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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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It is now well accepted that moderate levels of ROS are required for several cellular functions, including gene expression. The production of ROS is elevated in tumor cells as a consequence of increased metabolic rate, gene mutation and relative hypoxia, and excess ROS are quenched by increased antioxidant enzymatic and nonenzymatic pathways in the same cells. Moderate increases of ROS contribute to several pathologic conditions, among which are tumor promotion and progression, as they are involved in different signaling pathways and induce DNA mutation. However, ROS are also able to trigger programmed cell death (PCD). Our review will emphasize the molecular mechanisms useful for the development of therapeutic strategies that are based on modulating ROS levels to treat cancer. 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J., Ursini, F. & Maiorino, M. An overview of mechanisms of redox signaling. J. Mol. Cell. Cardiol. 73, 2–9 (2014).",{"doi":1215},"10.1016\u002Fj.yjmcc.2014.01.018",{"id":28,"text":1217,"url":28,"identifiers":1218},"Bedard, K. & Krause, K.-H. The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology. Physiol. Rev. 87, 245–313 (2007).",{"doi":1219},"10.1152\u002Fphysrev.00044.2005",{"id":28,"text":1221,"url":28,"identifiers":1222},"Vander Heiden, M., Cantley, L. & Thompson, C. Understanding the Warburg effect: the metabolic requirements of cell proliferation. Science 324, 1029–1033 (2009).",{"doi":1223},"10.1126\u002Fscience.1160809",{"id":28,"text":1225,"url":28,"identifiers":1226},"Finkel, T. Signal transduction by reactive oxygen species. J. Cell Biol. 194, 7–15 (2011).",{"doi":1227},"10.1083\u002Fjcb.201102095",{"id":28,"text":1229,"url":28,"identifiers":1230},"Paradies, G. et al. 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Biochem. 86, 715–748 (2017).",{"doi":1865},"10.1146\u002Fannurev-biochem-061516-045037",false,{"id":1868,"createTime":1869,"updateTime":1869,"relativeEntities":1870,"slug":1871,"properties":1872,"entityType":991,"verifyStatus":26,"verifyTime":1869,"verifyNote":992,"languages":1887,"translateLanguages":28,"viewCount":32,"primaryUrl":1888,"fullTextUrl":28,"authors":1889,"publicationType":1138,"publisherRelationship":1945,"citationCount":2007,"citationInfo":2008,"publishDate":28,"publishYear":28,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":2015,"openAccess":28,"references":2016,"isForceReanalyzing":1866},"b9ef87ad-95f7-4583-8b77-8890067987bf","2024-09-25T02:23:54.796+00:00",[],"Mesenchymal-stem-cells-environmentally-responsive-therapeutics-for-regenerative-medicine",{"mag":1873,"pmc":1875,"openalex":1877,"abstract":1879,"title":1881,"pm":1883,"doi":1885},{"VOID":1874},"2074084795",{"VOID":1876},"3849579",{"VOID":1878},"W2074084795",{"EN":1880},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Mesenchymal stem cells (MSCs) are partially defined by their ability to differentiate into tissues including bone, cartilage and adipose \u003Cjats:italic>in vitro\u003C\u002Fjats:italic>, but it is their trophic, paracrine and immunomodulatory functions that may have the greatest therapeutic impact \u003Cjats:italic>in vivo\u003C\u002Fjats:italic>. Unlike pharmaceutical treatments that deliver a single agent at a specific dose, MSCs are site regulated and secrete bioactive factors and signals at variable concentrations in response to local microenvironmental cues. Significant progress has been made in understanding the biochemical and metabolic mechanisms and feedback associated with MSC response. The anti-inflammatory and immunomodulatory capacity of MSC may be paramount in the restoration of localized or systemic conditions for normal healing and tissue regeneration. Allogeneic MSC treatments, categorized as a drug by regulatory agencies, have been widely pursued, but new studies demonstrate the efficacy of autologous MSC therapies, even for individuals affected by a disease state. Safety and regulatory concerns surrounding allogeneic cell preparations make autologous and minimally manipulated cell therapies an attractive option for many regenerative, anti-inflammatory and autoimmune applications.\u003C\u002Fjats:p>",{"EN":1882},"Mesenchymal stem cells: environmentally responsive therapeutics for regenerative medicine",{"VOID":1884},"24232253",{"VOID":1886},"10.1038\u002Femm.2013.94",[31],"https:\u002F\u002Fwww.nature.com\u002Farticles\u002Femm201394",[1890,1909,1926],{"id":1891,"sortIndex":32,"researcher":28,"roles":1892,"affiliations":1893,"properties":1902,"displayName":1906,"givenName":28,"familyName":28},"b284489d-32d0-4404-a1c5-28468f88c5a0",[],[1894],{"id":1895,"sortIndex":32,"affiliation":1896,"properties":28},"fc1585d2-8c76-4c35-8df4-0b1b8173becd",{"id":1895,"createTime":28,"updateTime":28,"relativeEntities":1897,"slug":28,"properties":1898,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1901,"statistic":28},[],{"title":1899},{"EN":1900},"Celling Biosciences, Austin, TX, USA.",[],{"orcid":1903,"title":1905,"openalex":1907},{"VOID":1904},"https:\u002F\u002Forcid.org\u002F0000-0002-2297-2703",{"EN":1906},"Matthew B. 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The field of cancer metabolism subsequently revealed additional metabolic alterations in cancer by focusing on central carbon metabolism, including the citric acid cycle and pentose phosphate pathway. Recent reports have, however, uncovered substantial non-carbon metabolism contributions to cancer cell viability and growth. Amino acids, nutrients vital to the survival of all cell types, experience reprogrammed metabolism in cancer. This review outlines the diverse roles of amino acids within the tumor and in the tumor microenvironment. Beyond their role in biosynthesis, they serve as energy sources and help maintain redox balance. In addition, amino acid derivatives contribute to epigenetic regulation and immune responses linked to tumorigenesis and metastasis. 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O., Wind, F. & Negelein, E. 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Life Sci. 65, 3699–3724 (2008).",{"doi":5360},"10.1007\u002Fs00018-008-8295-8",{"id":28,"text":5362,"url":28,"identifiers":5363},"Locasale, J. W. Serine, glycine and one-carbon units: cancer metabolism in full circle. Nat. Rev. Cancer 13, 572–583 (2013).",{"doi":5364},"10.1038\u002Fnrc3557",{"id":28,"text":5366,"url":28,"identifiers":5367},"Shuvalov, O. et al. One-carbon metabolism and nucleotide biosynthesis as attractive targets for anticancer therapy. Oncotarget 8, 23955–23977 (2017).",{"doi":5368},"10.18632\u002Foncotarget.15053",{"id":28,"text":5370,"url":28,"identifiers":5371},"Lu, S., Chen, G. L., Ren, C., Kwabi-Addo, B. & Epner, D. E. Methionine restriction selectively targets thymidylate synthase in prostate cancer cells. Biochem. Pharm. 66, 791–800 (2003).",{"doi":5372},"10.1016\u002FS0006-2952(03)00406-4",{"id":28,"text":5374,"url":28,"identifiers":5375},"Pegg, A. E. Mammalian polyamine metabolism and function. IUBMB Life 61, 880–894 (2009).",{"doi":5376},"10.1002\u002Fiub.230",{"id":28,"text":5378,"url":28,"identifiers":5379},"Greene, L. I. et al. A role for tryptophan-2,3-dioxygenase in CD8 T-cell suppression and evidence of tryptophan catabolism in breast cancer patient plasma. Mol. Cancer Res. 17, 131–139 (2019).",{"doi":5380},"10.1158\u002F1541-7786.MCR-18-0362",{"id":28,"text":5382,"url":28,"identifiers":5383},"Fallarino, F. et al. Modulation of tryptophan catabolism by regulatory T cells. Nat. Immunol. 4, 1206–1212 (2003).",{"doi":5384},"10.1038\u002Fni1003",{"id":28,"text":5386,"url":28,"identifiers":5387},"DiNatale, B. C. et al. Kynurenic acid is a potent endogenous aryl hydrocarbon receptor ligand that synergistically induces interleukin-6 in the presence of inflammatory signaling. Toxicol. Sci. 115, 89–97 (2010).",{"doi":5388},"10.1093\u002Ftoxsci\u002Fkfq024",{"id":28,"text":5390,"url":28,"identifiers":5391},"Opitz, C. A. et al. An endogenous tumour-promoting ligand of the human aryl hydrocarbon receptor. Nature 478, 197–203 (2011).",{"doi":5392},"10.1038\u002Fnature10491",{"id":28,"text":5394,"url":28,"identifiers":5395},"Nguyen, N. T. et al. Aryl hydrocarbon receptor negatively regulates dendritic cell immunogenicity via a kynurenine-dependent mechanism. Proc. Natl Acad. Sci. USA 107, 19961–19966 (2010).",{"doi":5396},"10.1073\u002Fpnas.1014465107",{"id":28,"text":5398,"url":28,"identifiers":5399},"Mezrich, J. D. et al. An interaction between kynurenine and the aryl hydrocarbon receptor can generate regulatory T cells. J. Immunol. 185, 3190–3198 (2010).",{"doi":5400},"10.4049\u002Fjimmunol.0903670",{"id":28,"text":5402,"url":28,"identifiers":5403},"Vaughn, A. E. & Deshmukh, M. Glucose metabolism inhibits apoptosis in neurons and cancer cells by redox inactivation of cytochrome c. Nat. Cell Biol. 10, 1477–1483 (2008).",{"doi":5404},"10.1038\u002Fncb1807",{"id":28,"text":5406,"url":28,"identifiers":5407},"Chung, W. J. et al. Inhibition of cystine uptake disrupts the growth of primary brain tumors. J. Neurosci. 25, 7101–7110 (2005).",{"doi":5408},"10.1523\u002FJNEUROSCI.5258-04.2005",{"id":28,"text":5410,"url":28,"identifiers":5411},"Lo, M., Ling, V., Wang, Y. Z. & Gout, P. W. The xc- cystine\u002Fglutamate antiporter: a mediator of pancreatic cancer growth with a role in drug resistance. Br. J. Cancer 99, 464–472 (2008).",{"doi":5412},"10.1038\u002Fsj.bjc.6604485",{"id":28,"text":5414,"url":28,"identifiers":5415},"Fan, J. et al. Quantitative flux analysis reveals folate-dependent NADPH production. Nature 510, 298–302 (2014).",{"doi":5416},"10.1038\u002Fnature13236",{"id":28,"text":5418,"url":28,"identifiers":5419},"Ulanovskaya, O. A., Zuhl, A. M. & Cravatt, B. F. NNMT promotes epigenetic remodeling in cancer by creating a metabolic methylation sink. Nat. Chem. Biol. 9, 300–306 (2013).",{"doi":5420},"10.1038\u002Fnchembio.1204",{"id":28,"text":5422,"url":28,"identifiers":5423},"Maddocks, O. D. K. et al. Modulating the therapeutic response of tumours to dietary serine and glycine starvation. Nature 544, 372–376 (2017).",{"doi":5424},"10.1038\u002Fnature22056",{"id":28,"text":5426,"url":28,"identifiers":5427},"Pietrocola, F., Galluzzi, L., Bravo-San Pedro, J. M., Madeo, F. & Kroemer, G. Acetyl coenzyme A: a central metabolite and second messenger. Cell Metab. 21, 805–821 (2015).",{"doi":5428},"10.1016\u002Fj.cmet.2015.05.014",{"id":28,"text":5430,"url":28,"identifiers":5431},"Son, S. M. et al. Leucine signals to mTORC1 via its metabolite acetyl-coenzyme A. Cell Metab. 29, 192–201.e197 (2019).",{"doi":5432},"10.1016\u002Fj.cmet.2018.08.013",{"id":28,"text":5434,"url":28,"identifiers":5435},"Wu, Z. et al. TPO-induced metabolic reprogramming drives liver metastasis of colorectal cancer CD110+ tumor-initiating cells. 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Cancer Res. 25, 1462–1471 (2019).",{"doi":6016},"10.1158\u002F1078-0432.CCR-18-2882",{"id":6018,"createTime":6019,"updateTime":6019,"relativeEntities":6020,"slug":6021,"properties":6022,"entityType":991,"verifyStatus":26,"verifyTime":6037,"verifyNote":992,"languages":6038,"translateLanguages":28,"viewCount":32,"primaryUrl":6039,"fullTextUrl":28,"authors":6040,"publicationType":1138,"publisherRelationship":6094,"citationCount":856,"citationInfo":6155,"publishDate":6158,"publishYear":6156,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":6159,"openAccess":28,"references":6160,"isForceReanalyzing":1866},"8cf48d94-94b6-4b51-af69-11a64f7231fc","2024-09-30T02:08:20.529+00:00",[],"Intracellular-sensing-of-viral-genomes-and-viral-evasion",{"mag":6023,"pmc":6025,"openalex":6027,"abstract":6029,"title":6031,"pm":6033,"doi":6035},{"VOID":6024},"2995721821",{"VOID":6026},"6906418",{"VOID":6028},"W2995721821",{"EN":6030},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>During viral infection, virus-derived cytosolic nucleic acids are recognized by host intracellular specific sensors. The efficacy of this recognition system is crucial for triggering innate host defenses, which then stimulate more specific adaptive immune responses against the virus. Recent studies show that signal transduction pathways activated by sensing proteins are positively or negatively regulated by many modulators to maintain host immune homeostasis. However, viruses have evolved several strategies to counteract\u002Fevade host immune reactions. These systems involve viral proteins that interact with host sensor proteins and prevent them from detecting the viral genome or from initiating immune signaling. In this review, we discuss key regulators of cytosolic sensor proteins and viral proteins based on experimental evidence.\u003C\u002Fjats:p>",{"EN":6032},"Intracellular sensing of viral genomes and viral evasion",{"VOID":6034},"31827068",{"VOID":6036},"10.1038\u002Fs12276-019-0299-y","2024-09-30T02:08:20.528+00:00",[31],"https:\u002F\u002Fwww.nature.com\u002Farticles\u002Fs12276-019-0299-y",[6041,6060,6077],{"id":6042,"sortIndex":32,"researcher":28,"roles":6043,"affiliations":6044,"properties":6053,"displayName":6057,"givenName":28,"familyName":28},"47e90217-d6fa-44f9-b9fc-b11cca4b2c75",[],[6045],{"id":6046,"sortIndex":32,"affiliation":6047,"properties":28},"b04ddb94-55da-4051-adca-92d7d750dad0",{"id":6046,"createTime":28,"updateTime":28,"relativeEntities":6048,"slug":28,"properties":6049,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":6052,"statistic":28},[],{"title":6050},{"VI":6051},"College 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Science 350, 217–221 (2015).",{"doi":6795},"10.1126\u002Fscience.aab3369",{"id":28,"text":6797,"url":28,"identifiers":6798},"Chan, Y. K. & Gack, M. U. A phosphomimetic-based mechanism of dengue virus to antagonize innate immunity. Nat. Immunol. 17, 523–530 (2016).",{"doi":6799},"10.1038\u002Fni.3393",{"id":28,"text":6801,"url":28,"identifiers":6802},"Rui, Y. et al. Disruption of MDA5-mediated innate immune responses by the 3C proteins of coxsackievirus A16, coxsackievirus A6, and enterovirus D68. J. Virol. 91, e00546–17 (2017).",{},{"id":28,"text":6804,"url":28,"identifiers":6805},"Li, L. et al. Encephalomyocarditis virus 2C protein antagonizes interferon-beta signaling pathway through interaction with MDA5. Antivir. Res 161, 70–84 (2019).",{"doi":6806},"10.1016\u002Fj.antiviral.2018.10.010",{"id":28,"text":6808,"url":28,"identifiers":6809},"Kuo, R. L. et al. Role of enteroviral RNA-dependent RNA polymerase in regulation of MDA5-mediated interferon-beta activation. J. Virol. 93, e00132–19 (2019).",{},{"id":28,"text":6811,"url":28,"identifiers":6812},"Lahaye, X. et al. The capsids of HIV-1 and HIV-2 determine immune detection of the viral cDNA by the innate sensor cGAS in dendritic cells. Immunity 39, 1132–1142 (2013).",{"doi":6813},"10.1016\u002Fj.immuni.2013.11.002",{"id":28,"text":6815,"url":28,"identifiers":6816},"Dell'Oste, V. et al. Innate nuclear sensor IFI16 translocates into the cytoplasm during the early stage of in vitro human cytomegaloviral infection and is entrapped in the egressing virions during the late stage. J. Virol. 88, 6970–6982 (2014).",{"doi":6621},{"id":6818,"createTime":6819,"updateTime":6819,"relativeEntities":6820,"slug":6821,"properties":6822,"entityType":991,"verifyStatus":26,"verifyTime":6837,"verifyNote":992,"languages":6838,"translateLanguages":28,"viewCount":32,"primaryUrl":6839,"fullTextUrl":28,"authors":6840,"publicationType":1138,"publisherRelationship":6911,"citationCount":6972,"citationInfo":6973,"publishDate":6975,"publishYear":1203,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":6976,"openAccess":28,"references":6977,"isForceReanalyzing":1866},"21e5b24e-1c43-4473-9f2c-d4c5e08190fd","2024-10-05T09:13:27.500+00:00",[],"Combination-of-anti-angiogenic-therapy-and-immune-checkpoint-blockade-normalizes-vascular-immune-crosstalk-to-potentiate-cancer-immunity",{"mag":6823,"pmc":6825,"openalex":6827,"abstract":6829,"title":6831,"pm":6833,"doi":6835},{"VOID":6824},"3084409519",{"VOID":6826},"8080646",{"VOID":6828},"W3084409519",{"EN":6830},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Cancer immunotherapy with immune checkpoint inhibitors (ICIs) has revolutionized the treatment of advanced cancers. However, the tumor microenvironment (TME) functions as a formidable barrier that severely impairs the efficacy of ICIs. While the crosstalk between tumor vessels and immune cells determines the nature of anti-tumor immunity, it is skewed toward a destructive cycle in growing tumors. First, the disorganized tumor vessels hinder CD8\u003Cjats:sup>+\u003C\u002Fjats:sup>T cell trafficking into the TME, disable effector functions, and even kill T cells. Moreover, VEGF, the key driver of angiogenesis, interferes with the maturation of dendritic cells, thereby suppressing T cell priming, and VEGF also induces TOX-mediated exhaustion of CD8\u003Cjats:sup>+\u003C\u002Fjats:sup>T cells. Meanwhile, a variety of innate and adaptive immune cells contribute to the malformation of tumor vessels. Protumoral M2-like macrophages as well as T\u003Cjats:sub>H\u003C\u002Fjats:sub>2 and Treg cells secrete pro-angiogenic factors that accelerate uncontrolled angiogenesis and promote vascular immaturity. While CD8\u003Cjats:sup>+\u003C\u002Fjats:sup>T and CD4\u003Cjats:sup>+\u003C\u002Fjats:sup>T\u003Cjats:sub>H\u003C\u002Fjats:sub>1 cells suppress angiogenesis and induce vascular maturation by secreting IFN-γ, they are unable to infiltrate the TME due to malformed tumor vessels. These findings led to preclinical studies that demonstrated that simultaneous targeting of tumor vessels and immunity is a viable strategy to normalize aberrant vascular-immune crosstalk and potentiate cancer immunotherapy. Furthermore, this combination strategy has been evidently demonstrated through recent pivotal clinical trials, granted approval from FDA, and is now being used in patients with kidney, liver, lung, or uterine cancer. Overall, combining anti-angiogenic therapy and ICI is a valid therapeutic strategy that can enhance cancer immunity and will further expand the landscape of cancer treatment.\u003C\u002Fjats:p>",{"EN":6832},"Combination of anti-angiogenic therapy and immune checkpoint blockade normalizes vascular-immune crosstalk to potentiate cancer 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Diabetes 59, 850–860 (2010).",{"doi":7748},"10.2337\u002Fdb09-1342",{"id":7750,"createTime":7751,"updateTime":7751,"relativeEntities":7752,"slug":7753,"properties":7754,"entityType":991,"verifyStatus":26,"verifyTime":7751,"verifyNote":992,"languages":7769,"translateLanguages":28,"viewCount":32,"primaryUrl":7770,"fullTextUrl":28,"authors":7771,"publicationType":1138,"publisherRelationship":7808,"citationCount":7868,"citationInfo":7869,"publishDate":1209,"publishYear":1203,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":7871,"openAccess":28,"references":7872,"isForceReanalyzing":1866},"c58dbfbb-c3c2-4b1e-a7fc-5f199a32b454","2024-10-12T10:51:39.816+00:00",[],"Wnt-signaling-in-cancer-therapeutic-targeting-of-Wnt-signaling-beyond-%CE%B2-catenin-and-the-destruction-complex",{"mag":7755,"pmc":7757,"openalex":7759,"abstract":7761,"title":7763,"pm":7765,"doi":7767},{"VOID":7756},"3004712367",{"VOID":7758},"7062731",{"VOID":7760},"W3004712367",{"EN":7762},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Wnt\u002Fβ-catenin signaling is implicated in many physiological processes, including development, tissue homeostasis, and tissue regeneration. In human cancers, Wnt\u002Fβ-catenin signaling is highly activated, which has led to the development of various Wnt signaling inhibitors for cancer therapies. Nonetheless, the blockade of Wnt signaling causes side effects such as impairment of tissue homeostasis and regeneration. Recently, several studies have identified cancer-specific Wnt signaling regulators. In this review, we discuss the Wnt inhibitors currently being used in clinical trials and suggest how additional cancer-specific regulators could be utilized to treat Wnt signaling-associated cancer.\u003C\u002Fjats:p>",{"EN":7764},"Wnt signaling in cancer: therapeutic targeting of Wnt signaling beyond β-catenin and the destruction 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