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Journal of Medicine and Pharmacy","Tạp chí Y Dược học Cần Thơ",{"EN":581,"VI":582},"\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">04\u002F10\u002F2015 Ministry of Information and Communications allowed Can Tho journal of medicine and pharmacy to operate (102 \u002FGP-BTTTT)\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">07\u002F16\u002F2015 Can Tho journal of medicine and pharmacy is internationally recognized: ISSN 2354-1210\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">In 2016, The journal has been included in the list of medical science journals by The State Council for professorship which is awarded a work score of 0-0.5 points for a published article.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Can Tho Journal of Medicine and Pharmacy welcome original works that haven’t been submitted or published in other medical journals. Posts must contain content related to one of the journal’s categories.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The content published\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The journal is divided into 3 categories:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Scientific research article: are valuable scientific works, which have been researched and accepted.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Overview of medicine, biology and pharmacy: serving the objective of continuing training in the fields of medicine, biology and pharmacy; to systematize classical and modern knowledge.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Update information on new knowledge about medicine, biology, pharmacy in the country and in the world.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Scope\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Publication and introduction of scientific research in the fields:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Medicine (internal medicine, surgery, pediatrics, obstetrics and gynecology, odonto-stomatology, laboratory, oncology, traditional medicine, nursing).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Biology (genetics, biotechnology).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Pharmacology (pharmaceutics, drug quality analysis-control, synthetic pharmaceutical chemistry, biochemistry, pharmacognosy, botany, clinical pharmacy).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- To enhance the quality of undergraduate, postgraduate education, scientifically researching and meet the necessary treatment in hospital.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Introducing the updated domestic and oversea information about science technology to promote scientific research and exchanging technology in local, other universities.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Exchanging pharmaceutical and medical information for social health developing in the Mekong Delta and Vietnam.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The object\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Postgraduate students, student of Can Tho University of Medicine and Pharmacy, scientists from schools, research institutes, hospitals, health centers, pharmaceutical companies of the Mekong Delta; 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. Danh sách bài báo theo số Tạp chí được in ấn và phát hành trong năm định kỳ được công bố chính thức trên website: https:\u002F\u002Ftapchi.ctump.edu.vn\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>",{"VOID":584},"wcQ1uqwAAAAJ","2023-05-30T08:17:21.868+00:00",[],[588],{"id":589,"createTime":20,"updateTime":20,"relativeEntities":590,"slug":20,"properties":591,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":601,"parentIds":602,"statistic":20},"6413896b-eca9-442b-a73f-182a58a0ce40",[],{"title":592,"address":595,"country":598,"abbreviation":599},{"EN":593,"VI":594},"Can Tho University of Medicine and Pharmacy","Trường Đại học Y Dược Cần Thơ",{"EN":596,"VI":597},"No 179, Nguyen Van Cu street, An Khanh ward, Ninh Kieu district, Can Tho city, Vietnam","Số 179, đường Nguyễn Văn Cừ, phường An Khánh, quận Ninh Kiều, thành phố Cần Thơ, Việt Nam",{"VOID":117},{"VOID":600},"ctump","http:\u002F\u002Fwww.ctump.edu.vn\u002F",[],[],"https:\u002F\u002Ftapchi.ctump.edu.vn\u002Findex.php\u002Fctump",{"impactFactor":21,"impactFactorByYear":606,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":608,"totalPublicationByYear":609,"totalCitation":614,"totalCitationByYear":615,"totalCitationPerPublication":204,"totalCitationPerPublicationByYear":617,"hindexLast5Year":142,"hindex":142},{"2022":607,"2023":207,"2024":202},0.01,1556,{"2020":144,"2021":610,"2022":611,"2023":612,"2024":613,"2025":218},57,306,801,358,161,{"2021":241,"2022":374,"2023":616},99,{"2021":618,"2022":412,"2023":200},0.23,{"impactFactor":20,"impactFactorByYear":20,"i10Index":100,"i10IndexLast5Year":100,"totalPublication":620,"totalPublicationByYear":621,"totalCitation":620,"totalCitationByYear":622,"totalCitationPerPublication":99,"totalCitationPerPublicationByYear":625,"hindexLast5Year":146,"hindex":146},476,{"0":299,"2019":100,"2021":234,"2022":553,"2023":545,"2024":451,"2025":146,"2026":145},{"2021":101,"2022":100,"2023":255,"2024":623,"2025":454,"2026":624},136,83,{"2021":201,"2022":607,"2023":626,"2024":222,"2025":627,"2026":628},0.62,25.43,13.83,{"id":630,"createTime":631,"updateTime":476,"relativeEntities":632,"slug":633,"properties":634,"entityType":18,"verifyStatus":127,"verifyTime":20,"verifyNote":20,"languages":646,"translateLanguages":20,"viewCount":228,"subjectFields":647,"manageAffiliations":648,"indexDatabases":649,"url":650,"thumbnailPath":651,"statistic":652,"gsStatistic":688,"type":104,"analyzePriority":20},"6984a56a-db70-403b-9cc4-4013e1ceaffa","2023-05-09T06:47:40.346+00:00",[],"T%E1%BA%A1p%20ch%C3%AD%20Nghi%C3%AAn%20c%E1%BB%A9u%20n%C6%B0%E1%BB%9Bc%20ngo%C3%A0i",{"country":635,"issn":636,"title":638,"introduce":641,"gsId":644},{"VOID":117},{"VOID":637},"25252445",{"EN":639,"VI":640},"VNU Journal of Foreign Studies","Tạp chí Nghiên cứu nước ngoài",{"EN":642,"VI":643},"{\"ops\":[{\"insert\":\"\\n\\nThe \\n\"},{\"attributes\":{\"italic\":true},\"insert\":\"VNU Journal of Science\"},{\"insert\":\"\\n was established in 1985 for the publication of national and international research papers in all fields of natural sciences and technology, social sciences and humanities. Since then, the journal has grown in quality, size and scope and now comprises a dozen of serials spanning academic research. 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The current study reports a phase 1 trial to determine the maximum tolerated dose (MTD) and safety of AnvirzelTM in patients with advanced, refractory solid tumors. Patients were randomized to receive this agent by intramuscular injection at doses of 0.1, 0.2, 0.4 ml\u002Fm2\u002Fday with subsequent patients receiving 0.8 or 1.2 ml\u002Fm2\u002Fday sequentially. Eighteen patients were enrolled and completed at least one treatment cycle of three weeks. Most patients developed mild injection site pain (78%). Other toxicities included fatigue, nausea, and dyspnea. Traditional dose limiting toxicity was not seen, but the MTD was defined by injection volume as 0.8 ml\u002Fm2\u002Fday. No objective anti-tumor responses were seen. Anvirzel™ can be safely administered at doses up to 1.2 ml\u002Fm2\u002Fday, with the amount administered intramuscularly limited by volume. The recommended phase II dose level is 0.8 ml\u002Fm2\u002Fday.",{"EN":967},"Phase 1 trial of Anvirzel™ in patients with refractory solid tumors",{"VOID":969},"Langford SD, Boor PJ (1996) Oleander toxicity: An examination of human and animal toxic exposures. Toxicology 109(1):1–13\nManna SK, Sah NK, Newman R, Cismerps A, Aggarwal BB (2000) Oleandrin suppresses activation of nuclear transcription of factor-B, activator protein-2 and c-Jun NH2-terminal kinase. Cancer Res 60:3838–3847\nAbe F, Yamaguchi T (1978) Digitoxigenin oleandroside and 5α-Adynerin in the leaves of Nerium odorum. Chem Pharm Bull 26:3023–3027\nAbe F, Yamaguchi T (1979) Oleasides-novel cardenolies with an unusual framework on Nerium. Chem Pharm Bull 27:1604–1610\nWang X, Plomley JB, Newman RA, Cisneros A (2000) LC(MS(MS analyses of an oleander extract for cancer treatment. Anal Chem 72(15):3547–3552\nSmith JA, Madden T, Vijjeswarapu M, Newman RA (2001) Inhibition of export of fibroblast growth factor-2 (FGF-2) from the prostate cancer cell lines PC3 and DU 145 by Anvirzel and its cardiac glycoside component, oleandrin. Biochem Pharmacol 62(4):469–472\nJortani SA, Helm RA, Valdes R (1996) Inhibition of Na,K-ATPase by oleandrin and oleandrigenin, and their detection by digoxin immunoassays. Clin Chem 42:1654–1658\nPathak S, Multani AS, Narayan S, Kumar V, Newman RA (2000) Anvirzel, an extract of Nerium oleander, induces cell death in human but not murine cancer cells. Anticancer Drugs 11(6):455–463\nMcConkey DJ, Lin Y, Nutt LK, Ozel HZ, Newman RA (2000) Cardiac glycosides stimulate Ca increases and apoptosis in androgen-independent, metastatic human prostate adenocarcinoma cells. Cancer Res 60(14):3807–3812\nWHO (1979) Handbook for Reporting Results for Cancer Therapy. WHO, Geneva\nGupta A, Joshi P, Jortani SA, Valdes R Jr, Thorkelsson T, Verjee Z, Shemie S (1997) A case of nondigitalis cardiac glycoside toxicity. 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Potentialexplanations of the limited clinical success rate are given andrecommendations for the design of future studies provided.",{"EN":1131},"Development of Multidrug-Resistance Convertors: Sense or Nonsense?",{"VOID":1133},"Juliano RL, Ling V: A surface glycoprotein modulating drug permeability in chinese hamster ovary cell mutants. Biochem Biophys Acta 455: 152–162, 1976\nSharom, FJ: The P-glycoprotein efflux pump: how does it transport drugs? J Membr Biol 160: 161–175, 1997\nGottesman, MM, Pastan I: Biochemistry of multidrug resistance mediated by the multidrug transporter. Annu Rev Biochem 62: 385–427, 1993\nTwentyman PR: Transport proteins in drug resistance: biology and approaches to circumvention. J Intern Med 242: 133–137, 1997\nGermann UA: P-glycoprotein-a mediator of multidrug resistance in tumour cells. Eur J Cancer 32A: 927–944, 1996\nHiggins CF, Gottesman MM: Is the multidrug transporter a flippase? 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J Clin Invest 97: 2517–2524, 1996",{"VOID":1135},"10.1023\u002FA:1006487003814","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FA:1006487003814",[1138,1153,1166,1179],{"id":1139,"sortIndex":21,"researcher":20,"roles":1140,"affiliations":1141,"properties":1150},"5bb32bd9-addb-4c16-9576-19d3471bba59",[980],[1142],{"id":1143,"sortIndex":21,"affiliation":1144,"properties":20},"9e918a1d-6896-49f3-85cc-5224f87c035e",{"id":1143,"createTime":20,"updateTime":20,"relativeEntities":1145,"slug":20,"properties":1146,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1149,"statistic":20},[],{"title":1147},{"VI":1148},"Department of Medical Oncology, Rotterdam Cancer Institute (Daniel den Hoed Kliniek) and University Hospital, Rotterdam, the Netherlands",[],{"title":1151},{"VI":1152},"Lia van 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                       Objectives Several targeted therapies are available for metastatic neuroendocrine tumours (NETs) but no predictive factor of response to these treatments has been identified yet. Our aim was to identify and evaluate clinical, biological, histological and functional markers of response to everolimus. Methods We retrospectively reviewed 53 patients with NETs treated with everolimus (68 % in clinical trials). Clinical, biological and histological data were analyzed. The functional marker p-p70S6K, a main effector of the mTOR pathway, was studied by immunohistochemistry in 43 cases. Prognostic factors of progression-free survival (PFS) were studied by Kaplan Meier analysis. Results All patients had metastatic and progressive disease before everolimus treatment. Objective response was 9 % and median PFS was 8.1 (4.7–11.5) months. Hypercholesterolemia (HR = 0.13, p \u003C 0.0001) was associated with longer PFS, whereas presence of bone metastases (HR = 3.1, p \u003C 0.001) and overexpression of p-p70S6K by tumor cells (HR = 2.5, p = 0.01) were associated with shorter PFS under everolimus at multivariate analysis. Conclusion Clinical markers are not useful to predict response to everolimus. However, occurrence of hypercholesterolemia under treatment may be an early marker of response. Prospective studies are required to confirm these results and to assess whether p-p70S6K immunostaining is a prognostic or predictive marker of no-response to everolimus.",{"EN":1261},"Prediction of response to everolimus in neuroendocrine tumors: evaluation of clinical, biological and histological factors",{"EN":1263},"",{"VOID":1265},"Yao JC, Hassan M, Phan A, et al. (2008) One hundred years after “carcinoid”: epidemiology of and prognostic factors for neuroendocrine tumors in 35, 825 cases in the United States. J Clin Oncol Off J Am Soc Clin Oncol 26:3063–3072\nPavel ME, Hainsworth JD, Baudin E, et al. (2011) Everolimus plus octreotide long-acting repeatable for the treatment of advanced neuroendocrine tumours associated with carcinoid syndrome (RADIANT-2): a randomised, placebo-controlled, phase 3 study. Lancet 378:2005–2012\nYao JC, Fazio N, Singh S et al. (2016) Everolimus for the treatment of advanced, non-functional neuroendocrine tumours of the lung or gastrointestinal tract (RADIANT-4): a randomised, placebo-controlled, phase 3 study. Lancet 387(10022):968–77. doi: 10.1016\u002FS0140-6736(15)00817-X.\nYao JC, Shah MH, Ito T, et al. (2011) Everolimus for advanced pancreatic neuroendocrine tumors. N Engl J Med 364:514–523\nGalanis E, Buckner JC, Maurer MJ, et al. (2005) Phase II trial of temsirolimus (CCI-779) in recurrent glioblastoma multiforme: a north central cancer treatment group study. J Clin Oncol Off J Am Soc Clin Oncol 23:5294–5304\nLee CK, Marschner IC, Simes RJ, et al. (2012) Increase in cholesterol predicts survival advantage in renal cell carcinoma patients treated with temsirolimus. Clin Cancer Res: An Official Journal of the American Association for Cancer Research 18:3188–3196\nRavaud A, Urva SR, Grosch K, et al. (2014) Relationship between everolimus exposure and safety and efficacy: meta-analysis of clinical trials in oncology. Eur J Cancer 50:486–495\nNeshat MS, Mellinghoff IK, Tran C, et al. (2001) Enhanced sensitivity of PTEN-deficient tumors to inhibition of FRAP\u002FmTOR. Proc Natl Acad Sci U S A 98:10314–10319\nJanku F, Wheler JJ, Westin SN, et al. (2012) PI3K\u002FAKT\u002FmTOR inhibitors in patients with breast and gynecologic malignancies harboring PIK3CA mutations. J Clin Oncol Off J Am Soc Clin Oncol 30:777–782\nIyer G, Hanrahan AJ, Milowsky MI, et al. (2012) Genome sequencing identifies a basis for everolimus sensitivity. Science 338:221\nBollard J, Couderc C, Blanc M, et al. (2013) Antitumor effect of everolimus in preclinical models of high-grade gastroenteropancreatic neuroendocrine carcinomas. Neuroendocrinology 97:331–340\nCho D, Signoretti S, Dabora S, et al. (2007) Potential histologic and molecular predictors of response to temsirolimus in patients with advanced renal cell carcinoma. Clin Genitourin Cancer 5:379–385\nDuran I, Kortmansky J, Singh D, et al. (2006) A phase II clinical and pharmacodynamic study of temsirolimus in advanced neuroendocrine carcinomas. Br J Cancer 95:1148–1154\nYoon DH, Ryu MH, Park YS, et al. (2012) Phase II study of everolimus with biomarker exploration in patients with advanced gastric cancer refractory to chemotherapy including fluoropyrimidine and platinum. Br J Cancer 106:1039–1044\nLombard-Bohas C, Cariou B, Verges B, et al. (2014) Management of metabolic disorders induced by everolimus in patients with differentiated neuroendocrine tumors: expert proposals. Bull Cancer 101:175–183\nVerges B, Walter T, Cariou B (2014) ENDOCRINE SIDE EFFECTS OF ANTI-CANCER DRUGS effects of anti-cancer targeted therapies on lipid and glucose metabolism. Eur J Endocrinol 170:R43–R55\nBilimoria KY, Talamonti MS, Tomlinson JS, et al. (2008) Prognostic score predicting survival after resection of pancreatic neuroendocrine tumors: analysis of 3851 patients. Ann Surg 247:490–500\nKhan MS, Kirkwood A, Tsigani T, et al. (2013) Circulating tumor cells as prognostic markers in neuroendocrine tumors. J Clin Oncol Off J Am Soc Clin Oncol 31:365–372\nCapurso G, Archibugi L, Delle Fave G (2015) Molecular pathogenesis and targeted therapy of sporadic pancreatic neuroendocrine tumors. J Hepatobiliary Pancreat Sci 22(8):594–601. doi:10.1002\u002Fjhbp.210.\nMissiaglia E, Dalai I, Barbi S, et al. (2009) Pancreatic endocrine tumors: expression profiling evidences a role for AKT-mTOR pathway. J Clin Oncol Off J Am Soc Clin Oncol 28:245–255\nQian ZR, Ter-Minassian M, Chan JA, et al. (2013) Prognostic significance of MTOR pathway component expression in neuroendocrine tumors. J Clin Oncol Off J Am Soc Clin Oncol 31:3418–3425\nSharpe LJ, Brown AJ (2008) Rapamycin down-regulates LDL-receptor expression independently of SREBP-2. Biochem Biophys Res Commun 373:670–674\nCustodio AJ-FP, Alonso-Orduña V, López López C, Alonso T, Guillermo C, Carmona-Bayonas A, Álvarez-Escolá CSM, Capdevila J, Grande E, Barriuso J, Feliu J, Aller J (2015) Everolimus (EVE)-induced hyperglycemia (HG) in patients (pts) with advanced G1-G2 neuroendocrine tumors (NETs): clinical relevance and predictive value. ENETS - The European Neuroendocrine Tumor Society. Barcelona, In\nRugo HS, Hortobagyi GN, Yao J, Pavel M, Ravaud A, Franz D, Ringeisen F, Gallo J, Rouyrre N, Anak O, Motzer R (2016) Meta-analysis of stomatitis in clinical studies of everolimus: incidence and relationship with efficacy. Ann Oncol 27(3):519–525. doi:10.1093\u002Fannonc\u002Fmdv595.\nTempleton AJ, Dutoit V, Cathomas R, et al. 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The clinical benefit from ipilimumab can be hampered by the immure-related adverse events (irAEs) caused by dysregulation of host immune system. Ipilimumab associated hepatitis is also an important irAE, however, there have been limited descriptions of its clinicopathologic and imaging characteristics. We aim to describe the clinicopathologic and imaging characteristics of 6 patients who were diagnosed as ipilimumab associated hepatitis during the ipilimumab treatment for melanoma. The clinical features of these patients were as follows: (1) severe cases with systemic symptoms and highly increased level of liver function tests (LFTs), and (2) mild asymptomatic cases with mildly increased level of LFTs. In severe cases with ALT &gt;1,000&nbsp;IU\u002FL, imaging findings were characterized by mild hepatomegaly, periportal edema, and periportal lymphadenopathy, while mild cases showed normal imaging findings. This spectrum of imaging findings in our series was similar to that of common causes of acute hepatitis. Among 3 cases with pathologic specimen, two cases showed severe panlobular hepatitis with prominent perivenular infiltrate with endothelialitis, suggestive of predominant injury to hepatocytes, while the other case showed mild portal mononuclear infiltrate around proliferated bile ductules, suggestive of predominant injury to bile ducts. In summary, ipilimumab associated hepatitis may demonstrate variable imaging findings according to its clinical severity, and histologically may manifest either as a predominant injury to hepatocytes (acute hepatitis pattern) or as a predominant injury to bile ducts (biliary pattern).",{"EN":1677},"Ipilimumab associated hepatitis: imaging and clinicopathologic findings",{"VOID":1679},"citation_journal_title=N Engl J Med; citation_title=Improved survival with ipilimumab in patients with metastatic melanoma; citation_author=FS Hodi, SJ O’Day, DF McDermott; citation_volume=363; citation_issue=8; citation_publication_date=2010; citation_pages=711-723; citation_doi=10.1056\u002FNEJMoa1003466; citation_id=CR1\ncitation_journal_title=Semin Oncol; citation_title=Development of ipilimumab: contribution to a new paradigm for cancer immunotherapy; citation_author=A Hoos, R Ibrahim, A Korman; citation_volume=37; citation_issue=5; citation_publication_date=2010; citation_pages=533-546; citation_doi=10.1053\u002Fj.seminoncol.2010.09.015; citation_id=CR2\ncitation_journal_title=AJR Am J Roentgenol; citation_title=Radiologic aspects of immune-related tumor response criteria and patterns of immune-related adverse events in patients undergoing ipilimumab therapy; citation_author=KN O’Regan, JP Jagannathan, N Ramaiya, FS Hodi; citation_volume=197; citation_issue=2; citation_publication_date=2011; citation_pages=W241-W246; citation_doi=10.2214\u002FAJR.10.6032; citation_id=CR3\nWeber JS, Kahler KC, Hauschild A (2012) Management of immune-related adverse events and kinetics of response with ipilimumab. J Clin Oncol. doi:\n                    10.1200\u002FJCO.2012.41.6750\n                    \n                  \n                \ncitation_journal_title=Semin Oncol; citation_title=The emerging toxicity profiles of anti-CTLA-4 antibodies across clinical indications; citation_author=AM Giacomo, M Biagioli, M Maio; citation_volume=37; citation_issue=5; citation_publication_date=2010; citation_pages=499-507; citation_doi=10.1053\u002Fj.seminoncol.2010.09.007; citation_id=CR5\ncitation_journal_title=Clin Nucl Med; citation_title=Ipilimumab-induced colitis on FDG PET\u002FCT; citation_author=A Lyall, HA Vargas, RD Carvajal, G Ulaner; citation_volume=37; citation_issue=6; citation_publication_date=2012; citation_pages=629-630; citation_doi=10.1097\u002FRLU.0b013e318248549a; citation_id=CR6\ncitation_journal_title=AJR Am J Roentgenol; citation_title=Radiologic manifestations of immune-related adverse events in patients with metastatic melanoma undergoing anti-CTLA-4 antibody therapy; citation_author=Y Bronstein, CS Ng, P Hwu, WJ Hwu; citation_volume=197; citation_issue=6; citation_publication_date=2011; citation_pages=W992-W1000; citation_doi=10.2214\u002FAJR.10.6198; citation_id=CR7\ncitation_journal_title=Radiographics; citation_title=The infected liver: radiologic-pathologic correlation; citation_author=KJ Mortele, E Segatto, PR Ros; citation_volume=24; citation_issue=4; citation_publication_date=2004; citation_pages=937-955; citation_doi=10.1148\u002Frg.244035719; citation_id=CR8\ncitation_journal_title=Dig Dis Sci; citation_title=Pathologic changes in ipilimumab-related hepatitis in patients with metastatic melanoma; citation_author=DE Kleiner, D Berman; citation_volume=57; citation_issue=8; citation_publication_date=2012; citation_pages=2233-2240; citation_doi=10.1007\u002Fs10620-012-2140-5; citation_id=CR9\ncitation_journal_title=Proc Natl Acad Sci U S A; citation_title=Cancer regression and autoimmunity induced by cytotoxic T lymphocyte-associated antigen 4 blockade in patients with metastatic melanoma; citation_author=GQ Phan, JC Yang, RM Sherry; citation_volume=100; citation_issue=14; citation_publication_date=2003; citation_pages=8372-8377; citation_doi=10.1073\u002Fpnas.1533209100; citation_id=CR10\ncitation_journal_title=Ann Oncol; citation_title=Efficacy and safety of ipilimumab monotherapy in patients with pretreated advanced melanoma: a multicenter single-arm phase II study; citation_author=SJ O’Day, M Maio, V Chiarion-Sileni; citation_volume=21; citation_issue=8; citation_publication_date=2010; citation_pages=1712-1717; citation_doi=10.1093\u002Fannonc\u002Fmdq013; citation_id=CR11\ncitation_journal_title=J Clin Oncol; citation_title=Resolution of severe ipilimumab-induced hepatitis after antithymocyte globulin therapy; citation_author=KD Chmiel, D Suan, C Liddle; citation_volume=29; citation_issue=9; citation_publication_date=2011; citation_pages=e237-e240; citation_doi=10.1200\u002FJCO.2010.32.2206; citation_id=CR12\ncitation_journal_title=Immunol Rev; citation_title=Twelve immunotherapy drugs that could cure cancers; citation_author=MA Cheever; citation_volume=222; citation_publication_date=2008; citation_pages=357-368; citation_doi=10.1111\u002Fj.1600-065X.2008.00604.x; 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USA",[],{"id":1698,"sortIndex":99,"affiliation":1699,"properties":1705},"3b43e3b0-6f8f-4e2f-9dd6-3c644f22e300",{"id":1698,"createTime":20,"updateTime":20,"relativeEntities":1700,"slug":20,"properties":1701,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1704,"statistic":20},[],{"title":1702},{"VI":1703},"Department of Radiology and Research Institute of Radiology, University of Ulsan College of Medicine, Seoul Asan Medical Center, Seoul, Korea",[],{},{"title":1707},{"VI":1708},"Kim, Kyung 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the clear progress achieved in recent years in the treatment of MM, most patients eventually relapse and therefore novel therapeutic options are still necessary for these patients. In this regard, several drugs that target specific mechanisms of the tumor cells are currently being explored in the preclinical and clinical setting. This manuscripts offers a review of the rationale and current status of the antimyeloma activity of one of the most relevant examples of these targeted drugs: deacetylase inhibitors (DACi). Several studies have demonstrated the prooncogenic activity of deacetylases (DACs) through the targeting not only of histones but also of non histone proteins relevant to tumor progression, such as p53, E2F family members, Bcl-6, Hsp90, HIF-1α or Nur77. This fact together with the DACs overexpression present in several tumors, has prompted the development of some DACi with potential antitumor effect. This situation is also evident in the case of MM as two mechanisms of DACi, the inhibition of the epigenetic inactivation of p53 and the blockade of the unfolded protein response, through the inhibition of the aggressome formation (by targeting DAC6) and the inactivation of the chaperone system (by acetylating HSP-90), provides the rationale for the exploration of the potential antimyeloma activity of these compounds. Several DACi with different chemical structure and different selectivity for targeting the DAC families have been tested in MM. Their preclinical activity in monotherapy has been quite exciting and has been described to be mediated by various mechanisms: the induction of apoptosis and cell cycle arrest mainly by the upregulation of p21; the interferece with the interaction between plasma cells and the microenvironment, by reducing the expression and signalling of several cytokines or by inhibiting angiogenesis. Finally they also have a role in protecting murine models from myeloma bone disease. Neverteless, the clinical activity in monotherapy of these drugs in relapsed\u002Frefractory MM patients has been very modest. This has prompted the development of combinations such as the one with bortezomib or lenalidomide and dexamethasone, which have already been taken into the clinics with positive preliminary results.",{"EN":1865},"The DAC system and associations with multiple myeloma",{"VOID":1867},"Kyle RA, Rajkumar SV (2004) Multiple myeloma. N Engl J Med 351:1860–1873\nPetrelli NJ, Winer EP, Brahmer J et al (2009) Clinical Cancer Advances 2009: major research advances in cancer treatment, prevention, and screening–a report from the American Society of Clinical Oncology. J Clin Oncol 27:6052–6069\nKyle RA, Rajkumar SV (2008) Multiple myeloma. Blood 111:2962–2972\nKumar SK, Rajkumar SV, Dispenzieri A et al (2008) Improved survival in multiple myeloma and the impact of novel therapies. Blood 111:2516–2520\nRichardson PG, Sonneveld P, Schuster MW et al (2005) Bortezomib or high-dose dexamethasone for relapsed multiple myeloma. N Engl J Med 352:2487–2498\nSinghal S, Mehta J, Desikan R et al (1999) Antitumor activity of thalidomide in refractory multiple myeloma. N Engl J Med 341:1565–1571\nDimopoulos M, Spencer A, Attal M et al (2007) Lenalidomide plus dexamethasone for relapsed or refractory multiple myeloma. N Engl J Med 357:2123–2132\nWeber DM, Chen C, Niesvizky R et al (2007) Lenalidomide plus dexamethasone for relapsed multiple myeloma in North America. N Engl J Med 357:2133–2142\nOcio EM, Mateos MV, Maiso P, Pandiella A, San-Miguel JF (2008) New drugs in multiple myeloma: mechanisms of action and phase I\u002FII clinical findings. Lancet Oncol 9:1157–1165\nMitsiades CS, Hideshima T, Chauhan D et al (2009) Emerging treatments for multiple myeloma: beyond immunomodulatory drugs and bortezomib. Semin Hematol 46:166–175\nGregoretti IV, Lee YM, Goodson HV (2004) Molecular evolution of the histone deacetylase family: functional implications of phylogenetic analysis. J Mol Biol 338:17–31\nDokmanovic M, Clarke C, Marks PA (2007) Histone deacetylase inhibitors: overview and perspectives. Mol Cancer Res 5:981–989\nde Ruijter AJ, van Gennip AH, Caron HN, Kemp S, van Kuilenburg AB (2003) Histone deacetylases (HDACs): characterization of the classical HDAC family. Biochem J 370:737–749\nWitt O, Deubzer HE, Milde T, Oehme I (2009) HDAC family: What are the cancer relevant targets? Cancer Lett 277:8–21\nBolden JE, Peart MJ, Johnstone RW (2006) Anticancer activities of histone deacetylase inhibitors. Nat Rev Drug Discov 5:769–784\nMinucci S, Pelicci PG (2006) Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer. Nat Rev Cancer 6:38–51\nXu WS, Parmigiani RB, Marks PA (2007) Histone deacetylase inhibitors: molecular mechanisms of action. 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Blood 113:3781–3791\nHurt EM, Thomas SB, Peng B, Farrar WL (2006) Reversal of p53 epigenetic silencing in multiple myeloma permits apoptosis by a p53 activator. Cancer Biol Ther 5:1154–1160\nDavenport EL, Moore HE, Dunlop AS et al (2007) Heat shock protein inhibition is associated with activation of the unfolded protein response pathway in myeloma plasma cells. Blood 110:2641–2649\nDavenport EL, Morgan GJ, Davies FE (2008) Untangling the unfolded protein response. Cell Cycle 7:865–869\nBennett EJ, Bence NF, Jayakumar R, Kopito RR (2005) Global impairment of the ubiquitin-proteasome system by nuclear or cytoplasmic protein aggregates precedes inclusion body formation. Mol Cell 17:351–365\nKopito RR (2000) Aggresomes, inclusion bodies and protein aggregation. Trends Cell Biol 10:524–530\nKawaguchi Y, Kovacs JJ, McLaurin A, Vance JM, Ito A, Yao TP (2003) The deacetylase HDAC6 regulates aggresome formation and cell viability in response to misfolded protein stress. 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Proc Natl Acad Sci USA 101:540–545\nLavelle D, Chen YH, Hankewych M, DeSimone J (2001) Histone deacetylase inhibitors increase p21(WAF1) and induce apoptosis of human myeloma cell lines independent of decreased IL-6 receptor expression. Am J Hematol 68:170–178\nCatley L, Weisberg E, Tai YT et al (2003) NVP-LAQ824 is a potent novel histone deacetylase inhibitor with significant activity against multiple myeloma. Blood 102:2615–2622\nKhan SB, Maududi T, Barton K, Ayers J, Alkan S (2004) Analysis of histone deacetylase inhibitor, depsipeptide (FR901228), effect on multiple myeloma. Br J Haematol 125:156–161\nKaiser M, Zavrski I, Sterz J et al (2006) The effects of the histone deacetylase inhibitor valproic acid on cell cycle, growth suppression and apoptosis in multiple myeloma. Haematologica 91:248–251\nSchwartz C, Palissot V, Aouali N et al (2007) Valproic acid induces non-apoptotic cell death mechanisms in multiple myeloma cell lines. Int J Oncol 30:573–582\nKitazoe K, Abe M, Hiasa M et al (2009) Valproic acid exerts anti-tumor as well as anti-angiogenic effects on myeloma. Int J Hematol 89:45–57\nNeri P, Tagliaferri P, Di Martino MT et al (2008) In vivo anti-myeloma activity and modulation of gene expression profile induced by valproic acid, a histone deacetylase inhibitor. Br J Haematol 143:520–531\nCatley L, Weisberg E, Kiziltepe T et al (2006) Aggresome induction by proteasome inhibitor bortezomib and alpha-tubulin hyperacetylation by tubulin deacetylase (TDAC) inhibitor LBH589 are synergistic in myeloma cells. Blood 108:3441–3449\nMaiso P, Carvajal-Vergara X, Ocio EM et al (2006) The histone deacetylase inhibitor LBH589 is a potent antimyeloma agent that overcomes drug resistance. Cancer Res 66:5781–5789\nOcio EM, Vilanova D, Atadja P et al (2009) In vitro and in vivo rationale for the triple combination of panobinostat (LBH589) and dexamethasone with either bortezomib or lenalidomide in multiple myeloma. Haematologica\nFeng R, Oton A, Mapara MY, Anderson G, Belani C, Lentzsch S (2007) The histone deacetylase inhibitor, PXD101, potentiates bortezomib-induced anti-multiple myeloma effect by induction of oxidative stress and DNA damage. Br J Haematol 139:385–397\nArts J, Angibaud P, Marien A et al (2007) R306465 is a novel potent inhibitor of class I histone deacetylases with broad-spectrum antitumoral activity against solid and haematological malignancies. Br J Cancer 97:1344–1353\nFeng R, Ma H, Hassig CA et al (2008) KD5170, a novel mercaptoketone-based histone deacetylase inhibitor, exerts antimyeloma effects by DNA damage and mitochondrial signaling. Mol Cancer Ther 7:1494–1505\nDeleu S, Lemaire M, Arts J et al (2009) The effects of JNJ-26481585, a novel hydroxamate-based histone deacetylase inhibitor, on the development of multiple myeloma in the 5T2MM and 5T33MM murine models. Leukemia 23:1894–1903\nTodoerti K, Barbui V, Pedrini O et al Pleiotropic anti-myeloma activity of ITF2357: inhibition of interleukin-6 receptor signaling and repression of miR-19a and miR-19b. Haematologica 95:260–269\nMandl-Weber S, Meinel F, Jankowsky R, Oduncu F, Schmidmaier R, Baumann P The novel inhibitor of histone deacetylase resminostat (RAS2410) inhibits proliferation and induces apoptosis in multiple myeloma (MM) cells. Br J Haematol\nFandy TE, Shankar S, Ross DD, Sausville E, Srivastava RK (2005) Interactive effects of HDAC inhibitors and TRAIL on apoptosis are associated with changes in mitochondrial functions and expressions of cell cycle regulatory genes in multiple myeloma. Neoplasia 7:646–657\nAkiyama M, Hideshima T, Hayashi T et al (2002) Cytokines modulate telomerase activity in a human multiple myeloma cell line. Cancer Res 62:3876–3882\nChen S, Dai Y, Pei XY, Grant S (2009) Bim upregulation by histone deacetylase inhibitors mediates interactions with the Bcl-2 antagonist ABT-737: evidence for distinct roles for Bcl-2, Bcl-xL, and Mcl-1. Mol Cell Biol 29:6149–6169\nDamiano JS, Cress AE, Hazlehurst LA, Shtil AA, Dalton WS (1999) Cell adhesion mediated drug resistance (CAM-DR): role of integrins and resistance to apoptosis in human myeloma cell lines. Blood 93:1658–1667\nHideshima T, Mitsiades C, Tonon G, Richardson PG, Anderson KC (2007) Understanding multiple myeloma pathogenesis in the bone marrow to identify new therapeutic targets. Nat Rev Cancer 7:585–598\nWolf JL, Siegel D, Matous J et al (2008) A Phase II Study of Oral Panobinostat (LBH589) in Adult Patients with Advanced Refractory Multiple Myeloma. ASH Annu Meet Abstr 112:2774\nRichardson P, Mitsiades C, Colson K et al (2008) Phase I trial of oral vorinostat (suberoylanilide hydroxamic acid, SAHA) in patients with advanced multiple myeloma. Leuk Lymphoma 49:502–507\nGalli M, Salmoiraghi S, Golay J et al A phase II multiple dose clinical trial of histone deacetylase inhibitor ITF2357 in patients with relapsed or progressive multiple myeloma. Ann Hematol 89:185–190\nNiesvizky R, Ely S, DiLiberto M et al (2005) Multicenter Phase II Trial of the Histone Deacetylase Inhibitor Depsipeptide (FK228) for the Treatment of Relapsed or Refractory Multiple Myeloma (MM). ASH Annu Meet Abstr 106:2574-\nCampbell RA, Sanchez E, Steinberg J et al Vorinostat enhances the antimyeloma effects of melphalan and bortezomib. Eur J Haematol 84:201–211\nDeleu S, Lemaire M, Arts J et al (2009) Bortezomib alone or in combination with the histone deacetylase inhibitor JNJ-26481585: effect on myeloma bone disease in the 5T2MM murine model of myeloma. Cancer Res 69:5307–5311\nHideshima T, Bradner JE, Wong J et al (2005) Small-molecule inhibition of proteasome and aggresome function induces synergistic antitumor activity in multiple myeloma. Proc Natl Acad Sci USA 102:8567–8572\nPei XY, Dai Y, Grant S (2004) Synergistic induction of oxidative injury and apoptosis in human multiple myeloma cells by the proteasome inhibitor bortezomib and histone deacetylase inhibitors. Clin Cancer Res 10:3839–3852\nBadros A, Burger AM, Philip S et al (2009) Phase I study of vorinostat in combination with bortezomib for relapsed and refractory multiple myeloma. Clin Cancer Res 15:5250–5257\nWeber D, Badros AZ, Jagannath S et al (2008) Vorinostat plus bortezomib for the treatment of relapsed\u002Frefractory multiple myeloma: early clinical experience. ASH Annu Meet Abstr 112:871\nWeber DM, Jagannath S, Sobecks R et al (2008) Combination of vorinostat plus bortezomib for the treatment of patients with multiple myeloma who have previously received bortezomib. ASH Annu Meet Abstr 112:3711\nSan-Miguel JF, Sezer O, Siegel D et al (2009) A phase IB, multi-center, open-label dose-escalation study of oral panobinostat (LBH589) and I.V. Bortezomib in patients with relapsed multiple myeloma. ASH Annu Meet Abstr 114:3852-\nHarrison SJ, Quach H, Yuen K et al (2008) High response rates with the combination of bortezomib, dexamethasone and the pan-histone deacetylase inhibitor romidepsin in patients with relapsed or refractory multiple myeloma in a phase I\u002FII clinical trial. ASH Annu Meet Abstr 112:3698\nVoorhees PM, Gasparetto C, Richards KL et al (2009) Vorinostat in combination with pegylated liposomal doxorubicin and bortezomib for patients with relapsed\u002Frefractory multiple myeloma: results of a phase I study. ASH Annu Meet Abstr 114:306-\nSpencer A, Lonial S, Taylor K et al (2009) Panobinostat and lenalidomide combination phase I trial in myeloma. Clin Lymphoma Myeloma. Abstract 329\nSiegel D, Weber DM, Mitsiades CS et al (2009) Combined vorinostat, lenalidomide and dexamethasone therapy in patients with relapsed or refractory multiple myeloma: a phase I study. ASH Annu Meet Abstr 114:305-\nBerenson JR, Yellin O, Boccia RV, Nassir Y, Rothstein S, Swift RA (2009) A phase I study of oral melphalan combined with LBH589 for patients with relapsed or refractory multiple myeloma (MM). ASH Annu Meet Abstr 114:1855-",{"VOID":1869},"10.1007\u002Fs10637-010-9589-x","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10637-010-9589-x",[1872,1896],{"id":1873,"sortIndex":21,"researcher":20,"roles":1874,"affiliations":1875,"properties":1893},"ec766b5f-a51c-4c89-a354-c254cf32df48",[980],[1876,1884],{"id":1877,"sortIndex":21,"affiliation":1878,"properties":20},"82346293-bfa9-4c32-a7fd-60bbdcc875c8",{"id":1877,"createTime":20,"updateTime":20,"relativeEntities":1879,"slug":20,"properties":1880,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1883,"statistic":20},[],{"title":1881},{"VI":1882},"University Hospital of Salamanca, Salamanca, Spain",[],{"id":1885,"sortIndex":99,"affiliation":1886,"properties":1892},"1758167b-478c-4a19-a854-34e6795aefab",{"id":1885,"createTime":20,"updateTime":20,"relativeEntities":1887,"slug":20,"properties":1888,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1891,"statistic":20},[],{"title":1889},{"VI":1890},"IBMCC-CSIC (Institute of Molecular and Cellular Biology of Cancer-Spanish National Research Council) Cancer Research Center, University of Salamanca, Salamanca, Spain",[],{},{"title":1894},{"VI":1895},"Enrique M. Ocio",{"id":1897,"sortIndex":99,"researcher":20,"roles":1898,"affiliations":1899,"properties":1913},"22e5cdbb-2cef-4c2e-9496-acf647fd5c4e",[980],[1900,1906],{"id":1877,"sortIndex":21,"affiliation":1901,"properties":20},{"id":1877,"createTime":20,"updateTime":20,"relativeEntities":1902,"slug":20,"properties":1903,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1905,"statistic":20},[],{"title":1904},{"VI":1882},[],{"id":1885,"sortIndex":99,"affiliation":1907,"properties":1912},{"id":1885,"createTime":20,"updateTime":20,"relativeEntities":1908,"slug":20,"properties":1909,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1911,"statistic":20},[],{"title":1910},{"VI":1890},[],{},{"title":1914},{"VI":1915},"Jesús F. San Miguel",{"url":1870,"publisher":1917,"properties":1967},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1918,"slug":10,"properties":1919,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1923,"manageAffiliations":1936,"indexDatabases":1947,"url":94,"thumbnailPath":20,"statistic":1962,"gsStatistic":20,"type":104,"analyzePriority":20},[],{"issn":1920,"title":1921,"eissn":1922},{"VOID":13},{"EN":15},{"VOID":17},[1924,1928,1932],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1925,"label":1926,"description":1927,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":1929,"label":1930,"description":1931,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":33},{},{"id":36,"createTime":20,"updateTime":20,"relativeEntities":1933,"label":1934,"description":1935,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":39},{},[1937,1942],{"id":43,"createTime":20,"updateTime":20,"relativeEntities":1938,"slug":20,"properties":1939,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1941,"statistic":20},[],{"title":1940},{"EN":47},[],{"id":50,"createTime":20,"updateTime":20,"relativeEntities":1943,"slug":20,"properties":1944,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1946,"statistic":20},[],{"title":1945},{"EN":54},[],[1948,1955],{"id":58,"indexDatabase":1949,"url":71,"indexYears":20,"academicFieldIds":1954,"indexDatabaseRanking":20},{"id":60,"createTime":20,"updateTime":20,"relativeEntities":1950,"label":1951,"description":1952,"key":67,"publicationTags":1953,"standard":20},[],{"EN":63,"VI":63},{"EN":65,"VI":66},[69,70],[73,74],{"id":76,"indexDatabase":1956,"url":87,"indexYears":88,"academicFieldIds":1961,"indexDatabaseRanking":93},{"id":78,"createTime":20,"updateTime":20,"relativeEntities":1957,"label":1958,"description":1959,"key":84,"publicationTags":1960,"standard":20},[],{"EN":81,"VI":81},{"EN":81,"VI":83},[86],[90,91,92],{"impactFactor":21,"impactFactorByYear":1963,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":97,"totalPublicationByYear":1964,"totalCitation":21,"totalCitationByYear":1965,"totalCitationPerPublication":21,"totalCitationPerPublicationByYear":1966,"hindexLast5Year":21,"hindex":21},{},{"1986":99,"1991":99,"1992":99,"1996":99,"1997":99,"1998":99,"2003":99,"2005":100,"2006":99,"2007":100,"2008":101,"2009":101,"2010":99,"2011":99,"2012":99,"2013":100,"2017":99,"2018":99,"2019":99,"2020":99,"2021":99,"2022":99,"2023":100},{},{},{"pages":1968,"volume":1970},{"VOID":1969},"28-35",{"VOID":1971},"28","2010-12-01",2010,[69,93],{"id":1976,"createTime":1977,"updateTime":1978,"relativeEntities":1979,"slug":1980,"properties":1981,"entityType":972,"verifyStatus":127,"verifyTime":1978,"verifyNote":974,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1990,"fullTextUrl":20,"authors":1991,"publicationType":1060,"publisherRelationship":2245,"citationCount":20,"citationInfo":20,"publishDate":2301,"publishYear":1498,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":2302,"openAccess":20,"references":20,"isForceReanalyzing":1120},"01c08901-105d-4d19-a9cb-9bcd39a59f40","2023-12-06T12:02:54.698+00:00","2025-02-08T00:18:55.726+00:00",[],"An-open-label-single-arm-phase-2-study-of-the-Aurora-kinase-A-inhibitor-alisertib-in-patients-with-advanced-urothelial-cancer",{"abstract":1982,"title":1984,"references":1986,"doi":1988},{"EN":1983},"\n                        Background Progress in developing effective salvage therapies for UC is warranted. Alisertib is an orally available, selective inhibitor of the aurora kinase A. Methods A single-group, phase 2 trial was conducted with alisertib 50 mg orally BID for 7 days, with 14d rest until disease progression (PD) (NCT02109328). The primary endpoint (EP) was RECIST 1.1 objective response-rate (ORR, H0 ≤ 5 %, H1 ≥ 20 %, α = 10 % and β = 20 %). Eligibility included failure of at least one platinum-based regimen. Results From 10\u002F2014 to 04\u002F2015, 22 patients were enrolled (20 evaluable for response), 8 (36.4 %) in second-line and 14 (63.6 %) beyond the second-line. Eight (36.4 %) had an ECOG-performance status 1–2. Two partial responses (PR, ORR: 9.1 %), 7 stable disease (SD) and 11 PD were obtained. Median follow-up was 8.3 months (IQR: 7–10.3), 6-month progression-free survival (PFS) was 13.6 % (95%CI: 4.8–39.0). Two SD are still receiving treatment after 11.5 and 6.3 months. Median overall survival (OS) was not reached (6-month OS: 59.1 %, 95%CI: 41.7–83.7). Hb \u003C 10 g\u002Fdl was significantly associated with shorter PFS and OS multivariably (p = 0.031 and p = 0.033). Tissue of the case with 11.5 month SD harbored a missense mutation of mTOR (E1813D), the nonsense mutation Q527STOP of TSC1, HER3 and TAF1L missense mutations. Grade 3–4 adverse events (AE) were: 40.9 % mucositis, 36.4 % fatigue, 18.2 % neutropenia (13.6 % febrile neutropenia). There were 2 treatment-related deaths. Conclusions The study did not meet the primary EP, yet sustained disease control was obtained in about 14 % of patients. The incidence of AE and the issue of patient selection are two major concerns.",{"EN":1985},"An open-label, single-arm, phase 2 study of the Aurora kinase A inhibitor alisertib in patients with advanced urothelial cancer",{"VOID":1987},"Powles T, Eder JP, Fine GD, et al. (2014) MPDL3280A (anti-PD-L1) treatment leads to clinical activity in metastatic bladder cancer. Nature 515:558–562\nPlimack ER, Bellmunt J, Gupta S, et al. (2015) Pembrolizumab (MK-3475) for advanced urothelial cancer: updated results and biomarker analysis from KEYNOTE-012. J Clin Oncol 33 (suppl; abstr 4502).\nPetrylak DP, Powles T, Bellmunt J, et al. (2015) A phase Is study of MPDL3280A (anti-PDL1): updated response and survival data in urothelial bladder cancer (UBC). J Clin Oncol 33 (suppl; abstr 4501).\nRosenberg J, Petrylak D, Abidoye O, et al. (2015) (21LBA) Atezolizumab in patients (pts) with locally-advanced or metastatic urothelial carcinoma (mUC): results from a pivotal multicenter phase II study (IMvigor 210). Eur J Cancer 51(Supplement 3):S720\nSonpavde G, Jones BS, Bellmunt J, et al. (2015) Future directions and targeted therapies in bladder cancer. Hematol Oncol Clin North Am 29:361–376\nRaggi D, Miceli R, Sonpavde G, et al. (2015) Second-line single-agent versus doublet chemotherapy as salvage therapy for metastatic urothelial cancer: a systematic review and meta-analysis. Ann Oncol. doi:10.1093\u002Fannonc\u002Fmdv509\nSonpavde G, Pond GR, Choueiri TK, et al. (2015) Single agent taxane versus taxane containing combination chemotherapy as salvage therapy for advanced urothelial carcinoma. Eur Urol. doi:10.1016\u002Fj.eururo.2015.07.042\nSen S, Zhou H, Zhang RD, et al. (2002) Amplification\u002Foverexpression of a mitotic kinase gene in human bladder cancer. J Natl Cancer Inst 94:1320–1329\nZhou N, Singh K, Mir MC, et al. (2013) The investigational Aurora kinase A inhibitor MLN8237 induces defects in cell viability and cell cycle progression in bladder cancer cells in vitro and in vivo. Clin Cancer Res 19:1717–1728\nCervantes A, Elez E, Desamparados R, et al. (2012) Phase I pharmacokinetic\u002Fpharmacodynamic study of MLN8237, an investigational, oral, selective Aurora A kinase inhibitor, in aptients with advanced solid tumors. Clin Cancer Res 18:4764–4774\nEisenhauer EA, Therasse P, Bogaerts J, et al. (2009) New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1). Eur J Cancer 45:228–247\nYoung H, Baum R, Cremerius U, et al. (1999) Measurement of clinical and subclinical tumour response using (18F)-fluorodeoxyglucose and positron emission tomography: review and 1999 EORTC recommendations. European Organization for the research and treatment of cancer (EORTC) PET study group. Eur J Cancer 35:1773–1782\nMelichar B, Adenis A, Lockhart AC, et al. (2015) Safety and activity of alisertib, an investigational Aurora kinase A inhibitor, in patients with breast cancer, small-cell lung cancer, non-small-cell lung cancer, head and neck squamous cell carcinoma, and gastro-oesophageal adenocarcinoma: five-arm phase 2 study. Lancet Oncol 16:395–405\nBarr PM, Li H, Spier C, et al. (2015) Phase II intergroup trial of alisertib in relapsed and refractory peripheral T-cell lymphoma and transformed mycosis fungoides: SWOG 1108. J Clin Oncol 33:2399–2404\nFriedberg JW, Mahadevan D, Cebula E, et al. (2013) Phase II study of alisertib, a selective Aurora A kinase inhibitor, in relapsed and refractory aggressive B- and T-cell non-Hodgkin lymphomas. J Clin Oncol 32:44–50\nMatulonis UA, Sharma S, Ghamande S, et al. (2012) Phase II study of MLN8237 (alisertib), an investigational Aurora A kinase inhibitor, in patients with platinum-resistant epithelial ovarian, fallopian tube, or primary peritoneal carcinoma. Gynecol Oncol 127:63–69\nStadler WM, Vaughn DJ, Sonpavde G, et al. (2014) An open-label, single-arm, phase 2 trial of the polo-like kinase inhibitor volasertib (BI 6727) in patients with locally advanced or metastatic urothelial cancer. Cancer 120:976–982\nBellmunt J, Choueiry TK, Fougeray R, et al. (2010) Prognostic factors in patients with advanced transitional cell carcinoma of the urothelial tract experiencing treatment failure with platinum-containing regimens. J Clin Oncol 28:1850–1855\nSonpavde G, Pond GR, Fougeray R, et al. (2013) Time from prior chemotherapy enhances prognostic risk grouping in the second-line setting of advanced urothelial carcinoma: a retrospective analysis of pooled, prospective phase 2 trials. Eur Urol 63:717–723\nSonpavde G, Pond GR, Rosenberg JE, et al. (2015) Improved 5-Factor Prognostic Classification of Patients Receiving Salvage Systemic Therapy for Advanced Urothelial Carcinoma. J Urol. doi:10.1016\u002Fj.juro.2015.07.111\nIyer G, Hanrahan AJ, Milowsky MI, et al. (2012) Genome sequencing identifies a basis for everolimus sensitivity. Science 338:221\nWagle N, Grabiner BC, Van Allen EM, et al. (2014) Activating mTOR mutations in a patient with an extraordinary response on a phase I trial of everolimus and pazopanib. Cancer Discov 4:546–553\nTentler JJ, Iokina AA, Tan AC, et al. (2015) p53 family members regulate phenotypic response to Aurora kinase A inhibition in triple-negative breast cancer. 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To investigate thehypothesis that a systemic agent designedto inhibit dihydropyrimidine dehydrogenase(DPD), the first enzyme in thefluoropyrimidine degradative pathway, couldimprove the effective amount of5-fluorouracil (5-FU) delivered to a tumorresulting in enhanced response. \nPatients and methods. Eligibility includedcytologically or pathologically verifieddiagnosis of colorectal cancer thatrecurred during or within 12 months ofcompletion of adjuvant therapy,representing patients generally consideredresistant to fluorinated pyrimidinetherapy. Stratification was into twocohorts: recurrence while receivingadjuvant therapy, and relapse within 12months of completing adjuvant therapy.Treatment consisted of 28 days of oraltherapy every five weeks with eniluraciland 5-FU administered in a 10:1 ratio. Thedaily dose of eniluracil was 10 mg\u002Fm2with 5-FU 1 mg\u002Fm2, divided into twodoses. \nResults. Twenty-five patientsare evaluable for response: 9 relapsedduring therapy and 16 relapsed within oneyear of adjuvant therapy. In the firstgroup, there was one partial response (9%;95% CI 0–41%); in the second cohort therewas one confirmed complete response (5%;95% CI 0–23%) and one unconfirmed partialresponse, for an overall response rate of10%. \nConclusions. This regimen lackssignificant activity in this targetpopulation. Pre-treatment intratumoral DPDexpression was not assessed, therefore themechanism of fluorinated pyrimidineresistance cannot be specificallyattributed to elevated DPD levels.Attempting restoration of chemotherapysensitivity through blockade of enzymes orsignal transduction molecules responsiblefor resistance is rational, provided thattumor target expression is the basis fortrial entry.",{"EN":2313},"Biochemical Modulation of 5-Fluorouacil Through Dihydropyrimidine Dehydrogenase Inhibition: a Southwest Oncology Group Phase II Trial of Eniluracil and 5-Fluorouracil in Advanced Resistant Colorectal Cancer",{"VOID":2315},"Poon MA, O'Connell MJ, Moertel CG, Wieand HS, Cullinan SA, Everson LK, Krook JE, Maillard JA, Laurie JA, Tschetter LK, Wiesenfield M: Biochemical modulation of fluorouracil: evidence of significant improvement of survival and quality of life in patients with advanced colorectal carcinoma. J Clin Oncol 7:1407–1418, 1989\nAdvanced Colorectal Cancer Meta-Analysis Project: Modulation of 5-fluorouracil by leucovorin in patients with advanced colorectal cancer: evidence in terms of response rate. J Clin Oncol 10:896–903, 1992\nLeichman CG, Fleming TR, Muggia FM, Tangen CM, Ardalan B, Doroshow JH, Meyers FJ, Holcombe RF, Weiss GR, Mangalik A, Macdonald JS: Phase II study of 5-FU and its modulation in advanced colorectal cancer: a Southwest Oncology Group study. J Clin Oncol 13(6):1303–1311, 1995\nCorfu-A Study Group: Phase III randomized study of two fluorouracil combinations with either interferon alfa-2a or leucovorin for advanced colorectal cancer. J Clin Oncol 13:921–928, 1995\nO'Dwyer PJ, Manola J, Valone FH, Ryan LM, Hines JD, Wadler S, Haller D, Arbuck SG, Weiner LM, Mayer RJ, Bebson AB III: Fluorouracil modulation in colorectal cancer: lack of improvement with N-phosphonacetyl-l-aspartic acid or oral leucovorin or interferon, but enhanced therapeutic index with weekly 24-hour infusion schedule - an Easter Cooperative Oncology Group\u002FCancer and Leukemia Group B study. J Clin Oncol 19:2413–2421, 2001.\nO'Connell MJ, Laurie JA, Kahn M, Fitzgibbons RJ Jr, Erlichman C, Shepherd L, Moertel CG, Kocha WI, Pazdur R, Weiand HS, Rubin J, Vukov AM, Donohue JH, Krook JE, Figueredo A: Prospectively randomized trial of postoperative adjuvant chemotherapy in patients with high-risk colon cancer. J Clin Oncol 16:295–300, 1998\nMoertel CG, Fleming TR, Macdonald JS, Haller DG, Laurie JA, Goodman PJ, Ungerleider JS, Emerson WA, Tormey DC, Glick JH, Veeder MH, Maillard JA: Levamisole and fluorouracil for adjuvant therapy of resected colon carcinoma. N Engl J Med 322:352–358, 1990\nHeggie GD, Sommadossi J-P, Cross DS, Huster WJ, Diasio RB: Clinical pharmacokinetics of 5-fluorouracil and its metabolites in plasma, urine and bile. Cancer Res 47:2203–2206, 1987\nShousong C, Yousef MR, Spector T: 5-ethynyluracil (776C85): modulation of 5-FU efficacy and therapeutic index in rats bearing advanced colorectal carcinoma. Cancer Res 54:1507–1510, 1994\nBaker SD, Khor SP, Adjei AA, Doucette M, Spector T, Donehower RC, Grochow LB, Sartorius SE, Noe DA, Hohneker JA, Rowinsky EK: Pharmacokinetic, oral bioavailability, and safety study of fluorouracil in patients treated with 776C85, an inactivator of dihydropyrimidine dehydrogenase. J Clin Onocl 14:3085–3096, 1996\nSchilsky RL, Hohneker JA, Ratain MJ, Janisch L, Smetzer L, Lucas VS, Khor SP, Diasio R, Von Hoff DD, Burris HA III: Phase I clinical and pharmacologic study of eniluracil plus fluorouracil in patients with advanced cancer. J Clin Oncol 16:1450–1457, 1998\nBurroughs Wellcome: 776C85: Updated (3\u002F95) summary of non-clinical and clinical (Phase I) data\nSlamon DJ, Leyland-Jones B, Shak S, Fuchs H, Paton V, Bajamonde A, Fleming T, Eiermann W, Wolter, J, Pegram M, Baselga J, Norton L: Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that overexpresses HER2. N Engl J Med 344:783–792, 2001\nBergsland E, Hurwitz H, Fehrenbacher L, Meropol NJ, Novotny WF, Gaudreault J, Lieberman G, Kabbinavar F: A Randomized Phase II trial comparing rhuMAb VEGF (recombinant humanized monoclonal antibody to vascular endothelial growth factor) plus 5-fluorouracil\u002Fleucovorin (FU\u002FLV) to FU\u002FLV alone in patients with metastatic colorectal cancer. Proc Am Soc Clin Oncol 19:939, 2000",{"VOID":2317},"10.1023\u002FA:1020662113061","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FA:1020662113061",[2320,2335,2348,2363,2378,2395,2410],{"id":2321,"sortIndex":21,"researcher":20,"roles":2322,"affiliations":2323,"properties":2332},"016fc97b-0083-4e09-938a-8ae6c6721405",[980],[2324],{"id":2325,"sortIndex":21,"affiliation":2326,"properties":20},"8c2e0daa-2743-4459-9f23-8c69c17b6ace",{"id":2325,"createTime":20,"updateTime":20,"relativeEntities":2327,"slug":20,"properties":2328,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2331,"statistic":20},[],{"title":2329},{"VI":2330},"Comprehensive Cancer Centers of the Desert, Palm Springs, USA",[],{"title":2333},{"VI":2334},"Cynthia G. Leichman",{"id":2336,"sortIndex":99,"researcher":20,"roles":2337,"affiliations":2338,"properties":2345},"ad2c777a-6f6f-4d18-bed3-3939a6ac1aac",[980],[2339],{"id":1538,"sortIndex":21,"affiliation":2340,"properties":20},{"id":1538,"createTime":20,"updateTime":20,"relativeEntities":2341,"slug":20,"properties":2342,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2344,"statistic":20},[],{"title":2343},{"VI":1543},[],{"title":2346},{"VI":2347},"Kari Chansky",{"id":2349,"sortIndex":100,"researcher":20,"roles":2350,"affiliations":2351,"properties":2360},"11fbae2f-61af-425c-9deb-fc1007f079a9",[980],[2352],{"id":2353,"sortIndex":21,"affiliation":2354,"properties":20},"4165ce99-f875-40be-9ce9-e517cae9a893",{"id":2353,"createTime":20,"updateTime":20,"relativeEntities":2355,"slug":20,"properties":2356,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2359,"statistic":20},[],{"title":2357},{"VI":2358},"St. Vincent's CCC, New York, USA",[],{"title":2361},{"VI":2362},"John S. Macdonald",{"id":2364,"sortIndex":101,"researcher":20,"roles":2365,"affiliations":2366,"properties":2375},"758b6758-d7a5-42a9-9a39-7e1175884d2a",[980],[2367],{"id":2368,"sortIndex":21,"affiliation":2369,"properties":20},"e75c9c78-5728-4789-8a92-67f545b11752",{"id":2368,"createTime":20,"updateTime":20,"relativeEntities":2370,"slug":20,"properties":2371,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2374,"statistic":20},[],{"title":2372},{"VI":2373},"University of Kentucky Medical Center, Lexington, USA",[],{"title":2376},{"VI":2377},"Michael A. Doukas",{"id":2379,"sortIndex":142,"researcher":20,"roles":2380,"affiliations":2381,"properties":2393},"832be778-0234-4bbe-bb64-4da9e5365b6c",[980],[2382],{"id":2383,"sortIndex":21,"affiliation":2384,"properties":2390},"49ac0a44-60a6-430a-916c-eca4080f055f",{"id":2383,"createTime":20,"updateTime":20,"relativeEntities":2385,"slug":20,"properties":2386,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2389,"statistic":20},[],{"title":2387},{"VI":2388},"Cleveland Clinic Foundation, Cleveland, United States",[],{"title":2391},{"VI":2392},"Cleveland Clinic Foundation, Cleveland, USA",{"title":2394},{"VI":1033},{"id":2396,"sortIndex":143,"researcher":20,"roles":2397,"affiliations":2398,"properties":2407},"a924434f-c1a4-482c-ad8e-f7583caf4ff2",[980],[2399],{"id":2400,"sortIndex":21,"affiliation":2401,"properties":20},"71b51a3e-2e7c-4255-a23f-e82321f2e48d",{"id":2400,"createTime":20,"updateTime":20,"relativeEntities":2402,"slug":20,"properties":2403,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2406,"statistic":20},[],{"title":2404},{"VI":2405},"Greenville CCOP, Greenville, USA",[],{"title":2408},{"VI":2409},"Jeffrey K. Giguere",{"id":2411,"sortIndex":145,"researcher":20,"roles":2412,"affiliations":2413,"properties":2422},"0d795273-6da8-4f28-bae7-27ff98ab3824",[980],[2414],{"id":2415,"sortIndex":21,"affiliation":2416,"properties":20},"6fe8bf52-8b3b-47cb-a5ca-dce8fed1d3a8",{"id":2415,"createTime":20,"updateTime":20,"relativeEntities":2417,"slug":20,"properties":2418,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2421,"statistic":20},[],{"title":2419},{"VI":2420},"MD Anderson Cancer Center, University of Texas, Houston, USA",[],{"title":2423},{"VI":2424},"James L. Abbruzzese",{"url":2318,"publisher":2426,"properties":2476},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2427,"slug":10,"properties":2428,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":2432,"manageAffiliations":2445,"indexDatabases":2456,"url":94,"thumbnailPath":20,"statistic":2471,"gsStatistic":20,"type":104,"analyzePriority":20},[],{"issn":2429,"title":2430,"eissn":2431},{"VOID":13},{"EN":15},{"VOID":17},[2433,2437,2441],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":2434,"label":2435,"description":2436,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":2438,"label":2439,"description":2440,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":33},{},{"id":36,"createTime":20,"updateTime":20,"relativeEntities":2442,"label":2443,"description":2444,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":39},{},[2446,2451],{"id":43,"createTime":20,"updateTime":20,"relativeEntities":2447,"slug":20,"properties":2448,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2450,"statistic":20},[],{"title":2449},{"EN":47},[],{"id":50,"createTime":20,"updateTime":20,"relativeEntities":2452,"slug":20,"properties":2453,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2455,"statistic":20},[],{"title":2454},{"EN":54},[],[2457,2464],{"id":58,"indexDatabase":2458,"url":71,"indexYears":20,"academicFieldIds":2463,"indexDatabaseRanking":20},{"id":60,"createTime":20,"updateTime":20,"relativeEntities":2459,"label":2460,"description":2461,"key":67,"publicationTags":2462,"standard":20},[],{"EN":63,"VI":63},{"EN":65,"VI":66},[69,70],[73,74],{"id":76,"indexDatabase":2465,"url":87,"indexYears":88,"academicFieldIds":2470,"indexDatabaseRanking":93},{"id":78,"createTime":20,"updateTime":20,"relativeEntities":2466,"label":2467,"description":2468,"key":84,"publicationTags":2469,"standard":20},[],{"EN":81,"VI":81},{"EN":81,"VI":83},[86],[90,91,92],{"impactFactor":21,"impactFactorByYear":2472,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":97,"totalPublicationByYear":2473,"totalCitation":21,"totalCitationByYear":2474,"totalCitationPerPublication":21,"totalCitationPerPublicationByYear":2475,"hindexLast5Year":21,"hindex":21},{},{"1986":99,"1991":99,"1992":99,"1996":99,"1997":99,"1998":99,"2003":99,"2005":100,"2006":99,"2007":100,"2008":101,"2009":101,"2010":99,"2011":99,"2012":99,"2013":100,"2017":99,"2018":99,"2019":99,"2020":99,"2021":99,"2022":99,"2023":100},{},{},{"pages":2477,"volume":2479},{"VOID":2478},"419-424",{"VOID":2480},"20","2002-11-01",2002,[69,93],{"id":2485,"createTime":2486,"updateTime":2487,"relativeEntities":2488,"slug":2489,"properties":2490,"entityType":972,"verifyStatus":127,"verifyTime":2487,"verifyNote":974,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":2499,"fullTextUrl":20,"authors":2500,"publicationType":1060,"publisherRelationship":2557,"citationCount":20,"citationInfo":20,"publishDate":2613,"publishYear":2614,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":2615,"openAccess":20,"references":20,"isForceReanalyzing":1120},"01ece309-d4e4-45d9-8d5f-6df0f465b90c","2023-12-06T16:45:46.723+00:00","2024-12-22T09:40:03.791+00:00",[],"The-clinical-efficiency-of-TACE-combined-with-simultaneous-computed-tomography-guided-radiofrequency-ablation-for-advanced-hepatocellular-carcinoma",{"abstract":2491,"title":2493,"references":2495,"doi":2497},{"EN":2492},"Background To investigate the clinical efficiency of transcatheter arterial chemoembolization (TACE) combined with radiofrequency ablation (RFA) for advanced hepatocellular carcinoma (HCC). Methods This retrospective study enrolled 177 HCC patients, and they were divided into TACE monotherapy group (n = 129) and TACE + RFA group (n = 48) between January 2015 and October 2017. The objective response rate (ORR), disease control rate (DCR), and the survival outcomes were compared between the TACE monotherapy and the treatment of TACE + RFA after propensity score matching (PSM). Results After PSM matching, the confounding factors had no significant differences between the 48 pairs of patients. The DCR was calculated as 33 (69 %) and 42 (88 %) for the TACE monotherapy group and TACE + RFA group, respectively (P \u003C 0.05). And the ORR was calculated as 23 (48 %) and 35 (73 %), respectively (P \u003C 0.05). Moreover, the PFS rate of the TACE + RFA group was significantly higher than the TACE alone group (P \u003C 0.001). Conclusions The treatment of TACE combined with RFA has better tumor response rate and survival rate than the TACE monotherapy for patients with advanced HCC.",{"EN":2494},"The clinical efficiency of TACE combined with simultaneous computed tomography‐guided radiofrequency ablation for advanced hepatocellular carcinoma",{"VOID":2496},"Ferenci P, Fried M, Labrecque D, Bruix J, Sherman M, Omata M, Heathcote J, Piratsivuth T, Kew M, Otegbayo JA, Zheng SS, Sarin S, Hamid SS, Modawi SB, Fleig W, Fedail S, Thomson A, Khan A, Malfertheiner P, Lau G, Carillo FJ, Krabshuis J, Le Mair A, World Gastroenterology Organization (2010) Hepatocellular carcinoma (HCC): a global perspective. J Clin Gastroenterol 44:239–245. https:\u002F\u002Fdoi.org\u002F10.1097\u002FMCG.0b013e3181d46ef2\nMazzanti R, Gramantieri L, Bolondi L (2008) Hepatocellular carcinoma: epidemiology and clinical aspects. Mol Aspects Med 29:130–143. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.mam.2007.09.008\nChen JG, Zhang SW (2011) Liver cancer epidemic in China: past, present and future. Semin Cancer Biol 21:59–69. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.semcancer.2010.11.002\nBruix J, Sherman M, American Association for the Study of Liver D (2011) Management of hepatocellular carcinoma: an update. Hepatology 53:1020–1022. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fhep.24199\nQin LX, Tang ZY (2002) The prognostic significance of clinical and pathological features in hepatocellular carcinoma. World J Gastroenterol 8:193–199. https:\u002F\u002Fdoi.org\u002F10.3748\u002Fwjg.v24.i35.4000\nde Baere T, Arai Y, Lencioni R, Geschwind JF, Rilling W, Salem R, Matsui O, Soulen MC (2016) Treatment of liver tumors with lipiodol TACE: technical recommendations from experts opinion. Cardiovasc Intervent Radiol 39:334–343. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs00270-015-1208-y\nCommittee AT, Navaneethan U, Thosani N, Goodman A, Manfredi M, Pannala R, Parsi MA, Smith ZL, Sullivan SA, Banerjee S, Maple JT (2017) Radiofrequency ablation devices. VideoGIE 2:252–259. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.vgie.2017.06.002\nPeng ZW, Zhang YJ, Liang HH, Lin XJ, Guo RP, Chen MS (2012) Recurrent hepatocellular carcinoma treated with sequential transcatheter arterial chemoembolization and RF ablation versus RF ablation alone: a prospective randomized trial. Radiology 262:689–700. https:\u002F\u002Fdoi.org\u002F10.1148\u002Fradiol.11110637\nTakuma Y, Takabatake H, Morimoto Y, Toshikuni N, Kayahara T, Makino Y, Yamamoto H (2013) Comparison of combined transcatheter arterial chemoembolization and radiofrequency ablation with surgical resection by using propensity score matching in patients with hepatocellular carcinoma within Milan criteria. Radiology 269:927–937. https:\u002F\u002Fdoi.org\u002F10.1148\u002Fradiol.13130387\nKrajewski KM, Nishino M, Ramaiya NH, Choueiri TK (2015) RECIST 1.1 compared with RECIST 1.0 in patients with advanced renal cell carcinoma receiving vascular endothelial growth factor-targeted therapy. AJR Am J Roentgenol 204:W282-W288. https:\u002F\u002Fdoi.org\u002F10.2214\u002FAJR.14.13236\nLiu X, Liao G, Luo X, Song W, Zhang H, Chen H, Cai S, Guo D (2020) Hepatocellular carcinoma with different areas of right retroperitoneal space invasion: evaluation of transcatheter arterial chemoembolization efficacy and blood supply characteristics. Front Oncol 10:539692. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffonc.2020.539692\nLivraghi T, Goldberg SN, Lazzaroni S, Meloni F, Ierace T, Solbiati L, Gazelle GS (2000) Hepatocellular carcinoma: radio-frequency ablation of medium and large lesions. Radiology 214:761–768. https:\u002F\u002Fdoi.org\u002F10.1148\u002Fradiology.214.3.r00mr02761\nChuan-Xing L, Xu H, Bao-Shan H, Yong L, Pei-Jian S, Xian-Yi Y, Xiao-Ning L, Li-Gong L (2011) Efficacy of therapy for hepatocellular carcinoma with portal vein tumor thrombus: chemoembolization and stent combined with iodine-125 seed. Cancer Biol Ther 12(10):865–871. https:\u002F\u002Fdoi.org\u002F10.4161\u002Fcbt.12.10.17676\nGarwood ER, Fidelman N, Hoch SE, Kerlan RK Jr, Yao FY (2013) Morbidity and mortality following transarterial liver chemoembolization in patients with hepatocellular carcinoma and synthetic hepatic dysfunction. Liver Transpl 19(2):164–173. https:\u002F\u002Fdoi.org\u002F10.1002\u002Flt.23552\nMirza AN, Fornage BD, Sneige N, Kuerer HM, Newman LA, Ames FC, Singletary SE (2001) Radiofrequency ablation of solid tumors. Cancer J 7:95–102\nAl-Sakere B, Bernat C, Andre F, Connault E, Opolon P, Davalos RV, Mir LM (2007) A study of the immunological response to tumor ablation with irreversible electroporation. Technol Cancer Res Treat 6(4):301–336. https:\u002F\u002Fdoi.org\u002F10.1177\u002F153303460700600406\nMauri G, Nicosia L, Xu Z, Di Pietro S, Monfardini L, Bonomo G, Varano GM, Prada F, Della Vigna P, Orsi F (2018) Focused ultrasound: tumour ablation and its potential to enhance immunological therapy to cancer. Br J Radiol 91(1083):20170641. https:\u002F\u002Fdoi.org\u002F10.1259\u002Fbjr.20170641\nKagawa T, Koizumi J, Kojima S, Nagata N, Numata M, Watanabe N, Watanabe T, Mine T, Tokai, RFA Study Group (2010) Transcatheter arterial chemoembolization plus radiofrequency ablation therapy for early stage hepatocellular carcinoma: comparison with surgical resection. Cancer 116:3638–3644. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fcncr.25142\nNi JY, Liu SS, Xu LF, Sun HL, Chen YT (2013) Meta-analysis of radiofrequency ablation in combination with transarterial chemoembolization for hepatocellular carcinoma. World J Gastroenterol 19:3872–3882. https:\u002F\u002Fdoi.org\u002F10.3748\u002Fwjg.v19.i24.3872\nYi Y, Zhang Y, Wei Q, Zhao L, Han J, Song Y, Ding Y, Lu G, Liu J, Ding H, Dai F, Tang X (2014) Radiofrequency ablation or microwave ablation combined with transcatheter arterial chemoembolization in treatment of hepatocellular carcinoma by comparing with radiofrequency ablation alone. Chin J Cancer Res 26(1):112–118. https:\u002F\u002Fdoi.org\u002F10.3978\u002Fj.issn.1000-9604.2014.02.09\nPeng ZW, Zhang YJ, Chen MS, Xu L, Liang HH, Lin XJ, Guo RP, Zhang YQ, Lau WY (2013) Radiofrequency ablation with or without transcatheter arterial chemoembolization in the treatment of hepatocellular carcinoma: a prospective randomized trial. J Clin Oncol 31(4):426–432. https:\u002F\u002Fdoi.org\u002F10.1200\u002FJCO.2012.42.9936\nAbdelaziz AO, Abdelmaksoud AH, Nabeel MM, Shousha HI, Cordie AA, Mahmoud ShH, Medhat E, Omran D, Elbaz TM (2017) Transarterial chemoembolization combined with either radiofrequency or microwave ablation in management of hepatocellular carcinoma. Asian Pac J Cancer Prev 18(1):189–194. https:\u002F\u002Fdoi.org\u002F10.22034\u002FAPJCP.2017.18.1.189",{"VOID":2498},"10.1007\u002Fs10637-021-01101-w","https:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs10637-021-01101-w",[2501,2516,2529,2544],{"id":2502,"sortIndex":21,"researcher":20,"roles":2503,"affiliations":2504,"properties":2513},"f2f3c9f5-919a-4c00-87d2-ca1707c3e4a9",[980],[2505],{"id":2506,"sortIndex":21,"affiliation":2507,"properties":20},"0d729c78-aeca-4c8d-844e-d1d0e56a8ffb",{"id":2506,"createTime":20,"updateTime":20,"relativeEntities":2508,"slug":20,"properties":2509,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2512,"statistic":20},[],{"title":2510},{"VI":2511},"Department of Hematology and Oncology (Key Discipline of Jiangsu Medicine), Medical School, Zhongda Hospital, Southeast University, Nanjing, People’s Republic of China",[],{"title":2514},{"VI":2515},"Peng Yuan",{"id":2517,"sortIndex":99,"researcher":20,"roles":2518,"affiliations":2519,"properties":2526},"8248ad83-8aba-4c6d-9eb0-264395567ea5",[980],[2520],{"id":2506,"sortIndex":21,"affiliation":2521,"properties":20},{"id":2506,"createTime":20,"updateTime":20,"relativeEntities":2522,"slug":20,"properties":2523,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2525,"statistic":20},[],{"title":2524},{"VI":2511},[],{"title":2527},{"VI":2528},"Fei 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