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Journal of Medicine and Pharmacy","Tạp chí Y Dược học Cần Thơ",{"EN":487,"VI":488},"\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":490},"wcQ1uqwAAAAJ","2023-05-30T08:17:21.868+00:00",[],[494],{"id":495,"createTime":28,"updateTime":28,"relativeEntities":496,"slug":28,"properties":497,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":507,"parentIds":508,"statistic":28},"6413896b-eca9-442b-a73f-182a58a0ce40",[],{"title":498,"address":501,"country":504,"abbreviation":505},{"EN":499,"VI":500},"Can Tho University of Medicine and Pharmacy","Trường Đại học Y Dược Cần Thơ",{"EN":502,"VI":503},"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":15},{"VOID":506},"ctump","http:\u002F\u002Fwww.ctump.edu.vn\u002F",[],[],"https:\u002F\u002Ftapchi.ctump.edu.vn\u002Findex.php\u002Fctump",{"impactFactor":32,"impactFactorByYear":512,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":514,"totalPublicationByYear":515,"totalCitation":520,"totalCitationByYear":521,"totalCitationPerPublication":108,"totalCitationPerPublicationByYear":523,"hindexLast5Year":45,"hindex":45},{"2022":513,"2023":111,"2024":106},0.01,1556,{"2020":47,"2021":516,"2022":517,"2023":518,"2024":519,"2025":122},57,306,801,358,161,{"2021":146,"2022":280,"2023":522},99,{"2021":524,"2022":318,"2023":104},0.23,{"impactFactor":28,"impactFactorByYear":28,"i10Index":123,"i10IndexLast5Year":123,"totalPublication":526,"totalPublicationByYear":527,"totalCitation":526,"totalCitationByYear":528,"totalCitationPerPublication":40,"totalCitationPerPublicationByYear":531,"hindexLast5Year":49,"hindex":49},476,{"0":205,"2019":123,"2021":139,"2022":459,"2023":451,"2024":357,"2025":49,"2026":48},{"2021":42,"2022":123,"2023":161,"2024":529,"2025":360,"2026":530},136,83,{"2021":105,"2022":513,"2023":532,"2024":127,"2025":533,"2026":534},0.62,25.43,13.83,{"id":536,"createTime":537,"updateTime":382,"relativeEntities":538,"slug":539,"properties":540,"entityType":25,"verifyStatus":26,"verifyTime":28,"verifyNote":28,"languages":552,"translateLanguages":28,"viewCount":133,"subjectFields":553,"manageAffiliations":554,"indexDatabases":555,"url":556,"thumbnailPath":557,"statistic":558,"gsStatistic":594,"type":55,"analyzePriority":28},"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":541,"issn":542,"title":544,"introduce":547,"gsId":550},{"VOID":15},{"VOID":543},"25252445",{"EN":545,"VI":546},"VNU Journal of Foreign Studies","Tạp chí Nghiên cứu nước ngoài",{"EN":548,"VI":549},"{\"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. 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SCIE","scie",[934,813],"SCIE","https:\u002F\u002Fmjl.clarivate.com\u002Fsearch-results?issn=0167-7659",[937],"248e54de-c562-4c06-8a10-d7f8a37c06fe",{"impactFactor":32,"impactFactorByYear":939,"i10Index":575,"i10IndexLast5Year":140,"totalPublication":946,"totalPublicationByYear":947,"totalCitation":948,"totalCitationByYear":949,"totalCitationPerPublication":976,"totalCitationPerPublicationByYear":977,"hindexLast5Year":156,"hindex":156},{"2012":940,"2013":462,"2014":40,"2015":941,"2016":335,"2017":444,"2018":942,"2019":943,"2020":944,"2021":237,"2022":945,"2023":442},1.2,0.92,1.21,1.84,2.53,3.19,1286,{"1982":51,"1983":127,"1984":199,"1985":126,"1986":357,"1987":352,"1988":146,"1989":146,"1990":131,"1991":122,"1992":128,"1993":128,"1994":129,"1995":122,"1996":202,"1997":199,"1998":352,"1999":140,"2000":140,"2001":122,"2002":135,"2003":147,"2004":134,"2005":352,"2006":201,"2007":434,"2008":132,"2009":136,"2010":149,"2011":201,"2012":436,"2013":352,"2014":152,"2015":149,"2016":147,"2017":201,"2018":141,"2019":137,"2020":208,"2021":434,"2022":150,"2023":50,"2024":323},18522,{"1982":950,"1983":859,"1984":951,"1985":952,"1987":953,"1988":132,"1989":146,"1990":954,"1991":955,"1992":684,"1993":956,"1994":957,"1995":958,"1996":959,"2004":960,"2005":961,"2006":962,"2007":963,"2008":964,"2009":965,"2010":966,"2011":207,"2012":967,"2013":968,"2014":969,"2015":970,"2016":971,"2017":572,"2018":972,"2019":973,"2020":974,"2021":975,"2022":430,"2023":353},478,327,303,111,939,201,121,207,576,147,524,520,1297,1080,192,4477,841,418,388,364,694,565,462,495,1068,144,14.4,{"1982":978,"1983":979,"1984":980,"1985":981,"1987":982,"1988":983,"1989":40,"1990":984,"1991":985,"1992":986,"1993":987,"1994":988,"1995":989,"1996":990,"2004":991,"2005":992,"2006":993,"2007":136,"2008":994,"2009":995,"2010":996,"2011":997,"2012":998,"2013":999,"2014":1000,"2015":1001,"2016":1002,"2017":1003,"2018":1004,"2019":1005,"2020":1006,"2021":1007,"2022":1008,"2023":340},31.87,21.53,20.44,25.25,3.36,2.15,37.56,8.74,9.17,6.72,10.89,25.04,4.59,23.82,15.76,31.63,6.86,186.54,18.28,1.56,8.2,11.76,8.47,15.09,18.23,18.66,11.85,13.03,17.23,3.2,3.35,{"meta":1010,"data":1012},{"total":1011},"1294",[1013,1120,1219,1346,1456,1717,1801,1887,2037,2138],{"id":1014,"createTime":1015,"updateTime":1016,"relativeEntities":1017,"slug":1018,"properties":1019,"entityType":1028,"verifyStatus":26,"verifyTime":1029,"verifyNote":1030,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1031,"fullTextUrl":28,"authors":1032,"publicationType":1064,"publisherRelationship":1065,"citationCount":28,"citationInfo":28,"publishDate":1116,"publishYear":1117,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1118,"openAccess":28,"references":28,"isForceReanalyzing":1119},"00745e5c-b166-4b38-a27f-c6ced40e6ea5","2024-01-30T18:25:09.998+00:00","2025-01-26T13:18:52.960+00:00",[],"microRNAs-and-lung-cancer-tumors-and-22-mers",{"abstract":1020,"title":1022,"references":1024,"doi":1026},{"EN":1021},"Work over the last decade has revealed novel regulatory mechanisms in pathological disease states that are mediated by microRNAs and has inspired researchers to begin elucidating the specific roles of miRNAs in the regulation of genes involved in cancer development and progression. Recently, miRNAs have been explored as therapeutic targets and diagnostic markers of cancer. In this paper, we review recent advances in the study of miRNAs involved in tumorigenesis, focusing on miRNA regulation of genes that have been demonstrated to play critical roles in lung cancer development. We discuss miRNA regulation of genes that play critical roles in the process of malignant transformation, angiogenesis and tumor metastasis, the dysregulation of miRNA expression in cancer development, and the development of miRNA-based diagnostics and therapeutics.",{"EN":1023},"microRNAs and lung cancer: tumors and 22-mers",{"VOID":1025},"Yekta, S., Shih, I. H., & Bartel, D. P. (2004). MicroRNA-directed cleavage of HOXB8 mRNA. Science, 304, 594–596.\nVasudevan, S., Tong, Y., & Steitz, J. A. (2007). Switching from repression to activation: microRNAs can up-regulate translation. Science, 318, 1931–1934.\nNovotny, G. W., Sonne, S. B., Nielsen, J. E., Jonstrup, S. P., Hansen, M. A., Skakkebaek, N. E., et al. (2007). Translational repression of E2F1 mRNA in carcinoma in situ and normal testis correlates with expression of the miR-17-92 cluster. Cell Death and Differentiation, 14, 879–882.\nHe, L., He, X., Lowe, S. W., & Hannon, G. J. (2007). microRNAs join the p53 network—Another piece in the tumour-suppression puzzle. Nature Reviews Cancer, 7, 819–822.\nCho, W. C. (2007). OncomiRs: The discovery and progress of microRNAs in cancers. Molecular Cancer, 6, 60.\nHwang, H. W., & Mendell, J. T. (2006). MicroRNAs in cell proliferation, cell death, and tumorigenesis. British Journal of Cancer, 94, 776–780.\nEsquela-Kerscher, A., & Slack, F. J. (2006). Oncomirs—microRNAs with a role in cancer. Nature Reviews Cancer, 6, 259–269.\nHebert, C., Norris, K., Scheper, M. A., Nikitakis, N., & Sauk, J. J. (2007). High mobility group A2 is a target for miRNA-98 in head and neck squamous cell carcinoma. Molecular Cancer, 6, 5.\nLee, D. Y., Deng, Z., Wang, C. H., & Yang, B. B. (2007). MicroRNA-378 promotes cell survival, tumor growth, and angiogenesis by targeting SuFu and Fus-1 expression. Proceedings of the National Academy of Sciences of the United States of America, 104, 20350–20355.\nO’Donnell, K. A., Wentzel, E. A., Zeller, K. I., Dang, C. V., & Mendell, J. T. (2005). c-Myc-regulated microRNAs modulate E2F1 expression. Nature, 435, 839–843.\nMercatelli, N., Coppola, V., Bonci, D., Miele, F., Costantini, A., Guadagnoli, M., et al. (2008). The inhibition of the highly expressed miR-221 and miR-222 impairs the growth of prostate carcinoma xenografts in mice. PLoS ONE, 3, e4029.\nFelicetti, F., Errico, M. C., Bottero, L., Segnalini, P., Stoppacciaro, A., Biffoni, M., et al. (2008). The promyelocytic leukemia zinc finger-microRNA-221\u002F-222 pathway controls melanoma progression through multiple oncogenic mechanisms. Cancer Research, 68, 2745–2754.\nWickramasinghe, N. S., Manavalan, T. T., Dougherty, S. M., Riggs, K. A., Li, Y., & Klinge, C. M. (2009). Estradiol downregulates miR-21 expression and increases miR-21 target gene expression in MCF-7 breast cancer cells. Nucleic Acids Research, 37, 2584–2595.\nYang, Y., Chaerkady, R., Beer, M. A., Mendell, J. T., & Pandey, A. (2009). Identification of miR-21 targets in breast cancer cells using a quantitative proteomic approach. Proteomics, 9, 1374–1384.\nSi, M. L., Zhu, S., Wu, H., Lu, Z., Wu, F., & Mo, Y. Y. (2007). miR-21-mediated tumor growth. Oncogene, 26, 2799–2803.\nYanaihara, N., Caplen, N., Bowman, E., Seike, M., Kumamoto, K., Yi, M., et al. (2006). Unique microRNA molecular profiles in lung cancer diagnosis and prognosis. Cancer Cell, 9, 189–198.\nTaylor, D. D., & Gercel-Taylor, C. (2008). MicroRNA signatures of tumor-derived exosomes as diagnostic biomarkers of ovarian cancer. Gynecologic Oncology, 110, 13–21.\nMitchell, P. S., Parkin, R. K., Kroh, E. M., Fritz, B. R., Wyman, S. K., Pogosova-Agadjanyan, E. L., et al. (2008). 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H., Han, J., Yang, Q., Aris, V., Soteropoulos, P., et al. (2007). MicroRNA let-7a down-regulates MYC and reverts MYC-induced growth in Burkitt lymphoma cells. Cancer Research, 67, 9762–9770.\nMayr, C., Hemann, M. T., & Bartel, D. P. (2007). Disrupting the pairing between let-7 and Hmga2 enhances oncogenic transformation. Science, 315, 1576–1579.\nMuntoni, A., & Reddel, R. R. (2005). The first molecular details of ALT in human tumor cells. Human Molecular Genetics, 14(Spec No. 2), R191–R196.\nMitomo, S., Maesawa, C., Ogasawara, S., Iwaya, T., Shibazaki, M., Yashima-Abo, A., et al. (2008). Downregulation of miR-138 is associated with overexpression of human telomerase reverse transcriptase protein in human anaplastic thyroid carcinoma cell lines. Cancer Science, 99, 280–286.\nGonzalo, S., Jaco, I., Fraga, M. F., Chen, T., Li, E., Esteller, M., et al. (2006). DNA methyltransferases control telomere length and telomere recombination in mammalian cells. Nature Cell Biology, 8, 416–424.\nBenetti, R., Gonzalo, S., Jaco, I., Munoz, P., Gonzalez, S., Schoeftner, S., et al. (2008). A mammalian microRNA cluster controls DNA methylation and telomere recombination via Rbl2-dependent regulation of DNA methyltransferases. Nature Structural & Molecular Biology, 15, 268–279.\nFabbri, M., Garzon, R., Cimmino, A., Liu, Z., Zanesi, N., Callegari, E., et al. (2007). MicroRNA-29 family reverts aberrant methylation in lung cancer by targeting DNA methyltransferases 3A and 3B. Proceedings of the National Academy of Sciences of the United States of America, 104, 15805–15810.\nHotchkiss, R. S., Strasser, A., McDunn, J. E., & Swanson, P. E. (2009). Cell death. New England Journal of Medicine, 361, 1570–1583.\nPorkka, K. P., Pfeiffer, M. J., Waltering, K. K., Vessella, R. L., Tammela, T. L., & Visakorpi, T. (2007). MicroRNA expression profiling in prostate cancer. Cancer Research, 67, 6130–6135.\nBottoni, A., Piccin, D., Tagliati, F., Luchin, A., Zatelli, M. C., & degli Uberti, E. C. (2005). miR-15a and miR-16-1 down-regulation in pituitary adenomas. Journal of Cellular Physiology, 204, 280–285.\nCimmino, A., Calin, G. A., Fabbri, M., Iorio, M. V., Ferracin, M., Shimizu, M., et al. (2005). miR-15 and miR-16 induce apoptosis by targeting BCL2. Proceedings of the National Academy of Sciences of the United States of America, 102, 13944–13949.\nMott, J. L., Kobayashi, S., Bronk, S. F., & Gores, G. J. (2007). mir-29 regulates Mcl-1 protein expression and apoptosis. Oncogene, 26, 6133–6140.\nCalin, G. A., Ferracin, M., Cimmino, A., Di Leva, G., Shimizu, M., Wojcik, S. E., et al. (2005). A microRNA signature associated with prognosis and progression in chronic lymphocytic leukemia. New England Journal of Medicine, 353, 1793–1801.\nCummins, J. M., He, Y., Leary, R. J., Pagliarini, R., Diaz, L. A., Jr., Sjoblom, T., et al. (2006). 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Oncogene, 26, 5017–5022.",{"VOID":1027},"10.1007\u002Fs10555-010-9204-9","PUBLICATION","2025-01-26T13:18:52.959+00:00","Auto Verify","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10555-010-9204-9",[1033,1049],{"id":1034,"sortIndex":32,"researcher":28,"roles":1035,"affiliations":1037,"properties":1046,"displayName":1048,"givenName":28,"familyName":28},"76db4db8-a239-4b82-ba8a-3aad43bc727b",[1036],"AUTHOR",[1038],{"id":1039,"sortIndex":32,"affiliation":1040,"properties":28},"4185e1ce-31eb-4a3f-9bfa-9f2bb5739f6f",{"id":1039,"createTime":28,"updateTime":28,"relativeEntities":1041,"slug":28,"properties":1042,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1045,"statistic":28},[],{"title":1043},{"VI":1044},"Harold C. Simmons Comprehensive Cancer Center, The University of Texas Southwestern Medical Center, Dallas, USA",[],{"title":1047},{"VI":1048},"Liqin Du",{"id":1050,"sortIndex":40,"researcher":28,"roles":1051,"affiliations":1052,"properties":1061,"displayName":1063,"givenName":28,"familyName":28},"12fa8cdc-3d7e-4c8b-bd4a-80474790a8c7",[1036],[1053],{"id":1054,"sortIndex":32,"affiliation":1055,"properties":28},"b265e2fa-a70f-4721-a221-f28b69646969",{"id":1054,"createTime":28,"updateTime":28,"relativeEntities":1056,"slug":28,"properties":1057,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1060,"statistic":28},[],{"title":1058},{"VI":1059},"Eugene McDermott Center for Human Growth and Development, The University of Texas Southwestern Medical Center, Dallas, USA",[],{"title":1062},{"VI":1063},"Alexander Pertsemlidis","ARTICLE",{"url":1031,"publisher":1066,"properties":1111},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1067,"slug":872,"properties":1068,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1071,"manageAffiliations":1080,"indexDatabases":1091,"url":28,"thumbnailPath":28,"statistic":1106,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1069,"title":1070},{"VOID":875},{"VOID":877},[1072,1076],{"id":881,"createTime":28,"updateTime":28,"relativeEntities":1073,"label":1074,"description":1075,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":884},{},{"id":887,"createTime":28,"updateTime":28,"relativeEntities":1077,"label":1078,"description":1079,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":890},{},[1081,1086],{"id":894,"createTime":28,"updateTime":28,"relativeEntities":1082,"slug":28,"properties":1083,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1085,"statistic":28},[],{"title":1084},{"EN":898},[],{"id":901,"createTime":28,"updateTime":28,"relativeEntities":1087,"slug":28,"properties":1088,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1090,"statistic":28},[],{"title":1089},{"EN":905},[907],[1092,1099],{"id":910,"indexDatabase":1093,"url":916,"indexYears":917,"academicFieldIds":1098,"indexDatabaseRanking":921},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":1094,"label":1095,"description":1096,"key":792,"publicationTags":1097,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[919,920],{"id":923,"indexDatabase":1100,"url":935,"indexYears":28,"academicFieldIds":1105,"indexDatabaseRanking":28},{"id":925,"createTime":28,"updateTime":28,"relativeEntities":1101,"label":1102,"description":1103,"key":932,"publicationTags":1104,"standard":28},[],{"EN":928,"VI":928},{"EN":930,"VI":931},[934,813],[937],{"impactFactor":32,"impactFactorByYear":1107,"i10Index":575,"i10IndexLast5Year":140,"totalPublication":946,"totalPublicationByYear":1108,"totalCitation":948,"totalCitationByYear":1109,"totalCitationPerPublication":976,"totalCitationPerPublicationByYear":1110,"hindexLast5Year":156,"hindex":156},{"2012":940,"2013":462,"2014":40,"2015":941,"2016":335,"2017":444,"2018":942,"2019":943,"2020":944,"2021":237,"2022":945,"2023":442},{"1982":51,"1983":127,"1984":199,"1985":126,"1986":357,"1987":352,"1988":146,"1989":146,"1990":131,"1991":122,"1992":128,"1993":128,"1994":129,"1995":122,"1996":202,"1997":199,"1998":352,"1999":140,"2000":140,"2001":122,"2002":135,"2003":147,"2004":134,"2005":352,"2006":201,"2007":434,"2008":132,"2009":136,"2010":149,"2011":201,"2012":436,"2013":352,"2014":152,"2015":149,"2016":147,"2017":201,"2018":141,"2019":137,"2020":208,"2021":434,"2022":150,"2023":50,"2024":323},{"1982":950,"1983":859,"1984":951,"1985":952,"1987":953,"1988":132,"1989":146,"1990":954,"1991":955,"1992":684,"1993":956,"1994":957,"1995":958,"1996":959,"2004":960,"2005":961,"2006":962,"2007":963,"2008":964,"2009":965,"2010":966,"2011":207,"2012":967,"2013":968,"2014":969,"2015":970,"2016":971,"2017":572,"2018":972,"2019":973,"2020":974,"2021":975,"2022":430,"2023":353},{"1982":978,"1983":979,"1984":980,"1985":981,"1987":982,"1988":983,"1989":40,"1990":984,"1991":985,"1992":986,"1993":987,"1994":988,"1995":989,"1996":990,"2004":991,"2005":992,"2006":993,"2007":136,"2008":994,"2009":995,"2010":996,"2011":997,"2012":998,"2013":999,"2014":1000,"2015":1001,"2016":1002,"2017":1003,"2018":1004,"2019":1005,"2020":1006,"2021":1007,"2022":1008,"2023":340},{"pages":1112,"volume":1114},{"VOID":1113},"109-122",{"VOID":1115},"29","2010-02-04",2010,[934,921],false,{"id":1121,"createTime":1122,"updateTime":1123,"relativeEntities":1124,"slug":1125,"properties":1126,"entityType":1028,"verifyStatus":26,"verifyTime":1123,"verifyNote":1030,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1135,"fullTextUrl":28,"authors":1136,"publicationType":1064,"publisherRelationship":1165,"citationCount":28,"citationInfo":28,"publishDate":1216,"publishYear":1217,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1218,"openAccess":28,"references":28,"isForceReanalyzing":1119},"00d38026-c6ec-48c8-8b1a-ec05ec15053d","2023-12-07T04:41:14.052+00:00","2024-12-18T18:41:02.921+00:00",[],"Cancer-associated-fibroblasts-as-key-regulators-of-the-breast-cancer-tumor-microenvironment",{"abstract":1127,"title":1129,"references":1131,"doi":1133},{"EN":1128},"Tumor cells exist in close proximity with non-malignant cells. Extensive and multilayered crosstalk between tumor cells and stromal cells tailors the tumor microenvironment (TME) to support survival, growth, and metastasis. Fibroblasts are one of the largest populations of non-malignant host cells that can be found within the TME of breast, pancreatic, and prostate tumors. Substantial scientific evidence has shown that these cancer-associated fibroblasts (CAFs) are not only associated with tumors by proximity but are also actively recruited to developing tumors where they can influence other cells of the TME as well as influencing tumor cell survival and metastasis. This review discusses the impact of CAFs on breast cancer biology and highlights their heterogeneity, origin and their role in tumor progression, ECM remodeling, therapy resistance, metastasis, and the challenges ahead of targeting CAFs to improve therapy response.",{"EN":1130},"Cancer-associated fibroblasts as key regulators of the breast cancer tumor microenvironment",{"VOID":1132},"Hanahan, D., & Weinberg, R. A. (2011). Hallmarks of cancer: the next generation. Cell, 144(5), 646–674. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.cell.2011.02.013.\nBainbridge, P. (2013). Wound healing and the role of fibroblasts. Journal of Wound Care, 22(8), 407–408, 410-412. https:\u002F\u002Fdoi.org\u002F10.12968\u002Fjowc.2013.22.8.407.\nKalluri. (2016). The biology and function of fibroblasts in cancer. Nature, 16(9), 582–598.\nUnsworth, A., Anderson, R., & Britt, K. (2014). Stromal fibroblasts and the immune microenvironment: partners in mammary gland biology and pathology? Journal of Mammary Gland Biology and Neoplasia, 19(2), 169–182. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs10911-014-9326-8.\nVisvader, J. E., & Stingl, J. (2014). Mammary stem cells and the differentiation hierarchy: current status and perspectives. Genes & Development, 28(11), 1143–1158. https:\u002F\u002Fdoi.org\u002F10.1101\u002Fgad.242511.114.\nPolyak, K., & Kalluri, R. (2010). The role of the microenvironment in mammary gland development and cancer. Cold Spring Harbor Perspectives in Biology, 2(11), a003244. https:\u002F\u002Fdoi.org\u002F10.1101\u002Fcshperspect.a003244.\nFleming, J. M., Long, E. L., Ginsburg, E., Gerscovich, D., Meltzer, P. S., & Vonderhaar, B. K. (2008). Interlobular and intralobular mammary stroma: genotype may not reflect phenotype. BMC Cell Biology, 9, 46. https:\u002F\u002Fdoi.org\u002F10.1186\u002F1471-2121-9-46.\nMorsing, M., Klitgaard, M. C., Jafari, A., Villadsen, R., Kassem, M., Petersen, O. W., et al. (2016). 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Cancer Research, 72(18), 4652–4661. https:\u002F\u002Fdoi.org\u002F10.1158\u002F0008-5472.can-12-0877.",{"VOID":1134},"10.1007\u002Fs10555-018-9768-3","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs10555-018-9768-3",[1137,1152],{"id":1138,"sortIndex":32,"researcher":28,"roles":1139,"affiliations":1140,"properties":1149,"displayName":1151,"givenName":28,"familyName":28},"fc7752d9-d285-48cd-a9b8-6e2150c6d64e",[1036],[1141],{"id":1142,"sortIndex":32,"affiliation":1143,"properties":28},"cfa56f9c-ae91-4590-9c19-29d2449e0795",{"id":1142,"createTime":28,"updateTime":28,"relativeEntities":1144,"slug":28,"properties":1145,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1148,"statistic":28},[],{"title":1146},{"EN":1147},"Department of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, The Netherlands",[],{"title":1150},{"VI":1151},"J. M. Houthuijzen",{"id":1153,"sortIndex":40,"researcher":28,"roles":1154,"affiliations":1155,"properties":1162,"displayName":1164,"givenName":28,"familyName":28},"47d85e19-b11e-4435-9efa-b2d8de9aa4c9",[1036],[1156],{"id":1142,"sortIndex":32,"affiliation":1157,"properties":28},{"id":1142,"createTime":28,"updateTime":28,"relativeEntities":1158,"slug":28,"properties":1159,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1161,"statistic":28},[],{"title":1160},{"EN":1147},[],{"title":1163},{"VI":1164},"J. Jonkers",{"url":1135,"publisher":1166,"properties":1211},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1167,"slug":872,"properties":1168,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1171,"manageAffiliations":1180,"indexDatabases":1191,"url":28,"thumbnailPath":28,"statistic":1206,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1169,"title":1170},{"VOID":875},{"VOID":877},[1172,1176],{"id":881,"createTime":28,"updateTime":28,"relativeEntities":1173,"label":1174,"description":1175,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":884},{},{"id":887,"createTime":28,"updateTime":28,"relativeEntities":1177,"label":1178,"description":1179,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":890},{},[1181,1186],{"id":894,"createTime":28,"updateTime":28,"relativeEntities":1182,"slug":28,"properties":1183,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1185,"statistic":28},[],{"title":1184},{"EN":898},[],{"id":901,"createTime":28,"updateTime":28,"relativeEntities":1187,"slug":28,"properties":1188,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1190,"statistic":28},[],{"title":1189},{"EN":905},[907],[1192,1199],{"id":910,"indexDatabase":1193,"url":916,"indexYears":917,"academicFieldIds":1198,"indexDatabaseRanking":921},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":1194,"label":1195,"description":1196,"key":792,"publicationTags":1197,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[919,920],{"id":923,"indexDatabase":1200,"url":935,"indexYears":28,"academicFieldIds":1205,"indexDatabaseRanking":28},{"id":925,"createTime":28,"updateTime":28,"relativeEntities":1201,"label":1202,"description":1203,"key":932,"publicationTags":1204,"standard":28},[],{"EN":928,"VI":928},{"EN":930,"VI":931},[934,813],[937],{"impactFactor":32,"impactFactorByYear":1207,"i10Index":575,"i10IndexLast5Year":140,"totalPublication":946,"totalPublicationByYear":1208,"totalCitation":948,"totalCitationByYear":1209,"totalCitationPerPublication":976,"totalCitationPerPublicationByYear":1210,"hindexLast5Year":156,"hindex":156},{"2012":940,"2013":462,"2014":40,"2015":941,"2016":335,"2017":444,"2018":942,"2019":943,"2020":944,"2021":237,"2022":945,"2023":442},{"1982":51,"1983":127,"1984":199,"1985":126,"1986":357,"1987":352,"1988":146,"1989":146,"1990":131,"1991":122,"1992":128,"1993":128,"1994":129,"1995":122,"1996":202,"1997":199,"1998":352,"1999":140,"2000":140,"2001":122,"2002":135,"2003":147,"2004":134,"2005":352,"2006":201,"2007":434,"2008":132,"2009":136,"2010":149,"2011":201,"2012":436,"2013":352,"2014":152,"2015":149,"2016":147,"2017":201,"2018":141,"2019":137,"2020":208,"2021":434,"2022":150,"2023":50,"2024":323},{"1982":950,"1983":859,"1984":951,"1985":952,"1987":953,"1988":132,"1989":146,"1990":954,"1991":955,"1992":684,"1993":956,"1994":957,"1995":958,"1996":959,"2004":960,"2005":961,"2006":962,"2007":963,"2008":964,"2009":965,"2010":966,"2011":207,"2012":967,"2013":968,"2014":969,"2015":970,"2016":971,"2017":572,"2018":972,"2019":973,"2020":974,"2021":975,"2022":430,"2023":353},{"1982":978,"1983":979,"1984":980,"1985":981,"1987":982,"1988":983,"1989":40,"1990":984,"1991":985,"1992":986,"1993":987,"1994":988,"1995":989,"1996":990,"2004":991,"2005":992,"2006":993,"2007":136,"2008":994,"2009":995,"2010":996,"2011":997,"2012":998,"2013":999,"2014":1000,"2015":1001,"2016":1002,"2017":1003,"2018":1004,"2019":1005,"2020":1006,"2021":1007,"2022":1008,"2023":340},{"pages":1212,"volume":1214},{"VOID":1213},"577-597",{"VOID":1215},"37","2018-11-21",2018,[934,921],{"id":1220,"createTime":1221,"updateTime":1222,"relativeEntities":1223,"slug":1224,"properties":1225,"entityType":1028,"verifyStatus":26,"verifyTime":1222,"verifyNote":1030,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1234,"fullTextUrl":28,"authors":1235,"publicationType":1064,"publisherRelationship":1292,"citationCount":28,"citationInfo":28,"publishDate":1343,"publishYear":1344,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1345,"openAccess":28,"references":28,"isForceReanalyzing":1119},"00e78c33-366b-4e8e-b3bc-206e8908e490","2023-12-11T03:02:47.911+00:00","2025-02-24T08:30:12.214+00:00",[],"Immunomodulating-antibodies-and-drugs-for-the-treatment-of-hematological-malignancies",{"abstract":1226,"title":1228,"references":1230,"doi":1232},{"EN":1227},"The aim of cancer immunotherapy is to induce immune cells to kill tumor and promote immunological memory that protects against tumor recurrence. Most current immunotherapies, such as monoclonal antibodies (mAb), target the tumor cells directly. Advances in our understanding of the immune system such as the role of co-stimulatory and co-inhibitory receptors, and the advent of new immunomodulatory agents provide new opportunities to target the immune system and enhance anti-tumor immune responses. These promising agents include immunomodulating mAbs, Toll-like receptor agonists, IMiDs, and cytokines. In this review, we discuss the current results of immunomodulating agents in the treatment of hematological malignancies and propose applications that include targeting of the innate and adaptive immune systems as well as combinations with tumor-specific mAbs.",{"EN":1229},"Immunomodulating antibodies and drugs for the treatment of hematological malignancies",{"VOID":1231},"Zou, W. (2005). Immunosuppressive networks in the tumour environment and their therapeutic relevance. Nature Reviews. 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Cutting edge: Expression of functional CD137 receptor by dendritic cells. Journal of Immunology, 168, 4262–4267.\nSznol, M., Hodi, F. S., Margolin, K., et al. (2008) Phase I study of BMS-663513, a fully human anti-CD137 agonist monoclonal antibody, in patients (pts) with advanced cancer (CA). J Clin Oncol.;26 (2008 ASCO Annual Meeting).\nHouot, R., Goldstein, M. J., Kohrt, H. E., et al. (2009). Therapeutic effect of CD137 immunomodulation in lymphoma and its enhancement by Treg depletion. Blood, 114, 3431–3438.\nMurillo, O., Arina, A., Hervas-Stubbs, S., et al. (2008). Therapeutic antitumor efficacy of antiCD137 agonistic monoclonal antibody in mouse models of myeloma. Clinical Cancer Research, 14, 6895–6906.\nGoebeler, M., Viardot, A., Noppeney, R., et al. (2010). CD3\u002FCD19 bispecific BiTE antibody blinatumomab treatment of non-Hodgkin lymphoma (NHL) patients: 60 μg\u002Fm2\u002Fd by continuous infusion is tolerable and results in durable responses. 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B., et al. (2009). A Phase I\u002FII study of lenalidomide in combination with rituximab in relapsed\u002Frefractory mantle cell lymphoma. ASH meeting, Abstr 2719.\nDutia, M., DeRoock, I., Chee, K., et al. (2010). Analysis of a phase 2 study of lenalidomide and rituximab in relapsed or refractory non-Hodgkin’s lymphoma. EHA meeting, abst # 0295.\nFowler, N. H., McLaughlin, P., Hagemeister, F. B., et al. (2010). Complete response rates with lenalidomide plus rituximab for untreated indolent B-cell non-hodgkin’s lymphoma. Journal of Clinical Oncology, 28, 15s.\nPlosker, G. L., & Figgitt, D. P. (2003). Rituximab: A review of its use in non-Hodgkin’s lymphoma and chronic lymphocytic leukaemia. Drugs, 63, 803–843.\nMcLaughlin, P., Grillo-Lopez, A. J., Link, B. K., et al. (1998). Rituximab chimeric anti-CD20 monoclonal antibody therapy for relapsed indolent lymphoma: Half of patients respond to a four-dose treatment program. Journal of Clinical Oncology, 16, 2825–2833.\nRosenberg, S. A., Lotze, M. T., Muul, L. M., et al. (1987). A progress report on the treatment of 157 patients with advanced cancer using lymphokine-activated killer cells and interleukin-2 or high-dose interleukin-2 alone. The New England Journal of Medicine, 316, 889–897.\nEisenbeis, C. F., Grainger, A., Fischer, B., et al. (2004). Combination immunotherapy of B-cell non-Hodgkin’s lymphoma with rituximab and interleukin-2: A preclinical and phase I study. Clinical Cancer Research, 10, 6101–6110.\nFriedberg, J. W., Neuberg, D., Gribben, J. G., et al. (2002). Combination immunotherapy with rituximab and interleukin 2 in patients with relapsed or refractory follicular non-Hodgkin’s lymphoma. British Journal Haematology, 117, 828–834.\nGluck, W. L., Hurst, D., Yuen, A., et al. (2004). Phase I studies of interleukin (IL)-2 and rituximab in B-cell non-Hodgkin’s lymphoma: IL-2 mediated natural killer cell expansion correlations with clinical response. Clinical Cancer Research, 10, 2253–2264.\nKhan, K. D., Emmanouilides, C., Benson, D. M., Jr., et al. (2006). A phase 2 study of rituximab in combination with recombinant interleukin-2 for rituximab-refractory indolent non-Hodgkin’s lymphoma. Clinical Cancer Research, 12, 7046–7053.\nBanks, R. E., Patel, P. M., & Selby, P. J. (1995). Interleukin 12: A new clinical player in cytokine therapy. British Journal of Cancer, 71, 655–659.\nYounes, A., Pro, B., Robertson, M. J., et al. (2004). Phase II clinical trial of interleukin-12 in patients with relapsed and refractory non-Hodgkin’s lymphoma and Hodgkin’s disease. Clinical Cancer Research, 10, 5432–5438.\nAnsell, S. M., Geyer, S. M., Maurer, M. J., et al. (2006). Randomized phase II study of interleukin-12 in combination with rituximab in previously treated non-Hodgkin’s lymphoma patients. Clinical Cancer Research, 12, 6056–6063.\nAndorsky, D. J., & Timmerman, J. M. (2008). Interleukin-21: Biology and application to cancer therapy. Expert Opinion on Biological Therapy, 8, 1295–1307.\nRoda, J. M., Joshi, T., Butchar, J. P., et al. (2007). The activation of natural killer cell effector functions by cetuximab-coated, epidermal growth factor receptor positive tumor cells is enhanced by cytokines. Clinical Cancer Research, 13, 6419–6428.\nVanderMolen, L. A., Steis, R. G., Duffey, P. L., et al. (1990). Low-versus high-dose interferon alfa-2a in relapsed indolent non-Hodgkin’s lymphoma. Journal of the National Cancer Institute, 82, 235–238.\nSacchi, S., Federico, M., Vitolo, U., et al. (2001). Clinical activity and safety of combination immunotherapy with IFN-alpha 2a and rituximab in patients with relapsed low grade non-Hodgkin’s lymphoma. Haematologica, 86, 951–958.\nDavis, T. A., Maloney, D. G., Grillo-Lopez, A. J., et al. (2000). Combination immunotherapy of relapsed or refractory low-grade or follicular non-Hodgkin’s lymphoma with rituximab and interferon-alpha-2a. Clinical Cancer Research, 6, 2644–2652.\nKimby, E., Jurlander, J., Geisler, C., et al. (2008). Long-term molecular remissions in patients with indolent lymphoma treated with rituximab as a single agent or in combination with interferon alpha-2a: A randomized phase II study from the Nordic Lymphoma Group. Leukaemia & Lymphoma, 49, 102–112.\nvan der Kolk, L. E., Grillo-Lopez, A. J., Baars, J. W., & van Oers, M. H. (2003). Treatment of relapsed Bcell non-Hodgkin’s lymphoma with a combination of chimeric anti-CD20 monoclonal antibodies (rituximab) and G-CSF: Final report on safety and efficacy. Leukemia, 17, 1658–1664.\nCartron, G., Zhao-Yang, L., Baudard, M., et al. (2008). Granulocyte-macrophage colonystimulating factor potentiates rituximab in patients with relapsed follicular lymphoma: Results of a phase II study. Journal of Clinical Oncology, 26, 2725–2731.\nHainsworth, J. D., Litchy, S., Barton, J. H., et al. (2003). Single-agent rituximab as first-line and maintenance treatment for patients with chronic lymphocytic leukemia or small lymphocytic lymphoma: A phase II trial of the Minnie Pearl Cancer Research Network. Journal of Clinical Oncology, 21, 1746–1751.\nHuhn, D., von Schilling, C., Wilhelm, M., et al. (2001). Rituximab therapy of patients with B-cell chronic lymphocytic leukemia. Blood, 98, 1326–1331.\nItala, M., Geisler, C. H., Kimby, E., et al. (2002). Standard-dose anti-CD20 antibody rituximab has efficacy in chronic lymphocytic leukaemia: Results from a Nordic multicentre study. European Journal of Haematology, 69, 129–134.\nMcLaughlin, P., Liu, N., Poindexter, N., et al. (2005). Rituximab plus GM-CSF (Leukine) for indolent lymphoma. Proceedings of the 9th International Conference on Malignant lymphomas. Annals of Oncology, 16, v68.\nKjaergaard, J., Tanaka, J., Kim, J. A., Rothchild, K., Weinberg, A., & Shu, S. (2000). Therapeutic efficacy of OX-40 receptor antibody depends on tumor immunogenicity and anatomic site of tumor growth. Cancer Research, 60, 5514–5521.\nPiconese, S., Valzasina, B., & Colombo, M. P. (2008). OX40 triggering blocks suppression by regulatory T cells and facilitates tumor rejection. The Journal of Experimental Medicine, 205, 825–839.\nWeinberg, A. D., Rivera, M. M., Prell, R., et al. (2000). Engagement of the OX-40 receptor in vivo enhances antitumor immunity. Journal of Immunology, 164, 2160–2169.\nKo, K., Yamazaki, S., Nakamura, K., et al. (2005). Treatment of advanced tumors with agonistic anti-GITR mAb and its effects on tumor-infiltrating Foxp3+CD25+CD4+ regulatory T cells. The Journal of Experimental Medicine, 202, 885–891.\nFrench, R. R., Taraban, V. Y., Crowther, G. R., et al. (2007). Eradication of lymphoma by CD8 T cells following anti-CD40 monoclonal antibody therapy is critically dependent on CD27 costimulation. Blood, 109, 4810–4815.\nSakanishi, T., & Yagita, H. (2010). Anti-tumor effects of depleting and non-depleting anti-CD27 monoclonal antibodies in immune-competent mice. Biochemical and Biophysical Research Communications, 393, 829–835.\nKwon, E. D., Hurwitz, A. A., Foster, B. A., et al. (1997). Manipulation of T cell costimulatory and inhibitory signals for immunotherapy of prostate cancer. Proceedings of the National Academy of Sciences of the United States of America, 94, 8099–8103.\nLeach, D. R., Krummel, M. F., & Allison, J. P. (1996). Enhancement of antitumor immunity by CTLA-4 blockade. Science, 271, 1734–1736.\nHirano, F., Kaneko, K., Tamura, H., et al. (2005). Blockade of B7-H1 and PD-1 by monoclonal antibodies potentiates cancer therapeutic immunity. Cancer Research, 65, 1089–1096.\nFrench, R. R., Chan, H. T., Tutt, A. L., & Glennie, M. J. (1999). CD40 antibody evokes a cytotoxic T-cell response that eradicates lymphoma and bypasses T-cell help. Natural Medicines, 5, 548–553.\nLaw, C. L., Gordon, K. A., Collier, J., et al. (2005). Preclinical antilymphoma activity of a humanized anti-CD40 monoclonal antibody, SGN-40. Cancer Research, 65, 8331–8338.\nRomagne, F., Andre, P., Spee, P., et al. (2009). Preclinical characterization of 1-7F9, a novel human anti-KIR receptor therapeutic antibody that augments natural killer-mediated killing of tumor cells. Blood, 114, 2667–2677.\nO’Mahony, D., Morris, J. C., Quinn, C., et al. (2007). A pilot study of CTLA-4 blockade after cancer vaccine failure in patients with advanced malignancy. Clinical Cancer Research, 13, 958–964.\nBashey, A., Medina, B., Corringham, S., et al. (2009). CTLA4 blockade with ipilimumab to treat relapse of malignancy after allogeneic hematopoietic cell transplantation. Blood, 113, 1581–1588.\nAnsell, S. M., Hurvitz, S. A., Koenig, P. A., et al. (2009). Phase I study of ipilimumab, an anti-CTLA-4 monoclonal antibody, in patients with relapsed and refractory B-cell non-Hodgkin lymphoma. Clinical Cancer Research, 15, 6446–6453.\nAnsell, S. M., Witzig, T. E., Kurtin, P. J., et al. (2002). Phase 1 study of interleukin-12 in combination with rituximab in patients with B-cell non-Hodgkin lymphoma. Blood, 99, 67–74.\nFerrajoli, A. (2009). Incorporating the use of GM-CSF in the treatment of chronic lymphocytic leukemia. Leukaemia & Lymphoma, 50, 514–516.",{"VOID":1233},"10.1007\u002Fs10555-011-9274-3","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs10555-011-9274-3",[1236,1251,1266,1279],{"id":1237,"sortIndex":32,"researcher":28,"roles":1238,"affiliations":1239,"properties":1248,"displayName":1250,"givenName":28,"familyName":28},"7166f284-915a-4c54-99e6-65dcf06c1be2",[1036],[1240],{"id":1241,"sortIndex":32,"affiliation":1242,"properties":28},"09f6c5a4-baa3-4e5b-80ad-d3ed2d022e74",{"id":1241,"createTime":28,"updateTime":28,"relativeEntities":1243,"slug":28,"properties":1244,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1247,"statistic":28},[],{"title":1245},{"VI":1246},"Service d’Hématologie Clinique & INSERM U917, Centre Hospitalier Universitaire de Rennes, Rennes, France",[],{"title":1249},{"VI":1250},"Roch Houot",{"id":1252,"sortIndex":40,"researcher":28,"roles":1253,"affiliations":1254,"properties":1263,"displayName":1265,"givenName":28,"familyName":28},"49781e8a-f01f-4b53-af76-f8c13d61f289",[1036],[1255],{"id":1256,"sortIndex":32,"affiliation":1257,"properties":28},"72c9892f-1f28-48ff-80e3-6a38eac04640",{"id":1256,"createTime":28,"updateTime":28,"relativeEntities":1258,"slug":28,"properties":1259,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1262,"statistic":28},[],{"title":1260},{"VI":1261},"Department of Medicine, Division of Oncology, Stanford University, Stanford, USA",[],{"title":1264},{"VI":1265},"Holbrook Kohrt",{"id":1267,"sortIndex":123,"researcher":28,"roles":1268,"affiliations":1269,"properties":1276,"displayName":1278,"givenName":28,"familyName":28},"b15575c4-b5df-473c-a39f-ac707d67b8ae",[1036],[1270],{"id":1256,"sortIndex":32,"affiliation":1271,"properties":28},{"id":1256,"createTime":28,"updateTime":28,"relativeEntities":1272,"slug":28,"properties":1273,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1275,"statistic":28},[],{"title":1274},{"VI":1261},[],{"title":1277},{"VI":1278},"Matthew J. 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Models are Necessary to Predict Therapy of Transplantable Tumors in Mice",{"VOID":1356},"10.1023\u002FA:1006140513233",{"EN":1358},"Rapid evaluation of new cytotoxic agents and biological response modifiers for therapy of cancer and elucidation of their mechanisms of action require the use of relevant animal models. It is well established that the faithful reproduction of the tumor microenvironment that allows the emergence of subpopulations of tumor cells with the biological and metastatic properties observed in clinical cancer occurs with orthotopic tumor models (transplantable and transgenic). This review summarizes the evidence that phenotypic properties of metastatic cells are governed by the expression of genes that are regulated by interaction with the relevant organ environment. While ectopic models of cancer allow rapid screening of new compounds and transgenic models afford opportunities to study early cellular and molecular events in tumor progression and metastasis, orthotopic transplantation of tumor cells remains an affordable, reproducible and reliable methodology for the study of organ-specific determinants of the biology and therapy of cancer.","http:\u002F\u002Flink.springer.com\u002F10.1023\u002FA:1006140513233",[1361,1376,1389],{"id":1362,"sortIndex":32,"researcher":28,"roles":1363,"affiliations":1364,"properties":1373,"displayName":1375,"givenName":28,"familyName":28},"b096212a-7f6b-4c33-804d-a1635aea8deb",[1036],[1365],{"id":1366,"sortIndex":32,"affiliation":1367,"properties":28},"b901cc12-36dc-45d8-8d27-3b9895c0650e",{"id":1366,"createTime":28,"updateTime":28,"relativeEntities":1368,"slug":28,"properties":1369,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1372,"statistic":28},[],{"title":1370},{"VI":1371},"Department of Cell Biology, The University of Texas M. D. Anderson Cancer Center, Houston, USA",[],{"title":1374},{"VI":1375},"Jerald J. Killion",{"id":1377,"sortIndex":40,"researcher":28,"roles":1378,"affiliations":1379,"properties":1386,"displayName":1388,"givenName":28,"familyName":28},"17050581-fcae-4dcf-8e1c-3f99033ab88c",[1036],[1380],{"id":1366,"sortIndex":32,"affiliation":1381,"properties":28},{"id":1366,"createTime":28,"updateTime":28,"relativeEntities":1382,"slug":28,"properties":1383,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1385,"statistic":28},[],{"title":1384},{"VI":1371},[],{"title":1387},{"VI":1388},"Robert Radinsky",{"id":1390,"sortIndex":123,"researcher":28,"roles":1391,"affiliations":1392,"properties":1399,"displayName":1401,"givenName":28,"familyName":28},"1c660b91-04af-4790-bae5-451d8eab4908",[1036],[1393],{"id":1366,"sortIndex":32,"affiliation":1394,"properties":28},{"id":1366,"createTime":28,"updateTime":28,"relativeEntities":1395,"slug":28,"properties":1396,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1398,"statistic":28},[],{"title":1397},{"VI":1371},[],{"title":1400},{"VI":1401},"Isaiah J. Fidler",{"url":1359,"publisher":1403,"properties":1448},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1404,"slug":872,"properties":1405,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1408,"manageAffiliations":1417,"indexDatabases":1428,"url":28,"thumbnailPath":28,"statistic":1443,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1406,"title":1407},{"VOID":875},{"VOID":877},[1409,1413],{"id":881,"createTime":28,"updateTime":28,"relativeEntities":1410,"label":1411,"description":1412,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":884},{},{"id":887,"createTime":28,"updateTime":28,"relativeEntities":1414,"label":1415,"description":1416,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":890},{},[1418,1423],{"id":894,"createTime":28,"updateTime":28,"relativeEntities":1419,"slug":28,"properties":1420,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1422,"statistic":28},[],{"title":1421},{"EN":898},[],{"id":901,"createTime":28,"updateTime":28,"relativeEntities":1424,"slug":28,"properties":1425,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1427,"statistic":28},[],{"title":1426},{"EN":905},[907],[1429,1436],{"id":910,"indexDatabase":1430,"url":916,"indexYears":917,"academicFieldIds":1435,"indexDatabaseRanking":921},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":1431,"label":1432,"description":1433,"key":792,"publicationTags":1434,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[919,920],{"id":923,"indexDatabase":1437,"url":935,"indexYears":28,"academicFieldIds":1442,"indexDatabaseRanking":28},{"id":925,"createTime":28,"updateTime":28,"relativeEntities":1438,"label":1439,"description":1440,"key":932,"publicationTags":1441,"standard":28},[],{"EN":928,"VI":928},{"EN":930,"VI":931},[934,813],[937],{"impactFactor":32,"impactFactorByYear":1444,"i10Index":575,"i10IndexLast5Year":140,"totalPublication":946,"totalPublicationByYear":1445,"totalCitation":948,"totalCitationByYear":1446,"totalCitationPerPublication":976,"totalCitationPerPublicationByYear":1447,"hindexLast5Year":156,"hindex":156},{"2012":940,"2013":462,"2014":40,"2015":941,"2016":335,"2017":444,"2018":942,"2019":943,"2020":944,"2021":237,"2022":945,"2023":442},{"1982":51,"1983":127,"1984":199,"1985":126,"1986":357,"1987":352,"1988":146,"1989":146,"1990":131,"1991":122,"1992":128,"1993":128,"1994":129,"1995":122,"1996":202,"1997":199,"1998":352,"1999":140,"2000":140,"2001":122,"2002":135,"2003":147,"2004":134,"2005":352,"2006":201,"2007":434,"2008":132,"2009":136,"2010":149,"2011":201,"2012":436,"2013":352,"2014":152,"2015":149,"2016":147,"2017":201,"2018":141,"2019":137,"2020":208,"2021":434,"2022":150,"2023":50,"2024":323},{"1982":950,"1983":859,"1984":951,"1985":952,"1987":953,"1988":132,"1989":146,"1990":954,"1991":955,"1992":684,"1993":956,"1994":957,"1995":958,"1996":959,"2004":960,"2005":961,"2006":962,"2007":963,"2008":964,"2009":965,"2010":966,"2011":207,"2012":967,"2013":968,"2014":969,"2015":970,"2016":971,"2017":572,"2018":972,"2019":973,"2020":974,"2021":975,"2022":430,"2023":353},{"1982":978,"1983":979,"1984":980,"1985":981,"1987":982,"1988":983,"1989":40,"1990":984,"1991":985,"1992":986,"1993":987,"1994":988,"1995":989,"1996":990,"2004":991,"2005":992,"2006":993,"2007":136,"2008":994,"2009":995,"2010":996,"2011":997,"2012":998,"2013":999,"2014":1000,"2015":1001,"2016":1002,"2017":1003,"2018":1004,"2019":1005,"2020":1006,"2021":1007,"2022":1008,"2023":340},{"pages":1449,"volume":1451},{"VOID":1450},"279-284",{"VOID":1452},"17","1998-09-01",1998,[934,921],{"id":1457,"createTime":1458,"updateTime":1459,"relativeEntities":1460,"slug":1461,"properties":1462,"entityType":1028,"verifyStatus":26,"verifyTime":1459,"verifyNote":1030,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1471,"fullTextUrl":28,"authors":1472,"publicationType":1064,"publisherRelationship":1663,"citationCount":28,"citationInfo":28,"publishDate":1714,"publishYear":1715,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1716,"openAccess":28,"references":28,"isForceReanalyzing":1119},"01185bd9-33e8-4acb-9b9d-3fc0d54bf8e7","2024-01-21T19:31:35.631+00:00","2025-01-15T02:26:48.162+00:00",[],"Cross-talk-between-the-microbiome-and-chronic-inflammation-in-esophageal-cancer-potential-driver-of-oncogenesis",{"abstract":1463,"title":1465,"references":1467,"doi":1469},{"EN":1464},"Esophageal cancer (EC) is frequently considered a lethal malignancy and is often identified at a later stage. It is one of the major causes of cancer-related deaths globally. The conventional treatment methods like chemotherapy, radiotherapy, and surgery offer limited efficacy and poor clinical outcome with a less than 25% 5-year survival rate. The poor prognosis of EC persists despite the growth in the development of diagnostic and therapeutic modalities to treat EC. This underlines the need to elucidate the complex molecular mechanisms that drive esophageal oncogenesis. Apart from the role of the tumor microenvironment and its structural and cellular components in tumorigenesis, mounting evidence points towards the involvement of the esophageal microbiome, inflammation, and their cross-talk in promoting esophageal cancer. 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cell lung cancer (NSCLC) is the major cause of cancer-related deaths in the USA and worldwide. Most patients present with advanced disease, and treatment options for these patients are generally limited to platinum-based chemotherapy and a few targeted therapies. Targeted agents currently in use for NSCLC inhibit oncogenic receptor tyrosine kinase pathways, such as the epidermal growth factor receptor (EGFR) pathway. While current EGFR-targeted agents, including erlotinib and gefitinib, may result in dramatic responses, they demonstrate efficacy in only a fraction of patients, and resistance to these agents frequently develops. In order to select patients most likely to benefit from blockade of EGFR pathways, investigators have focused on identifying molecular correlates of response to anti-EGFR therapy. New strategies to minimize the risk of resistance to EGFR inhibition have been employed in the development of next-generation EGFR tyrosine kinase inhibitors, such as PF00299804 and BIBW 2992; these include irreversibility of target binding, inhibition of multiple EGFR family receptors, and\u002For simultaneous inhibition of EGFR and other oncogenic pathways.",{"EN":1727},"Epidermal growth factor receptor inhibition in lung cancer: the evolving role of individualized therapy",{"VOID":1729},"World Health Organization. (2008). Fact sheet no. 310: the top ten causes of death. November 2008. http:\u002F\u002Fwww.who.int\u002Fmediacentre\u002Ffactsheets\u002Ffs310_2008.pdf. Accessed 8 Oct 2009.\nAmerican Cancer Society. (2009). Cancer facts & figures, 2009. Atlanta, GA: American Cancer Society, Inc.\nNational Comprehensive Cancer Network. (2009). NCCN Clinical Practice Guidelines in Oncology™: Non-Small Cell Lung Cancer V.1.2010. http:\u002F\u002Fwww.nccn.org\u002Fprofessionals\u002Fphysician_gls\u002FPDF\u002Fnscl.pdf. Accessed 15 Dec 2009.\nBreathnach, O. S., Freidlin, B., Conley, B., Green, M. R., Johnson, D. H., Gandara, D. R., et al. (2001). Twenty-two years of phase III trials for patients with advanced non-small-cell lung cancer: sobering results. Journal of Clinical Oncology, 19(6), 1734–1742.\nCarney, D. N. (2002). Lung cancer—time to move on from chemotherapy. New England Journal of Medicine, 346(2), 126–128.\nJohnson, D. H., Fehrenbacher, L., Novotny, W. F., Herbst, R. S., Nemunaitis, J. J., Jablons, D. M., et al. (2004). Randomized phase II trial comparing bevacizumab plus carboplatin and paclitaxel with carboplatin and paclitaxel alone in previously untreated locally advanced or metastatic non-small-cell lung cancer. Journal of Clinical Oncology, 22(11), 2184–2191.\nSandler, A., Gray, R., Perry, M. C., Brahmer, J., Schiller, J. H., Dowlati, A., et al. (2006). Paclitaxel-carboplatin alone or with bevacizumab for non-small-cell lung cancer. New England Journal of Medicine, 355(24), 2542–2550.\nSibilia, M., Kroismayr, R., Lichtenberger, B. M., Natarajan, A., Hecking, M., & Holcmann, M. (2007). The epidermal growth factor receptor: from development to tumorigenesis. Differentiation, 75(9), 770–787.\nHanahan, D., & Weinberg, R. A. (2000). The hallmarks of cancer. Cell, 100(1), 57–70.\nHirsch, F. R., Varella-Garcia, M., & Cappuzzo, F. (2009). Predictive value of EGFR and HER2 overexpression in advanced non-small-cell lung cancer. Oncogene, 28(Suppl 1), S32–S37.\nHirsch, F. R., Scagliotti, G. V., Langer, C. J., Varella-Garcia, M., & Franklin, W. A. (2003). Epidermal growth factor family of receptors in preneoplasia and lung cancer: perspectives for targeted therapies. Lung Cancer, 41(Suppl 1), S29–S42.\nGazdar, A. F. (2009). Personalized medicine and inhibition of EGFR signaling in lung cancer. New England Journal of Medicine, 361(10), 1018–1020.\nGrandal, M. V., & Madshus, I. H. (2008). Epidermal growth factor receptor and cancer: control of oncogenic signalling by endocytosis. Journal of Cellular and Molecular Medicine, 12(5A), 1527–1534.\nHerbst, R. S., Heymach, J. V., & Lippman, S. M. (2008). Lung cancer. New England Journal of Medicine, 359(13), 1367–1380.\nCiardiello, F., & Tortora, G. (2008). EGFR antagonists in cancer treatment. New England Journal of Medicine, 358(11), 1160–1174.\nLaskin, J. J., & Sandler, A. B. (2004). Epidermal growth factor receptor: a promising target in solid tumours. Cancer Treatment Reviews, 30(1), 1–17.\nHo, C., & Laskin, J. (2009). EGFR-directed therapies to treat non-small-cell lung cancer. Expert Opinion on Investigational Drugs, 18(8), 1133–1145.\nSolomon, B., Varella-Garcia, M., & Camidge, D. R. (2009). ALK gene rearrangements: a new therapeutic target in a molecularly defined subset of non-small cell lung cancer. Journal of Thoracic Oncology, 4(12), 1450–1454.\nMilano, A., De Iaffaioli, R. V., & Caponigro, F. (2007). Downstream intracellular effectors of epidermal growth factor receptor as targets for anticancer therapy. Expert Opinion on Therapeutic Targets, 11(6), 771–782.\nQuesnelle, K. M., Boehm, A. L., & Grandis, J. R. (2007). STAT-mediated EGFR signaling in cancer. Journal of Cellular Biochemistry, 102(2), 311–319.\nSilva, C. M. (2004). Role of STATs as downstream signal transducers in Src family kinase-mediated tumorigenesis. Oncogene, 23(48), 8017–8023.\nModi, S., & Seidman, A. D. (2002). An update on epidermal growth factor receptor inhibitors. Current Oncology Reports, 4(1), 47–55.\nHirsch, F. R., Varella-Garcia, M., Bunn, P. A., Jr., Di Maria, M. V., Veve, R., Bremmes, R. M., et al. (2003). Epidermal growth factor receptor in non-small-cell lung carcinomas: correlation between gene copy number and protein expression and impact on prognosis. Journal of Clinical Oncology, 21(20), 3798–3807.\nOhsaki, Y., Tanno, S., Fujita, Y., Toyoshima, E., Fujiuchi, S., Nishigaki, Y., et al. (2000). Epidermal growth factor receptor expression correlates with poor prognosis in non-small cell lung cancer patients with p53 overexpression. Oncology Reports, 7(3), 603–607.\nJohn, T., Liu, G., & Tsao, M. S. (2009). Overview of molecular testing in non-small-cell lung cancer: mutational analysis, gene copy number, protein expression and other biomarkers of EGFR for the prediction of response to tyrosine kinase inhibitors. Oncogene, 28(Suppl 1), S14–S23.\nEberhard, D. A., Giaccone, G., & Johnson, B. E. (2008). Biomarkers of response to epidermal growth factor receptor inhibitors in Non-Small-Cell Lung Cancer Working Group: standardization for use in the clinical trial setting. Journal of Clinical Oncology, 26(6), 983–994.\nHirsch, F. R., Varella-Garcia, M., Bunn, P. A., Jr., Franklin, W. A., Dziadziuszko, R., Thatcher, N., et al. (2006). Molecular predictors of outcome with gefitinib in a phase III placebo-controlled study in advanced non-small-cell lung cancer. Journal of Clinical Oncology, 24(31), 5034–5042.\nParra, H. S., Cavina, R., Latteri, F., Zucali, P. A., Campagnoli, E., Morenghi, E., et al. (2004). Analysis of epidermal growth factor receptor expression as a predictive factor for response to gefitinib ('Iressa', ZD1839) in non–small-cell lung cancer. British Journal of Cancer, 91(2), 208–212.\nPerez-Soler, R., Chachoua, A., Hammond, L. A., Rowinsky, E. K., Huberman, M., Karp, D., et al. (2004). Determinants of tumor response and survival with erlotinib in patients with non-small-cell lung cancer. Journal of Clinical Oncology, 22(16), 3238–3247.\nTsao, M. S., Sakurada, A., Cutz, J. C., Zhu, C. Q., Kamel-Reid, S., Squire, J., et al. (2005). 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Abstract 3.",{"VOID":1731},"10.1007\u002Fs10555-010-9201-z","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10555-010-9201-z",[1734],{"id":1735,"sortIndex":32,"researcher":28,"roles":1736,"affiliations":1737,"properties":1746,"displayName":1748,"givenName":28,"familyName":28},"74462d5b-6a66-418e-8659-6f36b1c7495b",[1036],[1738],{"id":1739,"sortIndex":32,"affiliation":1740,"properties":28},"0000ea1d-3744-4b2d-ba7c-4895279ab990",{"id":1739,"createTime":28,"updateTime":28,"relativeEntities":1741,"slug":28,"properties":1742,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1745,"statistic":28},[],{"title":1743},{"VI":1744},"Hamon Center for Therapeutic Oncology Research and Department of Pathology, University of Texas Southwestern Medical Center, Dallas, USA",[],{"title":1747},{"VI":1748},"Adi F. Gazdar",{"url":1732,"publisher":1750,"properties":1795},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1751,"slug":872,"properties":1752,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1755,"manageAffiliations":1764,"indexDatabases":1775,"url":28,"thumbnailPath":28,"statistic":1790,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1753,"title":1754},{"VOID":875},{"VOID":877},[1756,1760],{"id":881,"createTime":28,"updateTime":28,"relativeEntities":1757,"label":1758,"description":1759,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":884},{},{"id":887,"createTime":28,"updateTime":28,"relativeEntities":1761,"label":1762,"description":1763,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":890},{},[1765,1770],{"id":894,"createTime":28,"updateTime":28,"relativeEntities":1766,"slug":28,"properties":1767,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1769,"statistic":28},[],{"title":1768},{"EN":898},[],{"id":901,"createTime":28,"updateTime":28,"relativeEntities":1771,"slug":28,"properties":1772,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1774,"statistic":28},[],{"title":1773},{"EN":905},[907],[1776,1783],{"id":910,"indexDatabase":1777,"url":916,"indexYears":917,"academicFieldIds":1782,"indexDatabaseRanking":921},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":1778,"label":1779,"description":1780,"key":792,"publicationTags":1781,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[919,920],{"id":923,"indexDatabase":1784,"url":935,"indexYears":28,"academicFieldIds":1789,"indexDatabaseRanking":28},{"id":925,"createTime":28,"updateTime":28,"relativeEntities":1785,"label":1786,"description":1787,"key":932,"publicationTags":1788,"standard":28},[],{"EN":928,"VI":928},{"EN":930,"VI":931},[934,813],[937],{"impactFactor":32,"impactFactorByYear":1791,"i10Index":575,"i10IndexLast5Year":140,"totalPublication":946,"totalPublicationByYear":1792,"totalCitation":948,"totalCitationByYear":1793,"totalCitationPerPublication":976,"totalCitationPerPublicationByYear":1794,"hindexLast5Year":156,"hindex":156},{"2012":940,"2013":462,"2014":40,"2015":941,"2016":335,"2017":444,"2018":942,"2019":943,"2020":944,"2021":237,"2022":945,"2023":442},{"1982":51,"1983":127,"1984":199,"1985":126,"1986":357,"1987":352,"1988":146,"1989":146,"1990":131,"1991":122,"1992":128,"1993":128,"1994":129,"1995":122,"1996":202,"1997":199,"1998":352,"1999":140,"2000":140,"2001":122,"2002":135,"2003":147,"2004":134,"2005":352,"2006":201,"2007":434,"2008":132,"2009":136,"2010":149,"2011":201,"2012":436,"2013":352,"2014":152,"2015":149,"2016":147,"2017":201,"2018":141,"2019":137,"2020":208,"2021":434,"2022":150,"2023":50,"2024":323},{"1982":950,"1983":859,"1984":951,"1985":952,"1987":953,"1988":132,"1989":146,"1990":954,"1991":955,"1992":684,"1993":956,"1994":957,"1995":958,"1996":959,"2004":960,"2005":961,"2006":962,"2007":963,"2008":964,"2009":965,"2010":966,"2011":207,"2012":967,"2013":968,"2014":969,"2015":970,"2016":971,"2017":572,"2018":972,"2019":973,"2020":974,"2021":975,"2022":430,"2023":353},{"1982":978,"1983":979,"1984":980,"1985":981,"1987":982,"1988":983,"1989":40,"1990":984,"1991":985,"1992":986,"1993":987,"1994":988,"1995":989,"1996":990,"2004":991,"2005":992,"2006":993,"2007":136,"2008":994,"2009":995,"2010":996,"2011":997,"2012":998,"2013":999,"2014":1000,"2015":1001,"2016":1002,"2017":1003,"2018":1004,"2019":1005,"2020":1006,"2021":1007,"2022":1008,"2023":340},{"pages":1796,"volume":1798},{"VOID":1797},"37-48",{"VOID":1115},"2010-02-03",[934,921],{"id":1802,"createTime":1803,"updateTime":1804,"relativeEntities":1805,"slug":1806,"properties":1807,"entityType":1028,"verifyStatus":26,"verifyTime":1804,"verifyNote":1030,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1816,"fullTextUrl":28,"authors":1817,"publicationType":1064,"publisherRelationship":1833,"citationCount":28,"citationInfo":28,"publishDate":1884,"publishYear":1885,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":1886,"openAccess":28,"references":28,"isForceReanalyzing":1119},"01c3e93d-a9f0-4a58-8d79-5363ad9e1f5e","2024-01-20T23:21:01.533+00:00","2024-12-22T17:56:22.447+00:00",[],"Rb-E2F-A-two-edged-sword-in-the-melanocytic-system",{"abstract":1808,"title":1810,"references":1812,"doi":1814},{"EN":1809},"Rb is a tumor suppressor that represses the expression of E2F regulated genes required for cell cycle progression. It is inactivated in melanomas and other cancer cells by phosphorylation catalyzed by persistent cyclin dependent kinase (CDK) activity. CDK activity is sustained in melanoma cells mostly by the elimination of the CDK inhibitor p16INK4A and by high levels of cyclins whose expression is maintained by stimuli emanating from activated cell surface receptors and\u002For mutated intracellular intermediates, such as N-Ras and B-Raf. However, Rb also suppresses the expression of apoptosis genes, and its presence protects normal melanocytes from cell death. Its high expression in human melanoma cells and tumors suggests a similar role in malignant cells as well. The differential release and suppression of E2F transcriptional activity is likely to depend on promoter-specific E2F\u002FRb interaction. Phosphorylated Rb is displaced from cell cycle genes but not from others. 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Nature 391: 859–865, 1998",{"VOID":1815},"10.1007\u002Fs10555-005-1582-z","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10555-005-1582-z",[1818],{"id":1819,"sortIndex":32,"researcher":28,"roles":1820,"affiliations":1821,"properties":1830,"displayName":1832,"givenName":28,"familyName":28},"ee53b0f0-1328-49f6-9a8a-022e2202df46",[1036],[1822],{"id":1823,"sortIndex":32,"affiliation":1824,"properties":28},"16d590ca-0842-4910-88ed-46d9de8ddb21",{"id":1823,"createTime":28,"updateTime":28,"relativeEntities":1825,"slug":28,"properties":1826,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1829,"statistic":28},[],{"title":1827},{"VI":1828},"Department of Dermatology, Yale University School of Medicine, New Haven, USA",[],{"title":1831},{"VI":1832},"Ruth Halaban",{"url":1816,"publisher":1834,"properties":1879},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1835,"slug":872,"properties":1836,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1839,"manageAffiliations":1848,"indexDatabases":1859,"url":28,"thumbnailPath":28,"statistic":1874,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":1837,"title":1838},{"VOID":875},{"VOID":877},[1840,1844],{"id":881,"createTime":28,"updateTime":28,"relativeEntities":1841,"label":1842,"description":1843,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":884},{},{"id":887,"createTime":28,"updateTime":28,"relativeEntities":1845,"label":1846,"description":1847,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":890},{},[1849,1854],{"id":894,"createTime":28,"updateTime":28,"relativeEntities":1850,"slug":28,"properties":1851,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1853,"statistic":28},[],{"title":1852},{"EN":898},[],{"id":901,"createTime":28,"updateTime":28,"relativeEntities":1855,"slug":28,"properties":1856,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1858,"statistic":28},[],{"title":1857},{"EN":905},[907],[1860,1867],{"id":910,"indexDatabase":1861,"url":916,"indexYears":917,"academicFieldIds":1866,"indexDatabaseRanking":921},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":1862,"label":1863,"description":1864,"key":792,"publicationTags":1865,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[919,920],{"id":923,"indexDatabase":1868,"url":935,"indexYears":28,"academicFieldIds":1873,"indexDatabaseRanking":28},{"id":925,"createTime":28,"updateTime":28,"relativeEntities":1869,"label":1870,"description":1871,"key":932,"publicationTags":1872,"standard":28},[],{"EN":928,"VI":928},{"EN":930,"VI":931},[934,813],[937],{"impactFactor":32,"impactFactorByYear":1875,"i10Index":575,"i10IndexLast5Year":140,"totalPublication":946,"totalPublicationByYear":1876,"totalCitation":948,"totalCitationByYear":1877,"totalCitationPerPublication":976,"totalCitationPerPublicationByYear":1878,"hindexLast5Year":156,"hindex":156},{"2012":940,"2013":462,"2014":40,"2015":941,"2016":335,"2017":444,"2018":942,"2019":943,"2020":944,"2021":237,"2022":945,"2023":442},{"1982":51,"1983":127,"1984":199,"1985":126,"1986":357,"1987":352,"1988":146,"1989":146,"1990":131,"1991":122,"1992":128,"1993":128,"1994":129,"1995":122,"1996":202,"1997":199,"1998":352,"1999":140,"2000":140,"2001":122,"2002":135,"2003":147,"2004":134,"2005":352,"2006":201,"2007":434,"2008":132,"2009":136,"2010":149,"2011":201,"2012":436,"2013":352,"2014":152,"2015":149,"2016":147,"2017":201,"2018":141,"2019":137,"2020":208,"2021":434,"2022":150,"2023":50,"2024":323},{"1982":950,"1983":859,"1984":951,"1985":952,"1987":953,"1988":132,"1989":146,"1990":954,"1991":955,"1992":684,"1993":956,"1994":957,"1995":958,"1996":959,"2004":960,"2005":961,"2006":962,"2007":963,"2008":964,"2009":965,"2010":966,"2011":207,"2012":967,"2013":968,"2014":969,"2015":970,"2016":971,"2017":572,"2018":972,"2019":973,"2020":974,"2021":975,"2022":430,"2023":353},{"1982":978,"1983":979,"1984":980,"1985":981,"1987":982,"1988":983,"1989":40,"1990":984,"1991":985,"1992":986,"1993":987,"1994":988,"1995":989,"1996":990,"2004":991,"2005":992,"2006":993,"2007":136,"2008":994,"2009":995,"2010":996,"2011":997,"2012":998,"2013":999,"2014":1000,"2015":1001,"2016":1002,"2017":1003,"2018":1004,"2019":1005,"2020":1006,"2021":1007,"2022":1008,"2023":340},{"pages":1880,"volume":1882},{"VOID":1881},"339-356",{"VOID":1883},"24","2005-06-01",2005,[934,921],{"id":1888,"createTime":1889,"updateTime":1890,"relativeEntities":1891,"slug":1892,"properties":1893,"entityType":1028,"verifyStatus":26,"verifyTime":1890,"verifyNote":1030,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1902,"fullTextUrl":28,"authors":1903,"publicationType":1064,"publisherRelationship":1983,"citationCount":28,"citationInfo":28,"publishDate":2034,"publishYear":2035,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":2036,"openAccess":28,"references":28,"isForceReanalyzing":1119},"01cffb0f-374f-4b6e-a32d-5829abc268db","2023-12-11T16:50:51.301+00:00","2025-01-27T19:53:47.906+00:00",[],"Liquid-biopsy-for-monitoring-of-tumor-dormancy-and-early-detection-of-disease-recurrence-in-solid-tumors",{"abstract":1894,"title":1896,"references":1898,"doi":1900},{"EN":1895},"Cancer is one of the three leading causes of death worldwide. Even after successful therapy and achieving remission, the risk of relapse often remains. In this context, dormant residual cancer cells in secondary organs such as the bone marrow constitute the cellular reservoir from which late tumor recurrences arise. This dilemma leads the term of minimal residual disease, which reflects the presence of tumor cells disseminated from the primary lesion to distant organs in patients who lack any clinical or radiological signs of metastasis or residual tumor cells left behind after therapy that eventually lead to local recurrence. Disseminated tumor cells have the ability to survive in a dormant state following treatment and linger unrecognized for more than a decade before emerging as recurrent disease. They are able to breakup their dormant state and to readopt their proliferation under certain circumstances, which can finally lead to distant relapse and cancer-associated death. In recent years, extensive molecular and genetic characterization of disseminated tumor cells and blood-based biomarker has contributed significantly to our understanding of the frequency and prevalence of tumor dormancy. In this article, we describe the clinical relevance of disseminated tumor cells and highlight how latest advances in different liquid biopsy approaches can be used to detect, characterize, and monitor minimal residual disease in breast cancer, prostate cancer, and melanoma patients.",{"EN":1897},"Liquid biopsy for monitoring of tumor dormancy and early detection of disease recurrence in solid tumors",{"VOID":1899},"Schuurhuis, G. J., Heuser, M., Freeman, S., Bene, M. C., Buccisano, F., Cloos, J., et al. (2018). Minimal\u002Fmeasurable residual disease in AML: A consensus document from the European LeukemiaNet MRD Working Party. Blood, 131(12), 1275–1291. https:\u002F\u002Fdoi.org\u002F10.1182\u002Fblood-2017-09-801498\nSosa, M. S., Bragado, P., & Aguirre-Ghiso, J. A. 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EMT and stemness in tumor dormancy and outgrowth: Are they intertwined processes? Frontiers in Oncology, 8, 381. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffonc.2018.00381\nFelici, C., Mannavola, F., Stucci, L. S., Duda, L., Cafforio, P., Porta, C., et al. (2022). Circulating tumor cells from melanoma patients show phenotypic plasticity and metastatic potential in xenograft NO.DCB17 mice. BMC Cancer, 22(1), 754. https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs12885-022-09829-1\nVoit, C., Kron, M., Rademaker, J., Schwurzer-Voit, M., Sterry, W., Weber, L., et al. (2005). Molecular staging in stage II and III melanoma patients and its effect on long-term survival. Journal of Clinical Oncology, 23(6), 1218–1227. https:\u002F\u002Fdoi.org\u002F10.1200\u002FJCO.2005.04.098\nLucci, A., Hall, C. S., Patel, S. P., Narendran, B., Bauldry, J. B., Royal, R. E., et al. (2020). Circulating tumor cells and early relapse in node-positive melanoma. 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malnutrition (PEM) is common in cancer patients and may develop into the syndrome known as ‘cancer cachexia’. This is characterised by complex disturbances in carbohydrate, lipid, protein, and electrolyte metabolism. The actiology is equally complex, with host and therapeutic factors contributing to the reduced food intake and effects on host tissues. Anorexia is of prime importance, differing in its cause from one patient to another and often presenting a barrier to successful nutritional support. Further research is necessary to elucidate the interaction of central and peripheral factors that may be involved in the aetiology of anorexia. Because of the interplay of biochemical, physiological, and psychological consequences of cancer, the nutritional support of the patient presents a considerable challenge to the caring professions.",{"EN":2047},"Malignant disease: nutritional implications of disease and treatment",{"VOID":2049},"Blackburn GL, Bothe A: Assessment of malnutrition in cancer patients. 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University of Surrey, Guildford, U.K., 1986, pp 30–35",{"VOID":2051},"10.1007\u002FBF00144270","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00144270",[2054,2069],{"id":2055,"sortIndex":32,"researcher":28,"roles":2056,"affiliations":2057,"properties":2066,"displayName":2068,"givenName":28,"familyName":28},"7b60dce6-1836-43ac-a9d2-42dcdf1bd4be",[1036],[2058],{"id":2059,"sortIndex":32,"affiliation":2060,"properties":28},"7db7342c-e424-4f3f-b812-5909a141d820",{"id":2059,"createTime":28,"updateTime":28,"relativeEntities":2061,"slug":28,"properties":2062,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2065,"statistic":28},[],{"title":2063},{"VI":2064},"Division of Nursing Studies, Department of Biochemistry, University of Surrey, Guildford, U.K.",[],{"title":2067},{"VI":2068},"Susan Holmes",{"id":2070,"sortIndex":40,"researcher":28,"roles":2071,"affiliations":2072,"properties":2081,"displayName":2083,"givenName":28,"familyName":28},"74039b8c-b9b4-48b0-a8a5-76ecaa5efdfa",[1036],[2073],{"id":2074,"sortIndex":32,"affiliation":2075,"properties":28},"f4e7f4b6-9c5d-4f1b-8f0c-d80c8c2e316e",{"id":2074,"createTime":28,"updateTime":28,"relativeEntities":2076,"slug":28,"properties":2077,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2080,"statistic":28},[],{"title":2078},{"VI":2079},"Division of Nutrition and Food Science, Department of Biochemistry, University of Surrey, Guildford, U.K.",[],{"title":2082},{"VI":2083},"John W. T. Dickerson",{"url":2052,"publisher":2085,"properties":2130},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":2086,"slug":872,"properties":2087,"entityType":25,"verifyStatus":878,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":2090,"manageAffiliations":2099,"indexDatabases":2110,"url":28,"thumbnailPath":28,"statistic":2125,"gsStatistic":28,"type":55,"analyzePriority":28},[],{"issn":2088,"title":2089},{"VOID":875},{"VOID":877},[2091,2095],{"id":881,"createTime":28,"updateTime":28,"relativeEntities":2092,"label":2093,"description":2094,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":884},{},{"id":887,"createTime":28,"updateTime":28,"relativeEntities":2096,"label":2097,"description":2098,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":890},{},[2100,2105],{"id":894,"createTime":28,"updateTime":28,"relativeEntities":2101,"slug":28,"properties":2102,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2104,"statistic":28},[],{"title":2103},{"EN":898},[],{"id":901,"createTime":28,"updateTime":28,"relativeEntities":2106,"slug":28,"properties":2107,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2109,"statistic":28},[],{"title":2108},{"EN":905},[907],[2111,2118],{"id":910,"indexDatabase":2112,"url":916,"indexYears":917,"academicFieldIds":2117,"indexDatabaseRanking":921},{"id":786,"createTime":28,"updateTime":28,"relativeEntities":2113,"label":2114,"description":2115,"key":792,"publicationTags":2116,"standard":28},[],{"EN":789,"VI":789},{"EN":789,"VI":791},[794],[919,920],{"id":923,"indexDatabase":2119,"url":935,"indexYears":28,"academicFieldIds":2124,"indexDatabaseRanking":28},{"id":925,"createTime":28,"updateTime":28,"relativeEntities":2120,"label":2121,"description":2122,"key":932,"publicationTags":2123,"standard":28},[],{"EN":928,"VI":928},{"EN":930,"VI":931},[934,813],[937],{"impactFactor":32,"impactFactorByYear":2126,"i10Index":575,"i10IndexLast5Year":140,"totalPublication":946,"totalPublicationByYear":2127,"totalCitation":948,"totalCitationByYear":2128,"totalCitationPerPublication":976,"totalCitationPerPublicationByYear":2129,"hindexLast5Year":156,"hindex":156},{"2012":940,"2013":462,"2014":40,"2015":941,"2016":335,"2017":444,"2018":942,"2019":943,"2020":944,"2021":237,"2022":945,"2023":442},{"1982":51,"1983":127,"1984":199,"1985":126,"1986":357,"1987":352,"1988":146,"1989":146,"1990":131,"1991":122,"1992":128,"1993":128,"1994":129,"1995":122,"1996":202,"1997":199,"1998":352,"1999":140,"2000":140,"2001":122,"2002":135,"2003":147,"2004":134,"2005":352,"2006":201,"2007":434,"2008":132,"2009":136,"2010":149,"2011":201,"2012":436,"2013":352,"2014":152,"2015":149,"2016":147,"2017":201,"2018":141,"2019":137,"2020":208,"2021":434,"2022":150,"2023":50,"2024":323},{"1982":950,"1983":859,"1984":951,"1985":952,"1987":953,"1988":132,"1989":146,"1990":954,"1991":955,"1992":684,"1993":956,"1994":957,"1995":958,"1996":959,"2004":960,"2005":961,"2006":962,"2007":963,"2008":964,"2009":965,"2010":966,"2011":207,"2012":967,"2013":968,"2014":969,"2015":970,"2016":971,"2017":572,"2018":972,"2019":973,"2020":974,"2021":975,"2022":430,"2023":353},{"1982":978,"1983":979,"1984":980,"1985":981,"1987":982,"1988":983,"1989":40,"1990":984,"1991":985,"1992":986,"1993":987,"1994":988,"1995":989,"1996":990,"2004":991,"2005":992,"2006":993,"2007":136,"2008":994,"2009":995,"2010":996,"2011":997,"2012":998,"2013":999,"2014":1000,"2015":1001,"2016":1002,"2017":1003,"2018":1004,"2019":1005,"2020":1006,"2021":1007,"2022":1008,"2023":340},{"pages":2131,"volume":2133},{"VOID":2132},"357-381",{"VOID":2134},"6","1987-11-01",1987,[934,921],{"id":2139,"createTime":2140,"updateTime":2141,"relativeEntities":2142,"slug":2143,"properties":2144,"entityType":1028,"verifyStatus":26,"verifyTime":2141,"verifyNote":1030,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":2153,"fullTextUrl":28,"authors":2154,"publicationType":1064,"publisherRelationship":2196,"citationCount":28,"citationInfo":28,"publishDate":2247,"publishYear":2248,"citationAnalyzeStatus":878,"lastCitationAnalyze":28,"indexDatabases":2249,"openAccess":28,"references":28,"isForceReanalyzing":1119},"01f700e8-397d-46d7-9a39-273fe135a877","2024-02-10T19:25:42.203+00:00","2025-01-12T16:40:52.432+00:00",[],"Physiological-functions-of-MTA-family-of-proteins",{"abstract":2145,"title":2147,"references":2149,"doi":2151},{"EN":2146},"Although the functional significance of the metastasic tumor antigen (MTA) family of chromatin remodeling proteins in the pathobiology of cancer is fairly well recognized, the physiological role of MTA proteins continues to be an understudied research area and is just beginning to be recognized. Similar to cancer cells, MTA1 also modulates the expression of target genes in normal cells either by acting as a corepressor or coactivator. In addition, physiological functions of MTA proteins are likely to be influenced by its differential expression, subcellular localization, and regulation by upstream modulators and extracellular signals. This review summarizes our current understanding of the physiological functions of the MTA proteins in model systems. In particular, we highlight recent advances of the role MTA proteins play in the brain, eye, circadian rhythm, mammary gland biology, spermatogenesis, liver, immunomodulation and inflammation, cellular radio-sensitivity, and hematopoiesis and differentiation. Based on the growth of knowledge regarding the exciting new facets of the MTA family of proteins in biology and medicine, we speculate that the next burst of findings in this field may reveal further molecular regulatory insights of non-redundant functions of MTA coregulators in the normal physiology as well as in pathological conditions outside cancer.",{"EN":2148},"Physiological functions of MTA family of proteins",{"VOID":2150},"Toh, Y., Pencil, S. D., & Nicolson, G. L. (1994). A novel candidate metastasis-associated gene, mta1, differentially expressed in highly metastatic mammary adenocarcinoma cell lines. cDNA cloning, expression, and protein analyses. Journal of Biological Chemistry, 269(37), 22958–22963.\nToh, Y., Pencil, S. D., & Nicolson, G. L. (1995). Analysis of the complete sequence of the novel metastasis-associated candidate gene, mta1, differentially expressed in mammary adenocarcinoma and breast cancer cell lines. Gene, 159(1), 97–104.\nMazumdar, A., Wang, R. 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M., Kenyon, C., & Herman, R. K. (1999). EGL-27 is similar to a metastasis-associated factor and controls cell polarity and cell migration in C. elegans. Development, 126(5), 1055–1064.\nZimmerman, S. M., & Kim, S. K. (2014). The GATA transcription factor\u002FMTA-1 homolog egr-1 promotes longevity and stress resistance in Caenorhabditis elegans. Aging Cell, 13(2), 329–339.\nvon Zelewsky, T., Palladino, F., Brunschwig, K., Tobler, H., Hajnal, A., & Muller, F. (2000). The C. elegans Mi-2 chromatin-remodelling proteins function in vulval cell fate determination. Development, 127(24), 5277–5284.\nChen, Z., & Han, M. (2001). Role of C. elegans lin-40 MTA in vulval fate specification and morphogenesis. Development, 128(23), 4911–4921.\nBonifati, V., Rizzu, P., van Baren, M. J., Schaap, O., Breedveld, G. J., Krieger, E., et al. (2003). Mutations in the DJ-1 gene associated with autosomal recessive early-onset parkinsonism. Science, 299(5604), 256–259.\nReddy, S. D., Rayala, S. K., Ohshiro, K., Pakala, S. B., Kobori, N., Dash, P., et al. (2011). Multiple coregulatory control of tyrosine hydroxylase gene transcription. Proceedings of the National Academy of Sciences of the United States of America, 108(10), 4200–4205.\nThakur, M. K., & Ghosh, S. (2009). Interaction of estrogen receptor alpha transactivation domain with MTA1 decreases in old mouse brain. Journal of Molecular Neurosciences, 37(3), 269–273.\nAramaki, Y., Ogawa, K., Toh, Y., Ito, T., Akimitsu, N., Hamamoto, H., et al. (2005). Direct interaction between metastasis-associated protein 1 and endophilin 3. FEBS Letters, 579(17), 3731–3736.\nLee, C., Gyorgy, A., Maric, D., Sadri, N., Schneider, R. J., Barker, J. L., et al. (2008). Members of the NuRD chromatin remodeling complex interact with AUF1 in developing cortical neurons. Cerebral Cortex, 18(12), 2909–2919.\nSimpson, A., Uitto, J., Rodeck, U., & Mahoney, M. G. (2001). Differential expression and subcellular distribution of the mouse metastasis-associated proteins Mta1 and Mta3. Gene, 273(1), 29–39.\nPotts, R. C., Zhang, P., Wurster, A. L., Precht, P., Mughal, M. R., Wood, W. H., 3rd, et al. (2011). CHD5, a brain-specific paralog of Mi2 chromatin remodeling enzymes, regulates expression of neuronal genes. PloS One, 6(9), e24515.\nDel Bene, F., Tessmar-Raible, K., & Wittbrodt, J. (2004). Direct interaction of geminin and Six3 in eye development. Nature, 427(6976), 745–749.\nManavathi, B., Peng, S., Rayala, S. K., Talukder, A. H., Wang, M. H., Wang, R. A., et al. (2007). Repression of Six3 by a corepressor regulates rhodopsin expression. Proceedings of the National Academy of Sciences of the United States of America, 104(32), 13128–13133.\nMitton, K. P., Swain, P. K., Chen, S., Xu, S., Zack, D. J., & Swaroop, A. (2000). The leucine zipper of NRL interacts with the CRX homeodomain. A possible mechanism of transcriptional synergy in rhodopsin regulation. Journal of Biological Chemistry, 275(38), 29794–29799.\nQtaishat, N. M., Wiggert, B., & Pepperberg, D. R. (2005). Interphotoreceptor retinoid-binding protein (IRBP) promotes the release of all-trans retinol from the isolated retina following rhodopsin bleaching illumination. Experimental Eye Research, 81(4), 455–463.\nWallis, D. E., Roessler, E., Hehr, U., Nanni, L., Wiltshire, T., Richieri-Costa, A., et al. (1999). Mutations in the homeodomain of the human SIX3 gene cause holoprosencephaly. Nature Genetics, 22(2), 196–198.\nLi, D. Q., Pakala, S. B., Reddy, S. D., Peng, S., Balasenthil, S., Deng, C. X., et al. (2013). Metastasis-associated protein 1 is an integral component of the circadian molecular machinery. Nature Communication, 4, 2545.\nZhou, B., Ma, Q., Kong, S. W., Hu, Y., Campbell, P. H., McGowan, F. X., et al. (2009). Ackerman KG, Wu B, Zhou B, Tevosian SG, Pu WT.Fog2 is critical for cardiac function and maintenance of coronary vasculature in the adult mouse heart. Journal of Clinical Investigation, 119(6), 1462–1676.\nZhang, H., Stephens, L. C., & Kumar, R. (2006). Metastasis tumor antigen family proteins during breast cancer progression and metastasis in a reliable mouse model for human breast cancer. Clinical Cancer Research, 12(5), 1479–1486.\nLagutin, O. V., Zhu, C. C., Kobayashi, D., Topczewski, J., Shimamura, K., Puelles, L., et al. (2003). Six3 repression of Wnt signaling in the anterior neuroectoderm is essential for vertebrate forebrain development. Genes & Development, 17(3), 368–379.\nKumar, R., Balasenthil, S., Manavathi, B., Rayala, S. K., & Pakala, S. B. (2010). Metastasis-associated protein 1 and its short form variant stimulates Wnt1 transcription through promoting its derepression from Six3 corepressor. Cancer Research, 70(16), 6649–6658.\nZhang, H., Singh, R. R., Talukder, A. H., & Kumar, R. (2006). Metastatic tumor antigen 3 is a direct corepressor of the Wnt4 pathway. Genes & Development, 20(21), 2943–2948.\nLi, W., Zhang, J., Liu, X., Xu, R., & Zhang, Y. (2007). Correlation of appearance of metastasis-associated protein1 (Mta1) with spermatogenesis in developing mouse testis. Cell Tissue Research, 329(2), 351–362.\nLi, W., Liu, X. P., Xu, R. J., & Zhang, Y. Q. (2007). Immunolocalization assessment of metastasis-associated protein 1 in human and mouse mature testes and its association with spermatogenesis. Asian Journal of Andrology, 9(3), 345–352.\nLi, W., Wu, Z. Q., Zhao, J., Guo, S. J., Li, Z., Feng, X., et al. (2011). Transient protection from heat-stress induced apoptotic stimulation by metastasis-associated protein 1 in pachytene spermatocytes. PloS One, 6(10), e26013.\nZhang, S., Li, W., Zhu, C., Wang, X., Li, Z., Zhang, J., et al. (2012). Sertoli cell-specific expression of metastasis-associated protein 2 (MTA2) is required for transcriptional regulation of the follicle-stimulating hormone receptor (FSHR) gene during spermatogenesis. Journal of Biological Chemistry, 287(48), 40471–40483.\nAl-Bader, M. D., Kilarkaje, N., El-Farra, A., & Al-Abdallah, A. A. (2014). Expression and subcellular localization of metastasis-associated protein 1, its short form, and estrogen receptors in rat placenta. Reproductive Sciences. doi:10.1177\u002F1933719114549851.\nKwintkiewicz, J., Padilla-Banks, E., Jefferson, W. N., Jacobs, I. M., Wade, P. A., & Williams, C. J. (2012). Metastasis-associated protein 3 (MTA3) regulates G2\u002FM progression in proliferating mouse granulosa cells. Biology of Reproduction, 86(3), 1–8.\nPakala, S. B., Bui-Nguyen, T. M., Reddy, S. D., Li, D. Q., Peng, S., Rayala, S. K., et al. (2010). 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Inhibition of metastasis-associated gene 1 expression affects proliferation and osteogenic differentiation of immortalized human mesenchymal stem cells. Cell Proliferation, 44(2), 128–138.",{"VOID":2152},"10.1007\u002Fs10555-014-9514-4","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10555-014-9514-4",[2155,2170,2183],{"id":2156,"sortIndex":32,"researcher":28,"roles":2157,"affiliations":2158,"properties":2167,"displayName":2169,"givenName":28,"familyName":28},"2f7a72aa-7cfb-4e25-843f-2e08e315e64c",[1036],[2159],{"id":2160,"sortIndex":32,"affiliation":2161,"properties":28},"26b476b7-2955-453d-b54e-d83a20bd31d5",{"id":2160,"createTime":28,"updateTime":28,"relativeEntities":2162,"slug":28,"properties":2163,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2166,"statistic":28},[],{"title":2164},{"VI":2165},"Department of Biochemistry and Molecular Medicine, George Washington University, Washington, USA",[],{"title":2168},{"VI":2169},"Nirmalya 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