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other provinces and regions in Vietnam and other country.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Address\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Headquarters of Can Tho Journal of Medicine and Pharmacy, located Scientific Research and International Cooperation Office: 179 Nguyen Van Cu Street, An Khanh Ward, Ninh Kieu District, Can Tho City, Vietnam.\u003C\u002Fspan>\u003C\u002Fp>","\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Ngày 16\u002F7\u002F2015, Tạp chí Y Dược học Cần Thơ được cấp chỉ số quốc tế: ISSN 2354-1210.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 4\u002F2016, Tạp chí đã được Hội đồng Giáo sư ngành Y đưa vào danh sách các tạp chí khoa học Y học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Năm 2020 Tạp chí Y Dược học Cần Thơ đã được phê duyệt vào danh mục của các Hội đồng Giáo sư ngành Dược học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ ra 12 số\u002Fnăm, 180-200 trang\u002Fsố.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 12\u002F2022 Tạp chí Y Dược học Cần Thơ là thành viên của hệ thống Crossref và từ tháng 01\u002F2023 tạp chí thực hiện bình duyệt online kín 2 chiều nhằm tăng tính minh bạch, tin cậy của các công trình nghiên cứu khoa học và đảm bảo tốt nhất chất lượng khoa học của bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ, mục đích và phạm vi của tạp chí\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ và mục đích hoạt động của tạp chí: xuất bản nhằm mục đích phổ biến kết quả từ các đề tài nghiên cứu khoa học; giao lưu trao đổi khoa học, chia sẻ kinh nghiệm, học tập, đồng thời cập nhật thông tin khoa học mới trong các lĩnh vực y, sinh, dược học trong và ngoài nước.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phạm vi của tạp chí: Tạp chí xuất bản được chia thành 3 chuyên mục: (i) Bài báo nghiên cứu khoa học là kết quả công trình nghiên cứu khoa học có giá trị đã được triển khai nghiên cứu, (ii) Bài tổng quan y, sinh, dược học: phục vụ mục tiêu đào tạo liên tục trong lĩnh vực y, sinh, dược học; nhằm hệ thống hóa những kiến thức kinh điển và hiện đại; (iii) Thông tin cập nhật kiến thức mới về y, sinh, dược học trong nước và trên thế giới.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Chính sách truy cập mở\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ áp dụng chính sách truy cập mở đối với các bài báo đã xuất bản đến với độc giả, nhằm mở rộng cơ hội tiếp cận các kết quả nghiên cứu chất lượng cao và tăng cường trao đổi kiến thức. Tạp chí đăng tải trực tuyến (miễn phí) toàn văn các bài báo được công bố trên website của Tạp chí (https:\u002F\u002Ftapchi.ctump.edu.vn).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đạo đức xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ cam kết tuân thủ đạo đức xuất bản phù hợp với các hướng dẫn và tiêu chuẩn của the Committee on Publication Ethics (COPE), tuân thủ các nguyên tắc của COPE’s Core Practices, Best Practices Guidelines for Journal Editors và Guidelines on Good Publication Practices.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Bản thảo bài báo chỉ được chấp nhận khi được tác giả chịu trách nhiệm chính cam kết các nội dung sau: Các nội dung của bản thảo chưa được đăng tải toàn bộ hoặc một phần ở các tạp chí khác; Tất cả các tác giả đều có đóng góp một cách đáng kể vào quá trình nghiên cứu hoặc chuẩn bị bản thảo và cùng chịu trách nhiệm về các nội dung của bản thảo; Tuân thủ các biện pháp đảm bảo đạo đức nghiên cứu (ví dụ thỏa thuận đồng ý tham gia nghiên cứu).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Cam kết bảo mật\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí cam kết thực hiện và tuân thủ các quy định của luật và các văn bản hướng dẫn liên quan đến bảo mật thông tin cá nhân trên không gian mạng. Các thông tin mà người dùng (tác giả, độc giả, biên tập viên, người phản biện) nhập vào các biểu mẫu trên Hệ thống Quản lý xuất bản trực tuyến của tạp chí chỉ được sử dụng vào các mục đích đã được tuyên bố rõ ràng và sẽ không được cung cấp cho bất kỳ bên thứ ba nào khác, hay dùng vào bất kỳ mục đích nào khác.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phí gửi bài\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng bài: 1.000.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng nhanh: 1.500.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với tác giả là cán bộ viên chức thuộc Trường Đại học Y Dược Cần Thơ thì được hỗ trợ 50% lệ phí gửi đăng bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với sinh viên thực hiện đề tài nghiên cứu khoa học cấp trường được hỗ trợ 100% lệ phí đăng bài ( Tác giả gửi đính kèm “ Quyết định về việc giao tổ chức thực hiện đề tài nghiên cứu khoa học cấp Trường của sinh viên”).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Hình thức nộp lệ phí:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Tiền mặt:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Nộp trực tiếp tại Phòng Tài chính - Kế toán, Trường Đại học Y Dược Cần Thơ, số 179 Nguyễn Văn Cừ, P. An Khánh, Q. Ninh Kiều, thành phố Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Chuyển khoản:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tên Tài khoản: Trường ĐHYD Cần Thơ, Số TK: 0111000115668, tại ngân hàng Vietcombank chi nhánh Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Thời gian: Áp dụng từ ngày 01\u002F02\u002F2023.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">* Phí gửi bài không được hoàn trả khi bài viết bị từ chối hoặc tác giả xin rút bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Quy trình phản biện bài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ thực hiện quy trình phản biện kín hai chiều nghiêm ngặt. Danh tính của những người phản biện không được tiết lộ cho các tác giả và ngược lại. Quy trình thẩm định bài báo đăng gồm các bước sau:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tiếp nhận bản thảo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tác giả liên hệ gửi bản thảo đến Tạp chí qua hệ thống trực tuyến tại website: https:\u002F\u002Ftapchi.ctump.edu.vn. Hướng dẫn về cách đăng ký, gửi bài và chuẩn bị bản thảo được cung cấp trên website của Tạp chí.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sàng lọc sơ bộ\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sau khi Tòa soạn nhận được bài báo của tác giả, Ban Thư ký sẽ tiến hành kiểm tra sơ bộ bài báo (các yêu cầu về nội dung và hình thức). Những bài báo không đúng quy cách hoặc có nội dung không phù hợp hoặc vi phạm bản quyền sẽ bị từ chối (Ban Thư ký thông báo phản hồi đến tác giả trong vòng 1 tuần). Những bài báo đủ điều kiện, được Ban Thư ký tòa soạn chuyển đến Ban Biên tập có cùng chuyên môn với nội dung bài báo để đề xuất người phản biện. Thời gian kể từ khi Ban Biên tập nhận bài báo đến khi đề xuất người phản biện bài báo chậm nhất là 5 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Vòng phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký gửi bài và yêu cầu phản biện đến 02 phản biện độc lập.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Các phản biện gởi nhận xét cho Ban Thư ký. Thời gian từ khi gửi bài cho phản biện đến khi nhận ý kiến của phản biện tối đa là 20 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xử ký kết quả phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Nếu ý kiến đồng ý cho đăng và không cần chỉnh sửa, Ban Thư ký tiếp tục đăng bài theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Nếu ý kiến đồng ý đăng và cần chỉnh sửa, Ban Thư ký sẽ thông tin đến tác giả chỉnh sửa theo yêu cầu của người phản biện. Thời gian chỉnh sửa và gửi lại kéo dài không quá 2 tuần, từ khi tác giả bài báo nhận được thông tin (Quá trình này có thể lặp lại tối đa 2 lần\u002F1 bài báo). Khi có sự thống nhất, đồng ý của người phản biện; bài báo được tiếp tục đăng theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Những bài báo có chất lượng không đạt yêu cầu, cả 2 phản biện không đồng ý cho đăng sẽ bị Tòa soạn từ chối đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký tổng hợp các bản thảo đã được tác giả hoàn thiện sau thẩm định trình Ban Biên tập xem xét, Tổng Biên tập phê duyệt, quyết định bài đăng theo các tiêu chí: sự phù hợp nội dung với tôn chỉ và mục đích, thể loại bài viết (ưu tiên các bài có bài có nghiên cứu chuyên sâu, hàm lượng khoa học cao), đóng góp mới bài báo, bài báo được ưu tiên đăng trong số gần nhất của Tạp chí theo thứ tự: tính thời sự, chất lượng bài báo và thời gian gửi bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Ban Biên tập và Ban Thư ký biên tập bản thảo, chế bản, đọc rà soát lỗi. Thời gian hoàn thành từ 10-15 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Ban Thư ký có trách nhiệm thông báo cho tác giả bài báo (bằng e-mail) về tình hình phê duyệt bài báo, thời gian, số kỳ, tập xuất bản bài báo theo qui định.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">4. 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The main objectives of the journal include: providing an intellectual platform for Vietnamese and international scholars; promoting interdisciplinary studies in social sciences and humanities; becoming the leading journal in social sciences and humanities in Vietnam; being indexed by worldwide databases and having academic recognition internationally in the near future.\\nThe journal is currently indexed by Google Scholar, WorldCat, Open Archives, Cosmos Impact Factor, Advanced Sciences Index, Scientific Indexing Services, CrossRef, EBSCO Information Services and Vietnam National University’s digital archive.\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Journal of Social Sciences and Humanities-Vietnam\"},{\"insert\":\"\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"ISSN 2354-1172, email: tapchikhxhnv@gmail.com, tckhxhnv@vnu.edu.vn\"},{\"insert\":\"\\n\"}]}","{\"ops\":[{\"insert\":\"Được thành lập ngày 31\u002F8\u002F2015 (giấy phép hoạt động số 155\u002FGP-BVHTT ngày 11 tháng 5 năm 2015 của Bộ Thông tin và Truyền thông, mã số tiêu chuẩn quốc tế ISSN 2354-1172), Tạp chí Khoa học Xã hội và Nhân văn (Journal of Social Sciences and Humanities) là ấn phẩm khoa học chính thức, duy nhất của Trường Đại học Khoa học Xã hội và Nhân văn, ĐHQG Hà Nội, phát triển và kế thừa Chuyên san Khoa học Xã hội và Nhân văn, Tạp chí Khoa học, ĐHQG Hà Nội.\\nTạp chí xuất bản định kỳ (04 số tiếng Việt\u002Fnăm và 02 số tiếng Anh\u002Fnăm), có nhiệm vụ \"},{\"attributes\":{\"italic\":true},\"insert\":\"công bố, giới thiệu các công trình nghiên cứu khoa học khoa học xã hội và nhân văn của các tác giả là các nhà khoa học trong và ngoài nước, phục vụ giảng dạy, học tập và nghiên cứu khoa học\"},{\"insert\":\". 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Dev Med Child Neurol. 1985, 27: 293-304.",{"doi":1972},"10.1111\u002Fj.1469-8749.1985.tb04539.x",{"id":1974,"createTime":1975,"updateTime":1976,"relativeEntities":1977,"slug":1978,"properties":1979,"entityType":796,"verifyStatus":25,"verifyTime":1976,"verifyNote":797,"syncStatus":28,"languages":1998,"translateLanguages":1999,"viewCount":36,"primaryUrl":2000,"fullTextUrl":26,"authors":2001,"publicationType":1070,"publisherRelationship":2145,"citationCount":1483,"citationInfo":2170,"publishDate":2173,"publishYear":2174,"citationAnalyzeStatus":28,"lastCitationAnalyze":26,"indexDatabases":26,"openAccess":26,"references":2175,"isForceReanalyzing":1413},"5d0203d1-e843-42bc-b520-907249cdaedc","2024-04-17T17:44:19.005+00:00","2025-02-26T20:37:06.030+00:00",[],"Copy-number-variation-is-highly-correlated-with-differential-gene-expression-a-pan-cancer-study",{"mag":1980,"keywords":1982,"pmc":1984,"openalex":1986,"abstract":1988,"title":1991,"pm":1994,"doi":1996},{"VOID":1981},"2985789142",{"VI":1983},"Biến thể số lượng bản sao, biểu hiện gen, ung thư, sinh tin học, di truyền học.",{"VOID":1985},"6842483",{"VOID":1987},"W2985789142",{"VI":1989,"EN":1990},"\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n              \u003Cjats:sec>\n                \u003Cjats:title>Đặt vấn đề\u003C\u002Fjats:title>\n                \u003Cjats:p>Ung thư là một bệnh lý đa dạng với nhiều biến thể di truyền. Các dòng chứng cứ đã chỉ ra rằng sự biến đổi số lượng bản sao (CNVs) của một số gen tham gia vào việc phát triển và tiến triển của nhiều loại ung thư thông qua sự thay đổi mức độ biểu hiện gen của từng loại ung thư hoặc nhiều loại ung thư khác nhau. Tuy nhiên, nó vẫn chưa rõ liệu mối tương quan này có phải là một hiện tượng chung giữa nhiều loại ung thư hay không.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\n              \u003Cjats:sec>\n                \u003Cjats:title>Phương pháp\u003C\u002Fjats:title>\n                \u003Cjats:p>Trong nghiên cứu này, chúng tôi đã áp dụng một phương pháp sinh tin học tích hợp CNV và biểu hiện gen khác biệt một cách toán học trên 1025 dòng tế bào và 9159 mẫu bệnh nhân để phát hiện mối quan hệ tiềm năng của chúng.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\n              \u003Cjats:sec>\n                \u003Cjats:title>Kết quả\u003C\u002Fjats:title>\n                \u003Cjats:p>Kết quả của chúng tôi cho thấy có một mối tương quan chặt chẽ giữa CNV và biểu hiện gen khác biệt và số lượng bản sao thể hiện một ảnh hưởng tuyến tính tích cực lên biểu hiện gen cho phần lớn các gen, cho thấy rằng sự biến đổi di truyền tạo ra một hiệu ứng trực tiếp lên mức độ phiên mã gen. Một tập dữ liệu độc lập khác được sử dụng để xác nhận lại mối quan hệ giữa số lượng bản sao và mức độ biểu hiện. Phân tích thêm cho thấy các gen có ảnh hưởng tuyến tính tích cực chung lên biểu hiện gen được nhóm trong những con đường liên quan đến bệnh tật nhất định, điều này gợi ý sự tham gia của CNV vào bệnh sinh của các bệnh lý.","\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n              \u003Cjats:sec>\n                \u003Cjats:title>Background\u003C\u002Fjats:title>\n                \u003Cjats:p>Cancer is a heterogeneous disease with many genetic variations. Lines of evidence have shown copy number variations (CNVs) of certain genes are involved in development and progression of many cancers through the alterations of their gene expression levels on individual or several cancer types. However, it is not quite clear whether the correlation will be a general phenomenon across multiple cancer types.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\n              \u003Cjats:sec>\n                \u003Cjats:title>Methods\u003C\u002Fjats:title>\n                \u003Cjats:p>In this study we applied a bioinformatics approach integrating CNV and differential gene expression mathematically across 1025 cell lines and 9159 patient samples to detect their potential relationship.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\n              \u003Cjats:sec>\n                \u003Cjats:title>Results\u003C\u002Fjats:title>\n                \u003Cjats:p>Our results showed there is a close correlation between CNV and differential gene expression and the copy number displayed a positive linear influence on gene expression for the majority of genes, indicating that genetic variation generated a direct effect on gene transcriptional level. Another independent dataset is utilized to revalidate the relationship between copy number and expression level. Further analysis show genes with general positive linear influence on gene expression are clustered in certain disease-related pathways, which suggests the involvement of CNV in pathophysiology of diseases.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\n              \u003Cjats:sec>\n                \u003Cjats:title>Conclusions\u003C\u002Fjats:title>\n                \u003Cjats:p>This study shows the close correlation between CNV and differential gene expression revealing the qualitative relationship between genetic variation and its downstream effect, especially for oncogenes and tumor suppressor genes. It is of a critical importance to elucidate the relationship between copy number variation and gene expression for prevention, diagnosis and treatment of cancer.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>",{"VI":1992,"EN":1993},"Biến thể số lượng bản sao có mối tương quan cao với biểu hiện gen khác biệt: một nghiên cứu toàn diện về ung thư","Copy number variation is highly correlated with differential gene expression: a pan-cancer 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Global variation in copy number in the human genome. Nature. 2006;444:444–54.",{"doi":2179},"10.1038\u002Fnature05329",{"id":26,"text":2181,"url":26,"identifiers":2182},"Sachidanandam R, Weissman D, Schmidt SC, Kakol JM, Stein LD, Marth G, et al. A map of human genome sequence variation containing 1.42 million single nucleotide polymorphisms. Nature. 2001;409:928–33.",{"doi":2183},"10.1038\u002F35057149",{"id":26,"text":2185,"url":26,"identifiers":2186},"International HapMap C. The international HapMap project. Nature. 2003;426:789–96.",{"doi":2187},"10.1038\u002Fnature02168",{"id":26,"text":2189,"url":26,"identifiers":2190},"Iafrate AJ, Feuk L, Rivera MN, Listewnik ML, Donahoe PK, Qi Y, et al. Detection of large-scale variation in the human genome. Nat Genet. 2004;36:949–51.",{"doi":2191},"10.1038\u002Fng1416",{"id":26,"text":2193,"url":26,"identifiers":2194},"Sebat J, Lakshmi B, Troge J, Alexander J, Young J, Lundin P, et al. Large-scale copy number polymorphism in the human genome. 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Science. 2003, 302: 1578-1581. 10.1126\u002Fscience.1088477.",{"doi":2795},"10.1126\u002Fscience.1088477",{"id":26,"text":2797,"url":26,"identifiers":2798},"Shiffman D, Ellis SG, Rowland CM, Malloy MJ, Luke MM, Iakoubova OA, Pullinger CR, Cassano J, Aouizerat BE, Fenwick RG, Reitz RE, Catanese JJ, Leong DU, Zellner C, Sninsky JJ, Topol EJ, Devlin JJ, Kane JP: Identification of four gene variants associated with myocardial infarction. Am J Hum Genet. 2005, 77: 596-605. 10.1086\u002F491674.",{"doi":2799},"10.1086\u002F491674",{"id":26,"text":2801,"url":26,"identifiers":2802},"Ahmad F, Seidman JG, Seidman CE: The genetic basis for cardiac remodeling. Annu Rev Genomics Hum Genet. 2005, 6: 185-216. 10.1146\u002Fannurev.genom.6.080604.162132.",{"doi":2803},"10.1146\u002Fannurev.genom.6.080604.162132",{"id":26,"text":2805,"url":26,"identifiers":2806},"Roberts R: Genomics and cardiac arrhythmias. 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BMC Med Genet. 2007, 8 (Suppl 1): S1-",{"doi":1193},{"id":26,"text":2826,"url":26,"identifiers":2827},"Nava A, Canciani B, Daliento L, Miraglia G, Buja G, Fasoli G, Martini B, Scognamiglio R, Thiene G: Juvenile sudden death and effort ventricular tachycardias in a family with right ventricular cardiomyopathy. Int J Cardiol. 1988, 21: 111-126. 10.1016\u002F0167-5273(88)90212-4.",{"doi":2828},"10.1016\u002F0167-5273(88)90212-4",{"id":26,"text":2830,"url":26,"identifiers":2831},"McPherson R, Pertsemlidis A, Kavaslar N, Stewart A, Roberts R, Cox DR, Hinds DA, Pennacchio LA, Tybjaerg-Hansen A, Folsom AR, Boerwinkle E, Hobbs HH, Cohen JC: A common allele on chromosome 9 associated with coronary heart disease. Science. 2007, 316: 1488-1491. 10.1126\u002Fscience.1142447.",{"doi":2832},"10.1126\u002Fscience.1142447",{"id":26,"text":2834,"url":26,"identifiers":2835},"Helgadottir A, Thorleifsson G, Manolescu A, Gretarsdottir S, Blondal T, Jonasdottir A, Jonasdottir A, Sigurdsson A, Baker A, Palsson A, Masson G, Gudbjartsson D, Magnusson KP, Andersen K, Levey AI, Backman VM, Matthiasdottir S, Jonsdottir T, Palsson S, Einarsdottir H, Gunnarsdottir S, Gylfason A, Vaccarino V, Hooper WC, Reilly MP, Granger CB, Austin H, Rader DJ, Shah SH, Quyyumi AA, Gulcher JR, Thorgeirsson G, Thorsteinsdottir U, Kong A, Stefansson K: A Common Variant on Chromosome 9p21 Affects the Risk of Myocardial Infarction. Science. 2007",{},{"id":26,"text":2837,"url":26,"identifiers":2838},"Murray CJ, Lopez AD: Alternative projections of mortality and disability by cause 1990–2020: Global Burden of Disease Study. Lancet. 1997, 349: 1498-1504. 10.1016\u002FS0140-6736(96)07492-2.",{"doi":2839},"10.1016\u002FS0140-6736(96)07492-2",{"id":26,"text":2841,"url":26,"identifiers":2842},"Skol AD, Scott LJ, Abecasis GR, Boehnke M: Joint analysis is more efficient than replication-based analysis for two-stage genome-wide association studies. Nat Genet. 2006, 38: 209-213. 10.1038\u002Fng1706.",{"doi":2843},"10.1038\u002Fng1706",{"id":26,"text":2845,"url":26,"identifiers":2846},"Wang H, Thomas DC, Pe'er I, Stram DO: Optimal two-stage genotyping designs for genome-wide association scans. Genet Epidemiol. 2006, 30: 356-368. 10.1002\u002Fgepi.20150.",{"doi":2847},"10.1002\u002Fgepi.20150",{"id":26,"text":2849,"url":26,"identifiers":2850},"Tiso N, Stephan DA, Nava A, Bagattin A, Devaney JM, Stanchi F, Larderet G, Brahmbhatt B, Brown K, Bauce B, Muriago M, Basso C, Thiene G, Danieli GA, Rampazzo A: Identification of mutations in the cardiac ryanodine receptor gene in families affected with arrhythmogenic right ventricular cardiomyopathy type 2 (ARVD2). Hum Mol Genet. 2001, 10: 189-194. 10.1093\u002Fhmg\u002F10.3.189.",{"doi":2851},"10.1093\u002Fhmg\u002F10.3.189",{"id":26,"text":2853,"url":26,"identifiers":2854},"Klein RJ, Zeiss C, Chew EY, Tsai JY, Sackler RS, Haynes C, Henning AK, SanGiovanni JP, Mane SM, Mayne ST, Bracken MB, Ferris FL, Ott J, Barnstable C, Hoh J: Complement factor H polymorphism in age-related macular degeneration. Science. 2005, 308: 385-389. 10.1126\u002Fscience.1109557.",{"doi":2855},"10.1126\u002Fscience.1109557",{"id":2857,"createTime":2858,"updateTime":2859,"relativeEntities":2860,"slug":2861,"properties":2862,"entityType":796,"verifyStatus":25,"verifyTime":2871,"verifyNote":797,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36,"primaryUrl":2872,"fullTextUrl":26,"authors":2873,"publicationType":1070,"publisherRelationship":3108,"citationCount":629,"citationInfo":3133,"publishDate":3135,"publishYear":1100,"citationAnalyzeStatus":3136,"lastCitationAnalyze":3137,"indexDatabases":26,"openAccess":26,"references":3138,"isForceReanalyzing":1413},"63c487f5-63f7-40ce-805c-f173f4a5de27","2024-01-25T21:52:04.945+00:00","2026-05-28T09:23:09.354+00:00",[],"Genome-wide-association-study-for-subclinical-atherosclerosis-in-major-arterial-territories-in-the-NHLBI-s-Framingham-Heart-Study",{"abstract":2863,"title":2865,"doi":2867,"gsPaper":2869},{"EN":2864},"Subclinical atherosclerosis (SCA) measures in multiple arterial beds are heritable phenotypes that are associated with increased incidence of cardiovascular disease. We conducted a genome-wide association study (GWAS) for SCA measurements in the community-based Framingham Heart Study. Over 100,000 single nucleotide polymorphisms (SNPs) were genotyped (Human 100K GeneChip, Affymetrix) in 1345 subjects from 310 families. We calculated sex-specific age-adjusted and multivariable-adjusted residuals in subjects tested for quantitative SCA phenotypes, including ankle-brachial index, coronary artery calcification and abdominal aortic calcification using multi-detector computed tomography, and carotid intimal medial thickness (IMT) using carotid ultrasonography. We evaluated associations of these phenotypes with 70,987 autosomal SNPs with minor allele frequency ≥ 0.10, call rate ≥ 80%, and Hardy-Weinberg p-value ≥ 0.001 in samples ranging from 673 to 984 subjects, using linear regression with generalized estimating equations (GEE) methodology and family-based association testing (FBAT). Variance components LOD scores were also calculated. There was no association result meeting criteria for genome-wide significance, but our methods identified 11 SNPs with p \u003C 10-5 by GEE and five SNPs with p \u003C 10-5 by FBAT for multivariable-adjusted phenotypes. Among the associated variants were SNPs in or near genes that may be considered candidates for further study, such as rs1376877 (GEE p \u003C 0.000001, located in ABI2) for maximum internal carotid artery IMT and rs4814615 (FBAT p = 0.000003, located in PCSK2) for maximum common carotid artery IMT. Modest significant associations were noted with various SCA phenotypes for variants in previously reported atherosclerosis candidate genes, including NOS3 and ESR1. Associations were also noted of a region on chromosome 9p21 with CAC phenotypes that confirm associations with coronary heart disease and CAC in two recently reported genome-wide association studies. In linkage analyses, several regions of genome-wide linkage were noted, confirming previously reported linkage of internal carotid artery IMT on chromosome 12. All GEE, FBAT and linkage results are provided as an open-access results resource at \n                    http:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fprojects\u002Fgap\u002Fcgi-bin\u002Fstudy.cgi?id=phs000007\n                    \n                  . The results from this GWAS generate hypotheses regarding several SNPs that may be associated with SCA phenotypes in multiple arterial beds. Given the number of tests conducted, subsequent independent replication in a staged approach is essential to identify genetic variants that may be implicated in atherosclerosis.",{"EN":2866},"Genome-wide association study for subclinical atherosclerosis in major arterial territories in the NHLBI's Framingham Heart 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N Engl J Med. 1999, Cardiovascular Health Study Collaborative Research Group, 340: 14-22. 10.1056\u002FNEJM199901073400103.","https:\u002F\u002Fdoi.org\u002F10.1056\u002Fnejm199901073400103",{"mag":3270,"openalex":3271,"pm":3272,"doi":3273},"2316167515","W2316167515","9878640","10.1056\u002Fnejm199901073400103",{"id":26,"text":3275,"url":26,"identifiers":3276},"Fox CS, Polak JF, Chazaro I, Cupples A, Wolf PA, D'Agostino RA, O'Donnell CJ: Genetic and environmental contributions to atherosclerosis phenotypes in men and women: heritability of carotid intima-media thickness in the Framingham Heart Study. Stroke. 2003, 34: 397-401. 10.1161\u002F01.STR.0000048214.56981.6F.",{"doi":3277},"10.1161\u002F01.STR.0000048214.56981.6F",{"id":26,"text":3279,"url":26,"identifiers":3280},"O'Leary DH, Polak JF, Kronmal RA, Savage PJ, Borhani NO, Kittner SJ, Tracy R, Gardin JM, Price TR, Furberg CD: Thickening of the carotid wall. A marker for atherosclerosis in the elderly?. 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Science. 2006, 311: 933-10.1126\u002Fscience.311.5763.933a.",{},{"id":3318,"createTime":3319,"updateTime":3320,"relativeEntities":3321,"slug":3322,"properties":3323,"entityType":796,"verifyStatus":25,"verifyTime":3320,"verifyNote":797,"syncStatus":28,"languages":3342,"translateLanguages":3343,"viewCount":36,"primaryUrl":3344,"fullTextUrl":26,"authors":3345,"publicationType":1070,"publisherRelationship":3396,"citationCount":629,"citationInfo":3417,"publishDate":1486,"publishYear":1487,"citationAnalyzeStatus":3136,"lastCitationAnalyze":3419,"indexDatabases":26,"openAccess":26,"references":3420,"isForceReanalyzing":1413},"cf1718f4-85c7-4fc5-a220-4d34910e1034","2024-04-11T15:46:54.970+00:00","2025-01-25T23:32:05.300+00:00",[],"The-SDH-mutation-database-an-online-resource-for-succinate-dehydrogenase-sequence-variants-involved-in-pheochromocytoma-paraganglioma-and-mitochondrial-complex-II-deficiency",{"mag":3324,"keywords":3326,"pmc":3328,"openalex":3330,"abstract":3332,"title":3335,"pm":3338,"doi":3340},{"VOID":3325},"1863395362",{"VI":3327},"",{"VOID":3329},"1325269",{"VOID":3331},"W1863395362",{"VI":3333,"EN":3334},"\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Nền tảng\u003C\u002Fjats:title>\n            \u003Cjats:p>Các gen SDHA, SDHB, SDHC và SDHD mã hóa các tiểu đơn vị của succinate dehydrogenase (succinate: ubiquinone oxidoreductase), một thành phần của cả chu trình Krebs và chuỗi hô hấp ty thể. SDHA, một flavoprotein và SDHB, một protein sắt-lưu huỳnh cùng nhau tạo thành miền xúc tác, trong khi SDHC và SDHD mã hóa các neo màng cho phép phức hợp tham gia vào chuỗi hô hấp như phức hợp II. Các đột biến dòng germline của SDHD và SDHB là nguyên nhân chính của các dạng di truyền của các khối u paraganglioma và pheochromocytoma. Tiểu đơn vị lớn nhất, SDHA, bị đột biến ở những bệnh nhân mắc hội chứng Leigh và teo thị giác khởi phát muộn, nhưng vẫn chưa được xác định là yếu tố trong bệnh ung thư di truyền.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Mô tả\u003C\u002Fjats:title>\n            \u003Cjats:p>Cơ sở dữ liệu đột biến SDH dựa trên hệ thống Cơ sở dữ liệu Biến thể Mở (Leiden Open Variation Database - LOVD) mới được mô tả. Các biến thể hiện được mô tả trong cơ sở dữ liệu được trích xuất từ tài liệu đã xuất bản và trong một số trường hợp được chú thích để phù hợp với cách đặt tên đột biến hiện tại. Các nhà nghiên cứu cũng có thể gửi trực tiếp các biến thể trình tự mới qua mạng. Kể từ khi xác định SDHD, SDHC và SDHB như những gen ức chế khối u cổ điển vào năm 2000 và 2001, các nghiên cứu từ các nhóm nghiên cứu trên toàn thế giới đã xác định tổng cộng 120 biến thể. Tại đây, chúng tôi giới thiệu tất cả các biến thể trình tự liên quan đến paraganglioma và pheochromocytoma đã được báo cáo trong các gen này, ngoài tất cả các đột biến đã được báo cáo của SDHA. Cơ sở dữ liệu hiện đã có thể truy cập trực tuyến.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Kết luận\u003C\u002Fjats:title>\n            \u003Cjats:p>Cơ sở dữ liệu đột biến SDH cung cấp một công cụ và tài nguyên quý giá cho các bác sĩ lâm sàng liên quan đến việc điều trị bệnh nhân mắc paraganglioma-pheochromocytoma, các nhà di truyền học lâm sàng cần cái nhìn tổng quan về kiến thức hiện tại, và các nhà di truyền học cũng như các nhà nghiên cứu khác cần một nền tảng vững chắc để tiếp tục khám phá cả hai hội chứng khối u này và các kiểu hình liên quan đến SDHA.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>","\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Background\u003C\u002Fjats:title>\n            \u003Cjats:p>The SDHA, SDHB, SDHC and SDHD genes encode the subunits of succinate dehydrogenase (succinate: ubiquinone oxidoreductase), a component of both the Krebs cycle and the mitochondrial respiratory chain. SDHA, a flavoprotein and SDHB, an iron-sulfur protein together constitute the catalytic domain, while SDHC and SDHD encode membrane anchors that allow the complex to participate in the respiratory chain as complex II. Germline mutations of SDHD and SDHB are a major cause of the hereditary forms of the tumors paraganglioma and pheochromocytoma. The largest subunit, SDHA, is mutated in patients with Leigh syndrome and late-onset optic atrophy, but has not as yet been identified as a factor in hereditary cancer.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Description\u003C\u002Fjats:title>\n            \u003Cjats:p>The SDH mutation database is based on the recently described Leiden Open (source) Variation Database (LOVD) system. The variants currently described in the database were extracted from the published literature and in some cases annotated to conform to current mutation nomenclature. Researchers can also directly submit new sequence variants online. Since the identification of SDHD, SDHC, and SDHB as classic tumor suppressor genes in 2000 and 2001, studies from research groups around the world have identified a total of 120 variants. Here we introduce all reported paraganglioma and pheochromocytoma related sequence variations in these genes, in addition to all reported mutations of SDHA. The database is now accessible online.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Conclusion\u003C\u002Fjats:title>\n            \u003Cjats:p>The SDH mutation database offers a valuable tool and resource for clinicians involved in the treatment of patients with paraganglioma-pheochromocytoma, clinical geneticists needing an overview of current knowledge, and geneticists and other researchers needing a solid foundation for further exploration of both these tumor syndromes and SDHA-related phenotypes.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>",{"VI":3336,"EN":3337},"Cơ sở dữ liệu đột biến SDH: một tài nguyên trực tuyến cho các biến thể trình tự succinate dehydrogenase liên quan đến pheochromocytoma, paraganglioma và thiếu hụt phức hợp II ty thể","The SDH mutation database: an online resource for succinate dehydrogenase sequence variants involved in pheochromocytoma, paraganglioma and mitochondrial complex II deficiency",{"VOID":3339},"16288654",{"VOID":3341},"10.1186\u002F1471-2350-6-39",[102],[101],"https:\u002F\u002Fbmcmedgenet.biomedcentral.com\u002Farticles\u002F10.1186\u002F1471-2350-6-39",[3346,3366,3380],{"id":3347,"sortIndex":36,"researcher":26,"roles":3348,"affiliations":3349,"properties":3359},"9cc1646d-b878-4b66-a7de-bf6daeef911d",[],[3350],{"id":26,"sortIndex":36,"affiliation":3351,"properties":26},{"id":3352,"createTime":3353,"updateTime":3353,"relativeEntities":3354,"slug":3355,"properties":3356,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},"48ef2ac2-c500-40d4-86d8-f97914cd89b6","2024-04-11T15:46:55.000+00:00",[],"Department-of-Human-Genetics-Center-for-Human-and-Clinical-Genetics-Leiden-University-Medical-Center-P-O-Box-9503-2300-RA-Leiden-The-Netherlands",{"title":3357},{"EN":3358},"Department of Human Genetics, Center for Human and Clinical Genetics, Leiden University Medical Center, P.O. Box 9503, 2300 RA, Leiden, The Netherlands",{"openalex":3360,"orcid":3362,"title":3364},{"VOID":3361},"A5050931949",{"VOID":3363},"https:\u002F\u002Forcid.org\u002F0000-0002-8288-0050",{"EN":3365},"Jean‐Pierre Bayley",{"id":3367,"sortIndex":114,"researcher":26,"roles":3368,"affiliations":3369,"properties":3375},"16950aba-d4e8-4147-a545-39550bcb9192",[],[3370],{"id":26,"sortIndex":36,"affiliation":3371,"properties":26},{"id":3352,"createTime":3353,"updateTime":3353,"relativeEntities":3372,"slug":3355,"properties":3373,"entityType":98,"verifyStatus":28,"verifyTime":26,"verifyNote":26,"syncStatus":28,"languages":26,"translateLanguages":26,"viewCount":36},[],{"title":3374},{"EN":3358},{"openalex":3376,"title":3378},{"VOID":3377},"A5053681207",{"EN":3379},"Peter E.M. 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