOID":2288},"https:\u002F\u002Forcid.org\u002F0000-0001-8530-780X",{"EN":2290},"Claus Garbe",{"id":2292,"sortIndex":111,"researcher":26,"roles":2293,"affiliations":2294,"properties":2305},"1f30b546-879a-442f-9c36-2ed380fb7c7a",[],[2295],{"id":2296,"sortIndex":36,"affiliation":2297,"properties":26},"818b1c40-c781-4850-a1ea-41760d41dfb5",{"id":2298,"createTime":2299,"updateTime":2299,"relativeEntities":2300,"slug":2301,"properties":2302,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"fc880669-4aab-4a29-8be6-d1bbae0a9662","2024-10-08T15:08:20.204+00:00",[],"dDepartment-of-Medicine-University-of-Pittsburgh-Cancer-Institute-Pittsburgh-Pennsylvania-USA",{"title":2303},{"EN":2304},"dDepartment of Medicine, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania, USA",{"openalex":2306,"orcid":2308,"title":2310},{"VOID":2307},"A5007239425",{"VOID":2309},"https:\u002F\u002Forcid.org\u002F0000-0002-3570-4476",{"EN":2311},"John M. Kirkwood",{"id":2313,"sortIndex":115,"researcher":26,"roles":2314,"affiliations":2315,"properties":2322},"ca1ce68b-1b2f-46a1-959c-81e9d1fbf351",[],[2316],{"id":2317,"sortIndex":36,"affiliation":2318,"properties":26},"2cae443e-e393-4bc0-aaf7-99363460f91d",{"id":2277,"createTime":2278,"updateTime":2278,"relativeEntities":2319,"slug":2280,"properties":2320,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":2321},{"EN":2283},{"openalex":2323,"orcid":2325,"title":2327},{"VOID":2324},"A5056227404",{"VOID":2326},"https:\u002F\u002Forcid.org\u002F0000-0003-0019-2770",{"EN":2328},"Thomas 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2004, Global perspectives of contemporary epidemiological trends of cutaneous malignant melanoma, Br J Dermatol, 150, 179, 10.1111\u002Fj.1365-2133.2004.05708.x",{"doi":2417},"10.1111\u002Fj.1365-2133.2004.05708.x",{"id":26,"text":2419,"url":26,"identifiers":2420},"Molife, 2002, Adjuvant therapy of malignant melanoma, Crit Rev Oncol Hematol, 44, 81, 10.1016\u002FS1040-8428(02)00014-8",{"doi":2421},"10.1016\u002FS1040-8428(02)00014-8",{"id":26,"text":2423,"url":26,"identifiers":2424},"Wheatley, 2003, Does adjuvant interferon-alpha for high-risk melanoma provide a worthwhile benefit? A meta-analysis of the randomised trials, Cancer Treat Rev, 29, 241, 10.1016\u002FS0305-7372(03)00074-4",{"doi":2425},"10.1016\u002FS0305-7372(03)00074-4",{"id":26,"text":2427,"url":26,"identifiers":2428},"Mocellin, 2010, Interferon alpha adjuvant therapy in patients with high-risk melanoma: a systematic review and meta-analysis, J Natl Cancer Inst, 102, 493, 10.1093\u002Fjnci\u002Fdjq009",{"doi":2429},"10.1093\u002Fjnci\u002Fdjq009",{"id":26,"text":2431,"url":26,"identifiers":2432},"Eggermont, 2004, Re-evaluating the role of dacarbazine in metastatic melanoma: what have we learned in 30 years?, Eur J Cancer, 40, 1825, 10.1016\u002Fj.ejca.2004.04.030",{"doi":2433},"10.1016\u002Fj.ejca.2004.04.030",{"id":26,"text":2435,"url":26,"identifiers":2436},"Atkins, 1999, High-dose recombinant interleukin 2 therapy for patients with metastatic melanoma: analysis of 270 patients treated between 1985 and 1993, J Clin Oncol, 17, 2105, 10.1200\u002FJCO.1999.17.7.2105",{"doi":2437},"10.1200\u002FJCO.1999.17.7.2105",{"id":26,"text":2439,"url":26,"identifiers":2440},"Bajetta, 2006, Multicenter phase III randomized trial of polychemotherapy (CVD regimen) versus the same chemotherapy (CT) plus subcutaneous interleukin-2 and interferon-alpha2b in metastatic melanoma, Ann Oncol, 17, 571, 10.1093\u002Fannonc\u002Fmdl007",{"doi":2441},"10.1093\u002Fannonc\u002Fmdl007",{"id":26,"text":2443,"url":26,"identifiers":2444},"Ridolfi, 2002, Cisplatin, dacarbazine with or without subcutaneous interleukin-2, and interferon alpha-2b in advanced melanoma outpatients: results from an Italian multicenter phase III randomized clinical trial, J Clin Oncol, 20, 1600, 10.1200\u002FJCO.2002.20.6.1600",{"doi":2445},"10.1200\u002FJCO.2002.20.6.1600",{"id":26,"text":2447,"url":26,"identifiers":2448},"Atkins, 2008, Phase III trial comparing concurrent biochemotherapy with cisplatin, vinblastine, dacarbazine, interleukin-2, and interferon alfa-2b with cisplatin, vinblastine, and dacarbazine alone in patients with metastatic malignant melanoma (E3695): a trial coordinated by the Eastern Cooperative Oncology Group, J Clin Oncol, 26, 5748, 10.1200\u002FJCO.2008.17.5448",{"doi":2449},"10.1200\u002FJCO.2008.17.5448",{"id":26,"text":2451,"url":26,"identifiers":2452},"Lewis, 2006, Phase II multicenter study of neoadjuvant biochemotherapy for patients with stage III malignant melanoma, J Clin Oncol, 24, 3157, 10.1200\u002FJCO.2005.04.5344",{"doi":2453},"10.1200\u002FJCO.2005.04.5344",{"id":26,"text":2455,"url":26,"identifiers":2456},"Eigentler, 2003, Palliative therapy of disseminated malignant melanoma: a systematic review of 41 randomised clinical trials, Lancet Oncol, 4, 748, 10.1016\u002FS1470-2045(03)01280-4",{"doi":2457},"10.1016\u002FS1470-2045(03)01280-4",{"id":26,"text":2459,"url":26,"identifiers":2460},"Balch, 2009, Final version of 2009 AJCC melanoma staging and classification, J Clin Oncol, 27, 6199, 10.1200\u002FJCO.2009.23.4799",{"doi":2461},"10.1200\u002FJCO.2009.23.4799",{"id":26,"text":2463,"url":26,"identifiers":2464},"Garbe, 2010, Diagnosis and treatment of melanoma: European consensus-based interdisciplinary guideline, Eur J Cancer, 46, 270, 10.1016\u002Fj.ejca.2009.10.032",{"doi":2465},"10.1016\u002Fj.ejca.2009.10.032",{"id":26,"text":2467,"url":26,"identifiers":2468},"Coit, 2009, Melanoma, J Natl Compr Canc Netw, 7, 250, 10.6004\u002Fjnccn.2009.0020",{"doi":2469},"10.6004\u002Fjnccn.2009.0020",{"id":26,"text":2471,"url":26,"identifiers":2472},"Thomas, 2004, Excision margins in high-risk malignant melanoma, N Engl J Med, 350, 757, 10.1056\u002FNEJMoa030681",{"doi":2473},"10.1056\u002FNEJMoa030681",{"id":26,"text":2475,"url":26,"identifiers":2476},"Balch, 2000, Long-term results of a multi-institutional randomized trial comparing prognostic factors and surgical results for intermediate thickness melanomas (1.0 to 4.0 mm). Intergroup Melanoma Surgical Trial, Ann Surg Oncol, 7, 87, 10.1007\u002Fs10434-000-0087-9",{"doi":2477},"10.1007\u002Fs10434-000-0087-9",{"id":26,"text":2479,"url":26,"identifiers":2480},"Shah, 2007, Adjuvant therapy of melanoma, Cancer J, 13, 217, 10.1097\u002FPPO.0b013e318074dfd4",{"doi":2481},"10.1097\u002FPPO.0b013e318074dfd4",{"id":26,"text":2483,"url":26,"identifiers":2484},"Fecher, 2009, Where are we with adjuvant therapy of stage III and IV melanoma in 2009?, J Natl Compr Canc Netw, 7, 295, 10.6004\u002Fjnccn.2009.0022",{"doi":2485},"10.6004\u002Fjnccn.2009.0022",{"id":26,"text":2487,"url":26,"identifiers":2488},"Kirkwood, 1996, Interferon alfa-2b adjuvant therapy of high-risk resected cutaneous melanoma: the Eastern Cooperative Oncology Group Trial EST 1684, J Clin Oncol, 14, 7, 10.1200\u002FJCO.1996.14.1.7",{"doi":2489},"10.1200\u002FJCO.1996.14.1.7",{"id":26,"text":2491,"url":26,"identifiers":2492},"Creagan, 1995, Randomized, surgical adjuvant clinical trial of recombinant interferon alfa-2a in selected patients with malignant melanoma, J Clin Oncol, 13, 2776, 10.1200\u002FJCO.1995.13.11.2776",{"doi":2493},"10.1200\u002FJCO.1995.13.11.2776",{"id":26,"text":2495,"url":26,"identifiers":2496},"Kirkwood, 2000, High- and low-dose interferon alfa-2b in high-risk melanoma: first analysis of intergroup trial E1690\u002FS9111\u002FC9190, J Clin Oncol, 18, 2444, 10.1200\u002FJCO.2000.18.12.2444",{"doi":2497},"10.1200\u002FJCO.2000.18.12.2444",{"id":26,"text":2499,"url":26,"identifiers":2500},"Eggermont, 2005, Post-surgery adjuvant therapy with intermediate doses of interferon alfa 2b versus observation in patients with stage IIb\u002FIII melanoma (EORTC 18952): randomised controlled trial, Lancet, 366, 1189, 10.1016\u002FS0140-6736(05)67482-X",{"doi":2501},"10.1016\u002FS0140-6736(05)67482-X",{"id":26,"text":2503,"url":26,"identifiers":2504},"Hancock, 2004, Adjuvant interferon in high-risk melanoma: the AIM HIGH Study–United Kingdom Coordinating Committee on Cancer Research randomized study of adjuvant low-dose extended-duration interferon Alfa-2a in high-risk resected malignant melanoma, J Clin Oncol, 22, 53, 10.1200\u002FJCO.2004.03.185",{"doi":2505},"10.1200\u002FJCO.2004.03.185",{"id":26,"text":2507,"url":26,"identifiers":2508},"Pehamberger, 1998, Adjuvant interferon alfa-2a treatment in resected primary stage II cutaneous melanoma. Austrian Malignant Melanoma Cooperative Group, J Clin Oncol, 16, 1425, 10.1200\u002FJCO.1998.16.4.1425",{"doi":2509},"10.1200\u002FJCO.1998.16.4.1425",{"id":26,"text":2511,"url":26,"identifiers":2512},"Cascinelli, 2001, Effect of long-term adjuvant therapy with interferon alpha-2a in patients with regional node metastases from cutaneous melanoma: a randomised trial, Lancet, 358, 866, 10.1016\u002FS0140-6736(01)06068-8",{"doi":2513},"10.1016\u002FS0140-6736(01)06068-8",{"id":26,"text":2515,"url":26,"identifiers":2516},"Garbe, 2008, Adjuvant low-dose interferon α2a with or without dacarbazine compared with surgery alone: a prospective-randomized phase III DeCOG trial in melanoma patients with regional lymph node metastasis, Ann Oncol, 19, 1195, 10.1093\u002Fannonc\u002Fmdn001",{"doi":2517},"10.1093\u002Fannonc\u002Fmdn001",{"id":26,"text":2519,"url":26,"identifiers":2520},"Grob, 1998, Randomised trial of interferon alpha-2a as adjuvant therapy in resected primary melanoma thicker than 1.5 mm without clinically detectable node metastases. 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temozolomide (TMZ) in patients (pts) with advanced melanoma: an open-label, randomized, multicenter, phase II study, J Clin Oncol, 26",{},{"id":26,"text":2831,"url":26,"identifiers":2832},"U.S. National Institutes of Health, Comparison of AZD6244 in Combination With Dacarbazine Versus (vs) Dacarbazine Alone in BRAF Mutation Positive Melanoma Patients",{},{"id":26,"text":2834,"url":26,"identifiers":2835},"Infante, 2010, Safety and efficacy results from the first-in-human study of the oral MEK 1\u002F2 inhibitor GSK1120212, J Clin Oncol, 28",{},{"id":26,"text":2837,"url":26,"identifiers":2838},"Kirkwood, 2010, A phase II study of tasisulam sodium (LY573636) as second-line treatment for patients with unresectable or metastatic melanoma, J Clin Oncol, 28",{},{"id":26,"text":2840,"url":26,"identifiers":2841},"Dudley, 2003, Generation of tumor-infiltrating lymphocyte cultures for use in adoptive transfer therapy for melanoma patients, J Immunother, 26, 332, 10.1097\u002F00002371-200307000-00005",{"doi":2842},"10.1097\u002F00002371-200307000-00005",{"id":26,"text":2844,"url":26,"identifiers":2845},"Dudley, 2008, Adoptive cell therapy for patients with metastatic melanoma: evaluation of intensive myeloablative chemoradiation preparative regimens, J Clin Oncol, 26, 5233, 10.1200\u002FJCO.2008.16.5449",{"doi":2846},"10.1200\u002FJCO.2008.16.5449",{"id":26,"text":2848,"url":26,"identifiers":2849},"Dudley, 2005, Adoptive cell transfer therapy following non-myeloablative but lymphodepleting chemotherapy for the treatment of patients with refractory metastatic melanoma, J Clin Oncol, 23, 2346, 10.1200\u002FJCO.2005.00.240",{"doi":2850},"10.1200\u002FJCO.2005.00.240",{"id":26,"text":2852,"url":26,"identifiers":2853},"Besser, 2009, Minimally cultured or selected autologous tumor-infiltrating lymphocytes after a lympho-depleting chemotherapy regimen in metastatic melanoma patients, J Immunother, 32, 415, 10.1097\u002FCJI.0b013e31819c8bda",{"doi":2854},"10.1097\u002FCJI.0b013e31819c8bda",{"id":26,"text":2856,"url":26,"identifiers":2857},"Koike, 2008, Nonmyeloablative chemotherapy followed by T-cell adoptive transfer and dendritic cell-based vaccination results in rejection of established melanoma, J Immunother, 31, 402, 10.1097\u002FCJI.0b013e31816cabbb",{"doi":2858},"10.1097\u002FCJI.0b013e31816cabbb",{"id":26,"text":2860,"url":26,"identifiers":2861},"Wallen, 2009, Fludarabine modulates immune response and extends in vivo survival of adoptively transferred CD8 T cells in patients with metastatic melanoma, PLoS One, 4, e4749, 10.1371\u002Fjournal.pone.0004749",{"doi":2862},"10.1371\u002Fjournal.pone.0004749",{"id":26,"text":2864,"url":26,"identifiers":2865},"Hauschild, 2009, Phase III, randomized, double-blind study of elesclomol and paclitaxel versus paclitaxel alone in stage IV metastatic melanoma (MM), J Clin Oncol, 27",{},{"id":26,"text":2867,"url":26,"identifiers":2868},"Bedikian, 2010, Results of pooled analyses from two phase III trials of 1,085 patients (pts) with advanced melanoma: oblimersen (OBL) plus dacarbazine (DTIC) versus DTIC alone, J Clin Oncol, 28",{},{"id":26,"text":2870,"url":26,"identifiers":2871},"Cancer Research, U.K. A trial looking at bevacizumab after surgery for melanoma skin cancer (AVAST-M)",{},{"id":26,"text":2873,"url":26,"identifiers":2874},"U.S. National Institutes of Health, Efficacy and Safety Study of OncoVEXGM-CSF Compared to GM-CSF in Melanoma",{},{"id":2876,"createTime":2877,"updateTime":2878,"relativeEntities":2879,"slug":2880,"properties":2881,"entityType":826,"verifyStatus":25,"verifyTime":2898,"verifyNote":827,"syncStatus":28,"languages":2899,"translateLanguages":2900,"viewCount":36,"primaryUrl":2901,"fullTextUrl":26,"authors":2902,"publicationType":902,"publisherRelationship":2922,"citationCount":2959,"citationInfo":2960,"publishDate":2962,"publishYear":2963,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":2964,"isForceReanalyzing":1073},"a34c6cee-2bcb-4413-9fb8-70d102b10413","2024-10-05T05:39:56.895+00:00","2025-02-06T08:10:18.145+00:00",[],"VEGF-Receptor-Signaling-in-Tumor-Angiogenesis",{"mag":2882,"keywords":2884,"openalex":2886,"abstract":2888,"title":2891,"pm":2894,"doi":2896},{"VOID":2883},"2102140960",{"VI":2885},"VEGF, tyrosine kinase, angiogenesis, tumor growth, clinical studies",{"VOID":2887},"W2102140960",{"EN":2889,"VI":2890},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n               \u003Cjats:p>The growth of human tumors and development of metastases depend on the de novo formation of blood vessels. The formation of new blood vessels is tightly regulated by specific growth factors that target receptor tyrosine kinases (RTKs). Vascular endothelial growth factor (VEGF) and the Flk-1\u002FKDR RTK have been implicated as the key endothelial cell-specific factor signaling pathway required for pathological angiogenesis, including tumor neovascularization. Inhibition of the VEGF tyrosine kinase signaling pathway blocks new blood vessel formation in growing tumors, leading to stasis or regression of tumor growth. Advances in understanding the biology of angiogenesis have led to the development of several therapeutic modalities for the inhibition of the VEGF tyrosine kinase signaling pathway. A number of these modalities are under investigation in clinical studies to evaluate their potential to treat human cancers.\u003C\u002Fjats:p>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n               \u003Cjats:p>Sự phát triển của các khối u ở người và sự hình thành di căn phụ thuộc vào sự hình thành mạch máu mới de novo. Quá trình hình thành các mạch máu mới được điều chỉnh chặt chẽ bởi các yếu tố tăng trưởng cụ thể nhắm vào các thụ thể tyrosine kinase (RTKs). Yếu tố tăng trưởng nội mạch (VEGF) và RTK Flk-1\u002FKDR đã được xác định là con đường tín hiệu chính yếu tố cụ thể trên tế bào nội mạch cần thiết cho sự hình thành mạch máu bệnh lý, bao gồm việc hình thành mạch mới trong khối u. Việc ức chế con đường tín hiệu tyrosine kinase VEGF ngăn chặn sự hình thành mạch máu mới trong các khối u đang phát triển, dẫn đến tình trạng ngừng tăng trưởng hoặc suy thoái của khối u. Những tiến bộ trong việc hiểu biết về sinh học của quá trình sinh mạch đã dẫn đến sự phát triển của một số phương thức điều trị để ức chế con đường tín hiệu tyrosine kinase VEGF. Nhiều phương thức trong số này đang được nghiên cứu trong các thử nghiệm lâm sàng để đánh giá khả năng điều trị ung thư ở người.",{"EN":2892,"VI":2893},"VEGF Receptor Signaling in Tumor Angiogenesis","Điều Hòa Tín Hiệu Thụ Thể VEGF Trong Thoát Vị Khối U",{"VOID":2895},"10804084",{"VOID":2897},"10.1634\u002Ftheoncologist.5-suppl_1-3","2024-10-05T05:39:56.894+00:00",[102],[101],"https:\u002F\u002Facademic.oup.com\u002Foncolo\u002Farticle\u002F5\u002FS1\u002F3\u002F6385848",[2903],{"id":2904,"sortIndex":36,"researcher":26,"roles":2905,"affiliations":2906,"properties":2917},"99566aa0-fbfe-4d70-8048-24192875e1f3",[],[2907],{"id":2908,"sortIndex":36,"affiliation":2909,"properties":26},"8f992f14-f4cd-4da4-a9e4-30ba94ce4565",{"id":2910,"createTime":2911,"updateTime":2911,"relativeEntities":2912,"slug":2913,"properties":2914,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"c56cc842-9bac-41c9-b8ad-5128260a1f7a","2024-10-05T05:39:56.911+00:00",[],"SUGEN-Inc-South-San-Francisco-California-USA",{"title":2915},{"EN":2916},"SUGEN, Inc., South San Francisco, California, USA",{"openalex":2918,"title":2920},{"VOID":2919},"A5069477348",{"EN":2921},"Gerald McMahon",{"url":26,"publisher":2923,"properties":2953},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":2924,"slug":663,"properties":2925,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":2931,"manageAffiliations":2932,"indexDatabases":2933,"url":761,"thumbnailPath":26,"statistic":2948,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":2926,"issn":2927,"introduce":2928,"eissn":2929,"title":2930},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":663},[],[],[2934,2941],{"id":743,"indexDatabase":2935,"url":758,"indexYears":26,"academicFieldIds":2940,"indexDatabaseRanking":26},{"id":745,"createTime":746,"updateTime":747,"relativeEntities":2936,"label":2937,"description":2938,"key":754,"publicationTags":2939,"standard":26},[],{"EN":750,"VI":750},{"VI":752,"EN":753},[756,757],[760],{"id":722,"indexDatabase":2942,"url":735,"indexYears":736,"academicFieldIds":2947,"indexDatabaseRanking":741},{"id":724,"createTime":725,"updateTime":726,"relativeEntities":2943,"label":2944,"description":2945,"key":732,"publicationTags":2946,"standard":26},[],{"EN":729,"VI":729},{"EN":729,"VI":731},[734],[738,739,740],{"impactFactor":36,"impactFactorByYear":2949,"i10Index":252,"i10IndexLast5Year":59,"totalPublication":257,"totalPublicationByYear":2950,"totalCitation":770,"totalCitationByYear":2951,"totalCitationPerPublication":785,"totalCitationPerPublicationByYear":2952,"hindexLast5Year":159,"hindex":159},{"2012":764,"2013":59,"2014":114,"2015":50,"2017":125,"2018":765,"2019":766,"2020":517,"2021":767,"2022":768,"2023":59},{"1997":115,"2000":114,"2001":114,"2002":59,"2004":162,"2005":59,"2006":114,"2007":114,"2008":135,"2009":114,"2010":114,"2011":115,"2013":115,"2016":115,"2017":114,"2019":115,"2020":114,"2022":115},{"1997":772,"2000":773,"2001":143,"2002":774,"2004":775,"2005":776,"2006":777,"2007":778,"2008":779,"2009":780,"2010":781,"2011":652,"2013":142,"2016":782,"2017":783,"2019":784,"2020":258,"2022":135},{"1997":772,"2000":787,"2001":788,"2002":789,"2004":790,"2005":791,"2006":792,"2007":793,"2008":794,"2009":795,"2010":796,"2011":652,"2013":142,"2016":782,"2017":797,"2019":784,"2020":798,"2022":135},{"volume":2954,"pages":2956,"issue":2958},{"VOID":2955},"5",{"VOID":2957},"3-10",{"VOID":1262},484,{"total":2959,"publishYear":26,"statisticByYear":2961},{"2012":244,"2013":79,"2014":240,"2015":242,"2016":516,"2017":79,"2018":242,"2019":234,"2020":103,"2021":53,"2022":53,"2023":298,"2024":111},"2000-04-01",2000,[2965,2969,2972,2976,2980,2984,2988,2991,2993,2997,3000,3004,3008,3012,3016,3019,3023,3027,3031,3035,3039,3043,3047,3051,3055,3059,3063,3067,3071,3074,3078,3082,3086,3090,3093,3097,3101,3105,3108,3112,3116,3120,3123,3126,3129,3132,3136,3140,3144,3148,3152,3156,3160,3164,3168,3172,3176,3180,3184,3187,3191,3195,3198,3201,3205,3207,3210,3213,3216,3219,3222,3225,3228,3231,3234,3237,3241,3245,3248,3252,3256,3260,3263,3266,3269,3273,3277,3281,3284,3287,3290,3293],{"id":26,"text":2966,"url":26,"identifiers":2967},"Folkman, 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growth factor-beta 1 on in vitro angiogenesis, Exp Cell Res, 204, 356, 10.1006\u002Fexcr.1993.1043",{"doi":3015},"10.1006\u002Fexcr.1993.1043",{"id":26,"text":3017,"url":26,"identifiers":3018},"Gleave, 1993, Epidermal growth factor receptor-mediated autocrine and paracrine stimulation of human transitional cell carcinoma, Cancer Res, 53, 5300",{},{"id":26,"text":3020,"url":26,"identifiers":3021},"Ferrara, 1989, Pituitary follicular cells secrete a novel heparin-binding growth factor specific for vascular endothelial cells, Biochem Biophys Res Commun, 161, 851, 10.1016\u002F0006-291X(89)92678-8",{"doi":3022},"10.1016\u002F0006-291X(89)92678-8",{"id":26,"text":3024,"url":26,"identifiers":3025},"Leung, 1989, Vascular endothelial growth factor is a secreted angiogenic mitogen, Science, 246, 1306, 10.1126\u002Fscience.2479986",{"doi":3026},"10.1126\u002Fscience.2479986",{"id":26,"text":3028,"url":26,"identifiers":3029},"Ferrara, 1999, Clinical applications of angiogenic growth factors and 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Discovery and design of angiogenesis inhibitors that inhibit tyrosine kinase activities associated with VEGF, FGF, and PDGF receptors, Proc Am Assoc Cancer Res, 40, 68a",{},{"id":26,"text":3294,"url":26,"identifiers":3295},"Fabbro, 1999, Inhibitors of protein kinases: CGP 41251, a protein kinase inhibitor with potential as an anticancer agent, Pharmacol Ther, 82, 293, 10.1016\u002FS0163-7258(99)00005-4",{"doi":3296},"10.1016\u002FS0163-7258(99)00005-4",{"id":3298,"createTime":3299,"updateTime":3300,"relativeEntities":3301,"slug":3302,"properties":3303,"entityType":826,"verifyStatus":25,"verifyTime":3299,"verifyNote":827,"syncStatus":28,"languages":3319,"translateLanguages":3320,"viewCount":36,"primaryUrl":3321,"fullTextUrl":26,"authors":3322,"publicationType":902,"publisherRelationship":3465,"citationCount":3501,"citationInfo":3502,"publishDate":3504,"publishYear":3505,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":3506,"isForceReanalyzing":1073},"385ce7c8-d527-4766-9ef2-1be31831f7ca","2024-10-09T22:56:55.094+00:00","2025-02-06T08:11:17.041+00:00",[],"Ewing-s-Sarcoma-Family-of-Tumors-Current-Management",{"mag":3304,"keywords":3306,"openalex":3307,"abstract":3309,"title":3312,"pm":3315,"doi":3317},{"VOID":3305},"2160175915",{"VI":813},{"VOID":3308},"W2160175915",{"EN":3310,"VI":3311},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n               \u003Cjats:sec>\n                  \u003Cjats:title>Learning Objectives\u003C\u002Fjats:title>\n                  \u003Cjats:p>After completing this course, the reader will be able to: Describe the presentation, differential diagnosis, and prognosis for patients with Ewing's sarcoma.Explain the principles of multidisciplinary management of Ewing's sarcoma.Discuss the late effects of the therapy for Ewing's sarcoma.\u003C\u002Fjats:p>\n                  \u003Cjats:p>Access and take the CME test online and receive 1 AMA PRA category 1 credit at CME.TheOncologist.com\u003C\u002Fjats:p>\n                  \u003Cjats:p>Ewing's sarcoma is the second most frequent primary bone cancer, with approximately 225 new cases diagnosed each year in patients less than 20 years of age in North America. It is one of the pediatric small round blue cell tumors, characterized by strong membrane expression of CD99 in a chain-mail pattern and negativity for lymphoid (CD45), rhabdomyosarcoma (myogenin, desmin, actin) and neuroblastoma (neurofilament protein) markers. Pathognomonic translocations involving the ews gene on chromosome 22 and an ets-type gene, most commonly the fli1 gene on chromosome 11, are implicated in the great majority of cases. Clinical presentation is usually dominated by local bone pain and a mass. Imaging reveals a technetium pyrophosphate avid lesion that, on plain radiograph, is destructive, diaphyseal and classically causes layered periosteal calcification. Magnetic resonance best defines the extent of the lesion. Biopsy should be undertaken by an experienced orthopedic oncologist. Approximately three quarters of patients have initially localized disease. About two thirds survive disease-free. Management, preferably at a specialist center with a multi-disciplinary team, includes both local control—either surgery, radiation or a combination—and systemic chemotherapy. Chemotherapy includes cyclic combinations, incorporating vincristine, doxorubicin, cyclophosphamide, etoposide, ifosfamide and occasionally actinomycin D. Topotecan in combination with cyclophosphamide has shown preliminary activity. Patients with initially metastatic disease fare less well, with about one quarter surviving. Studies incorporating intensive therapy followed by stem cell infusion show no clear benefit. New approaches include anti-angiogenic therapy, particularly since vascular endothelial growth factor is an apparent downstream target of the ews-fli1 oncogene.\u003C\u002Fjats:p>\n               \u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n               \u003Cjats:sec>\n                  \u003Cjats:title>Mục tiêu học tập\u003C\u002Fjats:title>\n                  \u003Cjats:p>Sau khi hoàn thành khóa học này, người đọc sẽ có khả năng: Mô tả sự trình bày, chẩn đoán phân biệt và tiên lượng bệnh nhân mắc bệnh u Ewing. Giải thích các nguyên tắc quản lý đa chuyên khoa bệnh u Ewing. Thảo luận về các tác động muộn của liệu pháp điều trị cho bệnh u Ewing.\u003C\u002Fjats:p>\n                  \u003Cjats:p>Truy cập và làm bài kiểm tra CME trực tuyến và nhận 1 tín chỉ AMA PRA loại 1 tại CME.TheOncologist.com\u003C\u002Fjats:p>\n                  \u003Cjats:p>U Ewing là loại ung thư xương nguyên phát phổ biến thứ hai, với khoảng 225 trường hợp mới được chẩn đoán mỗi năm ở bệnh nhân dưới 20 tuổi tại Bắc Mỹ. Đây là một trong những khối u tế bào tròn nhỏ màu xanh ở trẻ em, có đặc điểm là biểu hiện mạnh mẽ của màng CD99 theo kiểu xích đu và âm tính với các dấu hiệu lympho (CD45), u cơ vân (myogenin, desmin, actin) và u nguyên bào thần kinh (protein neurofilament). Các chuyển vị đặc trưng liên quan đến gen ews trên nhiễm sắc thể 22 và một gen loại ets, thường là gen fli1 trên nhiễm sắc thể 11, có liên quan đến phần lớn các trường hợp. Triệu chứng lâm sàng thường bị chi phối bởi cơn đau xương tại chỗ và khối u. Hình ảnh cho thấy một tổn thương hấp thụ technetium pyrophosphate mà trên phim chụp không có chất cản quang có thể hủy hoại, nằm ở thân xương và theo kiểu cổ điển gây ra sự vôi hóa màng xương theo lớp. Chụp cộng hưởng từ giúp xác định tốt nhất mức độ tổn thương. Sinh thiết nên được thực hiện bởi một bác sĩ phẫu thuật ung thư xương có kinh nghiệm. Khoảng ba phần tư bệnh nhân có bệnh khu trú ngay từ đầu. Khoảng hai phần ba sống sót mà không có bệnh. Quản lý, lý tưởng là tại một trung tâm chuyên khoa với đội ngũ đa chuyên môn, bao gồm cả kiểm soát tại chỗ — phẫu thuật, xạ trị hoặc kết hợp và hóa trị toàn thân. Hóa trị bao gồm các phác đồ theo chu kỳ, kết hợp vincristine, doxorubicin, cyclophosphamide, etoposide, ifosfamide và đôi khi actinomycin D. Topotecan kết hợp với cyclophosphamide đã cho thấy hoạt động sơ bộ. Bệnh nhân có bệnh di căn ngay từ đầu có có triển vọng sống thấp hơn, với khoảng một phần tư sống sót. Các nghiên cứu kết hợp liệu pháp điều trị tích cực theo sau là truyền tế bào gốc cho thấy không có lợi ích rõ ràng. Các phương pháp mới bao gồm liệu pháp chống tăng sinh mạch, đặc biệt là khi yếu tố tăng trưởng nội mô mạch máu là một mục tiêu hạ lưu rõ ràng của gen ung thư ews-fli1.",{"EN":3313,"VI":3314},"Ewing's Sarcoma Family of Tumors: Current Management","Nhóm Khối U Ewing: Quản Lý Hiện Tại",{"VOID":3316},"16720851",{"VOID":3318},"10.1634\u002Ftheoncologist.11-5-503",[102],[101],"https:\u002F\u002Facademic.oup.com\u002Foncolo\u002Farticle\u002F11\u002F5\u002F503\u002F6397096",[3323,3345,3366,3387,3406,3425,3444],{"id":3324,"sortIndex":114,"researcher":26,"roles":3325,"affiliations":3326,"properties":3338},"fbf462a7-17ea-4ffa-add9-5000c5694b97",[],[3327],{"id":3328,"sortIndex":36,"affiliation":3329,"properties":26},"3498be6b-cc31-4e70-bafd-99d9cf641a0b",{"id":3330,"createTime":3331,"updateTime":3332,"relativeEntities":3333,"slug":3334,"properties":3335,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"02d79de7-3278-41e3-a6a4-dd626202cedd","2024-10-09T22:56:55.132+00:00","2025-06-11T16:13:21.135+00:00",[],"cUniversity-Children-s-Hospital-Basel-Basel-Switzerland",{"title":3336},{"EN":3337},"cUniversity Children's Hospital Basel, Basel, Switzerland",{"openalex":3339,"orcid":3341,"title":3343},{"VOID":3340},"A5001373279",{"VOID":3342},"https:\u002F\u002Forcid.org\u002F0009-0007-2534-6381",{"EN":3344},"Michael Paulussen",{"id":3346,"sortIndex":111,"researcher":26,"roles":3347,"affiliations":3348,"properties":3359},"f46272a0-1740-455b-af38-66a2fc63c7a3",[],[3349],{"id":3350,"sortIndex":36,"affiliation":3351,"properties":26},"e25fb947-d33d-4656-86f0-dc000ac08526",{"id":3352,"createTime":3353,"updateTime":3353,"relativeEntities":3354,"slug":3355,"properties":3356,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"746348b9-8b19-415b-91ca-14a1e0b524b3","2024-10-09T22:56:55.166+00:00",[],"e-Department-of-Radiotherapy-University-Hospital-Muenster-M%C3%BCnster-Germany",{"title":3357},{"EN":3358},"e Department of Radiotherapy, University Hospital Muenster, Münster, Germany",{"openalex":3360,"orcid":3362,"title":3364},{"VOID":3361},"A5052456706",{"VOID":3363},"https:\u002F\u002Forcid.org\u002F0000-0002-8007-5517",{"EN":3365},"Andreas Schuck",{"id":3367,"sortIndex":36,"researcher":26,"roles":3368,"affiliations":3369,"properties":3380},"d6bf7761-059a-4276-b00b-92880a2a3931",[],[3370],{"id":3371,"sortIndex":36,"affiliation":3372,"properties":26},"ebb4dd80-b1ba-4941-a4a5-4c3183507ab9",{"id":3373,"createTime":3374,"updateTime":3374,"relativeEntities":3375,"slug":3376,"properties":3377,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"7183ddf5-2ef0-4666-a086-74dbe39e269f","2024-10-09T22:56:55.109+00:00",[],"aSte-Justine-Hospital-University-of-Montreal-Montreal-Canada",{"title":3378},{"EN":3379},"aSte-Justine Hospital, University of Montreal, Montreal, Canada",{"openalex":3381,"orcid":3383,"title":3385},{"VOID":3382},"A5067299217",{"VOID":3384},"https:\u002F\u002Forcid.org\u002F0000-0003-2019-8627",{"EN":3386},"Mark L. 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1999, Cancer Incidence and Survival Among Children and Adolescents: United States SEER Program 1975–1995, 99",{},{"id":26,"text":3511,"url":26,"identifiers":3512},"Hense, 1999, Klin Padiatr, 211, 271, 10.1055\u002Fs-2008-1043799",{"doi":3513},"10.1055\u002Fs-2008-1043799",{"id":26,"text":3515,"url":26,"identifiers":3516},"Widhe, 2000, Initial symptoms and clinical features in osteosarcoma and Ewing sarcoma, J Bone Joint Surg Am, 82, 667, 10.2106\u002F00004623-200005000-00007",{"doi":3517},"10.2106\u002F00004623-200005000-00007",{"id":26,"text":3519,"url":26,"identifiers":3520},"Sneppen, 1984, Presenting symptoms and treatment delay in osteosarcoma and Ewing's sarcoma, Acta Radiol Oncol, 23, 159, 10.3109\u002F02841868409136005",{"doi":3521},"10.3109\u002F02841868409136005",{"id":26,"text":3523,"url":26,"identifiers":3524},"Craft, 1997, Long-term results from the first UKCCSG Ewing's Tumour Study (ET-1). United Kingdom Children's Cancer Study Group (UKCCSG) and the Medical Research Council Bone Sarcoma Working Party, Eur J Cancer, 33, 1061, 10.1016\u002FS0959-8049(97)00043-9",{"doi":3525},"10.1016\u002FS0959-8049(97)00043-9",{"id":26,"text":3527,"url":26,"identifiers":3528},"Ferrari, 2001, Ewing's sarcoma of bone: relation between clinical characteristics and staging, Oncol Rep, 8, 553",{},{"id":26,"text":3530,"url":26,"identifiers":3531},"Henk, 1998, et al. [Ewing sarcoma. Diagnostic imaging], Radiologe, 38, 509, 10.1007\u002Fs001170050386",{"doi":3532},"10.1007\u002Fs001170050386",{"id":26,"text":3534,"url":26,"identifiers":3535},"Tateishi, 2003, Chest wall tumors: radiologic findings and pathologic correlation: part 2. Malignant tumors, Radiographics, 23, 1491, 10.1148\u002Frg.236015527",{"doi":3536},"10.1148\u002Frg.236015527",{"id":26,"text":3538,"url":26,"identifiers":3539},"Frouge, 1988, The role of magnetic resonance imaging in the evaluation of Ewing sarcoma. A report of 27 cases, Skeletal Radiol, 17, 387, 10.1007\u002FBF00361656",{"doi":3540},"10.1007\u002FBF00361656",{"id":26,"text":3542,"url":26,"identifiers":3543},"Cohen, 1986, Efficacy of magnetic resonance imaging in 139 children with tumors, Arch Surg, 121, 522, 10.1001\u002Farchsurg.1986.01400050032004",{"doi":3544},"10.1001\u002Farchsurg.1986.01400050032004",{"id":26,"text":3546,"url":26,"identifiers":3547},"Mankin, 1996, The hazards of the biopsy, revisited. Members of the Musculoskeletal Tumor Society, J Bone Joint Surg Am, 78, 656, 10.2106\u002F00004623-199605000-00004",{"doi":3548},"10.2106\u002F00004623-199605000-00004",{"id":26,"text":3550,"url":26,"identifiers":3551},"Ewing, 1921, Diffuse endothelioma of bone, Proc N Y Pathol Soc, 21, 17",{},{"id":26,"text":3553,"url":26,"identifiers":3554},"Horowitz, 1992, Ewing's sarcoma, CA Cancer J Clin, 42, 300, 10.3322\u002Fcanjclin.42.5.300",{"doi":3555},"10.3322\u002Fcanjclin.42.5.300",{"id":26,"text":3557,"url":26,"identifiers":3558},"Tsokos, 1992, Peripheral primitive neuroectodermal tumors. Diagnosis, classification, and prognosis, Perspect Pediatr Pathol, 16, 27",{},{"id":26,"text":3560,"url":26,"identifiers":3561},"Dehner, 1993, Primitive neuroectodermal tumor and Ewing's sarcoma, Am J Surg Pathol, 17, 1, 10.1097\u002F00000478-199301000-00001",{"doi":3562},"10.1097\u002F00000478-199301000-00001",{"id":26,"text":3564,"url":26,"identifiers":3565},"Fellinger, 1991, Biochemical and genetic characterization of the HBA71 Ewing's sarcoma cell surface antigen, Cancer Res, 51, 336",{},{"id":26,"text":3567,"url":26,"identifiers":3568},"Ramani, 1993, Immunocytochemical study of 12E7 in small round-cell tumours of childhood: an assessment of its sensitivity and specificity, Histopathology, 23, 557, 10.1111\u002Fj.1365-2559.1993.tb01243.x",{"doi":3569},"10.1111\u002Fj.1365-2559.1993.tb01243.x",{"id":26,"text":3571,"url":26,"identifiers":3572},"Weidner, 1994, Immunohistochemical profile of monoclonal antibody O13: antibody that recognizes glycoprotein p30\u002F32MIC2 and is useful in diagnosing Ewing's sarcoma and peripheral neuroepithelioma, Am J Surg Pathol, 18, 486, 10.1097\u002F00000478-199405000-00008",{"doi":3573},"10.1097\u002F00000478-199405000-00008",{"id":26,"text":3575,"url":26,"identifiers":3576},"Navarro, 1994, Comparison of Ewing's sarcoma of bone and peripheral neuroepithelioma. An immunocytochemical and ultrastructural analysis of two primitive neuroectodermal neoplasms, Arch Pathol Lab Med, 118, 608",{},{"id":26,"text":3578,"url":26,"identifiers":3579},"Lizard-Nacol, 1989, Immunologic characterization of Ewing's sarcoma using mesenchymal and neural markers, Am J Pathol, 135, 847",{},{"id":26,"text":3581,"url":26,"identifiers":3582},"Dierick, 1993, The immunophenotype of Ewing's sarcoma. 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J Radiat Oncol Biol Phys, 42, 379, 10.1016\u002FS0360-3016(98)00228-4",{"doi":4084},"10.1016\u002FS0360-3016(98)00228-4",{"id":26,"text":4086,"url":26,"identifiers":4087},"Le Vu, 1998, Radiation dose, chemotherapy and risk of osteosarcoma after solid tumours during childhood, Int J Cancer, 77, 370, 10.1002\u002F(SICI)1097-0215(19980729)77:3\u003C370::AID-IJC11>3.0.CO;2-C",{"doi":4088},"10.1002\u002F(SICI)1097-0215(19980729)77:3\u003C370::AID-IJC11>3.0.CO;2-C",{"id":26,"text":4090,"url":26,"identifiers":4091},"Paulussen, 2001, Second malignancies after Ewing tumor treatment in 690 patients from a cooperative German\u002FAustrian\u002FDutch study, Ann Oncol, 12, 1619, 10.1023\u002FA:1013148730966",{"doi":4092},"10.1023\u002FA:1013148730966",{"id":26,"text":4094,"url":26,"identifiers":4095},"Friedman, 2002, Late effects of childhood cancer therapy, Pediatr Clin North Am, 49, 1083, 10.1016\u002FS0031-3955(02)00032-9",{"doi":4096},"10.1016\u002FS0031-3955(02)00032-9",{"id":26,"text":4098,"url":26,"identifiers":4099},"Nagarajan, 2003, Education, employment, insurance, and marital status among 694 survivors of pediatric lower extremity bone tumors: a report from the childhood cancer survivor study, Cancer, 97, 2554, 10.1002\u002Fcncr.11363",{"doi":4100},"10.1002\u002Fcncr.11363",{"id":26,"text":4102,"url":26,"identifiers":4103},"Fuchs, 2003, Complications in long-term survivors of Ewing sarcoma, Cancer, 98, 2687, 10.1002\u002Fcncr.11891",{"doi":4104},"10.1002\u002Fcncr.11891",{"id":4106,"createTime":4107,"updateTime":4108,"relativeEntities":4109,"slug":4110,"properties":4111,"entityType":826,"verifyStatus":25,"verifyTime":4107,"verifyNote":827,"syncStatus":28,"languages":4130,"translateLanguages":4131,"viewCount":36,"primaryUrl":4132,"fullTextUrl":26,"authors":4133,"publicationType":902,"publisherRelationship":4176,"citationCount":202,"citationInfo":4213,"publishDate":4215,"publishYear":3505,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":4216,"isForceReanalyzing":1073},"f516ae80-554e-4f70-9ccf-eb01b2bffd28","2024-09-02T05:03:24.045+00:00","2025-02-06T08:12:14.064+00:00",[],"Chemotherapeutic-Approaches-for-Targeting-Cell-Death-Pathways",{"mag":4112,"keywords":4114,"pmc":4116,"openalex":4118,"abstract":4120,"title":4123,"pm":4126,"doi":4128},{"VOID":4113},"2108300681",{"VI":4115},"chết tế bào, hóa trị liệu, apoptosis, hoại tử, tự thực bào, thảm họa phân bào, sự lão hóa",{"VOID":4117},"3132471",{"VOID":4119},"W2108300681",{"EN":4121,"VI":4122},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n               \u003Cjats:sec>\n                  \u003Cjats:title>Learning Objectives\u003C\u002Fjats:title>\n                  \u003Cjats:p>After completing this course, the reader will be able to: List the multiple cell death pathways that are activated in response to chemotherapeutic agents.Identify signaling molecules involved and morphological changes that occur in the different types of cell death pathways.Describe mechanisms targeted by novel chemotherapeutic agents.\u003C\u002Fjats:p>\n                  \u003Cjats:p>Access and take the CME test online and receive 1 AMA PRA category 1 credit at CME.TheOncologist.com\u003C\u002Fjats:p>\n                  \u003Cjats:p>For several decades, apoptosis has taken center stage as the principal mechanism of programmed cell death in mammalian tissues. It also has been increasingly noted that conventional chemotherapeutic agents not only elicit apoptosis but other forms of nonapoptotic death such as necrosis, autophagy, mitotic catastrophe, and senescence. This review presents background on the signaling pathways involved in the different cell death outcomes. A re-examination of what we know about chemotherapy-induced death is vitally important in light of new understanding of nonapoptotic cell death signaling pathways. If we can precisely activate or inhibit molecules that mediate the diversity of cell death outcomes, perhaps we can succeed in more effective and less toxic chemotherapeutic regimens.\u003C\u002Fjats:p>\n               \u003C\u002Fjats:sec>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n               \u003Cjats:sec>\n                  \u003Cjats:title>Mục Tiêu Học Tập\u003C\u002Fjats:title>\n                  \u003Cjats:p>Sau khi hoàn thành khóa học này, người đọc sẽ có thể: Liệt kê nhiều con đường xuất tử tế bào được kích hoạt để đáp ứng các tác nhân hóa trị liệu. Xác định các phân tử tín hiệu liên quan và các thay đổi hình thái xảy ra trong các loại con đường xuất tử tế bào khác nhau. Mô tả các cơ chế mà các tác nhân hóa trị liệu mới nhắm tới.\u003C\u002Fjats:p>\n                  \u003Cjats:p>Truy cập và làm bài kiểm tra CME trực tuyến và nhận 1 tín chỉ AMA PRA loại 1 tại CME.TheOncologist.com\u003C\u002Fjats:p>\n                  \u003Cjats:p>Trong vài thập kỷ qua, apoptosis đã trở thành tâm điểm như là cơ chế chủ yếu của sự chết tế bào theo chương trình trong các mô động vật có vú. Ngoài ra, ngày càng có nhiều ghi nhận cho rằng các tác nhân hóa trị liệu thông thường không chỉ kích thích apoptosis mà còn cả các hình thức chết tế bào phi apoptotic khác như hoại tử, tự thực bào, thảm họa phân bào và sự lão hóa. Bài viết tổng quan này trình bày bối cảnh về các con đường tín hiệu liên quan đến các kết cục chết tế bào khác nhau. Việc xem xét lại những gì chúng ta biết về cái chết tế bào do hóa trị liệu là rất quan trọng trong bối cảnh hiểu biết mới về các con đường tín hiệu chết tế bào phi apoptotic. Nếu chúng ta có thể kích hoạt hoặc ức chế chính xác các phân tử trung gian cho sự đa dạng của các kết cục chết tế bào, có lẽ chúng ta có thể thành công trong việc phát triển các phác đồ hóa trị liệu hiệu quả hơn và ít độc hại hơn.",{"EN":4124,"VI":4125},"Chemotherapeutic Approaches for Targeting Cell Death Pathways","Cách Tiếp Cận Hóa Trị Để Nhắm Đến Các Đường Dẫn Xuất Tử Ở Tế Bào",{"VOID":4127},"16614230",{"VOID":4129},"10.1634\u002Ftheoncologist.11-4-342",[102],[101],"https:\u002F\u002Facademic.oup.com\u002Foncolo\u002Farticle\u002F11\u002F4\u002F342\u002F6397072",[4134,4155],{"id":4135,"sortIndex":36,"researcher":26,"roles":4136,"affiliations":4137,"properties":4148},"7e4c51e0-8054-43db-b91c-440868f3f670",[],[4138],{"id":4139,"sortIndex":36,"affiliation":4140,"properties":26},"8b47b671-dafc-4403-a63d-9564619728e9",{"id":4141,"createTime":4142,"updateTime":4142,"relativeEntities":4143,"slug":4144,"properties":4145,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"7cd8dd59-96bc-49da-bc47-ba732770c292","2024-09-02T05:03:24.072+00:00",[],"a-National-Cancer-Institute-and-Food-and-Drug-Administration-Interagency-Oncology-Task-Force-Bethesda-Maryland-USA",{"title":4146},{"EN":4147},"a National Cancer Institute and Food and Drug Administration Interagency Oncology Task Force, Bethesda, Maryland, USA",{"openalex":4149,"orcid":4151,"title":4153},{"VOID":4150},"A5013371199",{"VOID":4152},"https:\u002F\u002Forcid.org\u002F0009-0002-2508-2391",{"EN":4154},"M. 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Zong",{"url":26,"publisher":4177,"properties":4207},{"id":659,"createTime":660,"updateTime":661,"relativeEntities":4178,"slug":663,"properties":4179,"entityType":24,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"subjectFields":4185,"manageAffiliations":4186,"indexDatabases":4187,"url":761,"thumbnailPath":26,"statistic":4202,"gsStatistic":26,"type":26,"analyzePriority":26},[],{"country":4180,"issn":4181,"introduce":4182,"eissn":4183,"title":4184},{"VOID":666},{"VOID":668},{"EN":670},{"VOID":672},{"EN":663},[],[],[4188,4195],{"id":743,"indexDatabase":4189,"url":758,"indexYears":26,"academicFieldIds":4194,"indexDatabaseRanking":26},{"id":745,"createTime":746,"updateTime":747,"relativeEntities":4190,"label":4191,"description":4192,"key":754,"publicationTags":4193,"standard":26},[],{"EN":750,"VI":750},{"VI":752,"EN":753},[756,757],[760],{"id":722,"indexDatabase":4196,"url":735,"indexYears":736,"academicFieldIds":4201,"indexDatabaseRanking":741},{"id":724,"createTime":725,"updateTime":726,"relativeEntities":4197,"label":4198,"description":4199,"key":732,"publicationTags":4200,"standard":26},[],{"EN":729,"VI":729},{"EN":729,"VI":731},[734],[738,739,740],{"impactFactor":36,"impactFactorByYear":4203,"i10Index":252,"i10IndexLast5Year":59,"totalPublication":257,"totalPublicationByYear":4204,"totalCitation":770,"totalCitationByYear":4205,"totalCitationPerPublication":785,"totalCitationPerPublicationByYear":4206,"hindexLast5Year":159,"hindex":159},{"2012":764,"2013":59,"2014":114,"2015":50,"2017":125,"2018":765,"2019":766,"2020":517,"2021":767,"2022":768,"2023":59},{"1997":115,"2000":114,"2001":114,"2002":59,"2004":162,"2005":59,"2006":114,"2007":114,"2008":135,"2009":114,"2010":114,"2011":115,"2013":115,"2016":115,"2017":114,"2019":115,"2020":114,"2022":115},{"1997":772,"2000":773,"2001":143,"2002":774,"2004":775,"2005":776,"2006":777,"2007":778,"2008":779,"2009":780,"2010":781,"2011":652,"2013":142,"2016":782,"2017":783,"2019":784,"2020":258,"2022":135},{"1997":772,"2000":787,"2001":788,"2002":789,"2004":790,"2005":791,"2006":792,"2007":793,"2008":794,"2009":795,"2010":796,"2011":652,"2013":142,"2016":782,"2017":797,"2019":784,"2020":798,"2022":135},{"volume":4208,"pages":4209,"issue":4211},{"VOID":2116},{"VOID":4210},"342-357",{"VOID":4212},"4",{"total":202,"publishYear":26,"statisticByYear":4214},{"2012":234,"2013":222,"2014":242,"2015":238,"2016":239,"2017":159,"2018":222,"2019":255,"2020":79,"2021":517,"2022":238,"2023":79,"2024":124},"2006-04-01",[4217,4221,4225,4229,4233,4237,4241,4245,4249,4253,4257,4261,4265,4269,4273,4277,4281,4285,4289,4293,4297,4301,4305,4309,4313,4317,4321,4325,4329,4333,4337,4341,4345,4349,4353,4357,4361,4365,4369,4373,4377,4381,4385,4389,4393,4397,4401,4405,4408,4412,4416,4420,4424,4428,4432,4436,4440,4444,4448,4452,4456,4460,4464,4468,4472,4476,4480,4484,4488,4492,4496,4500,4504,4508,4512,4516,4520,4524,4528,4532,4536,4540,4544,4547,4551,4555,4559,4563,4567,4571,4575,4579,4583,4587,4591,4595,4599,4603,4607,4611,4615,4619,4622,4626,4630,4634,4638,4642,4646,4650,4654,4658,4662,4666,4669,4673,4677,4681,4684,4688,4691,4694,4698,4702,4705,4709,4713,4717,4720,4723,4727,4731,4734,4738,4742,4746,4750,4754,4758,4762,4766,4770,4774,4778,4782,4786,4790,4793,4796,4800,4804,4808,4811,4815,4818,4822,4826,4830,4834,4838,4842,4846,4850,4854,4858,4862,4866,4870,4874,4878,4882,4886,4889,4893,4897,4901,4905,4909,4913,4917,4921,4925,4929,4932],{"id":26,"text":4218,"url":26,"identifiers":4219},"Brown, 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10.1126\u002Fscience.281.5381.1312",{"doi":4288},"10.1126\u002Fscience.281.5381.1312",{"id":26,"text":4290,"url":26,"identifiers":4291},"Lindsten, 2000, The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues, Mol Cell, 6, 1389, 10.1016\u002FS1097-2765(00)00136-2",{"doi":4292},"10.1016\u002FS1097-2765(00)00136-2",{"id":26,"text":4294,"url":26,"identifiers":4295},"Wei, 2001, Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death, Science, 292, 727, 10.1126\u002Fscience.1059108",{"doi":4296},"10.1126\u002Fscience.1059108",{"id":26,"text":4298,"url":26,"identifiers":4299},"Suzuki, 2000, Structure of Bax: coregulation of dimer formation and intracellular localization, Cell, 103, 645, 10.1016\u002FS0092-8674(00)00167-7",{"doi":4300},"10.1016\u002FS0092-8674(00)00167-7",{"id":26,"text":4302,"url":26,"identifiers":4303},"Scorrano, 2003, BAX and BAK regulation of endoplasmic reticulum Ca2+: a 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10.1126\u002Fscience.1096645",{"doi":4935},"10.1126\u002Fscience.1096645",{"id":4937,"createTime":4938,"updateTime":4938,"relativeEntities":4939,"slug":4940,"properties":4941,"entityType":826,"verifyStatus":25,"verifyTime":4955,"verifyNote":827,"syncStatus":28,"languages":4956,"translateLanguages":26,"viewCount":36,"primaryUrl":4957,"fullTextUrl":26,"authors":4958,"publicationType":902,"publisherRelationship":5013,"citationCount":5050,"citationInfo":5051,"publishDate":5053,"publishYear":5054,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":5055,"isForceReanalyzing":1073},"628ef31a-52db-4d03-a2dd-53a390e456d5","2024-09-27T20:49:42.494+00:00",[],"Expanding-Criteria-for-Resectability-of-Colorectal-Liver-Metastases",{"mag":4942,"keywords":4944,"openalex":4945,"abstract":4947,"title":4949,"pm":4951,"doi":4953},{"VOID":4943},"2158918006",{},{"VOID":4946},"W2158918006",{"EN":4948},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n               \u003Cjats:sec>\n                  \u003Cjats:title>Learning Objectives\u003C\u002Fjats:title>\n                  \u003Cjats:p>After completing this course, the reader will be able to: Identify the criteria for hepatic resection of colorectal metastases.Describe strategies for expanding the number of patients who may potentially benefit from hepatic resection.List the factors associated with poor prognosis following hepatic resection.\u003C\u002Fjats:p>\n                  \u003Cjats:p>CME Access and take the CME test online and receive 1 AMA PRA Category 1 Credit™ at CME.TheOncologist.com\u003C\u002Fjats:p>\n                  \u003Cjats:p>Surgical resection is the treatment of choice in patients with colorectal liver metastases, with 5-year survival rates reported in the range of 40%–58%. Over the past 10 years, there has been an impetus to expand the criteria for defining resectability for patients with colorectal metastases. In the past, such features as the number of metastases (three to four), the size of the tumor lesion, and a mandatory 1-cm margin of resection dictated who was “resectable.” More recently, the criteria for resectability have been expanded to include any patient in whom all disease can be removed with a negative margin and who has adequate hepatic volume\u002Freserve. Specifically, instead of resectability being defined by what is removed, decisions concerning resectability now center around what will remain after resection. Under this new paradigm, the number of patients with resectable disease can be expanded by increasing\u002Fpreserving hepatic reserve (e.g., portal vein embolization, two-stage hepatectomy), combining resection with ablation, and decreasing tumor size (preoperative chemotherapy). The criteria for resectability have also expanded to include patients with extrahepatic disease. Rather than being an absolute contraindication to surgery, patients with both intra- and extrahepatic disease should potentially be considered for resection based on strict selection criteria. The expansion of criteria for resectability of colorectal liver metastases requires a much more nuanced and sophisticated approach to the patient with advanced disease. A therapeutic approach that includes all aspects of multidisciplinary and multimodality care is required to select and treat this complex group of patients.\u003C\u002Fjats:p>\n               \u003C\u002Fjats:sec>",{"EN":4950},"Expanding Criteria for Resectability of Colorectal Liver Metastases",{"VOID":4952},"18245012",{"VOID":4954},"10.1634\u002Ftheoncologist.2007-0142","2024-09-27T20:49:42.493+00:00",[102],"https:\u002F\u002Facademic.oup.com\u002Foncolo\u002Farticle\u002F13\u002F1\u002F51\u002F6396574",[4959,4981,4996],{"id":4960,"sortIndex":115,"researcher":26,"roles":4961,"affiliations":4962,"properties":4974},"4a9b434f-a80d-455b-8941-c1781c5e8959",[],[4963],{"id":4964,"sortIndex":36,"affiliation":4965,"properties":26},"c3a0ef67-b5ab-4cab-8bf2-f1e106dad39c",{"id":4966,"createTime":4967,"updateTime":4968,"relativeEntities":4969,"slug":4970,"properties":4971,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"17decb26-4249-4703-86ca-9f82225da393","2023-12-18T02:17:15.372+00:00","2024-12-05T21:58:07.950+00:00",[],"Department-of-Surgery-Johns-Hopkins-University-School-of-Medicine-Baltimore-Maryland-USA",{"title":4972},{"VI":4973},"Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA",{"openalex":4975,"orcid":4977,"title":4979},{"VOID":4976},"A5075915892",{"VOID":4978},"https:\u002F\u002Forcid.org\u002F0000-0001-7360-7338",{"EN":4980},"Richard D. Schulick",{"id":4982,"sortIndex":114,"researcher":26,"roles":4983,"affiliations":4984,"properties":4991},"5b4883b8-d370-4181-933f-dbf60eb8f00a",[],[4985],{"id":4986,"sortIndex":36,"affiliation":4987,"properties":26},"5a3be8f8-d281-4bff-bbc3-e5163d551bed",{"id":4966,"createTime":4967,"updateTime":4968,"relativeEntities":4988,"slug":4970,"properties":4989,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":4990},{"VI":4973},{"openalex":4992,"title":4994},{"VOID":4993},"A5059338254",{"EN":4995},"Michael A. Choti",{"id":4997,"sortIndex":36,"researcher":26,"roles":4998,"affiliations":4999,"properties":5006},"80875399-0d4a-46c3-8ddd-8979dc8be8b5",[],[5000],{"id":5001,"sortIndex":36,"affiliation":5002,"properties":26},"bf76d8d4-931b-4265-b996-b6e10473c4b4",{"id":4966,"createTime":4967,"updateTime":4968,"relativeEntities":5003,"slug":4970,"properties":5004,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":5005},{"VI":4973},{"openalex":5007,"orcid":5009,"title":5011},{"VOID":5008},"A5058146274",{"VOID":5010},"https:\u002F\u002Forcid.org\u002F0000-0002-7994-9870",{"EN":5012},"Timothy M. 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I. 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