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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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In a single hybridization, CGH provides an overview of DNA sequence copy number changes (losses, deletions, gains, amplifications) in a tumor specimen and maps these changes on normal chromosomes. CGH is based on the in situ hybridization of differentially labeled \u003Cjats:italic>total genomic tumor\u003C\u002Fjats:italic> DNA and normal reference DNA to \u003Cjats:italic>normal\u003C\u002Fjats:italic> human metaphase chromosomes. After hybridization and fluorescent staining of the bound DNAs, copy number variations among the different sequences in the tumor DNA are detected by measuring the tumor\u002Fnormal fluorescence intensity ratio for each locus in the target metaphase chromosomes. CGH is in particular useful for analysis of DNA sequence copy number changes in common solid tumors where high‐quality metaphase preparations are often difficult to make, and where complex karyotypes with numerous markers, double minutes, and homogeneously stained chromosomal regions are common. CGH only detects changes that are present in a substantial proportion of tumor cells (i.e., clonal aberrations). It does not reveal translocations, inversions, and other aberrations that do not change copy number. At present, CGH is a research tool that complements previous methods for genetic analysis. CGH will advance our understanding of the genetic progression of cancer and highlight important genomic regions for further study. Direct clinical applications of CGH are possible, but will require further development and validation of the technique. We describe here our recent optimized procedures for CGH, including DNA labeling, hybridization, fluorescence microscopy, digital image analysis, data interpretation, and quality control, emphasizing those steps that are most critical. We will also assess sensitivity and resolution limits of CGH as well as discuss possible future technical improvements. \u003Cjats:italic>Genes Chromosom Cancer\u003C\u002Fjats:italic> 10:231–243 (1994). © 1994 Wiley‐Liss, Inc.\u003C\u002Fjats:p>",{"EN":962},"Optimizing comparative genomic hybridization for analysis of DNA sequence copy number changes in solid tumors",{"VOID":964},"7522536",{"VOID":966},"10.1002\u002Fgcc.2870100403","PUBLICATION","Auto 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DNA copy number alterations (CNAs), which occur frequently in breast cancer and define key pathogenetic events, are also potentially useful prognostic or predictive factors. Here, we report a genome‐wide array‐based comparative genomic hybridization (array CGH) survey of CNAs in 89 breast tumors from a patient cohort with locally advanced disease. Statistical analysis links distinct cytoband loci harboring CNAs to specific clinicopathological parameters, including tumor grade, estrogen receptor status, presence of \u003Cjats:italic>TP\u003C\u002Fjats:italic>\u003Cjats:italic>53\u003C\u002Fjats:italic> mutation, and overall survival. Notably, distinct spectra of CNAs also underlie the different subtypes of breast cancer recently defined by expression‐profiling, implying these subtypes develop along distinct genetic pathways. In addition, higher numbers of gains\u002Flosses are associated with the “basal‐like” tumor subtype, while high‐level DNA amplification is more frequent in “luminal‐B” subtype tumors, suggesting also that distinct mechanisms of genomic instability might underlie their pathogenesis. The identified CNAs may provide a basis for improved patient prognostication, as well as a starting point to define important genes to further our understanding of the pathobiology of breast cancer. 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mesothelioma (MM) is an aggressive cancer arising from mesothelial cells, mainly due to former asbestos exposure. Little is known about the microRNA (miRNA) expression of MM. miRNAs are small noncoding RNAs, which play an essential role in the regulation of gene expression. This study was carried out to analyze the miRNA expression profile of 17 MM samples using miRNA microarray. The analysis distinguished the overall miRNA expression profiles of tumor tissue and normal mesothelium. Differentially expressed miRNAs were found in tumor samples compared with normal sample. Twelve of them, let‐7b*, miR‐1228*, miR‐195*, miR‐30b*, miR‐32*, miR‐345, miR‐483‐3p, miR‐584, miR‐595, miR‐615‐3p, and miR‐885‐3p, were highly expressed whereas the remaining nine, let‐7e*, miR‐144*, miR‐203, miR‐340*, miR‐34a*, miR‐423, miR‐582, miR‐7‐1*, and miR‐9, were unexpressed or had severely reduced expression levels. Target genes for these miRNAs include the most frequently affected genes in MM such as \u003Cjats:italic>CDKN2A\u003C\u002Fjats:italic>, \u003Cjats:italic>NF2\u003C\u002Fjats:italic>, \u003Cjats:italic>JUN\u003C\u002Fjats:italic>, \u003Cjats:italic>HGF\u003C\u002Fjats:italic>, and \u003Cjats:italic>PDGFA\u003C\u002Fjats:italic>. Many of the miRNAs were located in chromosomal areas known to be deleted or gained in MM such as 8q24, 1p36, and 14q32. Furthermore, we could identify specific miRNAs for each histopathological subtype of MM. Regarding risk factors such as smoking status and asbestos exposure, significantly differentially expressed miRNAs were identified in smokers versus nonsmokers (miR‐379, miR‐301a, miR‐299‐3p, miR‐455‐3p, and miR‐127‐3p), but not in asbestos‐exposed patients versus nonexposed ones. 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AJ, 1987, tdic(9;12): A nonrandom chromosome abnormality in childhood B‐cell precursor acute lymphoblastic leukemia: A Pediatric Oncology Group Study, Blood, 70, 1962, 10.1182\u002Fblood.V70.6.1962.1962",{"doi":2063},"10.1182\u002Fblood.V70.6.1962.1962",{"id":28,"text":2065,"url":28,"identifiers":2066},"10.1073\u002Fpnas.87.17.6639",{"doi":2065},{"id":28,"text":2068,"url":28,"identifiers":2069},"10.1038\u002F359380a0",{"doi":2068},{"id":28,"text":2071,"url":28,"identifiers":2072},"ISCN, 1991, Guidelines for Cancer Cytogenetics: Supplement to An International System for Human Cytogenetics Nomenclature",{},{"id":28,"text":2074,"url":28,"identifiers":2075},"Krance RA, 1992, t(12;17)(p13;q21) in early pre‐B acute lymphoid leukemia, Leukemia, 6, 251",{},{"id":28,"text":2077,"url":28,"identifiers":2078},"10.1016\u002F0165-4608(92)90317-2",{"doi":2077},{"id":28,"text":2080,"url":28,"identifiers":2081},"Mitelman F, 1991, Catalog of Chromosome Aberrations in Cancer, 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genomic hybridization (CGH) makes it possible to detect losses and gains of DNA sequences along all chromosomes in a tumor specimen based on the hybridization of differentially labeled tumor and normal DNA to normal human metaphase chromosomes. In this study, CGH analysis was applied to the identification of genomic imbalances in 26 bladder cancers in order to gain information on the genetic events underlying the development and progression of this malignancy. Losses affecting 11p, 11q, 8p, 9, 17p, 3p, and 12q were all seen in more than 20% of the tumors. The minimal common region of loss in each chromosome was identified based on the analysis of overlapping deletions in different tumors. Gains of DNA sequences were most often found at chromosomal regions distinct from the locations of currently known oncogenes. The bands involved in more than 10% of the tumors were 8q21, 13q21‐q34, 1q31, 3q24‐q26, and 1p22. In conclusion, these CGH data highlight several previously unreported genetic alterations in bladder cancer. Further detailed studies of these regions with specific molecular genetic techniques may lead to the identification of tumor suppressor genes and oncogenes that play an important role in bladder tumorigenesis.\u003C\u002Fjats:p>",{"EN":2118},"Identification of gains and losses of DNA sequences in primary bladder cancer by comparative genomic 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VR, 1987, Tumor behavior in transitional cell carcinoma of the bladder in relation to chromosomal markers and histopathology, Cancer Res, 47, 6800",{},{"id":28,"text":2317,"url":28,"identifiers":2318},"10.1016\u002F0165-4608(86)90145-7",{"doi":2317},{"id":28,"text":2320,"url":28,"identifiers":2321},"10.1016\u002FS0889-8588(18)30361-7",{"doi":2320},{"id":28,"text":2323,"url":28,"identifiers":2324},"Cairns P, 1993, Preliminary mapping of the deleted region of chromosome 9 in bladder cancer, Cancer Res, 53, 1230",{},{"id":28,"text":2326,"url":28,"identifiers":2327},"10.1016\u002F0140-6736(93)91595-D",{"doi":2326},{"id":28,"text":2329,"url":28,"identifiers":2330},"Devilee P, 1991, Allelotype of human breast carcinoma: A second major site for loss of heterozygosity on chromosome 6q, Oncogene, 6, 1705",{},{"id":28,"text":1164,"url":28,"identifiers":2332},{"doi":1164},{"id":28,"text":2334,"url":28,"identifiers":2335},"10.1038\u002Fbjc.1993.51",{"doi":2334},{"id":28,"text":2337,"url":28,"identifiers":2338},"Gibas Z, 1984, Nonrandom chromosomal changes in transitional cell carcinoma of the bladder, Cancer Res, 44, 1257",{},{"id":28,"text":2340,"url":28,"identifiers":2341},"10.1002\u002Fijc.2910530409",{"doi":2340},{"id":28,"text":1170,"url":28,"identifiers":2343},{"doi":1170},{"id":28,"text":2345,"url":28,"identifiers":2346},"Kallioniemi O‐P, 1993, Comparative genomic hybridization: A rapid new method for detecting and mapping of DNA amplification in tumors, Semin Cancer Biol, 4, 41",{},{"id":28,"text":1179,"url":28,"identifiers":2348},{"doi":1179},{"id":28,"text":966,"url":28,"identifiers":2350},{"doi":966},{"id":28,"text":2352,"url":28,"identifiers":2353},"Knowles MA, 1993, Deletion mapping of chromosome 8 in cancers of the urinary bladder using restriction fragment length polymorphisms and microsatellite polymorphisms, Oncogene, 8, 1357",{},{"id":28,"text":2355,"url":28,"identifiers":2356},"Knowles MA, 1994, Allelotype of human bladder cancer, Cancer Res, 54, 531",{},{"id":28,"text":2358,"url":28,"identifiers":2359},"Matsumura K, 1992, Deletion of chromosome 17p loci in breast cancer detected by fluorescence in situ hybridization, Cancer Res, 52, 3474",{},{"id":28,"text":2361,"url":28,"identifiers":2362},"Morita R, 1991, Allelotype of renal carcinoma, Cancer Res, 51, 820",{},{"id":28,"text":2364,"url":28,"identifiers":2365},"PiperJ RutovitzD SudarD KallioniemiA KallioniemiO‐P WaldmanFM GrayJW PinkelD(1994)Computer image analysis of comparative genomic hybridization. Cytometry (in press).",{},{"id":28,"text":2367,"url":28,"identifiers":2368},"Sakamoto M, 1993, Comparative genomic hybridization and loss of heterozygosity studies in ovarian cancer, Am J Hum Genet, 53, 356",{},{"id":28,"text":2370,"url":28,"identifiers":2371},"Sano T, 1991, Frequent loss of heterozygosity on chromosomes 1q, 5q, and 17p in human gastric carcinomas, Cancer Res, 51, 2926",{},{"id":28,"text":2373,"url":28,"identifiers":2374},"Sato T, 1991, Allelotype of human ovarian cancer, Cancer Res, 51, 5118",{},{"id":28,"text":2376,"url":28,"identifiers":2377},"Sauter G, 1993, Heterogeneity of erbB‐2 amplification in bladder cancer, Cancer Res, 53, 2199",{},{"id":28,"text":2379,"url":28,"identifiers":2380},"Sauter G, 1994, Physical deletion of the p53 gene in bladder cancer: Detection by fluorescence in situ hybridization, Am J Pathol, 144, 756",{},{"id":28,"text":2382,"url":28,"identifiers":2383},"SauterG MochH CarrollP KerschmannR MihatschM WaldmanF(1994b)Chromosome 9 loss detected by fluorescence in situ hybridization in bladder cancer. Am J Pathol (in press).",{"doi":2384},"10.1002\u002Fijc.2910640205",{"id":28,"text":2386,"url":28,"identifiers":2387},"10.1016\u002F0165-4608(87)90028-8",{"doi":2386},{"id":28,"text":2389,"url":28,"identifiers":2390},"Tsuchiya E, 1992, Allelotype of non‐small cell lung carcinoma—Comparison between loss of heterozygosity in squamous cell carcinoma and adenocarcinoma, Cancer Res, 52, 2478",{},{"id":28,"text":2392,"url":28,"identifiers":2393},"10.1016\u002F0165-4608(88)90090-8",{"doi":2392},{"id":28,"text":2395,"url":28,"identifiers":2396},"10.1016\u002FS0022-5347(17)37212-9",{"doi":2395},{"id":2398,"createTime":2399,"updateTime":2399,"relativeEntities":2400,"slug":2401,"properties":2402,"entityType":967,"verifyStatus":26,"verifyTime":2415,"verifyNote":968,"languages":2416,"translateLanguages":28,"viewCount":32,"primaryUrl":2417,"fullTextUrl":28,"authors":2418,"publicationType":1099,"publisherRelationship":2632,"citationCount":2680,"citationInfo":2681,"publishDate":2310,"publishYear":2308,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":2683,"openAccess":28,"references":2684,"isForceReanalyzing":1208},"46e8a2e9-d3e7-428b-a4a4-9900c4f41d97","2024-09-21T23:41:32.220+00:00",[],"Chromosome-analysis-of-97-primary-breast-carcinomas-Identification-of-eight-karyotypic-subgroups",{"openalex":2403,"mag":2405,"abstract":2407,"title":2409,"pm":2411,"doi":2413},{"VOID":2404},"W2019663670",{"VOID":2406},"2019663670",{"EN":2408},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Chromosome banding analysis of 97 short‐term cultured primary breast carcinomas revealed clonal aberrations in 79 tumors, whereas 18 were karyotypically normal. In 34 of the 79 tumors with abnormalities, two to eight clones per case were detected; unrelated clones were present in 27 (34%) cases, whereas only related clones were found in seven. These findings indicate that a substantial proportion of breast carcinomas are of polyclonal origin. Altogether eight abnormalities were repeatedly identified both as sole chromosomal anomalies and as part of more complex karyotypes: the structural rearrangements i(1)(q10), der(1;16)(q10;p10), del(1)(q11–12), del(3)(p12–13p14–21), and del(6)(q21–22) and the numerical aberrations +7, +18, and +20. At least one of these changes was found in 41 (52%) of the karyotypically abnormal tumors. They identify a minimum number of cytogenetic subgroups in breast cancer and are likely to represent primary chromosome anomalies in this type of neoplasia. Other candidates for such a role are translocations of 3p12–13 and 4q21 with various partner chromosomes and inversions of chromosome 7, which also were seen repeatedly. Additional chromosomal aberrations that give the impression of occurring nonrandomly in breast carcinomas include structural rearrangements leading to partial monosomies for 1p, 8p, 11p, 11q, 15p, 17p, 19p, and 19q and losses of one copy of chromosomes X, 8, 9, 13, 14, 17, and 22. 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1981, Histological Typing of Breast Tumors",{},{"id":28,"text":2784,"url":28,"identifiers":2785},"TeixeiraMR PandisN BardiG AndersenJA MandahlN MitelmanF HeimS(1994)Cytogenetic analysis of multifocal breast carcinomas: Detection of karyotypically unrelated clones as well as clonal similarities between tumor foci. Br J Cancer (in press).",{"doi":2786},"10.1038\u002Fbjc.1994.421",{"id":28,"text":2788,"url":28,"identifiers":2789},"10.1002\u002Fgcc.2870070402",{"doi":2788},{"id":28,"text":2791,"url":28,"identifiers":2792},"10.1002\u002Fgcc.2870070403",{"doi":2791},{"id":28,"text":2794,"url":28,"identifiers":2795},"Zhang R, 1989, Rare clonal karyotypic variants in primary cultures of human breast carcinoma cells, Cancer Res, 49, 444",{},{"id":2797,"createTime":2798,"updateTime":2798,"relativeEntities":2799,"slug":2800,"properties":2801,"entityType":967,"verifyStatus":26,"verifyTime":2798,"verifyNote":968,"languages":2814,"translateLanguages":28,"viewCount":32,"primaryUrl":2815,"fullTextUrl":28,"authors":2816,"publicationType":1099,"publisherRelationship":3013,"citationCount":3062,"citationInfo":3063,"publishDate":3065,"publishYear":1781,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":3066,"openAccess":28,"references":3067,"isForceReanalyzing":1208},"58202ab1-02db-47a9-9da4-7dac6117cca3","2024-10-16T17:06:51.418+00:00",[],"Germline-hypermethylation-of-i-MLH1-i-and-i-EPCAM-i-deletions-are-a-frequent-cause-of-Lynch-syndrome",{"openalex":2802,"mag":2804,"abstract":2806,"title":2808,"pm":2810,"doi":2812},{"VOID":2803},"W2025785990",{"VOID":2805},"2025785990",{"EN":2807},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>It was shown that Lynch syndrome can be caused by germline hypermethylation of the \u003Cjats:italic>MLH1\u003C\u002Fjats:italic> and \u003Cjats:italic>MSH2\u003C\u002Fjats:italic> promoters. Furthermore, it has been demonstrated very recently that germline deletions of the 3′ region of \u003Cjats:italic>EPCAM\u003C\u002Fjats:italic> cause transcriptional read‐through which results in silencing of \u003Cjats:italic>MSH2\u003C\u002Fjats:italic> by hypermethylation. We wanted to determine the prevalence of germline \u003Cjats:italic>MLH1\u003C\u002Fjats:italic> promoter hypermethylation and of germline and somatic \u003Cjats:italic>MSH2\u003C\u002Fjats:italic> promoter hypermethylation in a large group of Lynch syndrome‐suspected patients. From a group of 331 Lynch Syndrome‐suspected patients we selected cases, who had no germline \u003Cjats:italic>MLH1\u003C\u002Fjats:italic>, \u003Cjats:italic>MSH2\u003C\u002Fjats:italic>, or \u003Cjats:italic>MSH6\u003C\u002Fjats:italic> mutation and whose tumors showed loss of MLH1 or MSH2, or, if staining was unavailable, had a tumor with microsatellite instability. Methylation assays were performed to test these patients for germline \u003Cjats:italic>MLH1\u003C\u002Fjats:italic> and\u002For \u003Cjats:italic>MSH2\u003C\u002Fjats:italic> promoter hypermethylation. Two patients with germline \u003Cjats:italic>MLH1\u003C\u002Fjats:italic> promoter hypermethylation and no patients with germline \u003Cjats:italic>MSH2\u003C\u002Fjats:italic> promoter hypermethylation were identified. In the subgroup screened for germline \u003Cjats:italic>MSH2\u003C\u002Fjats:italic> promoter hypermethylation, we identified 3 patients with somatic \u003Cjats:italic>MSH2\u003C\u002Fjats:italic> promoter hypermethylation in their tumors, which was caused by a germline \u003Cjats:italic>EPCAM\u003C\u002Fjats:italic> deletion. In the group of 331 Lynch Syndrome‐suspected patients, the frequencies of germline \u003Cjats:italic>MLH1\u003C\u002Fjats:italic> promoter hypermethylation and somatic \u003Cjats:italic>MSH2\u003C\u002Fjats:italic> promoter hypermethylation caused by germline \u003Cjats:italic>EPCAM\u003C\u002Fjats:italic> deletions are 0.6 and 0.9%, respectively. These mutations, therefore, seem to be rather infrequent. However, the contribution of germline \u003Cjats:italic>MLH1\u003C\u002Fjats:italic> hypermethylation and \u003Cjats:italic>EPCAM\u003C\u002Fjats:italic> deletions to the genetically proven Lynch syndrome cases in this cohort is very high. Previously 27 pathogenic mutations were identified; the newly identified mutations now represent 16% of all mutations. © 2009 Wiley‐Liss, Inc.\u003C\u002Fjats:p>",{"EN":2809},"Germline hypermethylation of \u003Ci>MLH1\u003C\u002Fi> and \u003Ci>EPCAM\u003C\u002Fi> deletions are a frequent cause of Lynch syndrome",{"VOID":2811},"19455606",{"VOID":2813},"10.1002\u002Fgcc.20678",[31],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fgcc.20678",[2817,2834,2851,2868,2887,2902,2917,2932,2947,2962,2979,2996],{"id":2818,"sortIndex":32,"researcher":28,"roles":2819,"affiliations":2820,"properties":2829,"displayName":2831,"givenName":28,"familyName":28},"7caf4a7c-70a8-46f2-9ece-cc9260bf0f30",[],[2821],{"id":2822,"sortIndex":32,"affiliation":2823,"properties":28},"00892b4f-b022-4c50-9a07-626ec0bc7463",{"id":2822,"createTime":28,"updateTime":28,"relativeEntities":2824,"slug":28,"properties":2825,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2828,"statistic":28},[],{"title":2826},{"EN":2827},"Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands",[],{"title":2830,"openalex":2832},{"EN":2831},"Renée C. 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Thesis University of Groningen (http:\u002F\u002Firs.ub.rug.nl\u002Fppn\u002F182343367).",{},{"id":3147,"createTime":3148,"updateTime":3148,"relativeEntities":3149,"slug":3150,"properties":3151,"entityType":967,"verifyStatus":26,"verifyTime":3164,"verifyNote":968,"languages":3165,"translateLanguages":28,"viewCount":32,"primaryUrl":3166,"fullTextUrl":28,"authors":3167,"publicationType":1099,"publisherRelationship":3426,"citationCount":3062,"citationInfo":3475,"publishDate":3478,"publishYear":3476,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":3479,"openAccess":28,"references":3480,"isForceReanalyzing":1208},"a7c93c13-be99-4542-a660-310930f905d4","2024-09-21T02:20:54.857+00:00",[],"Gene-dosage-alterations-revealed-by-cDNA-microarray-analysis-in-cervical-cancer-Identification-of-candidate-amplified-and-overexpressed-genes",{"openalex":3152,"mag":3154,"abstract":3156,"title":3158,"pm":3160,"doi":3162},{"VOID":3153},"W2155098031",{"VOID":3155},"2155098031",{"EN":3157},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Cervical cancer (CC) cells exhibit complex karyotypic alterations, which is consistent with deregulation of numerous critical genes in its formation and progression. To characterize this karyotypic complexity at the molecular level, we used cDNA array comparative genomic hybridization (aCGH) to analyze 29 CC cases and identified a number of over represented and deleted genes. The aCGH analysis revealed at least 17 recurrent amplicons and six common regions of deletions. These regions contain several known tumor‐associated genes, such as those involved in transcription, apoptosis, cytoskeletal remodeling, ion‐transport, drug metabolism, and immune response. Using the fluorescence in situ hybridization (FISH) approach we demonstrated the presence of high‐level amplifications at the 8q24.3, 11q22.2, and 20q13 regions in CC cell lines. To identify amplification‐associated genes that correspond to focal amplicons, we examined one or more genes in each of the 17 amplicons by Affymetrix U133A expression arrays and semiquantitative reverse‐transcription PCR (RT‐PCR) in 31 CC tumors. This analysis exhibited frequent and robust upregulated expression in CC relative to normal cervix for genes \u003Cjats:italic>EPHB2\u003C\u002Fjats:italic> (1p36), \u003Cjats:italic>CDCA8\u003C\u002Fjats:italic> (1p34.3), \u003Cjats:italic>AIM2\u003C\u002Fjats:italic> (1q22‐23), \u003Cjats:italic>RFC4\u003C\u002Fjats:italic>, \u003Cjats:italic>MUC4\u003C\u002Fjats:italic>, and \u003Cjats:italic>HRASLS\u003C\u002Fjats:italic> (3q27‐29), \u003Cjats:italic>SKP2\u003C\u002Fjats:italic> (5p12‐13), \u003Cjats:italic>CENTD3\u003C\u002Fjats:italic> (5q31.3), \u003Cjats:italic>PTK2, RECQL4\u003C\u002Fjats:italic> (8q24), \u003Cjats:italic>MMP1\u003C\u002Fjats:italic> and \u003Cjats:italic>MMP13\u003C\u002Fjats:italic> (11q22.2), \u003Cjats:italic>AKT1\u003C\u002Fjats:italic> (14q32.3), \u003Cjats:italic>ABCC3\u003C\u002Fjats:italic> (17q21‐22), \u003Cjats:italic>SMARCA4\u003C\u002Fjats:italic> (19p13.3) \u003Cjats:italic>LIG1\u003C\u002Fjats:italic> (19q13.3), \u003Cjats:italic>UBE2C\u003C\u002Fjats:italic> (20q13.1), \u003Cjats:italic>SMC1L1\u003C\u002Fjats:italic> (Xp11), \u003Cjats:italic>KIF4A\u003C\u002Fjats:italic> (Xq12), \u003Cjats:italic>TMSNB\u003C\u002Fjats:italic> (Xq22), and \u003Cjats:italic>CSAG2\u003C\u002Fjats:italic> (Xq28). Thus, the gene dosage and expression profiles generated here have enabled the identification of focal amplicons characteristic for the CC genome and facilitated the validation of relevant genes in these amplicons. These data, thus, form an important step toward the identification of biologically relevant genes in CC pathogenesis. 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of tumors utilizing next‐generation sequencing methods, including assessment of the number of somatic mutations (tumor mutational burden [TMB]), is currently at the forefront of the field of personalized medicine. Recent clinical studies have associated high TMB with improved patient response rates and survival benefit from immune checkpoint inhibitors; hence, TMB is emerging as a biomarker of response for these immunotherapy agents. However, variability in current methods for TMB estimation and reporting is evident, demonstrating a need for standardization and harmonization of TMB assessment methodology across assays and centers. Two uniquely placed organizations, Friends of Cancer Research (Friends) and the Quality Assurance Initiative Pathology (QuIP), have collaborated to coordinate efforts for international multistakeholder initiatives to address this need. Friends and QuIP, who have partnered with several academic centers, pharmaceutical organizations, and diagnostic companies, have adopted complementary, multidisciplinary approaches toward the goal of proposing evidence‐based recommendations for achieving consistent TMB estimation and reporting in clinical samples across assays and centers. Many factors influence TMB assessment, including preanalytical factors, choice of assay, and methods of reporting. Preliminary analyses highlight the importance of targeted gene panel size and composition, and bioinformatic parameters for reliable TMB estimation. Herein, Friends and QuIP propose recommendations toward consistent TMB estimation and reporting methods in clinical samples across assays and centers. These recommendations should be followed to minimize variability in TMB estimation and reporting, which will ensure reliable and reproducible identification of patients who are likely to benefit from immune checkpoint inhibitors.\u003C\u002Fjats:p>",{"EN":3606},"Tumor mutational burden standardization initiatives: Recommendations for consistent tumor mutational burden assessment in clinical samples to guide immunotherapy treatment decisions",{"VOID":3608},"30664300",{"VOID":3610},"10.1002\u002Fgcc.22733",[31],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fgcc.22733",[3614,3633,3650,3669,3686,3703,3718],{"id":3615,"sortIndex":32,"researcher":28,"roles":3616,"affiliations":3617,"properties":3626,"displayName":3630,"givenName":28,"familyName":28},"3ab2e6e5-9b4a-4270-8815-8a4bb20bb9d6",[],[3618],{"id":3619,"sortIndex":32,"affiliation":3620,"properties":28},"7dc09ff2-f507-4040-b272-2435acc27a08",{"id":3619,"createTime":28,"updateTime":28,"relativeEntities":3621,"slug":28,"properties":3622,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3625,"statistic":28},[],{"title":3623},{"EN":3624},"Institute of Pathology, University Hospital Heidelberg (on behalf of QuIP® GmbH, Berlin, Germany)  Heidelberg Germany",[],{"orcid":3627,"title":3629,"openalex":3631},{"VOID":3628},"https:\u002F\u002Forcid.org\u002F0000-0003-1001-103X",{"EN":3630},"Albrecht Stenzinger",{"VOID":3632},"A5026607584",{"id":3634,"sortIndex":40,"researcher":28,"roles":3635,"affiliations":3636,"properties":3645,"displayName":3647,"givenName":28,"familyName":28},"8a1ad7cf-3235-47d8-98be-4220849e355c",[],[3637],{"id":3638,"sortIndex":32,"affiliation":3639,"properties":28},"cdb0afcc-1386-46fd-aa89-a07cae9f19f2",{"id":3638,"createTime":28,"updateTime":28,"relativeEntities":3640,"slug":28,"properties":3641,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3644,"statistic":28},[],{"title":3642},{"EN":3643},"Science Policy, Friends of Cancer Research Washington District of Columbia",[],{"title":3646,"openalex":3648},{"EN":3647},"Jeffrey D. 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