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Journal of Medicine and Pharmacy","Tạp chí Y Dược học Cần Thơ",{"EN":629,"VI":630},"\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":632},"wcQ1uqwAAAAJ","2023-05-30T08:17:21.868+00:00",[],[636],{"id":637,"createTime":20,"updateTime":20,"relativeEntities":638,"slug":20,"properties":639,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":649,"parentIds":650,"statistic":20},"6413896b-eca9-442b-a73f-182a58a0ce40",[],{"title":640,"address":643,"country":646,"abbreviation":647},{"EN":641,"VI":642},"Can Tho University of Medicine and Pharmacy","Trường Đại học Y Dược Cần Thơ",{"EN":644,"VI":645},"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":176},{"VOID":648},"ctump","http:\u002F\u002Fwww.ctump.edu.vn\u002F",[],[],"https:\u002F\u002Ftapchi.ctump.edu.vn\u002Findex.php\u002Fctump",{"impactFactor":21,"impactFactorByYear":654,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":656,"totalPublicationByYear":657,"totalCitation":662,"totalCitationByYear":663,"totalCitationPerPublication":265,"totalCitationPerPublicationByYear":665,"hindexLast5Year":203,"hindex":203},{"2022":655,"2023":268,"2024":263},0.01,1556,{"2020":205,"2021":658,"2022":659,"2023":660,"2024":661,"2025":279},57,306,801,358,161,{"2021":301,"2022":427,"2023":664},99,{"2021":666,"2022":465,"2023":261},0.23,{"impactFactor":20,"impactFactorByYear":20,"i10Index":280,"i10IndexLast5Year":280,"totalPublication":668,"totalPublicationByYear":669,"totalCitation":668,"totalCitationByYear":670,"totalCitationPerPublication":198,"totalCitationPerPublicationByYear":673,"hindexLast5Year":207,"hindex":207},476,{"0":354,"2019":280,"2021":294,"2022":602,"2023":594,"2024":503,"2025":207,"2026":206},{"2021":200,"2022":280,"2023":314,"2024":671,"2025":506,"2026":672},136,83,{"2021":262,"2022":655,"2023":674,"2024":284,"2025":675,"2026":676},0.62,25.43,13.83,{"id":678,"createTime":679,"updateTime":527,"relativeEntities":680,"slug":681,"properties":682,"entityType":18,"verifyStatus":186,"verifyTime":20,"verifyNote":20,"languages":694,"translateLanguages":20,"viewCount":289,"subjectFields":695,"manageAffiliations":696,"indexDatabases":697,"url":698,"thumbnailPath":699,"statistic":700,"gsStatistic":734,"type":213,"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":683,"issn":684,"title":686,"introduce":689,"gsId":692},{"VOID":176},{"VOID":685},"25252445",{"EN":687,"VI":688},"VNU Journal of Foreign Studies","Tạp chí Nghiên cứu nước ngoài",{"EN":690,"VI":691},"{\"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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Although, the main text structure may vary based on the review subtopics, the articles should be formatted according to suitable Templates as research articles.\"},{\"attributes\":{\"align\":\"justify\"},\"insert\":\"\\n\"},{\"insert\":\"\\n\"}]}","{\"ops\":[{\"insert\":\"Tạp chí Khoa học Trường ĐHSP Hà Nội 2 nhằm mục đích cung cấp một nền tảng liên ngành của sự phổ biến những tiến bộ của khoa học và công nghệ. Tạp chí xuất bản các bài báo gốc có giá trị khoa học hoặc công nghệ trong tất cả các lĩnh vực khoa học tự nhiên, xã hội hoặc giáo dục.\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Chuyên san Khoa học tự nhiên và công nghệ:\"},{\"insert\":\" Là các bài báo mô tả những phát hiện có giá trị trong vật lý, toán học, hóa học, sinh học; giải quyết các vấn đề kỹ thuật hoặc công nghệ.\"},{\"attributes\":{\"list\":\"bullet\"},\"insert\":\"\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Chuyên san Khoa học Xã hội và Nhân văn:\"},{\"insert\":\" là các bài báo xuất bản chất lượng cao trong các lĩnh vực khác nhau của khoa học xã hội và nghiên cứu phát triển con người.\"},{\"attributes\":{\"list\":\"bullet\"},\"insert\":\"\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Chuyên san Khoa học giáo dục:\"},{\"insert\":\" là các bài báo xuất bản trong lĩnh vực khoa học giáo dục và các ứng dụng của tiến bộ vào giáo dục để cải thiện và nâng cao giáo dục khoa học ở tất cả các cấp.\"},{\"attributes\":{\"list\":\"bullet\"},\"insert\":\"\\n\"},{\"insert\":\"Tạp chí trường ĐHSP Hà Nội 2 xuất bản được phản biện kín, xét duyệt bởi ít nhất 02 chuyên gia, và được đánh giá, chọn lựa từ ban biên tập và Tổng biên tập.\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Các loại bài báo\"},{\"insert\":\":\\nBài báo nghiên cứu:\"},{\"attributes\":{\"list\":\"ordered\"},\"insert\":\"\\n\"},{\"insert\":\"Báo cáo học thuật về nghiên cứu ban đầu chưa từng được xuất bản ở bất kỳ nơi nào, hay bằng bất kỳ ngôn ngữ nào khác. Bản thảo thích hợp, nên chứa các phần sau theo thứ tự: Tiêu đề, Tác giả, Liên kết tác giả, Địa chỉ email của tác giả tương ứng, Tóm tắt, Từ khóa, Danh pháp (nếu có), Giới thiệu, Thử nghiệm, Lý thuyết, Kết quả và thảo luận, Kết luận, Xung đột quan tâm, Lời cảm ơn (nếu có), Tài liệu tham khảo, Phụ lục (nếu có). Bản xuất bản trước phải được định dạng theo Mẫu (phiên bản MS-Word).\\n2. Bài báo tổng quan:\\nNgoài các bài phê bình được mời, các bài phê bình tài liệu, bài phê bình có hệ thống và bài phê bình sẽ được chấp nhận để xem xét. Bản thảo cần được soạn thảo và sắp xếp theo trình tự yêu cầu: Tên sách, Tên tác giả, Liên kết, Địa chỉ email, Tóm tắt, Từ khóa, Nội dung chính, Kết luận, Xung đột lợi ích, Lời cảm ơn (nếu có), Tài liệu tham khảo. Mặc dù, cấu trúc văn bản chính có thể thay đổi dựa trên các chủ đề phụ của bài đánh giá, các bài báo nên được định dạng theo các Mẫu phù hợp như các bài báo nghiên cứu.\\n\"}]}",{"VOID":862},"YPoBvsIAAAAJ",[],[],[],"https:\u002F\u002Fsj.hpu2.edu.vn\u002Findex.php\u002Fjournal","\u002Fapi\u002Fpublic\u002Ffile\u002Fpublisher\u002F954132b5-ca74-461c-b819-45ad6e49a404\u002F2790ef1d0a7d7a40a504c2fc1647f670.jpg",{"impactFactor":21,"impactFactorByYear":869,"i10Index":21,"i10IndexLast5Year":21,"totalPublication":476,"totalPublicationByYear":871,"totalCitation":290,"totalCitationByYear":872,"totalCitationPerPublication":666,"totalCitationPerPublicationByYear":873,"hindexLast5Year":280,"hindex":280},{"2024":870},0.17,{"2022":292,"2023":127,"2024":297},{"2022":503,"2023":283,"2024":280},{"2022":322,"2023":372,"2024":318},{"impactFactor":20,"impactFactorByYear":20,"i10Index":203,"i10IndexLast5Year":203,"totalPublication":477,"totalPublicationByYear":875,"totalCitation":307,"totalCitationByYear":876,"totalCitationPerPublication":877,"totalCitationPerPublicationByYear":878,"hindexLast5Year":204,"hindex":204},{"0":280,"2022":290,"2023":292,"2024":118,"2025":300},{"2023":204,"2024":292,"2025":122,"2026":127},1.22,{"2023":270,"2024":487,"2025":879},4.56,{"id":881,"createTime":882,"updateTime":883,"relativeEntities":884,"slug":885,"properties":886,"entityType":18,"verifyStatus":186,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":118,"subjectFields":898,"manageAffiliations":899,"indexDatabases":907,"url":947,"thumbnailPath":20,"statistic":948,"gsStatistic":980,"type":213,"analyzePriority":20},"21ccdb34-414d-420f-8a60-a592a2fa848e","2023-05-29T10:42:53.358+00:00","2026-08-27T01:57:29.560+00:00",[],"Vietnam-Journal-of-Earth-Sciences",{"country":887,"eissn":888,"issn":890,"title":892,"introduce":894,"gsId":896},{"VOID":176},{"VOID":889},"26159783",{"VOID":891},"08667187",{"EN":893},"Vietnam Journal of Earth Sciences",{"EN":895},"Science of the Earth, formerly Vietnam Journal of Earth Sciences, is a peer-reviewed journal to publish high-quality articles on the entire range of earth sciences and the environment, focused on the Asia Pacific region and their correlations and connections to the globe. The journal publishes fundamental and applied research in earth sciences and the environment, including geology, geophysics, geography, soil science, hydrology, meteorology, oceanography, petroleum, geohazards, environmental sciences, environmental engineering, sustainable development, geoinformatics, geodesy, GIS, and remote sensing.",{"VOID":897},"5htfr3YAAAAJ",[],[900],{"id":230,"createTime":20,"updateTime":20,"relativeEntities":901,"slug":20,"properties":902,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":239,"parentIds":906,"statistic":20},[],{"title":903,"country":904,"abbreviation":905},{"EN":234,"VI":235},{"VOID":176},{"VOID":238},[],[908,920,931],{"id":909,"indexDatabase":910,"url":915,"indexYears":916,"academicFieldIds":917,"indexDatabaseRanking":919},"6ace2085-a177-4a27-b309-8813b832111e",{"id":86,"createTime":20,"updateTime":20,"relativeEntities":911,"label":912,"description":913,"key":92,"publicationTags":914,"standard":20},[],{"EN":89,"VI":89},{"EN":89,"VI":91},[94],"https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002F21101039869","2018-2024",[918],"1689391c-5702-4349-aaa7-d720ee4321fc","NONE",{"id":921,"indexDatabase":922,"url":927,"indexYears":928,"academicFieldIds":929,"indexDatabaseRanking":20},"dadb15a8-ee22-41c2-a287-49e969d9a998",{"id":245,"createTime":20,"updateTime":20,"relativeEntities":923,"label":924,"description":925,"key":251,"publicationTags":926,"standard":20},[],{"EN":248,"VI":248},{"EN":250,"VI":250},[253],"https:\u002F\u002Fasean-cites.org\u002Fjournal_info?jid=10629","2016-2022",[930],"e04f14cf-280b-4aa8-b711-b77ddd79cbaf",{"id":932,"indexDatabase":933,"url":944,"indexYears":20,"academicFieldIds":945,"indexDatabaseRanking":20},"06f278ee-37b9-41eb-a9b0-3d2d77fa502b",{"id":934,"createTime":20,"updateTime":20,"relativeEntities":935,"label":936,"description":938,"key":941,"publicationTags":942,"standard":20},"88bab0f7-443b-476c-a72a-7fa5222da393",[],{"EN":937,"VI":937},"ISI\u002FESCI  - 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However, the immunomodulatory molecules CD11b and CD64, are highly associated with leukemogenesis. Hence, the prognostic value of them and their potential biological functions merit further investigation. Flow cytometry was operated to detect immunophenotypic molecules from AML bone marrow samples. Multivariate cox regression, Kaplan-Meier analyses, and nomogram were conducted to predict survival. Transcriptomic data, lymphocyte subsets, and immunohistochemical staining were incorporated to identify potential biological functions of prognostic immunophenotype in acute myeloid leukemia (AML). We classified 315 newly diagnosed AML patients of our center based on the expression of CD11b and CD64. The CD11b+CD64+ populations were identified as independent risk factors for overall survival and event-free survival of AML, exhibiting specific clinicopathological features. The predictive models based on CD11b+CD64+ showed high classification performance. In addition, the CD11b+CD64+ subset, characterized by high inhibitory immune checkpoints, M2-macrophage infiltration, low anti-tumor effector cells infiltration, as well as abnormal somatic mutation landscape, presented a distinctive tumor microenvironmental landscape. The CD11b+CD64+ population showd a higher expression of BCL2, and the drug sensitivity indicated that they presented a lower half-maximal inhibitory concentration value for BCL2 inhibitor, and could benefit more from the above medicine. This work might be of benefit to enhanced understanding of CD11b+CD64+ in the prognosis and leukemogenesis, and yielded novel biomarkers to guide immunotherapy and targeted therapy for AML.",{"EN":1009},"Comprehensive analysis of clinical prognostic features and tumor microenvironment landscape of CD11b+CD64+ patients with acute myeloid leukemia",{"VOID":1011},"F. Perna, S.H. Berman, R.K. Soni, J. Mansilla-Soto, J. Eyquem, M. Hamieh, R.C. Hendrickson, C.W. Brennan, M. 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Zhou","ARTICLE",{"url":1016,"publisher":1166,"properties":1220},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1167,"slug":10,"properties":1168,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1172,"manageAffiliations":1189,"indexDatabases":1200,"url":20,"thumbnailPath":20,"statistic":1215,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":1169,"title":1170,"eissn":1171},{"VOID":13},{"EN":15},{"VOID":17},[1173,1177,1181,1185],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1174,"label":1175,"description":1176,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":1178,"label":1179,"description":1180,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":33},{},{"id":36,"createTime":20,"updateTime":20,"relativeEntities":1182,"label":1183,"description":1184,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":39},{},{"id":42,"createTime":20,"updateTime":20,"relativeEntities":1186,"label":1187,"description":1188,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":45},{},[1190,1195],{"id":49,"createTime":20,"updateTime":20,"relativeEntities":1191,"slug":20,"properties":1192,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1194,"statistic":20},[],{"title":1193},{"EN":53},[55],{"id":57,"createTime":20,"updateTime":20,"relativeEntities":1196,"slug":20,"properties":1197,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1199,"statistic":20},[],{"title":1198},{"EN":61},[],[1201,1208],{"id":65,"indexDatabase":1202,"url":78,"indexYears":20,"academicFieldIds":1207,"indexDatabaseRanking":20},{"id":67,"createTime":20,"updateTime":20,"relativeEntities":1203,"label":1204,"description":1205,"key":74,"publicationTags":1206,"standard":20},[],{"EN":70,"VI":70},{"EN":72,"VI":73},[76,77],[80,81,82],{"id":84,"indexDatabase":1209,"url":95,"indexYears":96,"academicFieldIds":1214,"indexDatabaseRanking":102},{"id":86,"createTime":20,"updateTime":20,"relativeEntities":1210,"label":1211,"description":1212,"key":92,"publicationTags":1213,"standard":20},[],{"EN":89,"VI":89},{"EN":89,"VI":91},[94],[98,99,100,101],{"impactFactor":21,"impactFactorByYear":1216,"i10Index":117,"i10IndexLast5Year":118,"totalPublication":119,"totalPublicationByYear":1217,"totalCitation":134,"totalCitationByYear":1218,"totalCitationPerPublication":149,"totalCitationPerPublicationByYear":1219,"hindexLast5Year":118,"hindex":118},{"2012":105,"2013":106,"2014":107,"2015":108,"2016":109,"2017":110,"2018":111,"2019":112,"2020":113,"2021":114,"2022":115,"2023":116},{"2011":121,"2012":122,"2013":118,"2014":123,"2015":124,"2016":125,"2017":126,"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":133},{"2011":136,"2012":137,"2013":138,"2014":139,"2015":140,"2016":141,"2017":142,"2018":143,"2019":144,"2020":145,"2021":146,"2022":147,"2023":148},{"2011":151,"2012":152,"2013":153,"2014":154,"2015":155,"2016":156,"2017":157,"2018":158,"2019":159,"2020":160,"2021":161,"2022":162,"2023":163},{"pages":1221,"volume":1223},{"VOID":1222},"1253-1268",{"VOID":1224},"46","2023-04-18",2023,[76,102],false,{"id":1230,"createTime":1231,"updateTime":1232,"relativeEntities":1233,"slug":1234,"properties":1235,"entityType":1014,"verifyStatus":186,"verifyTime":1232,"verifyNote":1015,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1244,"fullTextUrl":20,"authors":1245,"publicationType":1164,"publisherRelationship":1376,"citationCount":20,"citationInfo":20,"publishDate":1435,"publishYear":1226,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":1436,"openAccess":20,"references":20,"isForceReanalyzing":1228},"00700b8b-e0bf-4d09-9dcf-84dc7edcc139","2024-01-11T15:20:01.915+00:00","2025-01-18T20:38:16.969+00:00",[],"Competition-between-p53-and-YY1-determines-PHGDH-expression-and-malignancy-in-bladder-cancer",{"abstract":1236,"title":1238,"references":1240,"doi":1242},{"EN":1237},"Serine metabolism is frequently dysregulated in many types of cancers and the tumor suppressor p53 is recently emerging as a key regulator of serine metabolism. However, the detailed mechanism remains unknown. Here, we investigate the role and underlying mechanisms of how p53 regulates the serine synthesis pathway (SSP) in bladder cancer (BLCA). Two BLCA cell lines RT-4 (WT p53) and RT-112 (p53 R248Q) were manipulated by applying CRISPR\u002FCas9 to examine metabolic differences under WT and mutant p53 status. Liquid chromatography-tandem mass spectrometry (LC-MS\u002FMS) and non-targeted metabolomics analysis were adopted to identify metabolomes changes between WT and p53 mutant BLCA cells. Bioinformatics analysis using the cancer genome atlas and Gene Expression Omnibus datasets and immunohistochemistry (IHC) staining was used to investigate PHGDH expression. Loss-of-function of PHGDH and subcutaneous xenograft model was adopted to investigate the function of PHGDH in mice BLCA. Chromatin immunoprecipitation (Ch-IP) assay was performed to analyze the relationships between YY1, p53, SIRT1 and PHGDH expression. SSP is one of the most prominent dysregulated metabolic pathways by comparing the metabolomes changes between wild-type (WT) p53 and mutant p53 of BLCA cells. TP53 gene mutation shows a positive correlation with PHGDH expression in TCGA-BLCA database. PHGDH depletion disturbs the reactive oxygen species homeostasis and attenuates the xenograft growth in the mouse model. Further, we demonstrate WT p53 inhibits PHGDH expression by recruiting SIRT1 to the PHGDH promoter. Interestingly, the DNA binding motifs of YY1 and p53 in the PHGDH promoter are partially overlapped which causes competition between the two transcription factors. This competitive regulation of PHGDH is functionally linked to the xenograft growth in mice. YY1 drives PHGDH expression in the context of mutant p53 and promotes bladder tumorigenesis, which preliminarily explains the relationship between high-frequency mutations of p53 and dysfunctional serine metabolism in bladder cancer.",{"EN":1239},"Competition between p53 and YY1 determines PHGDH expression and malignancy in bladder cancer",{"VOID":1241},"F. Massari, C. Ciccarese, M. Santoni, R. Iacovelli, R. Mazzucchelli, F. Piva, M. Scarpelli, R. Berardi, G. Tortora, A. Lopez-Beltran, L. Cheng, R. Montironi, Metabolic phenotype of bladder cancer. Cancer Treat. Rev. 45, 46–57 (2016). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ctrv.2016.03.005\nB.L. Woolbright, M. Ayres, J.A. Taylor III, Metabolic changes in bladder cancer. Urol. Oncol. 36, 327–337 (2018). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.urolonc.2018.04.010\nE.R. Kastenhuber, S.W. Lowe, Putting p53 in Context. Cell 170, 1062–1078 (2017). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cell.2017.08.028\nP. Berggren, G. Steineck, J. Adolfsson, J. Hansson, O. Jansson, P. Larsson, B. Sandstedt, H. Wijkstrom, K. Hemminki, p53 mutations in urinary bladder cancer. Br. J. Cancer 84, 1505–1511 (2001). https:\u002F\u002Fdoi.org\u002F10.1054\u002Fbjoc.2001.1823\nW.C. Kusser, X. Miao, B.W. Glickman, J.M. Friedland, N. Rothman, G.P. Hemstreet, J. Mellot, D.C. Swan, P.A. Schulte, R.B. Hayes, p53 mutations in human bladder cancer. Environ. Mol. Mutagen. 24, 156–160 (1994). https:\u002F\u002Fdoi.org\u002F10.1002\u002Fem.2850240303\nJ.C. Schroeder, K. Conway, Y. Li, K. Mistry, D.A. Bell, J.A. Taylor, p53 mutations in bladder cancer: evidence for exogenous versus endogenous risk factors. Cancer Res. 63, 7530–7538 (2003)\nJ. Liu, C. Zhang, W. Hu, Z. Feng, Tumor suppressor p53 and its mutants in cancer metabolism. Cancer Lett. 356, 197–203 (2015). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.canlet.2013.12.025\nP.A. Muller, K.H. Vousden, Mutant p53 in cancer: new functions and therapeutic opportunities. Cancer Cell 25, 304–317 (2014). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ccr.2014.01.021\nL. Sun, L. Song, Q. Wan, G. Wu, X. Li, Y. Wang, J. Wang, Z. Liu, X. Zhong, X. He, S. Shen, X. Pan, A. Li, Y. Wang, P. Gao, H. Tang, H. Zhang, Cmyc-mediated activation of serine biosynthesis pathway is critical for cancer progression under nutrient deprivation conditions. Cell. Res. 25, 429–444 (2015). https:\u002F\u002Fdoi.org\u002F10.1038\u002Fcr.2015.33\nQ. Li, J. Qiu, H. Yang, G. Sun, Y. Hu, D. Zhu, Z. Deng, X. Wang, J. Tang, R. Jiang, Kinesin family member 15 promotes cancer stem cell phenotype and malignancy via reactive oxygen species imbalance in hepatocellular carcinoma. Cancer Lett (2019). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.canlet.2019.11.008\nL. Wei, D. Lee, C.T. Law, M.S. Zhang, J. Shen, D.W. Chin, A. Zhang, F.H. Tsang, C.L. Wong, I.O. Ng, C.C. Wong, C.M. Wong, Genome-wide CRISPR\u002FCas9 library screening identified PHGDH as a critical driver for Sorafenib resistance in HCC. Nat. Commun. 10, 4681 (2019). https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41467-019-12606-7\nB. Zhang, A. Zheng, P. Hydbring, G. Ambroise, A.T. Ouchida, M. Goiny, H. Vakifahmetoglu-Norberg, E. Norberg, PHGDH defines a metabolic subtype in lung adenocarcinomas with poor prognosis. Cell. Rep. 19, 2289–2303 (2017). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.celrep.2017.05.067\nD. Samanta, Y. Park, S.A. Andrabi, L.M. Shelton, D.M. Gilkes, G.L. Semenza, PHGDH expression is required for mitochondrial redox homeostasis, breast Cancer stem cell maintenance, and lung metastasis. Cancer Res. 76, 4430–4442 (2016). https:\u002F\u002Fdoi.org\u002F10.1158\u002F0008-5472.CAN-16-0530\nE. Gronroos, A.A. Terentiev, T. Punga, J. Ericsson, YY1 inhibits the activation of the p53 tumor suppressor in response to genotoxic stress. Proc. Natl. Acad. Sci. U.S.A 101, 12165–12170 (2004). https:\u002F\u002Fdoi.org\u002F10.1073\u002Fpnas.0402283101\nC. Zhang, X. Zhang, W. Zhao, C. Zeng, W. Li, B. Li, X. Luo, J. Li, J. Jiang, B. Deng, D.W. McComb, Y. Dong, Chemotherapy drugs derived nanoparticles encapsulating mRNA encoding tumor suppressor proteins to treat triple-negative breast cancer. Nano Res. 12, 855–861 (2019). https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs12274-019-2308-9\nF.A. Ran, P.D. Hsu, J. Wright, V. Agarwala, D.A. Scott, F. Zhang, Genome engineering using the CRISPR-Cas9 system. Nat. Protoc. 8, 2281–2308 (2013). https:\u002F\u002Fdoi.org\u002F10.1038\u002Fnprot.2013.143\nJ. Shao, J. Lu, W. Zhu, H. Yu, X. Jing, Y.L. Wang, X. Wang, X.J. Wang, Derepression of LOXL4 inhibits liver cancer growth by reactivating compromised p53. Cell. Death Differ. 26, 2237–2252 (2019). https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41418-019-0293-x\nY. Wu, D. Liang, Y. Wang, M. Bai, W. Tang, S. Bao, Z. Yan, D. Li, J. Li, Correction of a genetic disease in mouse via use of CRISPR-Cas9. Cell. Stem Cell 13, 659–662 (2013). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.stem.2013.10.016\nJ.P. Zhang, X.L. Li, G.H. Li, W. Chen, C. Arakaki, G.D. Botimer, D. Baylink, L. Zhang, W. Wen, Y.W. Fu, J. Xu, N. Chun, W. Yuan, T. Cheng, X.B. Zhang (2017) Efficient precise knockin with a double cut HDR donor after CRISPR\u002FCas9-mediated double-stranded DNA cleavage. Genome Biol. 18, 35. https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs13059-017-1164-8\nX. Wang, R. Liu, X. Qu, H. Yu, H. Chu, Y. Zhang, W. Zhu, X. Wu, H. Gao, B. Tao, W. Li, J. Liang, G. Li, W. Yang, Alpha-ketoglutarate-activated NF-kappaB signaling promotes compensatory glucose uptake and brain Tumor Development. Mol. Cell 76(e147), 148–162 (2019). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.molcel.2019.07.007\nO.D. Maddocks, C.R. Berkers, S.M. Mason, L. Zheng, K. Blyth, E. Gottlieb, K.H. Vousden, Serine starvation induces stress and p53-dependent metabolic remodelling in cancer cells. Nature 493, 542–546 (2013). https:\u002F\u002Fdoi.org\u002F10.1038\u002Fnature11743\nY. Ou, S.J. Wang, L. Jiang, B. Zheng, W. Gu, p53 protein-mediated regulation of phosphoglycerate dehydrogenase (PHGDH) is crucial for the apoptotic response upon serine starvation. J. Biol. Chem. 290, 457–466 (2015). https:\u002F\u002Fdoi.org\u002F10.1074\u002Fjbc.M114.616359\nT. Terzian, Y.A. Suh, T. Iwakuma, S.M. Post, M. Neumann, G.A. Lang, C.S. Van Pelt, G. Lozano, The inherent instability of mutant p53 is alleviated by Mdm2 or p16INK4a loss. Genes Dev. 22, 1337–1344 (2008). https:\u002F\u002Fdoi.org\u002F10.1101\u002Fgad.1662908\nM. Halasi, M. Wang, T.S. Chavan, V. Gaponenko, N. Hay, A.L. Gartel, ROS inhibitor N-acetyl-L-cysteine antagonizes the activity of proteasome inhibitors. Biochem. J. 454, 201–208 (2013). https:\u002F\u002Fdoi.org\u002F10.1042\u002FBJ20130282\nA.M. Florea, D. 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Cell 67, 377–388 (1991). https:\u002F\u002Fdoi.org\u002F10.1016\u002F0092-8674(91)90189-6\nK.H. Lee, S. Evans, T.Y. Ruan, A.B. Lassar, SMAD-mediated modulation of YY1 activity regulates the BMP response and cardiac-specific expression of a GATA4\u002F5\u002F6-dependent chick Nkx2.5 enhancer. Development 131, 4709–4723 (2004). https:\u002F\u002Fdoi.org\u002F10.1242\u002Fdev.01344\nS. Wu, H. Wang, Y. Li, Y. Xie, C. Huang, H. Zhao, M. Miyagishi, V. Kasim, Transcription factor YY1 promotes cell proliferation by directly activating the pentose phosphate pathway. Cancer Res. 78, 4549–4562 (2018). https:\u002F\u002Fdoi.org\u002F10.1158\u002F0008-5472.CAN-17-4047",{"VOID":1243},"10.1007\u002Fs13402-023-00823-8","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs13402-023-00823-8",[1246,1270,1283,1296,1309,1322,1335,1350,1363],{"id":1247,"sortIndex":21,"researcher":20,"roles":1248,"affiliations":1249,"properties":1267,"displayName":1269,"givenName":20,"familyName":20},"1ff0822d-dd17-4b1d-b782-067083ef418a",[1021],[1250,1258],{"id":1251,"sortIndex":21,"affiliation":1252,"properties":20},"37f57a6d-a0e5-4f0c-b587-e525955b660c",{"id":1251,"createTime":20,"updateTime":20,"relativeEntities":1253,"slug":20,"properties":1254,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1257,"statistic":20},[],{"title":1255},{"VI":1256},"Precise Genome Engineering Centre, School of Life Sciences, Guangzhou University, 510006, Guangzhou, China",[],{"id":1259,"sortIndex":198,"affiliation":1260,"properties":1266},"dbfbe60e-8630-4150-96a9-9ba36c020bf3",{"id":1259,"createTime":20,"updateTime":20,"relativeEntities":1261,"slug":20,"properties":1262,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1265,"statistic":20},[],{"title":1263},{"VI":1264},"Department of Urology, Shanghai General Hospital, Shanghai Jiaotong University, Shanghai, China",[],{},{"title":1268},{"VI":1269},"Tiezhu Shi",{"id":1271,"sortIndex":198,"researcher":20,"roles":1272,"affiliations":1273,"properties":1280,"displayName":1282,"givenName":20,"familyName":20},"9501d9d8-7418-4a40-a5d4-52fac96bfc4b",[1021],[1274],{"id":1259,"sortIndex":21,"affiliation":1275,"properties":20},{"id":1259,"createTime":20,"updateTime":20,"relativeEntities":1276,"slug":20,"properties":1277,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1279,"statistic":20},[],{"title":1278},{"VI":1264},[],{"title":1281},{"VI":1282},"Zhihao Yuan",{"id":1284,"sortIndex":280,"researcher":20,"roles":1285,"affiliations":1286,"properties":1293,"displayName":1295,"givenName":20,"familyName":20},"7fc2b0c1-ff50-4dd1-b06a-e0371c368506",[1021],[1287],{"id":1251,"sortIndex":21,"affiliation":1288,"properties":20},{"id":1251,"createTime":20,"updateTime":20,"relativeEntities":1289,"slug":20,"properties":1290,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1292,"statistic":20},[],{"title":1291},{"VI":1256},[],{"title":1294},{"VI":1295},"Yanying He",{"id":1297,"sortIndex":200,"researcher":20,"roles":1298,"affiliations":1299,"properties":1306,"displayName":1308,"givenName":20,"familyName":20},"ff99a9bc-5ab3-4a7d-8372-f88d9b904d78",[1021],[1300],{"id":1259,"sortIndex":21,"affiliation":1301,"properties":20},{"id":1259,"createTime":20,"updateTime":20,"relativeEntities":1302,"slug":20,"properties":1303,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1305,"statistic":20},[],{"title":1304},{"VI":1264},[],{"title":1307},{"VI":1308},"Dongliang 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transcriptional profiling reveals cell heterogeneity and clinically relevant traits in intra-operatively collected patient-derived tissue. So far, single-cell studies have been constrained by the requirement for prospectively collected fresh or cryopreserved tissue. This limitation might be overcome by recent technical developments enabling single-cell analysis of FFPE tissue. We benchmark single-cell profiles from patient-matched fresh, cryopreserved and archival FFPE cancer tissue. We find that fresh tissue and FFPE routine blocks can be employed for the robust detection of clinically relevant traits on the single-cell level. Specifically, single-cell maps of fresh patient tissues and corresponding FFPE tissue blocks could be integrated into common low-dimensional representations, and cell subtype clusters showed highly correlated transcriptional strengths of signaling pathway, hallmark, and clinically useful signatures, although expression of single genes varied due to technological differences. FFPE tissue blocks revealed higher cell diversity compared to fresh tissue. In contrast, single-cell profiling of cryopreserved tissue was prone to artifacts in the clinical setting. Our analysis highlights the potential of single-cell profiling in the analysis of retrospectively and prospectively collected archival pathology cohorts and increases the applicability in translational research.",{"EN":1447},"Robust detection of clinically relevant features in single-cell RNA profiles of patient-matched fresh and formalin-fixed paraffin-embedded (FFPE) lung cancer tissue",{"EN":1449},"",{"VOID":1451},"A. Maynard, C.E. McCoach, J.K. Rotow, L. Harris, F. Haderk, D.L. Kerr et al., Therapy-induced evolution of human lung cancer revealed by single-cell RNA sequencing. Cell 182(5), 1232–1251.e22 (2020)\nB. Chen, C.R. Scurrah, E.T. McKinley, A.J. Simmons, M.A. Ramirez-Solano, X. Zhu et al., Differential pre-malignant programs and microenvironment chart distinct paths to malignancy in human colorectal polyps. Cell 184(26), 6262–6280.e26 (2021)\nY.C. Cohen, M. Zada, S.Y. Wang, C. Bornstein, E. David, A. Moshe et al., Identification of resistance pathways and therapeutic targets in relapsed multiple myeloma patients through single-cell sequencing. Nat. Med. 27(3), 491–503 (2021)\nL. Ma, M.O. Hernandez, Y. Zhao, M. Mehta, B. Tran, M. Kelly et al., Tumor cell biodiversity drives microenvironmental reprogramming in liver cancer. Cancer Cell 36(4), 418–430.e6 (2019)\nC.J. Hanley, S. Waise, M.J. Ellis, M.A. Lopez, W.Y. Pun, J. Taylor et al., Single-cell analysis reveals prognostic fibroblast subpopulations linked to molecular and immunological subtypes of lung cancer. Nat. Commun. 14(1), 387 (2023)\nC.A. Stewart, C.M. Gay, Y. Xi, S. Sivajothi, V. Sivakamasundari, J. Fujimoto et al., Single-cell analyses reveal increased intratumoral heterogeneity after the onset of therapy resistance in small-cell lung cancer. Nat. Cancer 1, 423–436 (2020)\nM. Slyper, C.B.M. Porter, O. Ashenberg, J. Waldman, E. Drokhlyansky, I. Wakiro et al., A single-cell and single-nucleus RNA-Seq toolbox for fresh and frozen human tumors. Nat. Med. 26(5), 792–802 (2020)\nA. Janesick, R. Shelansky, A.D. Gottscho, F. Wagner, M. Rouault, G. Beliakoff et al., High resolution mapping of the breast cancer tumor microenvironment using integrated single cell, spatial and in situ analysis of FFPE tissue. bioRxiv 2022.10.06.510405 (2022). https:\u002F\u002Fdoi.org\u002F10.1101\u002F2022.10.06.510405\nA.F. Vallejo, K. Harvey, T. Wang, K. Wise, L.M. Butler, J. Polo et al., snPATHO-seq: unlocking the FFPE archives for single nucleus RNA profiling. bioRxiv 2022.08.23.505054 (2022). https:\u002F\u002Fdoi.org\u002F10.1101\u002F2022.08.23.505054\nH. Chung, A. Melnikov, C. McCabe, E. Drokhlyansky, V.W. N., E.M. Magee et al., SnFFPE-Seq: towards scalable single nucleus RNA-Seq of formalin-fixed paraffin-embedded (FFPE) tissue. bioRxiv 2022.08.25.505257 (2022). https:\u002F\u002Fdoi.org\u002F10.1101\u002F2022.08.25.505257\nY. Hao, S. Hao, E. Andersen-Nissen, W.M. Mauck, S. Zheng, A. Butler et al., Integrated analysis of multimodal single-cell data. Cell 184(13), 3573–3587.e29 (2021)\nM.D. Young, S. Behjati, SoupX removes ambient RNA contamination from droplet-based single-cell RNA sequencing data. Gigascience 9(12), giaa151 (2020)\nM. Schubert, B. Klinger, M. Klünemann, A. Sieber, F. Uhlitz, S. Sauer et al., Perturbation-response genes reveal signaling footprints in cancer gene expression. Nat. Commun. 9(1), 20 (2018)\nA. Neuschulz, O. Bakina, V. Badillo-Lisakowski, P. Olivares-Chauvet, T. Conrad, M. Gotthardt et al., A single-cell RNA labeling strategy for measuring stress response upon tissue dissociation. Mol. Syst. Biol. 19(2), e11147 (2023)\nA. Liberzon, C. Birger, H. Thorvaldsdóttir, M. Ghandi, J.P. Mesirov, P. Tamayo, The molecular signatures database hallmark gene set collection. Cell Syst. 1, 417–425 (2015)\nP. Bischoff, A. Trinks, B. Obermayer, J.P. Pett, J. Wiederspahn, F. Uhlitz et al., Single-cell RNA sequencing reveals distinct tumor microenvironmental patterns in lung adenocarcinoma. Oncogene 40(50), 6748–6758 (2021)\nG.J. Yoshida, Regulation of heterogeneous cancer-associated fibroblasts: the molecular pathology of activated signaling pathways. J. Exp. Clin. Cancer Res. 39(1), 112 (2020)\nF. Castro, A.P. Cardoso, R.M. Gonçalves, K. Serre, M.J. Oliveira, Interferon-gamma at the crossroads of tumor immune surveillance or evasion. Front. Immunol. 9, 847 (2018)\nM.G. Dorrington, I.D.C. Fraser, NF-κB signaling in macrophages: dynamics, crosstalk, and signal integration. Front. Immunol. 10, 705 (2019)\nM. Orecchioni, Y. Ghosheh, A.B. Pramod, K. Ley, Macrophage polarization: different gene signatures in M1(Lps+) vs. classically and M2(LPS−) vs. alternatively activated macrophages. Front. Immunol. 10, 1084 (2019)\nX. Guo, Y. Zhang, L. Zheng, C. Zheng, J. Song, Q. Zhang et al., Global characterization of T cells in non-small-cell lung cancer by single-cell sequencing. Nat. Med. 24(7), 978–985 (2018)\nA.M. Gocher, C.J. Workman, D.A.A. Vignali, Interferon-γ: teammate or opponent in the tumour microenvironment? Nat. Rev. Immunol. 22(3), 158–172 (2021)\nR.C. Jones, J. Karkanias, M.A. Krasnow, A.O. Pisco, S.R. Quake, J. Salzman et al., The Tabula Sapiens: a multiple-organ, single-cell transcriptomic atlas of humans. Science 376(6594), eabl4896 (2022)\nJ.M. Chan, Á. Quintanal-Villalonga, V.R. Gao, Y. Xie, V. Allaj, O. Chaudhary et al., Signatures of plasticity, metastasis, and immunosuppression in an atlas of human small cell lung cancer. Cancer Cell 39(11), 1479–1496.e18 (2021)\nK.J. Travaglini, A.N. Nabhan, L. Penland, R. Sinha, A. Gillich, R.V. Sit et al., A molecular cell atlas of the human lung from single-cell RNA sequencing. Nature 587(7835), 619–625 (2020)",{"VOID":1453},"10.1007\u002Fs13402-024-00922-0","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs13402-024-00922-0",[1456,1471,1486,1499,1514,1535,1556,1575,1600],{"id":1457,"sortIndex":21,"researcher":20,"roles":1458,"affiliations":1459,"properties":1468,"displayName":1470,"givenName":20,"familyName":20},"92ac2465-32c2-41a7-913d-156b6bab378a",[1021],[1460],{"id":1461,"sortIndex":21,"affiliation":1462,"properties":20},"c45fab55-3df3-4665-831d-de171047cfbb",{"id":1461,"createTime":20,"updateTime":20,"relativeEntities":1463,"slug":20,"properties":1464,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1467,"statistic":20},[],{"title":1465},{"VI":1466},"Bioportal Single Cells, Berlin Institute of Health at Charité – Universitätsmedizin Berlin, Berlin, Germany",[],{"title":1469},{"VI":1470},"Alexandra 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Bischoff",{"url":20,"publisher":1628,"properties":20},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1629,"slug":10,"properties":1630,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1634,"manageAffiliations":1651,"indexDatabases":1662,"url":20,"thumbnailPath":20,"statistic":1677,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":1631,"title":1632,"eissn":1633},{"VOID":13},{"EN":15},{"VOID":17},[1635,1639,1643,1647],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1636,"label":1637,"description":1638,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":1640,"label":1641,"description":1642,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":33},{},{"id":36,"createTime":20,"updateTime":20,"relativeEntities":1644,"label":1645,"description":1646,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":39},{},{"id":42,"createTime":20,"updateTime":20,"relativeEntities":1648,"label":1649,"description":1650,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":45},{},[1652,1657],{"id":49,"createTime":20,"updateTime":20,"relativeEntities":1653,"slug":20,"properties":1654,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1656,"statistic":20},[],{"title":1655},{"EN":53},[55],{"id":57,"createTime":20,"updateTime":20,"relativeEntities":1658,"slug":20,"properties":1659,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1661,"statistic":20},[],{"title":1660},{"EN":61},[],[1663,1670],{"id":65,"indexDatabase":1664,"url":78,"indexYears":20,"academicFieldIds":1669,"indexDatabaseRanking":20},{"id":67,"createTime":20,"updateTime":20,"relativeEntities":1665,"label":1666,"description":1667,"key":74,"publicationTags":1668,"standard":20},[],{"EN":70,"VI":70},{"EN":72,"VI":73},[76,77],[80,81,82],{"id":84,"indexDatabase":1671,"url":95,"indexYears":96,"academicFieldIds":1676,"indexDatabaseRanking":102},{"id":86,"createTime":20,"updateTime":20,"relativeEntities":1672,"label":1673,"description":1674,"key":92,"publicationTags":1675,"standard":20},[],{"EN":89,"VI":89},{"EN":89,"VI":91},[94],[98,99,100,101],{"impactFactor":21,"impactFactorByYear":1678,"i10Index":117,"i10IndexLast5Year":118,"totalPublication":119,"totalPublicationByYear":1679,"totalCitation":134,"totalCitationByYear":1680,"totalCitationPerPublication":149,"totalCitationPerPublicationByYear":1681,"hindexLast5Year":118,"hindex":118},{"2012":105,"2013":106,"2014":107,"2015":108,"2016":109,"2017":110,"2018":111,"2019":112,"2020":113,"2021":114,"2022":115,"2023":116},{"2011":121,"2012":122,"2013":118,"2014":123,"2015":124,"2016":125,"2017":126,"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":133},{"2011":136,"2012":137,"2013":138,"2014":139,"2015":140,"2016":141,"2017":142,"2018":143,"2019":144,"2020":145,"2021":146,"2022":147,"2023":148},{"2011":151,"2012":152,"2013":153,"2014":154,"2015":155,"2016":156,"2017":157,"2018":158,"2019":159,"2020":160,"2021":161,"2022":162,"2023":163},"2024-02-01",2024,[76,102],{"id":1686,"createTime":1687,"updateTime":1688,"relativeEntities":1689,"slug":1690,"properties":1691,"entityType":1014,"verifyStatus":186,"verifyTime":1688,"verifyNote":1015,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1700,"fullTextUrl":20,"authors":1701,"publicationType":1164,"publisherRelationship":1778,"citationCount":20,"citationInfo":20,"publishDate":1838,"publishYear":1839,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":1840,"openAccess":20,"references":20,"isForceReanalyzing":1228},"00f731be-be40-49f6-b142-550ec369334d","2024-02-06T09:49:49.570+00:00","2025-02-20T07:36:43.472+00:00",[],"Leptin-induced-signaling-pathways-in-cancer-cell-migration-and-invasion",{"abstract":1692,"title":1694,"references":1696,"doi":1698},{"EN":1693},"Increasing evidence indicates that obesity is associated with tumor development and progression. Leptin is an adipocyte-related hormone with a key role in energy metabolism and whose circulating levels are elevated in obesity. The effect of leptin on cancer progression and metastasis and its underlying mechanisms are still unclear. Leptin can impact various steps in tumor metastasis, including epithelial-mesenchymal transition, cell adhesion to the extracellular matrix (ECM), and proteolysis of ECM components. To do so, leptin binds to its receptor (OB-Rb) to activate signaling pathways and downstream effectors that participate in tumor cell invasion as well as distant metastasis. In this review, we describe metastasis steps in detail and characterize metastasis-related molecules activated by leptin, which may help to develop a roadmap that guides future work. In addition, we conclude that a profound understanding of the fundamental molecular processes that contribute to leptin-induced metastasis may pave the way for the development of new prognostic molecules and appropriate approaches to the treatment of obesity-related cancers.",{"EN":1695},"Leptin-induced signaling pathways in cancer cell migration and invasion",{"VOID":1697},"I. Vucenik, J.P. Stains, Obesity and cancer risk: evidence, mechanisms, and recommendations. Ann. N. Y. Acad. Sci. 1271, 37–43 (2012)\nE.-J. Choi, H.-R. Kim, J.-H. Kie, B.-I. Moon and J.-Y. Seoh, Attenuation of obesity and related metabolic disorders by the individual or combination treatment with IL-2\u002Fanti-IL-2 complex and hyperbaric oxygen. bioRxiv. 351841 (2018)\nM.I. Goran, G.D. Ball, M.L. Cruz, Obesity and risk of type 2 diabetes and cardiovascular disease in children and adolescents. J. Clin. Endocrinol. Metab. 88, 1417–1427 (2003)\nA. Khodabakhshi, M. Ghayour-Mobarhan, H. Rooki, R. Vakili, S. 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Mashhad University of Medical Sciences, Mashhad, Iran",[],{},{"title":1761},{"VI":1762},"Mohsen Azimi-Nejad",{"id":1764,"sortIndex":200,"researcher":20,"roles":1765,"affiliations":1766,"properties":1775,"displayName":1777,"givenName":20,"familyName":20},"b338ee26-9172-46ab-bbee-449d9eb3161b",[1021],[1767],{"id":1768,"sortIndex":21,"affiliation":1769,"properties":20},"beab38ae-ab2e-4a0c-8347-6c37c3a5d890",{"id":1768,"createTime":20,"updateTime":20,"relativeEntities":1770,"slug":20,"properties":1771,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1774,"statistic":20},[],{"title":1772},{"VI":1773},"Surgical Oncology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran",[],{"title":1776},{"VI":1777},"Seyed Isaac Hashemy",{"url":1700,"publisher":1779,"properties":1833},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1780,"slug":10,"properties":1781,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":1785,"manageAffiliations":1802,"indexDatabases":1813,"url":20,"thumbnailPath":20,"statistic":1828,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":1782,"title":1783,"eissn":1784},{"VOID":13},{"EN":15},{"VOID":17},[1786,1790,1794,1798],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":1787,"label":1788,"description":1789,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":1791,"label":1792,"description":1793,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":33},{},{"id":36,"createTime":20,"updateTime":20,"relativeEntities":1795,"label":1796,"description":1797,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":39},{},{"id":42,"createTime":20,"updateTime":20,"relativeEntities":1799,"label":1800,"description":1801,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":45},{},[1803,1808],{"id":49,"createTime":20,"updateTime":20,"relativeEntities":1804,"slug":20,"properties":1805,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1807,"statistic":20},[],{"title":1806},{"EN":53},[55],{"id":57,"createTime":20,"updateTime":20,"relativeEntities":1809,"slug":20,"properties":1810,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1812,"statistic":20},[],{"title":1811},{"EN":61},[],[1814,1821],{"id":65,"indexDatabase":1815,"url":78,"indexYears":20,"academicFieldIds":1820,"indexDatabaseRanking":20},{"id":67,"createTime":20,"updateTime":20,"relativeEntities":1816,"label":1817,"description":1818,"key":74,"publicationTags":1819,"standard":20},[],{"EN":70,"VI":70},{"EN":72,"VI":73},[76,77],[80,81,82],{"id":84,"indexDatabase":1822,"url":95,"indexYears":96,"academicFieldIds":1827,"indexDatabaseRanking":102},{"id":86,"createTime":20,"updateTime":20,"relativeEntities":1823,"label":1824,"description":1825,"key":92,"publicationTags":1826,"standard":20},[],{"EN":89,"VI":89},{"EN":89,"VI":91},[94],[98,99,100,101],{"impactFactor":21,"impactFactorByYear":1829,"i10Index":117,"i10IndexLast5Year":118,"totalPublication":119,"totalPublicationByYear":1830,"totalCitation":134,"totalCitationByYear":1831,"totalCitationPerPublication":149,"totalCitationPerPublicationByYear":1832,"hindexLast5Year":118,"hindex":118},{"2012":105,"2013":106,"2014":107,"2015":108,"2016":109,"2017":110,"2018":111,"2019":112,"2020":113,"2021":114,"2022":115,"2023":116},{"2011":121,"2012":122,"2013":118,"2014":123,"2015":124,"2016":125,"2017":126,"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":133},{"2011":136,"2012":137,"2013":138,"2014":139,"2015":140,"2016":141,"2017":142,"2018":143,"2019":144,"2020":145,"2021":146,"2022":147,"2023":148},{"2011":151,"2012":152,"2013":153,"2014":154,"2015":155,"2016":156,"2017":157,"2018":158,"2019":159,"2020":160,"2021":161,"2022":162,"2023":163},{"pages":1834,"volume":1836},{"VOID":1835},"243-260",{"VOID":1837},"42","2019-03-15",2019,[76,102],{"id":1842,"createTime":1843,"updateTime":1844,"relativeEntities":1845,"slug":1846,"properties":1847,"entityType":1014,"verifyStatus":186,"verifyTime":1844,"verifyNote":1015,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1856,"fullTextUrl":20,"authors":1857,"publicationType":1164,"publisherRelationship":1996,"citationCount":20,"citationInfo":20,"publishDate":2056,"publishYear":2057,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":2058,"openAccess":20,"references":20,"isForceReanalyzing":1228},"011d34e9-caaa-4183-9bf4-975620244f82","2024-01-26T06:52:52.867+00:00","2025-01-15T16:32:27.718+00:00",[],"Functional-relationship-between-CFTR-and-RAC3-expression-for-maintaining-cancer-cell-stemness-in-human-colorectal-cancer",{"abstract":1848,"title":1850,"references":1852,"doi":1854},{"EN":1849},"CFTR mutations not only cause cystic fibrosis, but also increase the risk of colorectal cancer. A putative role of CFTR in colorectal cancer patients without cystic fibrosis has so far, however, not been investigated. RAC3 is a nuclear receptor coactivator that has been found to be overexpressed in several human tumors, and to be required for maintaining cancer stemness. Here, we investigated the functional relationship between CFTR and RAC3 for maintaining cancer stemness in human colorectal cancer. Cancer stemness was investigated by analysing the expression of stem cell markers, clonogenic growth and selective retention of fluorochrome, using stable transfection of shCFTR or shRAC3 in HCT116 colorectal cancer cells. In addition, we performed pathway enrichment and network analyses in both primary human colorectal cancer samples (TCGA, Xena platform) and Caco-2 colorectal cancer cells including (1) CD133+ or CD133- side populations and (2) CFTRwt or CFTRmut cells (ConsensusPathDB, STRING, Cytoscape, GeneMANIA). We found that the CD133+ side population expresses higher levels of RAC3 and CFTR than the CD133- side population. RAC3 overexpression increased CFTR expression, whereas CFTR downregulation inhibited the cancer stem phenotype. CFTR mRNA levels were found to be increased in colorectal cancer samples from patients without cystic fibrosis compared to those with CFTR mutations, and this correlated with an increased expression of RAC3. The expression pattern of a gene set involved in inflammatory response and nuclear receptor modulation in CD133+ Caco-2 cells was found to be shared with that in CFTRwt Caco-2 cells. These genes may contribute to colorectal cancer development. CFTR may play a non-tumor suppressor role in colorectal cancer development and maintenance involving enhancement of the expression of a set of genes related to cancer stemness and development in patients without CFTR mutations.",{"EN":1851},"Functional relationship between CFTR and RAC3 expression for maintaining cancer cell stemness in human colorectal cancer",{"VOID":1853},"K.J. Anderson, R.T. Cormier, P.M. Scott, Role of ion channels in gastrointestinal cancer. World J. Gastroenterol. 25, 5732–5772 (2019). https:\u002F\u002Fdoi.org\u002F10.3748\u002Fwjg.v25.i38.5732\nA.G. Palma, L. Galizia, B.A. Kotsias, G.I. Marino, CFTR channel in oocytes from Xenopus laevis and its regulation by xShroom1 protein. Eur. J. Physiol. 468, 871–880 (2016). https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs00424-016-1800-2\nD.G. Tang, Understanding cancer stem cell heterogeneity and plasticity. Cell Res. 22, 457–472 (2012). doi:https:\u002F\u002Fdoi.org\u002F10.1038\u002Fcr.2012.13\nP. Scott, K. Anderson, M. Singhania, R. Cormier, Cystic fibrosis, CFTR, and colorectal cancer. Int. J. Mol. Sci. 21, 2891 (2020). https:\u002F\u002Fdoi.org\u002F10.3390\u002Fijms21082891\nB.L. Than, J.F. Linnekamp, T.K. Starr, D.A. Largaespada, A. Rod, Y. Zhang, V. Bruner, J. Abrahante, A. Schumann, T. Luczak, J. Walter, A. Niemczyk, M.G. O’Sullivan, J.P. Medema, R.J. Fijneman, G.A. Meijer, E. Van den Broek, C.A. Hodges, P.M. Scott, L. Vermeulen, R.T. Cormier, CFTR is a tumor suppressor gene in murine and human intestinal cancer. Oncogene 35, 4179–4187 (2016). https:\u002F\u002Fdoi.org\u002F10.1038\u002Fonc.2015.483\nB.B. Tysnes, R. Bjerkvig, Cancer initiation and progression: involvement of stem cells and the microenvironment. Biochim. Biophys. Acta 1775, 283–297 (2007). doi:https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.bbcan.2007.01.001\nC.T. Jordan, M.L. Guzman, M. Noble, Cancer stem cells. N. Engl. J. Med. 355, 1253–1261 (2006)\nC. Sakakura, A. Hagiwara, R. Yasuoka, Y. Fujita, M. Nakanishi, K. Masuda, A. Kimura, Y. Nakamura, J. Inazawa, T. Abe, H. Yamagishi, Amplification and over-expression of the AIB1 nuclear receptor co-activator gene in primary gastric cancers. Int. J. Cancer 89, 217–223 (2000)\nS. Anzick, J. Kononen, R. Walker, D. Azorsa, M. Tanner, X. Guan, G. Sauter, O. Kallioniemi, J. Trent, P. Meltzer, AIB1, a steroid receptor coactivator amplified in breast and ovarian cancer. Science 277, 965–968 (1997)\nR.T. Henke, B.R. Haddad, S.E. Kim, J.D. Rone, A. Mani, J.M. Jessup, A. Wellstein, A. Maitra, A.T. Riegel, Overexpression of the nuclear receptor coactivator AIB1 (SRC-3) during progression of pancreatic adenocarcinoma. Clin. Cancer Res. 10, 6134–6142 (2004)\nH.J. Zhou, J. Yan, W. Luo, G. Ayala, S.H. Lin, H. Erdem, M. Ittmann, S.Y. Tsai, M.J. Tsai, SRC-3 is required for prostate cancer cell proliferation and survival. Cancer Res. 65, 7976–7983 (2005)\nL.C. Panelo, M.S. Machado, M.F. Rubio, F. Jaworski, C.V. Alvarado, L.A. Paz, A.J. Urtreger, E. Vazquez, M.A. Costas, High RAC3 expression levels are required for induction and maintaining of cancer cell stemness. Oncotarget 9, 5848–5860 (2018). doi:https:\u002F\u002Fdoi.org\u002F10.18632\u002Foncotarget.23635\nM.S. Machado, F.D. Rosa, M.C. Lira, A.J. Urtreger, M.F. Rubio, M.A. Costas, The inflammatory cytokine TNF contributes with RAC3-induced malignant transformation. EXCLI J. 17, 1030–1042 (2018). https:\u002F\u002Fdoi.org\u002F10.17179\u002Fexcli2018-1759\nS. Werbajh, I. Nojek, R. Lanz, M.A. Costas, RAC-3 is a NF-kB coactivator. FEBS Lett. 485, 195–199 (2000)\nG.P. Colo, R.R. Rosato, S. Grant, M.A. Costas, RAC3 down-regulation sensitizes human chronic myeloid leukemia cells to TRAIL-induced apoptosis. FEBS Lett. 581, 5075–5081 (2007)\nG.P. Colo, M.F. Rubio, I.M. Nojek, S.E. Werbajh, P.C. Echeverria, C.V. Alvarado, V.E. Nahmod, M.D. Galigniana, M.A. Costas, The p160 nuclear receptor co-activator RAC3 exerts an anti-apoptotic role through a cytoplasmatic action. Oncogene 27, 2430–2444 (2008)\nP.N. Fernandez Larrosa, M. Ruiz Grecco, D. Mengual Gomez, C.V. Alvarado, L.C. Panelo, M.F. Rubio, D.F. Alonso, D.E. Gomez and M.A. Costas. RAC3 more than a nuclear receptor coactivator: a key inhibitor of senescence that is downregulated in aging. Cell Death Dis 6, e1902 (2015) https:\u002F\u002Fdoi.org\u002F10.1038\u002Fcddis.2015.218\nM.F. Rubio, M.C. Lira, F.D. Rosa, A.D. Sambresqui, Salazar Guemes and M.A. Costas. RAC3 influences the chemoresistance of colon cancer cells through autophagy and apoptosis inhibition. Cancer Cell Int. 17, 111 (2017). https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs12935-017-0483-x\nG. Ma, Y. Ren, K. Wang, J. He, SRC-3 has a role in cancer other than as a nuclear receptor coactivator. Int. J. Biol. Sci. 7, 664–672 (2011)\nC.V. Alvarado, M.F. Rubio, P.N. Fernandez Larrosa, L. Panelo, P.J. Azurmendi, M. Ruiz Grecco, G.A. Martínez-Noël, M.A. Costas, The levels of RAC3 expression are up regulated by TNF in the inflammatory response. FEBS Open Bio 4, 450–457 (2014). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.fob.2014.04.009\nN. Ameen, J. Alexis, P. Salas, Cellular localization of the cystic fibrosis transmembrane conductance regulator in mouse intestinal tract. Histochem. Cell Biol. 114, 69–75 (2000). doi:https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs004180000164\nA.M. Strubberg, J. Liu, N.M. Walker, C.D. Stefanski, R.J. MacLeod, S.T. Magness, L.L. Clarke, Cftr modulates Wnt\u002Fbeta-catenin signaling and stem cell proliferation in murine intestine. Cell. Mol. Gastroenterol. Hepatol. 5, 253–271 (2018). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jcmgh.2017.11.013\nG.M. Seigel, L.M. Campbell, High-throughput microtiter assay for Hoechst 33342 dye uptake. Cytotechnology 45, 155–160 (2004). doi:https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs10616-004-7256-9\nS. Hao, E.A. Roesch, A. Perez, R.L. Weiner, L.C. Henderson, L. Cummings, P. Consiglio, J. Pajka, A. Eisenberg, L. Yeh, C.U. Cotton, M.L. Drumm, Inactivation of CFTR by CRISPR\u002FCas9 alters transcriptional regulation of inflammatory pathways and other networks. J. Cyst. Fibros. 19, 34–39 (2020). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jcf.2019.05.003\nR. Herwig, C. Hardt, M. Lienhard, A. Kamburov, Analyzing and interpreting genome data at the network level with ConsensusPathDB. Nat. Protoc. 11, 1889–1907 (2016). https:\u002F\u002Fdoi.org\u002F10.1038\u002Fnprot.2016.117\nM.J. Goldman, B. Craft, M. Hastie, K. Repecka, F. McDade, A. Kamath, A. Banerjee, Y. Luo, D. Rogers, A.N. Brooks, J. Zhu, D. Haussler, Visualizing and interpreting cancer genomics data via the Xena platform. Nat. Biotechnol. 38, 675–678 (2020). https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41587-020-0546-8\nX. Yu, Y. Lin, X. Yan, Q. Tian, L. Li, E.H. Lin, CD133, Stem cells, and cancer stem cells: Myth or reality? Curr. Colorect. Cancer Rep. 7, 253–259 (2011). https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs11888-011-0106-1\nK. Liu, X. Zhang, J.T. Zhang, L.L. Tsang, X. Jiang, H.C. Chan, Defective CFTR- beta-catenin interaction promotes NF-kappaB nuclear translocation and intestinal inflammation in cystic fibrosis. Oncotarget 7, 64030–64042 (2016). doi:https:\u002F\u002Fdoi.org\u002F10.18632\u002Foncotarget.11747\nL. Zeng, Q. Xiao, M. Chen, A. Margariti, D. Martin, A. Ivetic, H. Xu, J. Mason, W. Wang, G. Cockerill, K. Mori, J.Y. Li, S. Chien, Y. Hu, Q. Xu, Vascular endothelial cell growth-activated XBP1 splicing in endothelial cells is crucial for angiogenesis. Circulation 127, 1712–1722 (2013). doi:https:\u002F\u002Fdoi.org\u002F10.1161\u002FCIRCULATIONAHA.112.001337\nP. Li, J. Singh, Y. Sun, X. Ma, P. Yuan, CFTR constrains the differentiation from mouse embryonic stem cells to intestine lineage cells. Biochem. Biophys. Res. Commun. 510, 322–328 (2019). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.bbrc.2019.01.100\nR.A. Padua, N. Warren, D. Grimshaw, M. Smith, C. Lewis, J. Whittaker, P. Laidler, P. Wright, A. Douglas-Jones, P. Fenaux, A. Sharma, K. Horgan and R. West. The cystic fibrosis delta F508 gene mutation and cancer. Hum. Mut. 10, 45–48 (1997). https:\u002F\u002Fdoi.org\u002F10.1002\u002F(SICI)1098-1004(1997)10:1\u003C45::AID-HUMU6>3.0.CO;2-L\nR.L. Jakab, A.M. Collaco, N.A. Ameen, Physiological relevance of cell-specific distribution patterns of CFTR, NKCC1, NBCe1, and NHE3 along the crypt-villus axis in the intestine. Am. J. Physiol. 300, G82–G98 (2011). https:\u002F\u002Fdoi.org\u002F10.1152\u002Fajpgi.00245.2010\nN. Barker, J.H. van Es, J. Kuipers, P. Kujala, M. van den Born, M. Cozijnsen, A. Haegebarth, J. Korving, H. Begthel, P.J. Peters, H. Clevers, Identification of stem cells in small intestine and colon by marker gene Lgr5. Nature 449, 1003–1007 (2007). doi:https:\u002F\u002Fdoi.org\u002F10.1038\u002Fnature06196\nU. Bedi, V.K. Mishra, D. Wasilewski, C. Scheel, S.A. Johnsen, Epigenetic plasticity: a central regulator of epithelial-to-mesenchymal transition in cancer. Oncotarget 5, 2016–2029 (2014). doi:https:\u002F\u002Fdoi.org\u002F10.18632\u002Foncotarget.1875\nX. Yang, T. Yan, Y. Gong, X. Liu, H. Sun, W. Xu, C. Wang, D. Naren, Y. Zheng, High CFTR expression in Philadelphia chromosome-positive acute leukemia protects and maintains continuous activation of BCR-ABL and related signaling pathways in combination with PP2A. Oncotarget 8, 24437–24448 (2017). https:\u002F\u002Fdoi.org\u002F10.18632\u002Foncotarget.15510\nG.I. Marino, B.A. Kotsias, Cystic fibrosis transmembrane regulator (CFTR) in human trophoblast BeWo cells and its relation to cell migration. Placenta 35, 92–98 (2014). doi:https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.placenta.2013.12.004\nA.M. Crane, P. Kramer, J.H. Bui, W.J. Chung, X.S. Li, M.L. Gonzalez-Garay, F. Hawkins, W. Liao, D. Mora, S. Choi, J. Wang, H.C. Sun, D.E. Paschon, D.Y. Guschin, P.D. Gregory, D.N. Kotton, M.C. Holmes, E.J. Sorscher, B.R. Davis, Targeted correction and restored function of the CFTR gene in cystic fibrosis induced pluripotent stem cells. Stem Cell Rep. 4, 569–577 (2015). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.stemcr.2015.02.005\nJ.T. Zhang, Y. Wang, J.J. Chen, X.H. Zhang, J.D. Dong, L.L. Tsang, X.R. Huang, Z. Cai, H.Y. Lan, X.H. Jiang, H.C. Chan, Defective CFTR leads to aberrant beta-catenin activation and kidney fibrosis. Sci. Rep. 7, 5233 (2017). https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41598-017-05435-5\nZ. Li, CD133: a stem cell biomarker and beyond. Exp. Hematol. Oncol. 2, 17 (2013). https:\u002F\u002Fdoi.org\u002F10.1186\u002F2162-3619-2-17\nJ.M. Loo, A. Scherl, A. Nguyen, F.Y. Man, E. Weinberg, Z. Zeng, L. Saltz, P.B. Paty, S.F. Tavazoie, Extracellular metabolic energetics can promote cancer progression. Cell 160, 393–406 (2015). https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cell.2014.12.018",{"VOID":1855},"10.1007\u002Fs13402-021-00589-x","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs13402-021-00589-x",[1858,1873,1886,1899,1912,1934,1956,1976],{"id":1859,"sortIndex":21,"researcher":20,"roles":1860,"affiliations":1861,"properties":1870,"displayName":1872,"givenName":20,"familyName":20},"fcf2929b-b837-4d7e-81b1-7c8858a8a6a8",[1021],[1862],{"id":1863,"sortIndex":21,"affiliation":1864,"properties":20},"66238fd3-7f56-4f49-af5d-c3a598e495a7",{"id":1863,"createTime":20,"updateTime":20,"relativeEntities":1865,"slug":20,"properties":1866,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1869,"statistic":20},[],{"title":1867},{"VI":1868},"Laboratorio de Biología Molecular y Apoptosis, Instituto de Investigaciones Médicas Alfredo Lanari, IDIM-UBA-CONICET, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina",[],{"title":1871},{"VI":1872},"Alejandra Graciela Palma",{"id":1874,"sortIndex":198,"researcher":20,"roles":1875,"affiliations":1876,"properties":1883,"displayName":1885,"givenName":20,"familyName":20},"3236b232-0bef-43d8-b965-7158fb08bd57",[1021],[1877],{"id":1863,"sortIndex":21,"affiliation":1878,"properties":20},{"id":1863,"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":1882,"statistic":20},[],{"title":1881},{"VI":1868},[],{"title":1884},{"VI":1885},"Mileni Soares Machado",{"id":1887,"sortIndex":280,"researcher":20,"roles":1888,"affiliations":1889,"properties":1896,"displayName":1898,"givenName":20,"familyName":20},"804e75b1-5f29-43a0-9c6d-24804701efa1",[1021],[1890],{"id":1863,"sortIndex":21,"affiliation":1891,"properties":20},{"id":1863,"createTime":20,"updateTime":20,"relativeEntities":1892,"slug":20,"properties":1893,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1895,"statistic":20},[],{"title":1894},{"VI":1868},[],{"title":1897},{"VI":1898},"María Cecilia 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transforming growth factor (TGF)-β superfamily comprises cytokines such as TGF-β and Bone Morphogenetic Proteins (BMPs), which have a critical role in a multitude of biological processes. In breast cancer, high levels of TGF-β are associated with poor outcome, whereas inhibition of TGF-β-signaling reduces metastasis. In contrast, BMP-7 inhibits bone metastasis of breast cancer cells. In this study, we investigated the effect of BMP-7 on TGF-β-induced invasion in a 3 dimensional invasion assay. BMP-7 inhibited TGF-β-induced invasion of the metastatic breast cancer cell line MCF10CA1a, but not of its premalignant precursor MCF10AT in a spheroid invasion model. The inhibitory effect appears to be specific for BMP-7, as its closest homolog, BMP-6, did not alter the invasion of MCF10CA1a spheroids. To elucidate the mechanism by which BMP-7 inhibits TGF-β-induced invasion, we analyzed invasion-related genes. BMP-7 inhibited TGF-β-induced expression of integrin αvβ3 in the spheroids. Moreover, targeting of integrins by a chemical inhibitor or knockdown of integrin β3 negatively affected TGF-β-induced invasion. On the other hand, overexpression of integrin β3 counteracted the inhibitory effect of BMP7 on TGF-β-induced invasion. Thus, BMP-7 may exert anti-invasive actions by inhibiting TGF-β-induced expression of integrin β3.",{"EN":2069},"BMP-7 inhibits TGF-β-induced invasion of breast cancer cells through inhibition of integrin β3 expression",{"VOID":2071},"citation_journal_title=Nature; citation_title=The pathogenesis of cancer metastasis; citation_author=G Poste, IJ Fidler; citation_volume=283; citation_publication_date=1980; citation_pages=139-146; citation_doi=10.1038\u002F283139a0; citation_id=CR1\ncitation_journal_title=Nat. Rev. Canc.; citation_title=Role of integrins in cell invasion and migration; citation_author=JD Hood, DA Cheresh; citation_volume=2; citation_publication_date=2002; citation_pages=91-100; citation_doi=10.1038\u002Fnrc727; citation_id=CR2\ncitation_journal_title=Nat. Rev. Mol. Cell. 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cancer is one of the most aggressive cancers. Preclinical and clinical data indicate that Notch 1 ligand jagged1 (JAG1) plays a pro-oncogenic role in several malignant cancers. As yet, however, the role of JAG1 in pancreatic cancer is poorly understood. The objective of the present study was to investigate JAG1 as a therapeutic target in human pancreatic cancer. Expression levels of Notch signaling molecules were assessed using GEO datasets and Western blot analysis, respectively. Anti-tumor effects following JAG1 silencing were evaluated using in vitro and in vivo assays. Prognostic implications were assessed using GEO datasets. Using GEO datasets and Western blot analysis we detected significantly higher JAG1 mRNA and protein expression levels in pancreatic cancer compared to normal pancreatic tissues. JAG1 silencing significantly restrained the growth, migration and invasion of pancreatic cancer cells through the induction of apoptosis and blockade of various kinases independent of the Notch1 pathway. Combined JAG1 silencing and gemcitabine treatment showed synergistic anti-viability effects in human pancreatic cancer cells. JAG1 silencing also resulted in significant anti-cancer effects in vivo and high JAG1 expression was found to be associated with an adverse prognosis in pancreatic cancer patients. From our data we conclude that JAG1 may be a promising therapeutic target in pancreatic cancer.",{"EN":2326},"Association of Jagged1 expression with malignancy and prognosis in human pancreatic cancer",{"VOID":2328},"R. Siegel, J. Ma, Z. Zou, A. Jemal, Cancer statistics, 2014. CA Cancer J Clin 64, 9–29 (2014)\nJ. Schmidt, U. Abel, J. Debus, S. Harig, K. Hoffmann, T. Herrmann, D. Bartsch, J. Klein, U. Mansmann, D. Jager, L. Capussotti, R. Kunz, M.W. Buchler, Open-label, multicenter, randomized phase iii trial of adjuvant chemoradiation plus interferon alfa-2b versus fluorouracil and folinic acid for patients with resected pancreatic adenocarcinoma. Am J Clin Oncol 30, 4077–4083 (2012)\nN. Bardeesy, R.A. DePinho, Pancreatic cancer biology and genetics. Nat Rev Cancer 2, 897–909 (2002)\nC.E. Cano, Y. Motoo, J.L. Iovanna, Epithelial-to-mesenchymal transition in pancreatic adenocarcinoma. ScientificWorldJournal 10, 1947–1957 (2010)\nD. Singh, G. Upadhyay, R.K. Srivastava, S. Shankar, Recent advances in pancreatic cancer: Biology, treatment, and prevention. Biochim Biophys Acta 1856, 13–27 (2015)\nL. Miele, T. Golde, B. Osborne, Notch signaling in cancer. Curr Mol Med 6, 905–918 (2006)\nS. Weijzen, P. Rizzo, M. Braid, R. Vaishnav, S.M. Jonkheer, A. Zlobin, B.A. Osborne, S. Gottipati, J.C. Aster, W.C. Hahn, M. Rudolf, K. Siziopikou, W.M. Kast, L. Miele, Activation of notch-1 signaling maintains the neoplastic phenotype in human ras-transformed cells. Nat Med 8, 979–986 (2002)\nM. Reedijk, S. Odorcic, L. Chang, H. Zhang, N. Miller, D.R. McCready, G. Lockwood, S.E. Egan, High-level coexpression of jag1 and notch1 is observed in human breast cancer and is associated with poor overall survival. Cancer Res 65, 8530–8537 (2005)\nN. Sethi, X. Dai, C.G. Winter, Y. Kang, Tumor-derived jagged1 promotes osteolytic bone metastasis of breast cancer by engaging notch signaling in bone cells. Cancer Cell 19, 192–205 (2011)\nY. Dai, G. Wilson, B. Huang, M. Peng, G. Teng, D. Zhang, R. Zhang, M.P. Ebert, J. Chen, B.C. Wong, K.W. Chan, J. George, L. Qiao, Silencing of jagged1 inhibits cell growth and invasion in colorectal cancer. Cell Death Dis 5, e1170 (2014)\nB.W. Purow, R.M. Haque, M.W. Noel, Q. Su, M.J. Burdick, J. Lee, T. Sundaresan, S. Pastorino, J.K. Park, I. Mikolaenko, D. Maric, C.G. Eberhart, H.A. Fine, Expression of notch-1 andits ligands, delta-like-1 and jagged-1, is critical for glioma cell survival and proliferation. Cancer Res 65, 2353–2363 (2005)\nJ.T. Lin, M.K. Chen, K.T. Yeh, C.S. Chang, T.H. Chang, C.Y. Lin, Y.C. Wu, B.W. Su, K.D. Lee, P.J. 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AnnOncol 23, 1919–1925 (2012)",{"VOID":2330},"10.1007\u002Fs13402-020-00527-3","https:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs13402-020-00527-3",[2333,2348,2363],{"id":2334,"sortIndex":21,"researcher":20,"roles":2335,"affiliations":2336,"properties":2345,"displayName":2347,"givenName":20,"familyName":20},"100b0b2b-fee3-40b9-8adc-9a46eab83f02",[1021],[2337],{"id":2338,"sortIndex":21,"affiliation":2339,"properties":20},"c05edccc-c39d-403b-9403-48231b3e9f9e",{"id":2338,"createTime":20,"updateTime":20,"relativeEntities":2340,"slug":20,"properties":2341,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2344,"statistic":20},[],{"title":2342},{"VI":2343},"Department of Applied Life Science, SARI, Jeju National University, Jeju-do, Republic of Korea",[],{"title":2346},{"VI":2347},"Jungwhoi 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Jeju National University, Jeju-do, Republic of Korea",[],{},{"title":2383},{"VI":2384},"Jae Hoon Kim",{"url":2331,"publisher":2386,"properties":2440},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2387,"slug":10,"properties":2388,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":2392,"manageAffiliations":2409,"indexDatabases":2420,"url":20,"thumbnailPath":20,"statistic":2435,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":2389,"title":2390,"eissn":2391},{"VOID":13},{"EN":15},{"VOID":17},[2393,2397,2401,2405],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":2394,"label":2395,"description":2396,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":2398,"label":2399,"description":2400,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":33},{},{"id":36,"createTime":20,"updateTime":20,"relativeEntities":2402,"label":2403,"description":2404,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":39},{},{"id":42,"createTime":20,"updateTime":20,"relativeEntities":2406,"label":2407,"description":2408,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":45},{},[2410,2415],{"id":49,"createTime":20,"updateTime":20,"relativeEntities":2411,"slug":20,"properties":2412,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2414,"statistic":20},[],{"title":2413},{"EN":53},[55],{"id":57,"createTime":20,"updateTime":20,"relativeEntities":2416,"slug":20,"properties":2417,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2419,"statistic":20},[],{"title":2418},{"EN":61},[],[2421,2428],{"id":65,"indexDatabase":2422,"url":78,"indexYears":20,"academicFieldIds":2427,"indexDatabaseRanking":20},{"id":67,"createTime":20,"updateTime":20,"relativeEntities":2423,"label":2424,"description":2425,"key":74,"publicationTags":2426,"standard":20},[],{"EN":70,"VI":70},{"EN":72,"VI":73},[76,77],[80,81,82],{"id":84,"indexDatabase":2429,"url":95,"indexYears":96,"academicFieldIds":2434,"indexDatabaseRanking":102},{"id":86,"createTime":20,"updateTime":20,"relativeEntities":2430,"label":2431,"description":2432,"key":92,"publicationTags":2433,"standard":20},[],{"EN":89,"VI":89},{"EN":89,"VI":91},[94],[98,99,100,101],{"impactFactor":21,"impactFactorByYear":2436,"i10Index":117,"i10IndexLast5Year":118,"totalPublication":119,"totalPublicationByYear":2437,"totalCitation":134,"totalCitationByYear":2438,"totalCitationPerPublication":149,"totalCitationPerPublicationByYear":2439,"hindexLast5Year":118,"hindex":118},{"2012":105,"2013":106,"2014":107,"2015":108,"2016":109,"2017":110,"2018":111,"2019":112,"2020":113,"2021":114,"2022":115,"2023":116},{"2011":121,"2012":122,"2013":118,"2014":123,"2015":124,"2016":125,"2017":126,"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":133},{"2011":136,"2012":137,"2013":138,"2014":139,"2015":140,"2016":141,"2017":142,"2018":143,"2019":144,"2020":145,"2021":146,"2022":147,"2023":148},{"2011":151,"2012":152,"2013":153,"2014":154,"2015":155,"2016":156,"2017":157,"2018":158,"2019":159,"2020":160,"2021":161,"2022":162,"2023":163},{"pages":2441,"volume":2443},{"VOID":2442},"821-834",{"VOID":2444},"43","2020-06-01",2020,[76,102],{"id":2449,"createTime":2450,"updateTime":2451,"relativeEntities":2452,"slug":2453,"properties":2454,"entityType":1014,"verifyStatus":186,"verifyTime":2451,"verifyNote":1015,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":2463,"fullTextUrl":20,"authors":2464,"publicationType":1164,"publisherRelationship":2636,"citationCount":20,"citationInfo":20,"publishDate":2696,"publishYear":2697,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":2698,"openAccess":20,"references":20,"isForceReanalyzing":1228},"01e65352-9ed3-409a-af79-2b99a93ba34b","2023-11-26T00:47:14.694+00:00","2025-02-17T09:05:00.214+00:00",[],"FSCN1-induced-PTPRF-dependent-tumor-microenvironment-inflammatory-reprogramming-promotes-lung-adenocarcinoma-progression-via-regulating-macrophagic-glycolysis",{"abstract":2455,"title":2457,"references":2459,"doi":2461},{"EN":2456},"Macrophages (MΦs) play a dual role in the promotion and suppression of lung adenocarcinoma (LUAD), the function of which is influenced by the metabolic status. The role of protein tyrosine phosphatase receptor type F (PTPRF) in cancer has not been elucidated, and its role in MΦs remains to be seen. The Seahorse XFe 96 Cell Flow Analyzer detected glucose metabolism in tumor cells and macrophages. The expressions of FSCN1, M-CSF, IL4, PTPRF and IGF1 in macrophages were detected by Western blotting and qRT-PCR. Binding of FSCN1 and IGF1R was detected by co-immunoprecipitation. The tumor status in animals was observed using the IVIS Lumina III imaging system. We found that Fascin Actin-Bundling Protein 1 (FSCN1) activates the PI3K-AKT and JAK-STAT signaling pathways in LUAD cells via binding to IGF-1R, thereby promoting the secretion of cytokines such as IL4 and M-CSF. IL4 and M-CSF promote the expression of PTPRF in MΦs, leading to M2 polarization of MΦs by increasing glucose intake and lactate production. In return, M2-type MΦs act on LUAD cells by secreting cytokines such as IGF-1, CCL2, and IL10, which ultimately promote tumor progression. In vivo experiments proved that the knockdown of FSCN1 in A549 cells and PTPRF in MΦs greatly reduced LUAD proliferative and metastatic capacity, which was consistent with the in vitro findings. This study investigated the reprogramming effects of FSCN1 and PTPRF on inflammatory cytokines in the LUAD microenvironment, revealing potential mechanisms by which FSCN1 and PTPRF promote tumor progression and providing a new experimental basis for LUAD treatment.",{"EN":2458},"FSCN1 induced PTPRF-dependent tumor microenvironment inflammatory reprogramming promotes lung adenocarcinoma progression via regulating macrophagic glycolysis",{"VOID":2460},"H. Sung, J. Ferlay, R.L. Siegel, M. Laversanne, I. Soerjomataram, A. Jemal et al., Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J. Clin. 71, 209–249 (2021)\nR.S. Herbst, D. Morgensztern, C. Boshoff, The biology and management of non-small cell lung cancer. 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Akutsu et al., miR-145, miR-133a and miR-133b: Tumor-suppressive miRNAs target FSCN1 in esophageal squamous cell carcinoma. Int. J. Cancer 127, 2804–2814 (2010)\nJ. Liang, Z. Liu, X. Wei, L. Zhou, Y. Tang, C. Zhou et al., Expression of FSCN1 and FOXM1 are associated with poor prognosis of adrenocortical carcinoma patients. BMC Cancer 19, 1165 (2019)\nS.J. Kim, D.C. Kim, M.C. Kim, G.J. Jung, K.H. Kim, J.S. Jang et al., Fascin expression is related to poor survival in gastric cancer. Pathol. Int. 62, 777–784 (2012)\nC.-Q. Wang, C.-H. Tang, Y. Wang, L. Jin, Q. Wang, X. Li et al., FSCN1 gene polymorphisms: biomarkers for the development and progression of breast cancer. Sci. Rep. 7, 15887 (2017)\nM. Zhang, Z. Zhao, X. Duan, P. Chen, Z. Peng, H. Qiu, FSCN1 predicts survival and is regulated by a PI3K-dependent mechanism in renal cell carcinoma. J. Cell Physiol. 233, 4748–4758 (2018)\nD. Soulieres, F.R. Hirsch, F.A. Shepherd, W. Bordogna, P. Delmar, D.S. 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Physiol. 79, 541–566 (2017)\nI. Vitale, G. Manic, L.M. Coussens, G. Kroemer, L. Galluzzi, Macrophages and Metabolism in the Tumor Microenvironment. Cell Metab. 30, 36–50 (2019)\nM. Wenes, M. Shang, M. Di Matteo, J. Goveia, R. Martin-Perez, J. Serneels et al., Macrophage Metabolism Controls Tumor Blood Vessel Morphogenesis and Metastasis. Cell Metab. 24, 701–715 (2016)\nD.G. DeNardo, B. Ruffell, Macrophages as regulators of tumour immunity and immunotherapy. Nat. Rev. Immunol. 19, 369–382 (2019)\nA. Schmall, H.M. Al-Tamari, S. Herold, M. Kampschulte, A. Weigert, A. Wietelmann et al., Macrophage and cancer cell cross-talk via CCR2 and CX3CR1 is a fundamental mechanism driving lung cancer. Am. J. Respir. Crit. Care Med. 191, 437–447 (2015)\nS. Saha, I.N. Shalova, S.K. Biswas, Metabolic regulation of macrophage phenotype and function. Immunol. Rev. 280, 102–111 (2017)\nL. Zhu, Q. Zhao, T. Yang, W. Ding, Y. Zhao, Cellular metabolism and macrophage functional polarization. Int. Rev. 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Psarra, S.F. Magkouta et al., CSF1\u002FCSF1R signaling mediates malignant pleural effusion formation. 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its extremely poor prognosis, there is a pressing need for an improved understanding of the biology of glioblastoma multiforme (GBM), including the roles of tumor subpopulations that may contribute to their growth rate and therapy resistance. The most malignant phenotypes of GBM have been ascribed to the presence of subpopulations of cancer stem cells (CSCs), which are resistant to chemotherapeutic drugs and ionizing radiation and which promote invasiveness and metastasis. The mechanisms by which the CSC state is obtained and by which it promotes tumor maintenance are only beginning to emerge. We hypothesize that M2 polarized macrophages may affect CSC phenotypes via cell-cell communication. We investigated the interplay between glioma CSCs and macrophages via co-culture. The invasiveness of CSCs in the absence and presence of macrophages was assessed using collagen degradation and Transwell migration assays. The role of STAT3 as a CSC phenotypic mediator was assessed using siRNA-mediated gene silencing. We found that the levels of a M2 macrophage-specific secreted cytokine, TGF-β1, were elevated in the presence of CSCs, regardless of whether the cells were plated as contacting or non-contacting co-cultures. In addition, we found that the co-culture resulted in enhanced expression of M2 markers in macrophages that were previously polarized to the M1 phenotype. siRNA-mediated STAT3 silencing was found to reduce the chemo-responsiveness and migratory abilities of the CSCs. Combination treatment of STAT3 siRNA and DNA alkylating agents was found to further abrogate CSC functions. Our data indicate that the co-culture of CSCs and macrophages results in bi-directional signaling that alters the phenotypes of both cell types. These results provide an explanation for recently observed effects of macrophages on GBM tumor cell growth, motility and therapeutic resistance, and suggest potential therapeutic strategies to disrupt the CSC phenotype by impairing its communication with macrophages.",{"EN":2709},"Crosstalk between M2 macrophages and glioma stem cells",{"VOID":2711},"Z. Li, J.W. Lee, D. Mukherjee, J. Ji, S.P. Jeswani, K.L. Black, J.S. Yu, Immunotherapy targeting glioma stem cells--insights and perspectives. Expert. Opin. Biol. Ther. 12, 165–178 (2012)\nM. Staberg, S.R. Michaelsen, R.D. Rasmussen, M. Villingshoj, H.S. Poulsen, P. Hamerlik, Inhibition of histone deacetylases sensitizes glioblastoma cells to lomustine. Cell. Oncol. 40, 21–32 (2017)\nD. Matias, J. Balca-Silva, L.G. Dubois, B. Pontes, V.P. Ferrer, L. Rosario, A. do Carmo, J. Echevarria-Lima, A.B. Sarmento-Ribeiro, M.C. Lopes, V. Moura-Neto, Dual treatment with shikonin and temozolomide reduces glioblastoma tumor growth, migration and glial-to-mesenchymal transition. Cell. Oncol. 40, 247–261 (2017)\nH.D. Hemmati, I. Nakano, J.A. Lazareff, M. Masterman-Smith, D.H. Geschwind, M. Bronner-Fraser, H.I. Kornblum, Cancerous stem cells can arise from pediatric brain tumors. Proc. Natl. Acad. Sci. U. S. A. 100, 15178–15183 (2003)\nB. Ortensi, M. Setti, D. Osti, G. Pelicci, Cancer stem cell contribution to glioblastoma invasiveness. Stem Cell Res. Ther. 4, 18 (2013)\nA. Chavez-Gonzalez, B. Bakhshinejad, K. Pakravan, M.L. Guzman, S. Babashah, Novel strategies for targeting leukemia stem cells: Sounding the death knell for blood cancer. Cell. Oncol. (Dordr.) 40, 1–20 (2017)\nJ.M. Heddleston, M. Hitomi, M. Venere, W.A. Flavahan, K. Yang, Y. Kim, S. Minhas, J.N. Rich, A.B. Hjelmeland, Glioma stem cell maintenance: The role of the microenvironment. Curr. Pharm. Des. 17, 2386–2401 (2011)\nJ. Kolenda, S.S. Jensen, C. Aaberg-Jessen, K. Christensen, C. Andersen, N. Brunner, B.W. Kristensen, Effects of hypoxia on expression of a panel of stem cell and chemoresistance markers in glioblastoma-derived spheroids. J. Neuro-Oncol. 103, 43–58 (2011)\nZ. Li, H. Wang, C.E. Eyler, A.B. Hjelmeland, J.N. Rich, Turning cancer stem cells inside out: An exploration of glioma stem cell signaling pathways. J. Biol. Chem. 284, 16705–16709 (2009)\nR. Wang, K. Chadalavada, J. Wilshire, U. Kowalik, K.E. Hovinga, A. Geber, B. Fligelman, M. Leversha, C. 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Oncotarget 7, 86836–86856 (2016)",{"VOID":2713},"10.1007\u002Fs13402-017-0337-5","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs13402-017-0337-5",[2716,2731,2753],{"id":2717,"sortIndex":21,"researcher":20,"roles":2718,"affiliations":2719,"properties":2728,"displayName":2730,"givenName":20,"familyName":20},"3b9bcb84-47e1-4f72-8e74-98f6f45edcad",[1021],[2720],{"id":2721,"sortIndex":21,"affiliation":2722,"properties":20},"9be47cdc-f53d-4b56-8a08-2cb2d29be00b",{"id":2721,"createTime":20,"updateTime":20,"relativeEntities":2723,"slug":20,"properties":2724,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2727,"statistic":20},[],{"title":2725},{"EN":2726},"Department of Biomedical Engineering, Rutgers, The State University of New Jersey, Piscataway, USA",[],{"title":2729},{"VI":2730},"Leora M. Nusblat",{"id":2732,"sortIndex":198,"researcher":20,"roles":2733,"affiliations":2734,"properties":2750,"displayName":2752,"givenName":20,"familyName":20},"dee97561-09eb-4b45-bb6f-aa277a4feeff",[1021],[2735,2741],{"id":2721,"sortIndex":21,"affiliation":2736,"properties":20},{"id":2721,"createTime":20,"updateTime":20,"relativeEntities":2737,"slug":20,"properties":2738,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2740,"statistic":20},[],{"title":2739},{"EN":2726},[],{"id":2742,"sortIndex":198,"affiliation":2743,"properties":2749},"b61e12ad-85d0-4f64-8134-18304b950117",{"id":2742,"createTime":20,"updateTime":20,"relativeEntities":2744,"slug":20,"properties":2745,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2748,"statistic":20},[],{"title":2746},{"VI":2747},"Department of Biomedical Engineering, University of Wisconsin, Madison, USA",[],{},{"title":2751},{"VI":2752},"Molly J. Carroll",{"id":2754,"sortIndex":280,"researcher":20,"roles":2755,"affiliations":2756,"properties":2772,"displayName":2774,"givenName":20,"familyName":20},"69d5354b-c4e3-4db8-9b3e-6e22ee3dd5cb",[1021],[2757,2763],{"id":2721,"sortIndex":21,"affiliation":2758,"properties":20},{"id":2721,"createTime":20,"updateTime":20,"relativeEntities":2759,"slug":20,"properties":2760,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2762,"statistic":20},[],{"title":2761},{"EN":2726},[],{"id":2764,"sortIndex":198,"affiliation":2765,"properties":2771},"58ffe5a2-776b-449d-97b4-6e9ee8d81f54",{"id":2764,"createTime":20,"updateTime":20,"relativeEntities":2766,"slug":20,"properties":2767,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2770,"statistic":20},[],{"title":2768},{"EN":2769},"Department of Chemical and Biochemical Engineering, Rutgers, The State University of New Jersey, Piscataway, USA",[],{},{"title":2773},{"VI":2774},"Charles M. Roth",{"url":2714,"publisher":2776,"properties":2830},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2777,"slug":10,"properties":2778,"entityType":18,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":21,"subjectFields":2782,"manageAffiliations":2799,"indexDatabases":2810,"url":20,"thumbnailPath":20,"statistic":2825,"gsStatistic":20,"type":20,"analyzePriority":20},[],{"issn":2779,"title":2780,"eissn":2781},{"VOID":13},{"EN":15},{"VOID":17},[2783,2787,2791,2795],{"id":24,"createTime":20,"updateTime":20,"relativeEntities":2784,"label":2785,"description":2786,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":27},{},{"id":30,"createTime":20,"updateTime":20,"relativeEntities":2788,"label":2789,"description":2790,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":33},{},{"id":36,"createTime":20,"updateTime":20,"relativeEntities":2792,"label":2793,"description":2794,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":39},{},{"id":42,"createTime":20,"updateTime":20,"relativeEntities":2796,"label":2797,"description":2798,"parentId":20,"standard":20,"scholarHubFieldId":20},[],{"EN":45},{},[2800,2805],{"id":49,"createTime":20,"updateTime":20,"relativeEntities":2801,"slug":20,"properties":2802,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2804,"statistic":20},[],{"title":2803},{"EN":53},[55],{"id":57,"createTime":20,"updateTime":20,"relativeEntities":2806,"slug":20,"properties":2807,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2809,"statistic":20},[],{"title":2808},{"EN":61},[],[2811,2818],{"id":65,"indexDatabase":2812,"url":78,"indexYears":20,"academicFieldIds":2817,"indexDatabaseRanking":20},{"id":67,"createTime":20,"updateTime":20,"relativeEntities":2813,"label":2814,"description":2815,"key":74,"publicationTags":2816,"standard":20},[],{"EN":70,"VI":70},{"EN":72,"VI":73},[76,77],[80,81,82],{"id":84,"indexDatabase":2819,"url":95,"indexYears":96,"academicFieldIds":2824,"indexDatabaseRanking":102},{"id":86,"createTime":20,"updateTime":20,"relativeEntities":2820,"label":2821,"description":2822,"key":92,"publicationTags":2823,"standard":20},[],{"EN":89,"VI":89},{"EN":89,"VI":91},[94],[98,99,100,101],{"impactFactor":21,"impactFactorByYear":2826,"i10Index":117,"i10IndexLast5Year":118,"totalPublication":119,"totalPublicationByYear":2827,"totalCitation":134,"totalCitationByYear":2828,"totalCitationPerPublication":149,"totalCitationPerPublicationByYear":2829,"hindexLast5Year":118,"hindex":118},{"2012":105,"2013":106,"2014":107,"2015":108,"2016":109,"2017":110,"2018":111,"2019":112,"2020":113,"2021":114,"2022":115,"2023":116},{"2011":121,"2012":122,"2013":118,"2014":123,"2015":124,"2016":125,"2017":126,"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":133},{"2011":136,"2012":137,"2013":138,"2014":139,"2015":140,"2016":141,"2017":142,"2018":143,"2019":144,"2020":145,"2021":146,"2022":147,"2023":148},{"2011":151,"2012":152,"2013":153,"2014":154,"2015":155,"2016":156,"2017":157,"2018":158,"2019":159,"2020":160,"2021":161,"2022":162,"2023":163},{"pages":2831,"volume":2833},{"VOID":2832},"471-482",{"VOID":2834},"40","2017-06-22",2017,[76,102],{"id":2839,"createTime":2840,"updateTime":2841,"relativeEntities":2842,"slug":2843,"properties":2844,"entityType":1014,"verifyStatus":186,"verifyTime":2841,"verifyNote":1015,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":2853,"fullTextUrl":20,"authors":2854,"publicationType":1164,"publisherRelationship":3088,"citationCount":20,"citationInfo":20,"publishDate":3147,"publishYear":2697,"citationAnalyzeStatus":19,"lastCitationAnalyze":20,"indexDatabases":3148,"openAccess":20,"references":20,"isForceReanalyzing":1228},"021f2b1d-920a-4853-a56d-a19b167a248d","2024-01-08T07:35:01.642+00:00","2025-01-31T16:09:51.406+00:00",[],"Application-of-circulating-tumour-cells-to-predict-response-to-treatment-in-head-and-neck-cancer",{"abstract":2845,"title":2847,"references":2849,"doi":2851},{"EN":2846},"Local recurrence and metastasis remain the major causes of death in head and neck cancer (HNC) patients. Circulating tumour cells (CTCs) are shed from primary and metastatic sites into the circulation system and have been reported to play critical roles in the metastasis and recurrence of HNC. Here, we explored the use of CTCs to predict the response to treatment and disease progression in HNC patients. Blood samples were collected at diagnosis from HNC patients (n = 119). CTCs were isolated using a spiral microfluidic device and were identified using immunofluorescence staining. Correlation of baseline CTC numbers to 13-week PET-CT data and multidisciplinary team consensus data were conducted. CTCs were detected in 60\u002F119 (50.4%) of treatment naïve HNC patients at diagnosis. Baseline CTC numbers were higher in stage III vs. stage I-II p16-positive oropharyngeal cancers (OPCs) and other HNCs (p = 0.0143 and 0.032, respectively). In addition, we found that baseline CTC numbers may serve as independent predictors of treatment response, even after adjusting for other conventional prognostic factors. CTCs were detected in 10 out of 11 patients exhibiting incomplete treatment responses. We found that baseline CTC numbers are correlated with treatment response in patients with HNC. The expression level of cell-surface vimentin (CSV) on CTCs was significantly higher in patients with persistent or progressive disease, thus providing additional prognostic information for stratifying the risk at diagnosis in HNC patients. The ability to detect CTCs at diagnosis allows more accurate risk stratification, which in the future may be translated into better patient selection for treatment intensification and\u002For de-intensification strategies.",{"EN":2848},"Application of circulating tumour cells to predict response to treatment in head and neck cancer",{"VOID":2850},"L.Q.M. Chow, Head and Neck Cancer. N Engl. J. 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