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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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Creation of human tumour cells with defined genetic elements. Nature 1999; 400: 464–8.\nBondy GP, Wilson S, Chambers AF. Experimental metastatic ability of H-ras-transformed NIH3T3 cells. Cancer Res 1985; 45: 6005–9.\nMuschel RJ, Williams JE, Lowy DR et al. Harvey ras induction of metastatic potential depends upon oncogene activation and the type of recipient cell. Am J Pathol 1985; 121: 1–8.\nThorgeirsson UP, Turpeenniemi-Hujanen T, Williams JE et al. NIH\u002F3T3 cells transfected with human tumor DNA containing activated ras oncogenes express the metastatic phenotype in nude mice. Mol Cell Biol 1985; 5: 259–62.\nSteeg PS, Bevilacqua G, Kopper L et al. Evidence for a novel gene associated with low tumor metastatic potential. J Natl Cancer Inst 1988; 80: 200–4.\nWelch DR, Wei LL. Genetic and epigenetic regulation of human breast cancer progression and metastasis. Endocrine-related Cancer 1998; 5: 155–97.\nYoshida BA, Sokoloff M, Welch DR et al. 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intraperitoneal aerosol chemotherapy (PIPAC) represents a novel approach to deliver intraperitoneal chemotherapy. We report our experience with PIPAC in patients with peritoneal metastasis (PM) from gastric cancer (GC). Data from GC patients (n = 20) included in the prospective PIPAC-OPC1 and PIPAC-OPC2 studies are reported. All patients had received prior systemic chemotherapy. The mean peritoneal cancer index (PCI) was 10.5 (range 0–39) and nine patients had diffuse GC. PIPAC with cisplatin 7.5 mg\u002Fm2 and doxorubicin 1.5 mg\u002Fm2 were administered at 4–6-week intervals. Outcome criteria were objective tumour response, survival and adverse events. Twenty patients had 52 PIPAC procedures with a median follow-up of 10.4 months (3.3–26.5). Median survival from the time of PM diagnosis and after the first PIPAC procedure was 11.5 months and 4.7 months, respectively. Fourteen patients had repeated PIPAC (> 2), and the objective tumour response according to the histological peritoneal regression grading score (PRGS) was observed in 36%, whereas 36% had stable disease. Ten patients completed the three prescheduled sessions (per protocol group) and 40% of those displayed an objective tumour response, while 20% had stable disease. Only minor postoperative complications were noted, and none were considered causally related to the PIPAC treatment. PIPAC with low-dose cisplatin and doxorubicin can induce a quantifiable objective tumour response in selected patients with PM from GC. Survival data are encouraging and warrant further clinical studies.",{"EN":1137},"Pressurized intraperitoneal aerosol chemotherapy (PIPAC) of peritoneal metastasis from gastric cancer: a descriptive cohort study",{"VOID":1139},"International WCRF (2019) Worldwide cancer data https:\u002F\u002Fwww.wcrf.org\u002Fdietandcancer\u002Fcancer-trends\u002Fworldwide-cancer-data2018 [updated Jan. 2019; cited 2019 Jan]. https:\u002F\u002Fwww.wcrf.org\u002Fdietandcancer\u002Fcancer-trends\u002Fworldwide-cancer-data.\nYonemura Y, Endou Y, Sasaki T et al (2010) Surgical treatment for peritoneal carcinomatosis from gastric cancer. Eur J Surg Oncol 36(12):1131–1138. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ejso.2010.09.006\nGlehen O, Gilly FN, Arvieux C et al (2010) Peritoneal carcinomatosis from gastric cancer: a multi-institutional study of 159 patients treated by cytoreductive surgery combined with perioperative intraperitoneal chemotherapy. Ann Surg Oncol 17(9):2370–2377. https:\u002F\u002Fdoi.org\u002F10.1245\u002Fs10434-010-1039-7\nEl-Sedfy A, Brar SS, Coburn NG (2014) Current role of minimally invasive approaches in the treatment of early gastric cancer. World J Gastroenterol 20(14):3880–3888. https:\u002F\u002Fdoi.org\u002F10.3748\u002Fwjg.v20.i14.3880\nSugarbaker PH (2016) Cytoreductive surgery and hyperthermic intraperitoneal chemotherapy in the management of gastrointestinal cancers with peritoneal metastases: progress toward a new standard of care. Cancer Treat Rev 48:42–49. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ctrv.2016.06.007\nKitayama J, Ishigami H, Yamaguchi H et al (2018) Treatment of patients with peritoneal metastases from gastric cancer. Ann Gastroenterol Surg 2(2):116–123. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fags3.12060\nIshigami H, Fujiwara Y, Fukushima R et al (2018) Phase III Trial comparing intraperitoneal and intravenous paclitaxel plus S-1 versus cisplatin plus S-1 in patients with gastric cancer with peritoneal metastasis: PHOENIX-GC Trial. J Clin Oncol 36(19):1922–1929. https:\u002F\u002Fdoi.org\u002F10.1200\u002FJCO.2018.77.8613\nMiyashiro I, Furukawa H, Sasako M et al (2011) Randomized clinical trial of adjuvant chemotherapy with intraperitoneal and intravenous cisplatin followed by oral fluorouracil (UFT) in serosa-positive gastric cancer versus curative resection alone: final results of the Japan Clinical Oncology Group trial JCOG9206-2. Gastric Cancer 14(3):212–218. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs10120-011-0027-3\nSarela AI, Miner TJ, Karpeh MS et al (2006) Clinical outcomes with laparoscopic stage M1, unresected gastric adenocarcinoma. Ann Surg 243(2):189–195. https:\u002F\u002Fdoi.org\u002F10.1097\u002F01.sla.0000197382.43208.a5\nEsquis P, Consolo D, Magnin G et al (2006) High intra-abdominal pressure enhances the penetration and antitumor effect of intraperitoneal cisplatin on experimental peritoneal carcinomatosis. Ann Surg 244(1):106–112. https:\u002F\u002Fdoi.org\u002F10.1097\u002F01.sla.0000218089.61635.5f\nShinkai M, Imano M, Chiba Y et al (2018) Intraperitoneal and systemic chemotherapy for patients with gastric cancer with peritoneal metastasis: a Phase II Trial. Anticancer Res 38(10):5975–5981. https:\u002F\u002Fdoi.org\u002F10.21873\u002Fanticanres.12945\nSolass W, Kerb R, Murdter T et al (2014) Intraperitoneal chemotherapy of peritoneal carcinomatosis using pressurized aerosol as an alternative to liquid solution: first evidence for efficacy. Ann Surg Oncol 21(2):553–559. https:\u002F\u002Fdoi.org\u002F10.1245\u002Fs10434-013-3213-\nNowacki M, Alyami M, Villeneuve L et al (2018) Multicenter comprehensive methodological and technical analysis of 832 pressurized intraperitoneal aerosol chemotherapy (PIPAC) interventions performed in 349 patients for peritoneal carcinomatosis treatment: an international survey study. Eur J Surg Oncol 44(7):991–996. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ejso.2018.02.014\nGraversen M, Detlefsen S, Bjerregaard JK et al (2018) Prospective, single-center implementation and response evaluation of pressurized intraperitoneal aerosol chemotherapy (PIPAC) for peritoneal metastasis. Ther Adv Med Oncol. https:\u002F\u002Fdoi.org\u002F10.1177\u002F1758835918777036\nGraversen M, Lundell L, Fristrup C, Pfeiffer P, Mortensen MB (2018) Pressurized intraperitoneal aerosol chemotherapy (PIPAC) as an outpatient procedure. Pleura Peritoneum. https:\u002F\u002Fdoi.org\u002F10.1515\u002Fpp-2018-0128\nGarg PK, Jara M, Alberto M, Rau B (2019) The role of Pressurized IntraPeritoneal Aerosol Chemotherapy in the management of gastric cancer: a systematic review. Pleura Peritoneum 4(1):20180127\nStruller F, Horvath P, Solass W et al (2019) Pressurized intraperitoneal aerosol chemotherapy with low-dose cisplatin and doxorubicin (PIPAC C\u002FD) in patients with gastric cancer and peritoneal metastasis: a phase II study. Ther Adv Med Oncol 11:1758835919846402. https:\u002F\u002Fdoi.org\u002F10.1177\u002F1758835919846402\nSolass W, Sempoux C, Detlefsen S et al (2016) Peritoneal sampling and histological assessment of therapeutic response in peritoneal metastasis: proposal of the Peritoneal Regression Grading Score (PRGS). Pleura Peritoneum 1(2):99–107. https:\u002F\u002Fdoi.org\u002F10.1515\u002Fpp-2016-0011\nClavien PA, Strasberg SM (2009) Severity grading of surgical complications. Ann Surg 250(2):197–198. https:\u002F\u002Fdoi.org\u002F10.1097\u002FSLA.0b013e3181b6dcab\nNational Institutes of Health NCI (2009) Common Terminology Criteria for Adverse Events (CTCAE). 4.0 [published Online First: 28.05.2009]\nSolass W, Sempoux C, Carr N et al (2019) Reproducibility of the Peritoneal Regression Grading Score (PRGS) for assessment of response to therapy in peritoneal metastasis. Histopathology 74(7):1014–1024. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fhis.13829\nLauren P (1965) The two histological main types of gastric carcinoma: diffuse and so-called intestinal-type carcinoma. An attempt at a histo-clinical classification. Acta Pathol Microbiol Scand 64:31–49\nThomassen I, van Gestel YR, van Ramshorst B et al (2014) Peritoneal carcinomatosis of gastric origin: a population-based study on incidence, survival and risk factors. Int J Cancer 134(3):622–628. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fijc.28373\nYang D, Hendifar A, Lenz C et al (2011) Survival of metastatic gastric cancer: significance of age, sex and race\u002Fethnicity. J Gastrointest Oncol 2(2):77–84. https:\u002F\u002Fdoi.org\u002F10.3978\u002Fj.issn.2078-6891.2010.025\nCoccolini F, Celotti A, Ceresoli M et al (2016) Hyperthermic intraperitoneal chemotherapy (HIPEC) and neoadjuvant chemotherapy as prophylaxis of peritoneal carcinosis from advanced gastric cancer-effects on overall and disease free survival. J Gastrointest Oncol 7(4):523–529. https:\u002F\u002Fdoi.org\u002F10.21037\u002Fjgo.2016.06.05\nKhomyakov VRA, Ivanov A, Bolotina L, Utkina A et al (2016) Bidirectional chemotherapy in gastric cancer with peritoneal metastasis combining intravenous XELOX with intraperitoneal chemotherapy with low-dose cisplatin and Doxorubicin administered as a pressurized aerosol: an open-label, Phase-2 study (PIPAC-GA2). Pleura Peritoneum 1(3):159–166\nGockel I, Jansen-Winkeln B, Haase L et al (2018) Pressurized intraperitoneal aerosol chemotherapy (PIPAC) in gastric cancer patients with peritoneal metastasis (PM): results of a single-center experience and register study. J Gastric Cancer 18(4):379–391. https:\u002F\u002Fdoi.org\u002F10.5230\u002Fjgc.2018.18.e37\nGraversen M, Detlefsen S, Pfeiffer P et al (2018) Severe peritoneal sclerosis after repeated pressurized intraperitoneal aerosol chemotherapy with oxaliplatin (PIPAC OX): report of two cases and literature survey. Clin Exp Metastasis 35(3):103–108. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs10585-018-9895-9\nTempfer CB, Hilal Z, Dogan A et al (2018) Concentrations of cisplatin and doxorubicin in ascites and peritoneal tumor nodules before and after pressurized intraperitoneal aerosol chemotherapy (PIPAC) in patients with peritoneal metastasis. Eur J Surg Oncol 44(7):1112–1117. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ejso.2018.04.020",{"VOID":1141},"10.1007\u002Fs10585-020-10023-5","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10585-020-10023-5",[1144,1168,1206,1235,1257,1277,1306],{"id":1145,"sortIndex":32,"researcher":28,"roles":1146,"affiliations":1147,"properties":1165,"displayName":1167,"givenName":28,"familyName":28},"4ba0e5b5-5869-40ac-9b12-26eea6e7e984",[1036],[1148,1156],{"id":1149,"sortIndex":32,"affiliation":1150,"properties":28},"c90696cc-d596-45c6-a44a-ede0f1da48a2",{"id":1149,"createTime":28,"updateTime":28,"relativeEntities":1151,"slug":28,"properties":1152,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1155,"statistic":28},[],{"title":1153},{"VI":1154},"Odense PIPAC Center, Odense University Hospital, Odense, Denmark",[],{"id":1157,"sortIndex":40,"affiliation":1158,"properties":1164},"417b667d-2106-4c7d-8d99-ae19328652ef",{"id":1157,"createTime":28,"updateTime":28,"relativeEntities":1159,"slug":28,"properties":1160,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1163,"statistic":28},[],{"title":1161},{"VI":1162},"Department of Surgery, Upper GI and HPB Section, Odense University Hospital, Odense, Denmark",[],{},{"title":1166},{"VI":1167},"S. 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growth and metastatic behavior of three human tumor cell lines and a human colon carcinoma previously passagedin vivo were compared between nude mice and scid mice after xenotransplantation. The three human tumor lines included a bladder carcinoma (T24B), a melanoma (RPMI 7931) and alacZ gene-transduced breast cancer (MDA-MB-435 BAG). ThelacZ gene codes for β-galactosidase, which can be stained blue with chromogenic substrate X-gal, thus allowing the highly sensitive detection and quantitative examination of human cancer metastasis in host mice. Adult (7–14 weeks) NMRI nude and C.B-17 SCID mice were inoculated with 0.5–5 × 106 tumor cells s.c. Comparable take rate, latent period and growth rate of implanted tumors were observed in nude and scid mice for each of the cell lines tested. At the time of autopsy, which varied from 6 to 11 weeks after inoculation, a significantly higher incidence of spontaneous lung metastasis was discovered in scid mice (96%) than in age-matched nude mice (27%, totalP \u003C 0.001).In vitro assays for NK cell-mediated cytotoxicity revealed no significant differences between the two strains of mice. Our results suggest that nude and scid mice are equally suitable for propagating human tumors. However, the metastatic capacity of human tumor cells appears to be better expressed in scid mice. Scid mice may therefore provide an advantageous model for the study of human tumor metastasis.",{"EN":1409},"Comparative studies between nude and scid mice on the growth and metastatic behavior of xenografted human tumors",{"VOID":1411},"Fogh J, Fogh JM and Orfeo T, 1977, One hundred and twenty-seven cultured human tumor cell lines producing tumors in nude mice.Journal of the National Cancer Institute,59, 221–225.\nGiovanella BC, Stehlin JS, Williams LJ Jr, Lee SS and Shepard RC, 1978, Hetero-transplantation of human cancers into nude mice: a model system for human cancer chemotherapy.Cancer,42, 2269–2281.\nSharkey FE and Fogh J, 1979, Metastasis of human tumors in athymic nude mice.International Journal of Cancer,24, 733–738.\nSordat BCM, Ueyama Y and Fogh J, Metastasis of tumors xenografted in the nude mouse. In: Fogh J and Giovanella BC, eds.The Nude Mouse in Experimental and Clinical Research, vol. 2. New York: Academic Press, 1982, pp. 95–147.\nHanna N and Fidler IJ, 1981, Expression of metastatic potential of allogenic and xenogeneic neoplasms in young nude mice.Cancer Research,41, 438–444.\nKozlowski JM, Fidler IJ, Campbell D, Xu ZL, Kaighn ME and Hart IR, 1984, Metastatic behavior of human tumor cell lines grown in nude mouse.Cancer Research,44, 3522–3529.\nFidler IJ, 1986, Rationale and methods for the use of nude mice to study the biology and therapy of human cancer metastasis.Cancer and Metastasis Reviews,5, 29–49.\nHanna N, Davis TW and Fidler IJ, 1982, Environmental and genetic factors determine the level of NK activity of nude mice and affect their suitability as models for experimental metastasis.International Journal of Cancer,30, 371–376.\nDoré JF, Bailly M and Bertrand S, 1987, Metastasis of human tumors in experimental animals.Anticancer Research,7, 997–1004.\nFidler IJ, Pollack VA and Hanna N, The use of nude mice for studies of cancer metastasis. In: Sordat B, ed.Immune-Deficient Animals. 4th Inter national Workshop on Immune-Deficient Animals in Experimental Research, Chexbres 1982. Basel: Karger, 1984, pp. 328–338.\nHanna N, 1980, Expression of metastatic potential of tumor cells in young nude mice is correlated with low levels of natural killer cell-mediated cytotoxicity.International Journal of Cancer,26, 675–680.\nClark EA, Schultz LD and Pollack SB, 1981, Mutations in mice that influence natural killer (NK) cell activity.Immunogenetics,12, 601–613.\nFodstad Ø, Hansen CT, Cannon GB, Statham CN, Lichtenstein GR and Boyd MR, 1984, Lack of correlation between natural killer activity and tumor growth control in nude mice with different immune defects.Cancer Research,44, 4403–4408.\nNaito S, Giavazzi R, Walker SM, Itoh K, Mayo J and Fidler IJ, 1987, Growth and metastatic behaviour of human tumor cells implanted into nude and beige nude mice.Clinical and Experimental Metastasis,5, 135–146.\nZietman AL, Sugiyama E, Ramsay JR,et al., 1991, A comparative study on the xenotransplantability of human solid tumors into mice with different immune deficiencies.International Journal of Cancer,47, 755–759.\nSchuler W, Weiler IJ, Schuler A,et al., 1986, Rearrangement of antigen receptor genes is defective in mice with severe combined immune deficiency.Cell,46, 963–972.\nBosma GC, Custer RP and Bosma JM, 1983, A severe combined immunodeficiency mutation in the mouse.Nature,301, 527–530.\nMosier DE, Gulizia RJ, Baird SM and Wilson DB, 1988, Transfer of a functional human immune system to mice with severe combined immunodeficiency.Nature,335, 256–259.\nPhillips RA, Jewett MAS and Gallic BL, 1989, Growth of human tumors in immune-deficient scid mice and nude mice.Current Topics in Microbiology and Immunology,152, 258–263.\nGhetie MA, Richardson J, Tucker T, Jones D, Uhr JW and Vitetta ES, 1990, Disseminated or localized growth of a human B-cell tumor (Daudi) in scid mice.International Journal of Cancer,45, 481–485.\nReddy S, Piccione D, Takita H and Bankert RB, 1987, Human lung tumor growth established in the lung and subcutaneous tissue of mice with severe combined immunodeficiency.Cancer Research,47, 2456–2460.\nHill LL, Korngold R, Jaworsky C, Murphy G, McCue P and Berd D, 1991, Growth and metastasis of fresh human melanoma tissue in mice with severe combined immunodeficiency.Cancer Research,51, 4937–4041.\nNomura T, Takahama Y, Hongyo T,et al., 1990, Acid (severe combined immunodeficiency) mice as a new system to investigate metastasis of human tumors.Journal of Radiation Research Tokyo,31, 288–292.\nKieler J, Moore J, Biezowa B and Radzikowski C, 1971, Comparative studies of the cytologic and metabolic characteristics of C3H mouse cells during ‘spontaneous’ alteration and neoplastic conversionin vitro.Acta Pathologica Microbiologica Scandinavica,79, 529–544.\nGerner RE, Kitamura H and Moore GE, 1975, Studies of tumor cell lines derived from patients with malignant melanoma.Oncology,31, 31–43.\nBrünner N, Thompson EW, Spang-Thomsen M, Rygaard J, Danø K and Zwiebel JA, 1991,LacZ transduced human tumor xenografts as anin vivo model for the study of invasion and metastasis. (submitted toEuropean Journal of Cancer).\nBrinkley BR, Beall PT, Wible LJ, Mace ML, Turner DS and Cailleau RM, 1980, Variations in cell form and cytoskeleton in human breast carcinoma cellsin vitro.Cancer Research,40, 3118–3129.\nLin WC, Pretlow TP, Pretlow TG II and Culp LA, 1990, BacterialLacZ gene as a highly sensitive marker to detect micrometastasis formation during tumor progression.Cancer Research,50, 2808–2817.\nNolan GP, Fiering S, Nicolas J-F and Herzenberg LA, 1988, Fluorescence-activated cell analysis and sorting of viable mammalian cells based on β-Dgalactosidase activity after transduction of Escherichiacoli lacZ.Proceedings of the National Academy of Sciences USA,85, 2603–2607.\nRygaard K and Spang-Thomsen M, Growth-a computer program for determination of mean growth curves and calculation of response of therapy to solid tumor xenografts. In: Wu B-q and Zhang J, eds.Immune-Deficient Animals in Experimental Medicine. 6th International Workshop on ImmunoDeficient Animals, Beijing 1988, Basel: Karger, 1989, pp. 301–306.\nBudzynski W, Chirigos M and Gruys E, 1987, Augmentation of natural cell activity in tumor-bearing and normal mice by MVE-2.Cancer Immunology and Immunotherapy,24, 253–258.\nVisfeldt J, Povlsen CO and Rygaard J, 1972, Chromosome analysis of human tumors following heterotransplantation to the mouse mutant nude.Acta Pathologica Microbiologica Scandinavica, Section A,80, 169–176.\nHarrison CJ, Diagnosis of malignancy from chromosome preparations. In: Rooney DE and Czepulkowski BH, eds.Human Cytogenetics, a Practical Approach. Oxford: IRL Press, 1986, pp. 144–150.\nBenn PA and Perle MA, Chromosome staining and banding techniques. In: Rooney DE and Czepulkowski BH, eds.Human Cytogenetics, a Practical Approach. Oxford: IRL Press, 1986 pp. 57–84.\nKyriazis AP, Dipersio L, Michael GJ, Pesce AJ and Stinnett JD, 1978, Growth patterns and metastatic behavior of human tumors growing in athymic mice.Cancer Research,38, 3186–3190.\nHerberman RB, Nunn ME and Lavrin DH, 1975, Natural cytotoxic reactivity of mouse lymphoid cells against syngeneic and allogeneic tumors. I. Distribution of reactivity and specificity.International Journal of Cancer,16, 216–229.\nFidler IJ, 1974, Inhibition of pulmonary metastasis by intravenous injection of specifically activated macrophages.Cancer Research,34, 1074–1078.\nLoveless SE and Heppner GH, 1983, Tumor-associated macrophages of mouse mammary tumors. I. Differential cytotoxicity of macrophages from meta static and nonmetastatic tumor.Journal of Immunology,131, 2074–2078.\nMartin SE and Martin WJ, 1975, Antitumor antibodies in normal mouse sera.International Journal of Cancer,15, 658–664.\nHanna N and Fidler IJ, 1981, Relationship between metastatic potential and resistance to natural killer cell-mediated cytotoxicity in the three murine tumor systems.Journal of the National Cancer Institute,66, 1183–1189.\nDorshkind K, Pollack SB, Bosma MJ and Phillips RA, 1985, Natural killer (NK) cells are present in mice with severe combined immunodeficiency (scid).Journal of Immunology,134, 3798–3801.\nPovlsen CO, Fialkow PJ, Klein E, Klein G, Rygaard J and Wiener F, 1973, Growth and antigenic properties of a biopsy-derived Burkitt's lymphoma in thymusless (nude) mice.International Journal of Cancer,11, 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previously established an experimental model of tumor progression using a weakly malignant rat mammary carcinoma cell line, ER-1. Using this model, we demonstrated that ER-1 cells converted into highly tumorigenic and metastatic cells, ERpP, by s.c. co-inoculation with plastic plates. We here compared in vitro biological properties associated with malignancy of ER-1 cells with those of ERpP cells which were highly malignant when inoculated into syngeneic rats. In vitro growth rate of ERpP cells was higher than that of ER-1 cells under a low nutrient condition. Invasion capacity of ERpP cells to rat lung endothelial cell monolayer or reconstituted basement membrane, Matrigel, was higher than that of ER-1 cells. Migration of ERpP cells toward fibronectin or laminin was also significantly higher than that of ER-1 cells.There was no difference in gelatinolytic or plasminogen activator activity detected in conditioned media between ER-1 and ERpP cells. Furthermore, we found that ER-1 cells communicated better among themselves and with normal fibroblasts through gap junctions compared to ERpP cells. These results suggest that growth advan-tage in a poor nutrient condition, enhancement of cell motility, and loss or decrease of junctional communication may be associated with tumor progression of ER-1 cells. © Rapid Science 1998",{"EN":1571},"Characterization of the progressive sublines derived from a weakly malignant cloned cell line, ER-1, co-inoculated subcutaneously with a foreign body",{"VOID":1573},"Foulds L, 1957, Tumor progression. Cancer Res, 17, 355-6.\nNowell PC, 1986, Mechanisms of tumor progression. Cancer Res, 46, 2203-7.\nPitot HC, 1989, Progression: the terminal stage in carcinogenesis. Jpn J Cancer Res, 80, 599-607.\nNicolson GL, 1987, Tumor cell instability, diversification, and progression to the metastatic phenotype: from oncogene to oncofetal expression. Cancer Res, 47, 1473-87.\nHamada J, Takeichi N, Okada F, et al. 1992, Progression of weakly malignant clone cells derived from rat mammary carcinoma by host cells reactive to plastic plates. Jpn J Cancer Res, 83, 483-90.\nLi X, Nagayasu H, Hamada J, Hosokawa M and Takeichi N, 1993, Enhancement of tumorigenicity and invasion capacity of rat mammary adenocarcinoma cells by epidermal growth factor and transforming growth factor-β. Jpn J Cancer Res, 84, 1145-9.\nHamada J, Takeichi N and Kobayashi H, 1988, Metastatic capacity and intercellular communication between normal cells and metastatic cell clones derived from a rat mammary carcinoma. Cancer Res, 48, 5129-32.\nNakajima M, Welch DR, Belloni PN and Nicolson GL, 1987, Degradation of basement membrane type IV collagen and lung subendothelial matrix by rat mammary adenocarcinoma cell clones of differing metastatic potentials. Cancer Res, 47, 4869-76.\nAlbini A, Iwamoto Y, Kleinman HK, et al. 1987, A rapid in vitroassay for quantitating the invasive potential of tumor cells. Cancer Res, 47, 3239-45.\nNakajima M, DeChavigny A, Johnson CE, Hamada J, Stein CA and Nicolson GL, 1991, Suramin. A potent inhibitor of melanoma heparanase and invasion. J Biol Chem, 266, 9661-6.\nOhigashi H, Shinkai K, Mukai M, et al. 1989, In vitroinvasion of endothelial cell monolayer by rat ascites hepatoma cells. Jpn J Cancer Res, 80, 818-21.\nRepesh LA, 1989, A new in vitroassay for quantitating tumor cell invasion. Invasion Metastasis, 9, 192-208.\nHamada J, Cavanaugh PG, Lotan O and Nicolson GL, 1992, Separable growth and migration factors for large-cell lymphoma cells secreted by microvascular endothelial cells derived from target organs for metastasis. Br J Cancer, 66, 349-54.\nHoussen C and Dowdle EB, 1980, Electrophoretic analysis of plasminogen activators in polyacrylamide gels containing sodium dodecyl sulfate and copolymerized substrate. Analyt Biochem, 102, 196-202.\nLaemmli UK, 1970, Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature, 227, 680-5.\nRen J, Hamada J, Okada F, et al. 1990, Correlation between the presence of microvilli and the growth of metastatic potential of tumor cells. Jpn J Cancer Res, 81920-6.\nKishimoto T, Tavassoli M, Green R and Jacobsen DW, 1987, Receptors for transferrin and transcobalamin II display segregated distribution on microvilli of leukemia L1210 cells. Biochem Biophys Res Commun, 146, 1102-8.\nMori S, Akiyama T, Morishita Y, et al. 1987, Light and electron microscopical demonstration of c-erbB-2 gene product-like immunoreactivity in human malignant tumors. Virchows Arch, B, 54, 8-15.\nSporn MB and Roberts AB, 1986, Peptide growth factors and inflammation, tissue repair and cancer. J Clin Invest, 78, 329-32.\nWahl SM, Wong H and McCartney-Francis N, 1989, Role of growth factors in inflammation and repair. J Cell Biochem, 40, 193-9.\nBabior BM and Woodman RC, 1990, Chronic granulomatous disease. Semin Hematol, 27, 247-59.\nHamada J, Takeichi N, Ren J and Kobayashi H, 1991, Junctional communication of highly and weakly metastatic variant clones from a rat mammary carcinoma in primary and metastatic sites. Invasion Metastasis, 11, 149-57.\nNicolson GL, Dulski KM and Trosko JE, 1988, Loss of intercellular junctional communication correlates with metastatic potential in mammary adenocarcinoma cells. Proc Natl Acad Sci USA, 85, 473-6.\nEnomoto T, Sasaki Y, Shiba Y, Kanno Y and Yamasaki H, 1981, Tumor promoters cause a rapid and reversible inhibition of the formation and maintenance of electrical cell coupling in culture. Proc Natl Acad Sci USA, 78,5628-32.\nYotti LP, Chang CC and Trosko JE, 1979, Elimination of metabolic cooperation in Chinese hamster cells by a tumor promoter. Science, 206, 1089-91.\nEnomoto T and Yamasaki H, 1985, Phorbol estermediated inhibition of intercellular communication in BALB\u002Fc3T3 cells: relationship to enhancement of cell transformation. Cancer Res, 45, 2681-8.\nChow DA, 1984, Variant generation and selection: an in vitromodel of tumor progression. Int J Cancer, 33, 541-5.\nMadhukar BV, Oh SY, Chang CC, Wade M and Trosko JE, 1989, Altered regulation of intercellular communication by epidermal growth factor, transforming growth factor-β, and peptide hormones in normal keratinocytes. Carcinogenesis, 10, 13-20.",{"VOID":1575},"10.1023\u002FA:1006505211766","2024-12-05T19:35:03.651+00:00","Author affiliation is blank","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FA:1006505211766",[1580,1595,1610,1623,1630,1643,1656],{"id":1581,"sortIndex":32,"researcher":28,"roles":1582,"affiliations":1583,"properties":1592,"displayName":1594,"givenName":28,"familyName":28},"f5febd8e-9a38-4cef-801e-ddfc1c48bf7f",[1036],[1584],{"id":1585,"sortIndex":32,"affiliation":1586,"properties":28},"7638b079-3338-4ff5-87fd-3f4ade4c8bf1",{"id":1585,"createTime":28,"updateTime":28,"relativeEntities":1587,"slug":28,"properties":1588,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1591,"statistic":28},[],{"title":1589},{"VI":1590},"Division of Cell Biology, Cancer Institute, Hokkaido University School of Medicine, Sapporo, Japan",[],{"title":1593},{"VI":1594},"Jun-ichi 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Takeichi",{"url":1578,"publisher":1664,"properties":1714},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":1665,"slug":872,"properties":1666,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":1670,"manageAffiliations":1683,"indexDatabases":1694,"url":28,"thumbnailPath":28,"statistic":1709,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"issn":1667,"title":1668,"eissn":1669},{"VOID":875},{"EN":877},{"VOID":879},[1671,1675,1679],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":1672,"label":1673,"description":1674,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},{"id":889,"createTime":28,"updateTime":28,"relativeEntities":1676,"label":1677,"description":1678,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":892},{},{"id":895,"createTime":28,"updateTime":28,"relativeEntities":1680,"label":1681,"description":1682,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":898},{},[1684,1689],{"id":902,"createTime":28,"updateTime":28,"relativeEntities":1685,"slug":28,"properties":1686,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1688,"statistic":28},[],{"title":1687},{"EN":906},[908],{"id":910,"createTime":28,"updateTime":28,"relativeEntities":1690,"slug":28,"properties":1691,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1693,"statistic":28},[],{"title":1692},{"EN":914},[],[1695,1702],{"id":918,"indexDatabase":1696,"url":924,"indexYears":925,"academicFieldIds":1701,"indexDatabaseRanking":930},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":1697,"label":1698,"description":1699,"key":781,"publicationTags":1700,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[927,928,929],{"id":932,"indexDatabase":1703,"url":944,"indexYears":28,"academicFieldIds":1708,"indexDatabaseRanking":28},{"id":934,"createTime":28,"updateTime":28,"relativeEntities":1704,"label":1705,"description":1706,"key":941,"publicationTags":1707,"standard":28},[],{"EN":937,"VI":937},{"EN":939,"VI":940},[943,813],[946],{"impactFactor":32,"impactFactorByYear":1710,"i10Index":953,"i10IndexLast5Year":199,"totalPublication":954,"totalPublicationByYear":1711,"totalCitation":956,"totalCitationByYear":1712,"totalCitationPerPublication":977,"totalCitationPerPublicationByYear":1713,"hindexLast5Year":200,"hindex":200},{"2012":173,"2013":438,"2014":341,"2015":695,"2016":949,"2017":950,"2018":696,"2019":319,"2020":951,"2021":705,"2022":346,"2023":952},{"1983":147,"1984":134,"1985":128,"1986":135,"1987":130,"1988":139,"1989":142,"1990":202,"1991":133,"1992":281,"1993":141,"1994":148,"1995":150,"1996":516,"1997":139,"1998":280,"1999":564,"2000":325,"2002":689,"2003":207,"2004":137,"2005":50,"2006":278,"2007":162,"2008":560,"2009":434,"2010":196,"2011":206,"2012":332,"2013":436,"2014":149,"2015":206,"2016":142,"2017":131,"2018":206,"2019":196,"2020":141,"2021":149,"2022":201,"2023":202,"2024":135},{"1983":611,"1984":132,"1985":280,"1986":201,"1987":131,"1988":958,"1989":959,"1990":148,"1991":565,"1992":960,"1993":961,"1994":962,"1995":684,"1996":963,"1998":358,"2003":612,"2004":964,"2005":965,"2006":966,"2007":563,"2008":967,"2009":968,"2010":969,"2011":970,"2012":971,"2013":972,"2014":973,"2015":974,"2016":962,"2017":49,"2018":359,"2019":975,"2020":522,"2021":140,"2022":976,"2023":45},{"1983":979,"1984":980,"1985":981,"1986":185,"1987":982,"1988":983,"1989":984,"1990":985,"1991":986,"1992":987,"1993":988,"1994":989,"1995":990,"1996":991,"1998":442,"2003":992,"2004":993,"2005":994,"2006":995,"2007":996,"2008":997,"2009":998,"2010":999,"2011":1000,"2012":1001,"2013":1002,"2014":1003,"2015":1004,"2016":1005,"2017":320,"2018":1006,"2019":1007,"2020":1008,"2021":424,"2022":1009,"2023":104},{"pages":1715,"volume":1717},{"VOID":1716},"291-298",{"VOID":1718},"16","1998-04-01",1998,[943,930],{"id":1723,"createTime":1724,"updateTime":1725,"relativeEntities":1726,"slug":1727,"properties":1728,"entityType":1028,"verifyStatus":26,"verifyTime":1725,"verifyNote":1030,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":1739,"fullTextUrl":28,"authors":1740,"publicationType":1064,"publisherRelationship":1979,"citationCount":28,"citationInfo":28,"publishDate":2030,"publishYear":2031,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":2032,"openAccess":28,"references":28,"isForceReanalyzing":1126},"00596cd6-2952-4edf-97e8-601e972e9e65","2024-04-06T03:34:18.997+00:00","2025-01-08T22:54:14.571+00:00",[],"PLXDC2-enhances-invadopodium-formation-to-promote-invasion-and-metastasis-of-gastric-cancer-cells-via-interacting-with-PTP1B",{"abstract":1729,"title":1731,"keywords":1733,"references":1735,"doi":1737},{"EN":1730},"Plexin-domain containing 2 (PLXDC2) has been reported as an oncoprotein in several human malignancies. However, its expression and roles in gastric cancer remain largely unclear. In this study, we found that PLXDC2 was highly expressed in gastric cancer tissues, and the expression levels were positively correlated with clinicopathological features, but negatively with the patients’ outcome. Cox regression analysis identified PLXDC2 as an independent prognostic indicator for the patients. Knockdown of PLXDC2 markedly suppressed the in vitro invasion and in vivo metastasis of gastric cancer cells, while overexpression of PLXDC2 resulted in opposite effects. Mechanistically, PLXDC2 enhanced the level of phosphorylated Cortactin (p-Cortactin) by physically interacting with protein tyrosine phosphatase 1B (PTP1B), an important dephosphorylase, to prevent its dephosphorylating of p-Cortactin, thereby promoting the formation of invadopodia. Collectively, our results indicate that PLXDC2 contributes to the invasion and metastasis of gastric cancer by inhibiting PTP1B to facilitate the invadopodium formation, and may serve as a potential prognostic biomarker and a therapeutic target for this disease.",{"EN":1732},"PLXDC2 enhances invadopodium formation to promote invasion and metastasis of gastric cancer cells via interacting with PTP1B",{"EN":1734},"",{"VOID":1736},"Siegel RL, Miller KD, Fuchs HE, Jemal A (2021) Cancer Statistics, 2021. CA Cancer J Clin 71:7–33. https:\u002F\u002Fdoi.org\u002F10.3322\u002Fcaac.21654\nZheng RS, Sun KX, Zhang SW, Zeng HM, Zou XN, Chen R et al (2019) Report of cancer epidemiology in China, 2015. Zhonghua Zhong Liu Za Zhi 41:19–28. https:\u002F\u002Fdoi.org\u002F10.3760\u002Fcma.j.issn.0253-3766.2019.01.005\nVan Cutsem E, Sagaert X, Topal B, Haustermans K, Prenen H (2016) Gastric cancer. Lancet 388:2654–2664. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS0140-6736(16)30354-3\nHarada K, Lopez A, Shanbhag N, Badgwell B, Baba H, Ajani J (2018) Recent advances in the management of gastric adenocarcinoma patients. F1000Res. https:\u002F\u002Fdoi.org\u002F10.12688\u002Ff1000research.15133.1\nLeighton PA, Mitchell KJ, Goodrich LV, Lu X, Pinson K, Scherz P et al (2001) Defining brain wiring patterns and mechanisms through gene trapping in mice. Nature 410:174–179. https:\u002F\u002Fdoi.org\u002F10.1038\u002F35065539\nSt Croix B, Rago C, Velculescu V, Traverso G, Romans KE, Montgomery E et al (2000) Genes expressed in human tumor endothelium. Science 289:1197–1202. https:\u002F\u002Fdoi.org\u002F10.1126\u002Fscience.289.5482.1197\nMiller-Delaney SF, Lieberam I, Murphy P, Mitchell KJ (2011) Plxdc2 is a mitogen for neural progenitors. PLoS ONE 6:e14565. https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0014565\nCheng G, Zhong M, Kawaguchi R, Kassai M, Al-Ubaidi M, Deng J et al (2014) Identification of PLXDC1 and PLXDC2 as the transmembrane receptors for the multifunctional factor PEDF. Elife 3:e05401. https:\u002F\u002Fdoi.org\u002F10.7554\u002FeLife.05401\nDavies G, Cunnick GH, Mansel RE, Mason MD, Jiang WG (2004) Levels of expression of endothelial markers specific to tumour-associated endothelial cells and their correlation with prognosis in patients with breast cancer. Clin Exp Metastasis 21:31–37. https:\u002F\u002Fdoi.org\u002F10.1023\u002Fb:clin.0000017168.83616.d0\nYamamoto N, Eguchi A, Hirokawa Y, Ogura S, Sugimoto K, Iwasa M et al (2020) Expression pattern of plexin domain containing 2 in human hepatocellular carcinoma. Monoclon Antib Immunodiagn Immunother 39:57–60. https:\u002F\u002Fdoi.org\u002F10.1089\u002Fmab.2019.0050\nLavorato-Rocha AM, Akagi EM, de Melo MB, Rodrigues IS, Botelho MC, Marchi FA et al (2016) An integrative approach uncovers biomarkers that associate with clinically relevant disease outcomes in vulvar carcinoma. Mol Cancer Res 14:720–729. https:\u002F\u002Fdoi.org\u002F10.1158\u002F1541-7786.MCR-15-0366\nWang Y, Li H (2018) Identification of proteins associated with paclitaxel resistance of epithelial ovarian cancer using iTRAQ-based proteomics. Oncol Lett 15:9793–9801. https:\u002F\u002Fdoi.org\u002F10.3892\u002Fol.2018.8600\nGuan Y, Du Y, Wang G, Gou H, Xue Y, Xu J et al (2021) Overexpression of PLXDC2 in stromal cell-associated M2 macrophages is related to EMT and the progression of gastric cancer. Front Cell Dev Biol 9:673295. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffcell.2021.673295\nDavis S, Meltzer PS (2007) GEOquery: a bridge between the gene expression omnibus (GEO) and bioconductor. Bioinformatics 23:1846–1847\nDennis G Jr, Sherman BT, Hosack DA, Yang J, Gao W, Lane HC et al (2003) DAVID: database for annotation, visualization, and integrated discovery. Genome Biol 4:P3\nChen M, Yu X, Xu J, Ma J, Chen X, Chen B et al (2019) Association of gene polymorphisms with primary open angle glaucoma: a systematic review and meta-analysis. Invest Ophthalmol Vis Sci 60:1105–1121. https:\u002F\u002Fdoi.org\u002F10.1167\u002Fiovs.18-25922\nBao G, Wang N, Li R, Xu G, Liu P, He B (2016) Glycoprotein non-metastaticmelanoma protein B promotes glioma motility and angiogenesis through the Wnt\u002Fbeta-catenin signaling pathway. 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Cancer Metastasis Rev 28:137–149. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs10555-008-9176-1\nWeaver AM (2006) Invadopodia: specialized cell structures for cancer invasion. Clin Exp Metastasis 23:97–105. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs10585-006-9014-1\nEddy RJ, Weidmann MD, Sharma VP, Condeelis JS (2017) Tumor cell invadopodia: invasive protrusions that orchestrate metastasis. Trends Cell Biol 27:595–607. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.tcb.2017.03.003\nJeannot P, Besson A (2020) Cortactin function in invadopodia. Small GTPases 11:256–270. https:\u002F\u002Fdoi.org\u002F10.1080\u002F21541248.2017.1405773\nCastro-Castro A, Marchesin V, Monteiro P, Lodillinsky C, Rosse C, Chavrier P (2016) Cellular and molecular mechanisms of MT1-MMP-dependent cancer cell invasion. Annu Rev Cell Dev Biol 32:555–576. https:\u002F\u002Fdoi.org\u002F10.1146\u002Fannurev-cellbio-111315-125227\nWeed SA, Karginov AV, Schafer DA, Weaver AM, Kinley AW, Cooper JA et al (2000) Cortactin localization to sites of actin assembly in lamellipodia requires interactions with F-actin and the Arp2\u002F3 complex. J Cell Biol 151:29–40. https:\u002F\u002Fdoi.org\u002F10.1083\u002Fjcb.151.1.29\nStuible M, Dube N, Tremblay ML (2008) PTP1B regulates cortactin tyrosine phosphorylation by targeting Tyr446. J Biol Chem 283:15740–15746. https:\u002F\u002Fdoi.org\u002F10.1074\u002Fjbc.M710534200\nMertins P, Eberl HC, Renkawitz J, Olsen JV, Tremblay ML, Mann M et al (2008) Investigation of protein-tyrosine phosphatase 1B function by quantitative proteomics. Mol Cell Proteomics 7:1763–1777. https:\u002F\u002Fdoi.org\u002F10.1074\u002Fmcp.M800196-MCP200\nChiang AC, Massague J (2008) Molecular basis of metastasis. N Engl J Med 359:2814–2823. https:\u002F\u002Fdoi.org\u002F10.1056\u002FNEJMra0805239\nSaykali BA, El-Sibai M (2014) Invadopodia, regulation, and assembly in cancer cell invasion. Cell Commun Adhes 21:207–212. https:\u002F\u002Fdoi.org\u002F10.3109\u002F15419061.2014.923845\nFrom the American Association of Neurological Surgeons ASoNC, Interventional Radiology Society of Europe CIRACoNSESoMINTESoNESOSfCA, Interventions SoIRSoNS, World Stroke O, Sacks D, Baxter B et al (2018) Multisociety consensus quality improvement revised consensus statement for endovascular therapy of acute ischemic stroke. Int J Stroke 13:612–632. https:\u002F\u002Fdoi.org\u002F10.1177\u002F1747493018778713\nHamad HA, Enezei HH, Alrawas A, Zakuan NM, Abdullah NA, Cheah YK et al (2020) Identification of potential chemical substrates as fuel for hypoxic tumors that may be linked to invadopodium formation in hypoxia-induced MDA-MB-231 breast-cancer cell line. Molecules. https:\u002F\u002Fdoi.org\u002F10.3390\u002Fmolecules25173876\nChen L, Zhu M, Yu S, Hai L, Zhang L, Zhang C et al (2020) Arg kinase mediates CXCL12\u002FCXCR4-induced invadopodia formation and invasion of glioma cells. Exp Cell Res 389:111893. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.yexcr.2020.111893\nOgawa K, Lin Q, Li L, Bai X, Chen X, Chen H et al (2019) Aspartate beta-hydroxylase promotes pancreatic ductal adenocarcinoma metastasis through activation of SRC signaling pathway. J Hematol Oncol 12:144. https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs13045-019-0837-z\nLi Y, Zhang H, Gong H, Yuan Y, Li Y, Wang C et al (2018) miR-182 suppresses invadopodia formation and metastasis in non-small cell lung cancer by targeting cortactin gene. J Exp Clin Cancer Res 37:141. https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs13046-018-0824-1\nKe Y, Bao T, Zhou Q, Wang Y, Ge J, Fu B et al (2017) Discs large homolog 5 decreases formation and function of invadopodia in human hepatocellular carcinoma via Girdin and Tks5. Int J Cancer 141:364–376. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fijc.30730\nRajadurai CV, Havrylov S, Zaoui K, Vaillancourt R, Stuible M, Naujokas M et al (2012) Met receptor tyrosine kinase signals through a cortactin-Gab1 scaffold complex, to mediate invadopodia. J Cell Sci 125:2940–2953. https:\u002F\u002Fdoi.org\u002F10.1242\u002Fjcs.100834\nOser M, Mader CC, Gil-Henn H, Magalhaes M, Bravo-Cordero JJ, Koleske AJ et al (2010) Specific tyrosine phosphorylation sites on cortactin regulate Nck1-dependent actin polymerization in invadopodia. 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PLoS ONE 5:e13847. https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0013847\nOser M, Yamaguchi H, Mader CC, Bravo-Cordero JJ, Arias M, Chen X et al (2009) Cortactin regulates cofilin and N-WASp activities to control the stages of invadopodium assembly and maturation. J Cell Biol 186:571–587. https:\u002F\u002Fdoi.org\u002F10.1083\u002Fjcb.200812176\nSeals DF, Azucena EF Jr, Pass I, Tesfay L, Gordon R, Woodrow M et al (2005) The adaptor protein Tks5\u002FFish is required for podosome formation and function, and for the protease-driven invasion of cancer cells. Cancer Cell 7:155–165. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ccr.2005.01.006\nAbram CL, Seals DF, Pass I, Salinsky D, Maurer L, Roth TM et al (2003) The adaptor protein fish associates with members of the ADAMs family and localizes to podosomes of Src-transformed cells. J Biol Chem 278:16844–16851. https:\u002F\u002Fdoi.org\u002F10.1074\u002Fjbc.M300267200\nBuschman MD, Bromann PA, Cejudo-Martin P, Wen F, Pass I, Courtneidge SA (2009) The novel adaptor protein Tks4 (SH3PXD2B) is required for functional podosome formation. Mol Biol Cell 20:1302–1311. https:\u002F\u002Fdoi.org\u002F10.1091\u002Fmbc.E08-09-0949\nYu X, Zech T, McDonald L, Gonzalez EG, Li A, Macpherson I et al (2012) N-WASP coordinates the delivery and F-actin-mediated capture of MT1-MMP at invasive pseudopods. 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The difference in NKcell activity between patients with non-Hodgkin's lymphomas and Hodgkin's disease. Br J Haematol 1999; 104: 144–51.",{"id":28,"text":2223,"url":28,"identifiers":28},"Kirkwood JM, Richards T, Zarour HM et al. Immunomodulatory effects of high-dose and low-dose interferon alpha 2b in patients with high risk resected melanoma: the E2690 laboratory corollary of inter group adjuvant trial E16 90. Cancer 2002; 95: 1101–12.",{"id":28,"text":2225,"url":28,"identifiers":28},"Borrego F, Kabat J, Kim DK et al. Structure and function of major histocompatibility complex (MHC) class I specific receptors expressed on human natural killer (NK) cells. Mol Immunol, 2002; 38: 637–660.",{"id":28,"text":2227,"url":28,"identifiers":28},"Palmieri G, Morrone S, Lollini PL et al. TNF impairs in vivo and in vitro natural killer (NK) susceptibility of B16 melanoma cells. Scan J Immunol 1992; 35: 279–89.",{"id":28,"text":2229,"url":28,"identifiers":28},"Ross ME, Caligiuri MA. 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J Clin Oncol 1996; 14: 1690–6.",{"id":28,"text":2239,"url":28,"identifiers":28},"Conti L, Arista MC, Callopoli A et al. Flow cytometry evaluation of lymphocytes subsets in non-treated neoplastic patients. J Clin Exp Cancer Res 1995; 5: 257–64.",{"id":28,"text":2241,"url":28,"identifiers":28},"Konjevic G, Jurisic V, Spuzic I. Correction to the original lactate dehydrogenase (LDH) release assay for evaluation of NK cell cytotoxicity. J Immunol Meth, 1997; 200: 199–201.",{"id":28,"text":2243,"url":28,"identifiers":28},"Jurisic V, Spuzic I, Konjevic G. A comparison of NK cell activity with effects of TNF-alpha against K-562 cells, determined by LDH release assay. Cancer Lett 1999; 138: 67–72.",{"id":28,"text":2245,"url":28,"identifiers":28},"Johnston SR, Constenla DO, Moore J et al. Randomized phase II trial of BCDT [carmustine (BCNU), cisplatin, dacarbazine (DTIC) and tamoxifen] with or without interferon alpha (IFN-alpha) and interleukin (IL-2) in patients with metastatic melanoma. Br J Cancer 1998; 77: 1280–6.",{"id":28,"text":2247,"url":28,"identifiers":28},"Steinhauer EH, Doyle AT, Reed J, Kadish AS, Defective natural cytotoxicity in patients with cancer: Normal number of effector cells but decreased recycling capacity in patients with advanced disease. J Immunol 1982; 129: 2255–9.",{"id":28,"text":2249,"url":28,"identifiers":28},"Zea AH, Curti BD, Longo DL et al. Alterations in T cell receptor and signal transduction molecules in melanoma patients. Clin Cancer Res 1995; 1: 1327–35.",{"id":28,"text":2251,"url":28,"identifiers":28},"Kishi A, Ohmori M, Tomita S et al. Phenotypic and functional analyses of natural killer cells: Impaired NK activity partly due to the CD56+ cell dysfunction in cancer patients. Int J Immunother 1999; 15: 1–12.",{"id":28,"text":2253,"url":28,"identifiers":28},"Sibbit WL, Bankhurst AD, Jumonville AJ et al. Defects in natural killer activity and interferon response in human lung carcinoma and malignant melanoma. Cancer Res 1984; 44: 852–6.",{"id":28,"text":2255,"url":28,"identifiers":28},"Konjevic G, Jurisic V, Spuzic I. Association of NK cell dysfunction with changes in LDH characteristics of peripheral blood lymphocytes (PBL) in breast cancer patients. Breast Cancer Res Treat 2001; 66: 255–263",{"id":28,"text":2257,"url":28,"identifiers":28},"Krasagakis K, Tholke D, Farthmann B et al. Elevated plasma levels of transforming growth factor (TGF)-beta1 and TGF-beta2 in patients with disseminated malignant melanoma. Br J Cancer 1998; 77: 1492–4.",{"id":28,"text":2259,"url":28,"identifiers":28},"Hafner M, Orosz P, Kruger A, Mannel DN. TNF promotes metastasis by impairing natural killer cell activity. Int J Cancer 1996; 66: 388–92.",{"id":28,"text":2261,"url":28,"identifiers":28},"Barlozzari, T, Leonhardt J, Wiltrout RH et al. Direct evidence for the role of LGL in the inhibition of experimental tumor metastases. J Immunol 1985; 134: 2783–9.",{"id":28,"text":2263,"url":28,"identifiers":28},"Konjevic G, Spuzic I. Jurisic V. In-vitro effects of cytokines and cytokines receptors on the activity of NK cells. J BUON 1996; 1: 47–52.",{"id":28,"text":2265,"url":28,"identifiers":28},"Smyth MJ, Thia KY, Cretney E et al. Perforin is a major contributor to NK cell control of tumor metastasis. J Immunol 1999; 162: 6658–62.",{"id":28,"text":2267,"url":28,"identifiers":28},"Campbell JJ, Qin S, Unutmaz D et al. Unique subpopulations of CD56+ NK and NK-T peripheral blood lymphocytes identified by chemokine receptor expression repertoire. J Immunol 2001; 166: 6477–82.",{"id":28,"text":2269,"url":28,"identifiers":28},"Hersey P, Hasic E, Macdonald M et al. Effects of recombinant leukocyte interferon (rhIFN alpha A) on tumor growth and immune response in patients with metastatic melanoma. Br J Cancer 1985; 51: 815–26.",{"id":28,"text":2271,"url":28,"identifiers":28},"Eisenthal A, Skornick Y, Ron I et al. Phenotypic and functional pro-file of peripheral blood mononuclear cells isolated from melanoma patients undergoing combined immunotherapy and chemotherapy. Cancer Immunol Immunother 1993; 37: 367–72.",{"id":28,"text":2273,"url":28,"identifiers":28},"Verhagen A, Mackay IR, Rowley M, Tymms M. Comparison of augmentation of human natural killer cell cytotoxicity by interferon-alpha subtypes. Nat Immun Cell Growth Regul 1990; 9: 325–33.",{"id":28,"text":2275,"url":28,"identifiers":28},"Chakir H, Camilucci AA, Filion LG, Webb JR. Differentiation of murine NK cells into distinct subsets based on variable expression of the IL-12R beta 2 subunit. J Immunol 2000; 165: 4985–93.",{"id":28,"text":2277,"url":28,"identifiers":28},"Konjevic G, Schlesinger B, Cheng L et al. Analysis of perforin expression in human peripheral blood lymphocytes, CD56+ natural killer cell subsets and its induction by interleukin-2. Immunol Invest 1995; 24: 499–507.",{"id":28,"text":2279,"url":28,"identifiers":28},"Spaggiari GM, Contini P, Dondero A et al. Soluble HLA class I induces NK cell apoptosis upon the engagement of killer-activating HLA class I receptors through FasL-Fas interaction. Blood 2002; 100: 4098–107.",{"id":28,"text":2281,"url":28,"identifiers":28},"Golub SG, D'Amore PD, Rainey M. Systemic administration of human leukocyte interferon to melanoma patients. II. Cellular events associated with changes in natural killer cutotoxicity. J Nat Cancer Inst 1982; 68: 711–7.",{"id":28,"text":2283,"url":28,"identifiers":28},"Mogensen KE, Lewerenz M, Reboul J et al. The type I interferon receptor: Structure, function, and evolution of a family business. J Interferon Cytokine Res 1999; 19: 1069–98.",{"id":28,"text":2285,"url":28,"identifiers":28},"Bajetta, E, Di Leo A, Zampino MG et al. Multicenter randomized trial of dacarbazine alone or in combination with two different doses and schedules of interferon alfa-2a in the treatment of advanced melanoma. J Clin Oncol, 1994; 12: 806–11.",{"id":28,"text":2287,"url":28,"identifiers":28},"Atkins MB Immunotherapy and experimental approaches for metastatic melanoma. Melanoma 1998; 12: 877–902.",{"id":28,"text":2289,"url":28,"identifiers":28},"Aulitzky, WE, Aulitzky W, Gastl G et al. Acute effects of single dose of recombinant interferon-gamma on blood cell counts and lymphocyte subsets in patients with advanced renal cell cancer. J Interferon Res 1989; 9: 425–33.",{"id":28,"text":2291,"url":28,"identifiers":28},"Testi R, D'ambrosio D, De Maria R, Santoni A. The CD69 receptor: Multipurpose cell surface trigger for hematopoietic cells. Immunol Today 1994; 15: 479–83.",{"id":28,"text":2293,"url":28,"identifiers":28},"Yacyshyn-Bowen, MB, Poppema S, Berg A et al. CD69+ and HLADR+ activation antigens on peripheral blood lymphocyte populations in metastatic breast and ovarian cancer patients: Correlation with survival following active specific immunotherapy. Int J Cancer 1995; 61: 470–4.",{"id":28,"text":2295,"url":28,"identifiers":28},"Simms PE, Ellis TM. Utility of flow cytometric detection of CD69 expression as a rapid method for determining poly-and oligoclonal lymphocyte activation. Clin Diag Lab Immunol 1996; 3: 301–4.",{"id":28,"text":2297,"url":28,"identifiers":28},"Borrego F, Robertson MJ, Ritz J et al. CD69 is a stimulatory receptor for natural killer cell and its cytotoxic effect is blocked by CD94 inhibitory receptor. J Immunol 1999; 97: 159–65.",{"id":28,"text":2299,"url":28,"identifiers":28},"Pardoll DM, Topalian SL. The role of CD4 + T cell responses in antitumor immunity. Curr Opin Immunol 1998; 10: 588–94.",{"id":28,"text":2301,"url":28,"identifiers":28},"Hakansson A, Gustaffson B, Krysander L. et al. On down-regulation of the immune response to metastatic melanoma. Cancer Immunol Immunother 1999; 48: 253–62.",{"id":28,"text":2303,"url":28,"identifiers":28},"Boehm U, Klamp T, Groot M, Howard JC. Cellular responses to interferon-?. Annu Rev Immunol 1997; 15: 749–95.",{"id":28,"text":2305,"url":28,"identifiers":28},"Surman DR, Mark ED, Overwijk WW, Restifol NP. Cutting edge: CD4+ T cell control of CD8+ T cell reactivity to a model tumor antigen. J Immunol 2000; 164: 562–5.",{"id":28,"text":2307,"url":28,"identifiers":28},"Dobrzanski MJ, Reome JB, Dutton RW et al. Type 1 and type 2 CD8+ effectors T cell subpopulations promote long-term tumor immunity and protection to progressively growing tumor. Immunology 1999; 98: 535–40.",{"id":28,"text":2309,"url":28,"identifiers":28},"Bernengo MG, Lisa F, Meregalli M et al. Changes in T and B lymphocyte subpoulations before, during and after chemotherapy for malignant melanoma. Int J Tissue React 1984; 6: 505–11.",{"id":28,"text":2311,"url":28,"identifiers":28},"Pantaleo G, Koenig S, Baseler M et al. Defective clonogenic potential of CD8+ T-lymphocytes in patients with AIDS. Expansion in vivo of a non clonogenic CD3+CD8+DR+CD25-T cell population. J Immunol 1990; 144: 1696–704.",{"id":28,"text":2313,"url":28,"identifiers":28},"Funaro A, De Monte LB, Dianzani U et al. Human CD38 is associated to distinct molecules which mediate transmembrane signaling in different lineages. Eur J Immunol 1993; 23: 2407–11.",{"id":28,"text":2315,"url":28,"identifiers":28},"Mills CD, Kincaid K, Alt JM et al. M-1\u002FM-2 Macrophages and the Th1\u002FTh2 Paradigm. J Immunol 2000; 164: 6166–73.",{"id":28,"text":2317,"url":28,"identifiers":28},"Degiannis D, Koniavitou K. In vitro expression of activation markers and lymphocyte proliferation in response to interleukin 12: Effect of immunosuppressive agents. Transpl Proc 1996; 28: 3062–4.",{"id":28,"text":2319,"url":28,"identifiers":28},"Reveneau S, Arnould L, Jolimoy G et al. Changes in sIL-6R and s TNF-Rs release by PMNs and the serum levels in breast cancer patients at different stages of treatment. Cytokine 1998; 79: 540–3.",{"id":28,"text":2321,"url":28,"identifiers":28},"Zoll B, Lefterova P, Ebert O et al. Modulation of cell surface markers on NK-like T lymphocytes by using IL-2, IL-7 or IL-12 in vitro stimulation. Cytokine 2000; 12: 1385–90.",{"id":2323,"createTime":2324,"updateTime":2325,"relativeEntities":2326,"slug":2327,"properties":2328,"entityType":1028,"verifyStatus":26,"verifyTime":2325,"verifyNote":1030,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":2337,"fullTextUrl":28,"authors":2338,"publicationType":1064,"publisherRelationship":2470,"citationCount":28,"citationInfo":28,"publishDate":2526,"publishYear":2527,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":2528,"openAccess":28,"references":28,"isForceReanalyzing":1126},"0084979b-354a-418f-a842-6812b5fd7487","2024-01-24T05:19:23.699+00:00","2025-02-05T11:58:11.777+00:00",[],"BMP-signalling-controls-the-malignant-potential-of-ascites-derived-human-epithelial-ovarian-cancer-spheroids-via-AKT-kinase-activation",{"abstract":2329,"title":2331,"references":2333,"doi":2335},{"EN":2330},"Epithelial ovarian cancer (EOC) cells have the ability to form multi-cellular aggregates in malignant ascites which dramatically alters cell signalling, survival, and metastatic potential. Herein, we demonstrate that patient ascites-derived EOC cells down-regulate endogenous bone morphogenetic protein (BMP) signalling by decreasing BMP ligand expression when grown in suspension culture to form spheroids. Enforced BMP signalling in these cells via constitutively-active BMP type I ALK3QD receptor expression causes the formation of smaller, more loosely-aggregated spheroids. Additionally, ALK3QD-expressing spheroids have an increased rate of adhesion and dispersion upon reattachment to substratum. Inhibition of endogenous BMP signalling using recombinant Noggin or small molecule inhibitor LDN-193189, on the other hand, opposed these phenotypic changes. To identify potential targets that impact the phenotype of EOC spheroids due to activated BMP signalling, we performed genome-wide expression analyses using Affymetrix arrays. Using the online Connectivity Map resource, the BMP signalling gene expression signature revealed that the AKT pathway is induced by activated BMP signalling in EOC cells; this finding was further validated by phospho-AKT immuno-blotting. In fact, treatment of EOC spheroids with an AKT inhibitor, Akti-1\u002F2, reduced BMP-stimulated cell dispersion during reattachment as compared to controls. Thus, we have identified AKT as being one important downstream component of activated BMP signalling on EOC spheroid pathobiology, which may have important implications on the metastatic potential of this malignancy.",{"EN":2332},"BMP signalling controls the malignant potential of ascites-derived human epithelial ovarian cancer spheroids via AKT kinase activation",{"VOID":2334},"Lengyel E (2010) Ovarian cancer development and metastasis. Am J Pathol 177(3):1053–1064\nShield K, Ackland ML, Ahmed N, Rice GE (2009) Multicellular spheroids in ovarian cancer metastases: Biology and pathology. Gynecol Oncol 113(1):143–148\nKim TH, Mount CW, Gombotz WR, Pun SH (2010) The delivery of doxorubicin to 3-D multicellular spheroids and tumors in a murine xenograft model using tumor-penetrating triblock polymeric micelles. Biomaterials 31(28):7386–7397\nGrun B, Benjamin E, Sinclair J, Timms JF, Jacobs IJ, Gayther SA, Dafou D (2009) Three-dimensional in vitro cell biology models of ovarian and endometrial cancer. Cell Prolif 42(2):219–228\nKim JB (2005) Three-dimensional tissue culture models in cancer biology. Semin Cancer Biol 15(5):365–377\nHerrera B, van Dinther M, Ten Dijke P, Inman GJ (2009) Autocrine bone morphogenetic protein-9 signals through activin receptor-like kinase-2\u002FSmad1\u002FSmad4 to promote ovarian cancer cell proliferation. Cancer Res 69(24):9254–9262\nLe Page C, Puiffe ML, Meunier L, Zietarska M, de Ladurantaye M, Tonin PN, Provencher D, Mes-Masson AM (2009) BMP-2 signaling in ovarian cancer and its association with poor prognosis. J Ovarian Res 2:4\nMa Y, Ma L, Guo Q, Zhang S (2010) Expression of bone morphogenetic protein-2 and its receptors in epithelial ovarian cancer and their influence on the prognosis of ovarian cancer patients. J Exp Clin Cancer Res 29:85\nMoll F, Millet C, Noel D, Orsetti B, Bardin A, Katsaros D, Jorgensen C, Garcia M, Theillet C, Pujol P, Francois V (2006) Chordin is underexpressed in ovarian tumors and reduces tumor cell motility. FASEB J 20(2):240–250\nPils D, Wittinger M, Petz M, Gugerell A, Gregor W, Alfanz A, Horvat R, Braicu EI, Sehouli J, Zeillinger R, Mikulits W, Krainer M (2010) BAMBI is overexpressed in ovarian cancer and co-translocates with Smads into the nucleus upon TGF-beta treatment. Gynecol Oncol 117(2):189–197\nShepherd TG, Mujoomdar ML, Nachtigal MW (2010) Constitutive activation of BMP signalling abrogates experimental metastasis of OVCA429 cells via reduced cell adhesion. J Ovarian Res 3:5\nShepherd TG, Theriault BL, Nachtigal MW (2008) Autocrine BMP4 signalling regulates ID3 proto-oncogene expression in human ovarian cancer cells. Gene 414(1–2):95–105\nTheriault BL, Shepherd TG, Mujoomdar ML, Nachtigal MW (2007) BMP4 induces EMT and Rho GTPase activation in human ovarian cancer cells. Carcinogenesis 28(6):1153–1162\nDunfield LD, Dwyer EJ, Nachtigal MW (2002) TGF beta-induced Smad signaling remains intact in primary human ovarian cancer cells. Endocrinology 143(4):1174–1181\nWei X, Dombkowski D, Meirelles K, Pieretti-Vanmarcke R, Szotek PP, Chang HL, Preffer FI, Mueller PR, Teixeira J, MacLaughlin DT, Donahoe PK (2010) Mullerian inhibiting substance preferentially inhibits stem\u002Fprogenitors in human ovarian cancer cell lines compared with chemotherapeutics. Proc Natl Acad Sci USA 107(44):18874–18879\nShepherd TG, Theriault BL, Campbell EJ, Nachtigal MW (2006) Primary culture of ovarian surface epithelial cells and ascites-derived ovarian cancer cells from patients. Nat Protoc 1(6):2643–2649\nShepherd TG, Nachtigal MW (2003) Identification of a putative autocrine bone morphogenetic protein-signaling pathway in human ovarian surface epithelium and ovarian cancer cells. Endocrinology 144(8):3306–3314\nMurakami G, Watabe T, Takaoka K, Miyazono K, Imamura T (2003) Cooperative inhibition of bone morphogenetic protein signaling by Smurf1 and inhibitory Smads. Mol Biol Cell 14(7):2809–2817\nZhu H, Kavsak P, Abdollah S, Wrana JL, Thomsen GH (1999) A SMAD ubiquitin ligase targets the BMP pathway and affects embryonic pattern formation. Nature 400(6745):687–693\nIvascu A, Kubbies M (2007) Diversity of cell-mediated adhesions in breast cancer spheroids. Int J Oncol 31(6):1403–1413\nBoergermann JH, Kopf J, Yu PB, Knaus P (2010) Dorsomorphin and LDN-193189 inhibit BMP-mediated Smad, p38 and Akt signalling in C2C12 cells. Int J Biochem Cell Biol 42(11):1802–1807\nCuny GD, Yu PB, Laha JK, Xing X, Liu JF, Lai CS, Deng DY, Sachidanandan C, Bloch KD, Peterson RT (2008) Structure-activity relationship study of bone morphogenetic protein (BMP) signaling inhibitors. Bioorg Med Chem Lett 18(15):4388–4392\nLamb J (2007) The Connectivity Map: a new tool for biomedical research. Nature reviews 7(1):54–60\nLamb J, Crawford ED, Peck D, Modell JW, Blat IC, Wrobel MJ, Lerner J, Brunet JP, Subramanian A, Ross KN, Reich M, Hieronymus H, Wei G, Armstrong SA, Haggarty SJ, Clemons PA, Wei R, Carr SA, Lander ES, Golub TR (2006) The connectivity map: using gene-expression signatures to connect small molecules, genes, and disease. Science 313(5795):1929–1935\nZhang SD, Gant TW (2008) A simple and robust method for connecting small-molecule drugs using gene-expression signatures. BMC Bioinformatics 9:258\nArboleda MJ, Lyons JF, Kabbinavar FF, Bray MR, Snow BE, Ayala R, Danino M, Karlan BY, Slamon DJ (2003) Overexpression of AKT2\u002Fprotein kinase Bbeta leads to up-regulation of beta1 integrins, increased invasion, and metastasis of human breast and ovarian cancer cells. Cancer Res 63(1):196–206\nBast RC Jr, Hennessy B, Mills GB (2009) The biology of ovarian cancer: new opportunities for translation. Nature reviews 9(6):415–428\nCorrea RJ, Peart T, Valdes YR, DiMattia GE, Shepherd TG (2011) Modulation of AKT activity is associated with reversible dormancy in ascites-derived epithelial ovarian cancer spheroids. Carcinogenesis 33(1):49–58\nMeng Q, Xia C, Fang J, Rojanasakul Y, Jiang BH (2006) Role of PI3 K and AKT specific isoforms in ovarian cancer cell migration, invasion and proliferation through the p70S6K1 pathway. Cell Signal 18(12):2262–2271\nAhmed N, Thompson EW, Quinn MA (2007) Epithelial-mesenchymal interconversions in normal ovarian surface epithelium and ovarian carcinomas: an exception to the norm. J Cell Physiol 213(3):581–588\nTang MK, Zhou HY, Yam JW, Wong AS (2010) c-Met overexpression contributes to the acquired apoptotic resistance of nonadherent ovarian cancer cells through a cross talk mediated by phosphatidylinositol 3-kinase and extracellular signal-regulated kinase 1\u002F2. Neoplasia 12(2):128–138\nBalemans W, Van Hul W (2002) Extracellular regulation of BMP signaling in vertebrates: a cocktail of modulators. Dev Biol 250(2):231–250\nGoto K, Kamiya Y, Imamura T, Miyazono K, Miyazawa K (2007) Selective inhibitory effects of Smad6 on bone morphogenetic protein type I receptors. J Biol Chem 282(28):20603–20611\nItoh F, Asao H, Sugamura K, Heldin CH, ten Dijke P, Itoh S (2001) Promoting bone morphogenetic protein signaling through negative regulation of inhibitory Smads. EMBO J 20(15):4132–4142\nKamiya Y, Miyazono K, Miyazawa K (2010) Smad7 inhibits transforming growth factor-beta family type i receptors through two distinct modes of interaction. J Biol Chem 285(40):30804–30813\nCasey RC, Burleson KM, Skubitz KM, Pambuccian SE, Oegema TR Jr, Ruff LE, Skubitz AP (2001) Beta 1-integrins regulate the formation and adhesion of ovarian carcinoma multicellular spheroids. Am J Pathol 159(6):2071–2080\nKim YJ, Sauer C, Testa K, Wahl JK, Svoboda RA, Johnson KR, Wheelock MJ, Knudsen KA (2005) Modulating the strength of cadherin adhesion: evidence for a novel adhesion complex. J Cell Sci 118(Pt 17):3883–3894\nNapolitano AP, Chai P, Dean DM, Morgan JR (2007) Dynamics of the self-assembly of complex cellular aggregates on micromolded nonadhesive hydrogels. Tissue Eng 13(8):2087–2094\nTzanakakis ES, Hansen LK, Hu WS (2001) The role of actin filaments and microtubules in hepatocyte spheroid self-assembly. Cell Motil Cytoskeleton 48(3):175–189\nGamell C, Osses N, Bartrons R, Ruckle T, Camps M, Rosa JL, Ventura F (2008) BMP2 induction of actin cytoskeleton reorganization and cell migration requires PI3-kinase and Cdc42 activity. J Cell Sci 121(Pt 23):3960–3970\nBurleson KM, Boente MP, Pambuccian SE, Skubitz AP (2006) Disaggregation and invasion of ovarian carcinoma ascites spheroids. J Transl Med 4:6\nIwanicki M, Davidowitz R, Ng M, Besser A, Muranen T, Merritt M, Danuser G, Ince T, Brugge J (2011) Ovarian cancer spheroids use myosin-generated force to clear the mesothelium. Cancer Discov. doi:10.1158\u002F2159-8274.CD-11-0010\nDerynck R, Zhang YE (2003) Smad-dependent and Smad-independent pathways in TGF-beta family signalling. Nature 425(6958):577–584\nGuo X, Wang XF (2009) Signaling cross-talk between TGF-beta\u002FBMP and other pathways. Cell Res 19(1):71–88\nPerez VA, Ali Z, Alastalo TP, Ikeno F, Sawada H, Lai YJ, Kleisli T, Spiekerkoetter E, Qu X, Rubinos LH, Ashley E, Amieva M, Dedhar S, Rabinovitch M (2011) BMP promotes motility and represses growth of smooth muscle cells by activation of tandem Wnt pathways. J Cell Biol 192(1):171–188\nChen X, Liao J, Lu Y, Duan X, Sun W (2011) Activation of the PI3 K\u002FAkt pathway mediates bone morphogenetic protein 2-induced invasion of pancreatic cancer cells Panc-1. Pathol Oncol Res 17(2):257–261\nGraham TR, Odero-Marah VA, Chung LW, Agrawal KC, Davis R, Abdel-Mageed AB (2009) PI3 K\u002FAkt-dependent transcriptional regulation and activation of BMP-2-Smad signaling by NF-kappaB in metastatic prostate cancer cells. Prostate 69(2):168–180\nKang MH, Kang HN, Kim JL, Kim JS, Oh SC, Yoo YA (2009) Inhibition of PI3 kinase\u002FAkt pathway is required for BMP2-induced EMT and invasion. Oncol Rep 22(3):525–534\nKang MH, Kim JS, Seo JE, Oh SC, Yoo YA (2010) BMP2 accelerates the motility and invasiveness of gastric cancer cells via activation of the phosphatidylinositol 3-kinase (PI3 K)\u002FAkt pathway. Exp Cell Res 316(1):24–37\nLangenfeld EM, Kong Y, Langenfeld J (2005) Bone morphogenetic protein-2-induced transformation involves the activation of mammalian target of rapamycin. Mol Cancer Res 3(12):679–684\nDavidson B, Espina V, Steinberg SM, Florenes VA, Liotta LA, Kristensen GB, Trope CG, Berner A, Kohn EC (2006) Proteomic analysis of malignant ovarian cancer effusions as a tool for biologic and prognostic profiling. Clin Cancer Res 12(3 Pt 1):791–799\nSchilder RJ, Sill MW, Lee RB, Shaw TJ, Senterman MK, Klein-Szanto AJ, Miner Z, Vanderhyden BC (2008) Phase II evaluation of imatinib mesylate in the treatment of recurrent or persistent epithelial ovarian or primary peritoneal carcinoma: a Gynecologic Oncology Group Study. J Clin Oncol 26(20):3418–3425\nMassague J (2008) TGFbeta in Cancer. Cell 134(2):215–230",{"VOID":2336},"10.1007\u002Fs10585-011-9451-3","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10585-011-9451-3",[2339,2363,2385,2398,2436],{"id":2340,"sortIndex":32,"researcher":28,"roles":2341,"affiliations":2342,"properties":2360,"displayName":2362,"givenName":28,"familyName":28},"05522c6f-0dc7-4b13-bf86-e0138d088c2f",[1036],[2343,2351],{"id":2344,"sortIndex":32,"affiliation":2345,"properties":28},"b4d8bf3b-adcf-498a-8e27-d6650eb4b7c7",{"id":2344,"createTime":28,"updateTime":28,"relativeEntities":2346,"slug":28,"properties":2347,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2350,"statistic":28},[],{"title":2348},{"VI":2349},"Translational Ovarian Cancer Research Program, London Regional Cancer Program, London, Canada",[],{"id":2352,"sortIndex":40,"affiliation":2353,"properties":2359},"6c63cf6d-ff36-4998-b77c-b6e053ca733b",{"id":2352,"createTime":28,"updateTime":28,"relativeEntities":2354,"slug":28,"properties":2355,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2358,"statistic":28},[],{"title":2356},{"VI":2357},"Departments of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Canada",[],{},{"title":2361},{"VI":2362},"Teresa M. 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DiMattia",{"id":2437,"sortIndex":45,"researcher":28,"roles":2438,"affiliations":2439,"properties":2467,"displayName":2469,"givenName":28,"familyName":28},"d67b11ed-c9c2-43e9-b03d-66447b21e313",[1036],[2440,2446,2453,2460],{"id":2344,"sortIndex":32,"affiliation":2441,"properties":28},{"id":2344,"createTime":28,"updateTime":28,"relativeEntities":2442,"slug":28,"properties":2443,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2445,"statistic":28},[],{"title":2444},{"VI":2349},[],{"id":2352,"sortIndex":40,"affiliation":2447,"properties":2452},{"id":2352,"createTime":28,"updateTime":28,"relativeEntities":2448,"slug":28,"properties":2449,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2451,"statistic":28},[],{"title":2450},{"VI":2357},[],{},{"id":2416,"sortIndex":123,"affiliation":2454,"properties":2459},{"id":2416,"createTime":28,"updateTime":28,"relativeEntities":2455,"slug":28,"properties":2456,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2458,"statistic":28},[],{"title":2457},{"VI":2421},[],{},{"id":2425,"sortIndex":42,"affiliation":2461,"properties":2466},{"id":2425,"createTime":28,"updateTime":28,"relativeEntities":2462,"slug":28,"properties":2463,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2465,"statistic":28},[],{"title":2464},{"VI":2430},[],{},{"title":2468},{"VI":2469},"Trevor G. 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The purpose of this study is to investigate whether the detection of survivin-expressing CCC in the peripheral blood is also useful for predicting recurrence in patients with esophageal squamous cell carcinoma (ESCC). Blood samples obtained from 108 ESCC patients and 75 healthy volunteers were quantitatively investigated by a technique that detected reverse transcription-polymerase chain reaction products based on a hybridization-enzyme linked immunosorbent essay. Not all of the patients were available for the follow-up study. Only 48 patients who were treated with similar adjuvant therapy regimens were available and followed-up for 33 months after the initial assay test. Survivin-expressing CCC were detected in 51 (47.2%) patients. The presence of survivin-expressing CCC was found to be significantly associated with depth of invasion, vascular invasion, nodal status, and disease stages (P = 0.032, 0.019, 0.018, and 0.001, respectively). During the follow-up period, patients who had positive survivin expressions had a higher relapse rate and a shorter survival time than those who had negative survivin expressions (P = 0.002 and 0.016, respectively). Examination of survivin-expressing CCC could provide valuable information in the prediction of haematogenous recurrence as well as in the prognosis of ESCC.",{"EN":2537},"Detection of survivin-expressing circulating cancer cells in the peripheral blood of patients with esophageal squamous cell carcinoma and its clinical significance",{"VOID":2539},"Patel M, Ferry K, Franceschi D et al (2004) Esophageal carcinoma: current controversial topics. Cancer Invest 22:897–912. doi:10.1081\u002FCNV-200039672\nRoder JD, Stein HJ, Siewert JR (1995) Oesophageal carcinoma. In: Hermaneck P, Gospodarowicz MK, Henson DE (eds) Prognostic factors in cancer, UICC. Springer-Verlag, Berlin, p 37\nLee SJ, Lee KS, Yim YJ et al (2005) Recurrence of squamous cell carcinoma of the oesophagus after curative surgery: rates and patterns on imaging studies correlated with tumour location and pathological stage. Clin Radiol 60:547–554. doi:10.1016\u002Fj.crad.2004.09.002\nHuang P, Wang J, Guo Y et al (2003) Molecular detection of disseminated tumor cells in the peripheral blood in patients with gastrointestinal cancer. J Cancer Res Clin Oncol 129:192–198\nIkoma D, Ichikawa D, Ueda Y et al (2007) Circulating tumor cells and aberrant methylation as tumor markers in patients with esophageal cancer. Anticancer Res 27:535–539\nIto H, Kanda T, Nishimaki T et al (2004) Detection and quantification of circulating tumor cells in patients with esophageal cancer by real-time polymerase chain reaction. J Exp Clin Cancer Res 23:455–464\nKaganoi J, Shimada Y, Kano M et al (2004) Detection of circulating oesophageal squamous cancer cells in peripheral blood and its impact on prognosis. Br J Surg 91:1055–1060. doi:10.1002\u002Fbjs.4593\nKoike M, Hibi K, Kasai Y et al (2002) Molecular detection of circulating esophageal squamous cell cancer cells in the peripheral blood. Clin Cancer Res 8:2879–2882\nLiu Z, Jiang M, Zhao J et al (2007) Circulating tumor cells in preoperative esophageal cancer patients: quantitative assay system and potential clinical utility. Clin Cancer Res 13:2992–2997. doi:10.1158\u002F1078-0432.CCR-06-2072\nNakashima S, Natsugoe S, Matsumoto M et al (2003) Clinical significance of circulating tumor cells in blood by molecular detection and tumor markers in esophageal cancer. Surgery 133:162–169. doi:10.1067\u002Fmsy.2003.9\nChiou SK, Jones MK, Tarnawski AS (2003) Survivin–an anti-apoptosis protein: its biological roles and implications for cancer and beyond. Med Sci Monit 9:125–129\nAmbrosini G, Adida C, Altieri D (1997) A novel anti-apoptosis gene, survivin, expressed in cancer and lymphoma. Nat Med 3:917–921. doi:10.1038\u002Fnm0897-917\nGrabowski P, Kühnel T, Mühr-Wilkenshoff F et al (2003) Prognostic value of nuclear survivin expression in oesophageal squamous cell carcinoma. Br J Cancer 88:115–119. doi:10.1038\u002Fsj.bjc.6600696\nMega S, Miyamoto M, Li L et al (2006) Immunohistochemical analysis of nuclear survivin expression in esophageal squamous cell carcinoma. Dis Esophagus 19:355–359. doi:10.1111\u002Fj.1442-2050.2006.00604.x\nRosato A, Pivetta M, Parenti A et al (2006) Survivin in esophageal cancer: an accurate prognostic marker for squamous cell carcinoma but not adenocarcinoma. Int J Cancer 119:1717–1722. doi:10.1002\u002Fijc.21923\nYie SM, Luo B, Ye NY et al (2006) Detection of Survivin-expressing circulating cancer cells in the peripheral blood of breast cancer patients by a RT-PCR ELISA. Clin Exp Metastasis 23:279–289. doi:10.1007\u002Fs10585-006-9037-7\nYie SM, Lou B, Ye SR et al (2008) Detection of survivin-expressing circulating cancer cells (CCCs) in peripheral blood of patients with gastric and colorectal cancer reveals high risks of relapse. Ann Surg Oncol 15:3037–3082. doi:10.1245\u002Fs10434-008-0069-x\nYie SM, Lou B, Ye SR et al (2009) Clinical significance of detecting survivin-expressing circulating cancer cells in patients with non-small cell lung cancer. Lung Cancer 63:284–290. doi:10.1016\u002Fj.lungcan.2008.05.024\nWatanable H, Jass JR, Sobin LH (eds) (1990) Histological typing of esophageal and gastric tumors. Springer-Verlag, Berlin\nSobin H, Wittekind C (eds) (2002) UICC: TNM classification of malignant tumors, 6th edn. Wiley, New York\nYonenaga Y, Mori A, Onodera H et al (2005) Absence of smooth muscle actin-positive pericyte coverage of tumor vessels correlates with hematogenous metastasis and prognosis of colorectal cancer patients. Oncology 69:159–166\nMino-Miyagawa N, Kimura Y, Hamamoto K (1990) Tumor-antigen 4: its immunohistochemical distribution and tissue and serum concentrations in squamous cell carcinoma of the lung and esophagus. Cancer 66:1505–1512. doi:10.1002\u002F1097-0142(19901001)66:7\u003C1505::AID-CNCR2820660712>3.0.CO;2-V\nKatayama A, Mafune K, Tanaka Y et al (2003) Autopsy findings in patients after curative esophagectomy for esophageal carcinoma. J Am Coll Surg 196:866–873. doi:10.1016\u002FS1072-7515(03)00116-9\nJiao X, Krasna MJ (2002) Clinical significance of micrometastasis in lung and esophageal cancer: a new paradigm in thoracic oncology. Ann Thorac Surg 74:278–284. doi:10.1016\u002FS0003-4975(01)03376-8\nMehes G, Witt A, Kubista E et al (2001) Circulating breast cancer cells are frequently apoptotic. Am J Pathol 159:17–20\nBrablets T, Jung A, Spaderna S et al (2005) Migrating cancer stem cells-an integrated concept of malignant tumour progression. Nat Rev Cancer 5:744–749. doi:10.1038\u002Fnrc1694\nZhang T, Otevrel T, Gao ZQ et al (2001) Evidence that APC regulates survivin expression: a possible mechanism contributing to the stem cell origin of colon cancer. Cancer Res 61:8664–8667\nMoriai R, Asanuma K, Kobayashi D et al (2001) Quantitative analysis of the anti-apoptotic gene survivin expression in malignant haematopoietic cells. Anticancer Res 21:595–600\nTorre GC (1998) SCC antigen in malignant and nonmalignant squamous lesions. Tumour Biol 19:517–526. doi:10.1159\u002F000030045",{"VOID":2541},"10.1007\u002Fs10585-009-9274-7","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10585-009-9274-7",[2544,2559,2581,2594,2609,2622,2635,2648,2663,2676,2689],{"id":2545,"sortIndex":32,"researcher":28,"roles":2546,"affiliations":2547,"properties":2556,"displayName":2558,"givenName":28,"familyName":28},"8c273ff3-62c1-4e41-a7f0-cabeb3254b78",[1036],[2548],{"id":2549,"sortIndex":32,"affiliation":2550,"properties":28},"af37d72f-2769-47e5-993a-eb2a7526f565",{"id":2549,"createTime":28,"updateTime":28,"relativeEntities":2551,"slug":28,"properties":2552,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2555,"statistic":28},[],{"title":2553},{"VI":2554},"Core Laboratory, Sichuan Academy of Medical Sciences, Sichuan Provincial People’s Hospital, Chengdu, People’s Republic of China",[],{"title":2557},{"VI":2558},"Mei 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effects of treatment of human lung carcinoma cell line A 549 with recombinant DNA-derived human leukocyte interferons A (rIFN-αA) or D (rIFN-αD), and human lymphoblastoid interferon (Wellferon) onin vitro cell invasion were investigated in a quantitative invasion assay using human amnion. The A 549 cells treated with IFN for one day were incubated on the denuded basement membrane of the amnion in the absence of IFN, and cells which penetrated the full thickness of the connective tissue barrier were measured after 4 days. A dose-dependent inhibition of cell invasion was produced by the recombinant IFNs.The one day treatment of cells with 2·4 × 103 to 1·8 × 104 units\u002Fml of rIFN-αA resulted in a 60–80 per cent inhibition of invasiveness compared to untreated cells. After a one day exposure of cells to 2·2 × 104 units\u002Fml of rIFN-αD, cell invasion was reduced by approximately 70 per cent; a concentration of 4·4 × 103 units\u002Fml had no apparent effect. Similar treatment with lymphoblastoid IFN (6 × 104 units\u002Fml) had no significant effect on cell invasion. Accompanying the one day exposure to rIFN-αA (1·8 × 104 units\u002Fml) or rIFN-αD (2·2 × 104 units\u002Fml), (2′, 5′) oligo (A) synthetase activity was induced approximately 20-fold; a 4-fold induction of enzyme activity was found in cells exposed to lymphoblastoid IFN (6 × 104 units\u002Fml). After exposure of A 549 cells to the three IFNs at these concentrations, no significant alteration of the ability of the cells to attach to the basement membrane was found. Moreover, none of the one day IFN treatment regimens were cytocidal, and cell proliferation ability was not affected. This model system may be useful for investigating anti-invasive activity of other IFN types and subtypes.","Các tác động của việc điều trị dòng tế bào ung thư phổi người A 549 bằng interferon bạch cầu người tái tổ hợp A (rIFN-αA) hoặc D (rIFN-αD), và interferon lymphoblastoid người (Wellferon) đối với khả năng xâm lấn tế bào in vitro đã được khảo sát trong một bài kiểm tra xâm lấn định lượng sử dụng màng ối người. Các tế bào A 549 được điều trị bằng IFN trong một ngày đã được nuôi cấy trên màng đáy đã được làm trần của màng ối trong điều kiện không có IFN, và số tế bào xâm nhập qua toàn bộ độ dày của rào cản mô liên kết đã được đo sau 4 ngày. Việc sử dụng IFNs tái tổ hợp đã tạo ra sự ức chế khả năng xâm lấn tế bào theo liều lượng. Việc điều trị tế bào với 2·4 × 10^3 đến 1·8 × 10^4 đơn vị\u002Fml rIFN-αA trong một ngày đã dẫn đến sự ức chế 60-80% khả năng xâm lấn so với các tế bào không được điều trị. Sau khi tế bào được tiếp xúc một ngày với 2·2 × 10^4 đơn vị\u002Fml rIFN-αD, khả năng xâm lấn của tế bào giảm khoảng 70%; một nồng độ 4·4 × 10^3 đơn vị\u002Fml không có tác động rõ rệt. Việc điều trị tương tự với IFN lymphoblastoid (6 × 10^4 đơn vị\u002Fml) không có hiệu ứng đáng kể trên khả năng xâm lấn tế bào. Kèm theo việc tiếp xúc một ngày với rIFN-αA (1·8 × 10^4 đơn vị\u002Fml) hoặc rIFN-αD (2·2 × 10^4 đơn vị\u002Fml), hoạt động của oligo (A) synthetase (2′, 5′) đã được kích thích khoảng 20 lần; một sự kích thích 4 lần của hoạt động enzyme đã được tìm thấy trong các tế bào tiếp xúc với IFN lymphoblastoid (6 × 10^4 đơn vị\u002Fml). Sau khi tiếp xúc tế bào A 549 với ba loại IFNs ở các nồng độ này, không tìm thấy sự thay đổi đáng kể nào về khả năng gắn kết của các tế bào với màng đáy. Hơn nữa, không có chế độ điều trị IFN nào trong một ngày gây chết tế bào, và khả năng sinh sản của tế bào không bị ảnh hưởng. Hệ thống mô hình này có thể hữu ích trong việc nghiên cứu hoạt động chống xâm lấn của các loại và phân loại IFN khác.",{"EN":2772,"VI":2773},"Treatment with human recombinant leukocyte interferons inhibitsin vitro invasive ability of human lung carcinoma cells","Điều trị bằng interferon bạch cầu người tái tổ hợp ức chế khả năng xâm lấn in vitro của tế bào ung thư phổi người",{"VI":1734},{"VOID":2776},"Aguet, M., Gröbke, M., and Dreiding, P., 1984, Various human interferon a subclasses cross-react with common receptors: their binding affinities correlate with their specific biological activities.Virology, 132, 211–216.\nBaron, S., 1966, The biological significance of the interferon system.Interferons, edited by N. Finter (Amsterdam: North-Holland), pp. 291–292.\nBernacki, R. J., Niedbala, M. 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W., 1981, The structure of eight distinct cloned human leukocyte interferon cDNAs.Nature, 290, 20–26.\nGoeddel, D. V., Yelverton, E., Ullrich, A., Heynecker, H. L., Miozzari, G., Holmes, W., Seeburg, P. H., Dull, T., May, L., Stebbing, N., Crea, R., Moada, S., Candliss, R. M., Sloma, A., Tabor, J. M., Gross, M., Familletti, P. C., and Pestka, S., 1980, Human leukocyte interferon produced byE. coli is biologically active.Nature, 287, 411–415.\nGreen, J. A., Cooperband, S. R., and Kibrick, S., 1969, Immune specific induction of interferon production in cultures of human blood lymphocytes.Science, 164, 1415–1417.\nGrossberg, J. E., and Taylor, J. L., 1984, Interferon effects on cell differentiation.Interferon, Volume 3: Mechanisms of Production and Action, edited by N. B. Finter and R. M. Friedman (Amsterdam: Elsevier), pp. 299–317.\nHill, N. O., 1984, Background to human interferon.Recombinant DNA Products: Insulin, Interferon and Growth Hormone, edited by A. P. Bollan (Boca Raton, Florida: CRC Press), pp. 67–74.\nJones, P. A., and Declerck, Y. A., 1980, Destruction of extracellular matrices containing glycoproteins, elastin and collagen by metastatic human tumor cells.Cancer Research, 40, 3222–3231.\nKimchi, A., Shure, H., and Revel, M., 1979, Regulation of lymphocyte mitogenesis by (2′–5′) oligo-isoadenylate.Nature, 282, 849–851.\nKirkwood, J. M., and Ernstoff, M. S., 1984, Interferons in the treatment of human cancer.Journal of Clinical Oncology, 2, 336–352.\nKrim, M., 1980, Towards therapy with interferons. Part 1. Interferons: production and properties.Blood, 55, 875–884.\nLaszlo, J., Huang, A. T., Brenckman, W. D., Jeffs, C., Koren, H., Cianciolo, G., Metzgar, R., Cashdollar, W., Cox, E., Buckley, III, C. E., Tso, C. Y., and Lucas, Jr, V. S., 1983, Phase I study of pharmacological and immunological effects of human lymphoblastoid interferon given to patients with cancer.Cancer Research, 43, 4458–4466.\nLiotta, L. A., Garbisa, S., and Tryggvason, K., 1982, Biochemical mechanisms involved in tumor cell penetration of the basement membrane.Tumor Invasion and Metastasis, edited by L. A. Liotta and I. R. Hart (The Hague: Martinus Nijhoff), pp. 319–333.\nLiotta, L. A., Rao, C. N., and Barsky, S. H., 1983, Tumor invasion and the extracellular matrix.Laboratory Investigation, 49, 636–649.\nLiotta, L. A., Tryggvason, K., Garbisa, S., Hart, I., Foltz, C. M., and Shafie, S., 1980, Metastatic potential correlates with enzymatic degradation of basement membrane collagen.Nature, 284, 67–68.\nLowry, O. H., Rosebrough, N. J., Farr, A. L., and Randall, R. J., 1951, Protein measurement with the Folin phenol reagent,Journal of Biological Chemistry, 193, 265–275.\nMasucci, M. G., Szigeti, R., Klein, E., Klein, G., Gruest, J., Montagnier, L., Taira, H., Hall, A., Nagata, S., and Weissmann, C., 1980, Effect of interferon α 1 fromE. coli on some cell functions.Science, 209, 1431–1435.\nMerlin, G., Revel, M., and Wallbach, D., 1981, The interferon-induced enzymes oligoisoadenylate synthetase: rapid determination of itsin vitro products.Analytical Biochemistry, 110, 190–196.\nNagata, S., Mantel, N., and Weissmann, C., 1980a, The structure of one of the eight or more distinct chromosomal genes for human interferon-α.Nature, 287, 401–408.\nNagata, S., Taira, H., Hall, A., Johnsrud, I., Streuli, M., Ecdosi, J., Boll, W., Cantell, K., and Weissmann, C., 1980b, Synthesis inE. coli of a polypeptide with human leukocyte activity.Nature, 284, 316–320.\nNakajima, M., Custead, S. E., Welch, D. R., and Nicolson, G. L., 1984, Type IV collagenolysis: Relation to metastatic properties of rat 13762 mammary adenocarcinoma metastatic cell clones.American Association for Cancer Research Proceedings, 244, 162.\nNicolson, G. L., 1982, Metastatic tumor cell attachment and invasion assay utilizing vascular endothelial cell monolayers.Journal of Histochemistry and Cytochemistry, 30, 214–220.\nRusso, R. G., Foltz, C. M., and Liotta, L. A., 1983, New invasion assay using endothelial cells grown on native human basement membrane.Clinical and Experimental Metastasis, 1, 115–127.\nRusso, R. G., Thorgeirsson, U., and Liotta, L. A., 1982,In vitro quantitative assay of invasion using human amnion.Tumor Invasion and Metastases, edited by L. A. Liotta and I. R. Hart (The Hague: Martinus Nijhoff), pp. 173–187.\nSiegal, G. P., Thorgeirsson, U. P., Russo, R. G., Wallace, D. M., Liotta, L. A., and Berger, S. L., 1982, Interferon enhancement of the invasive capacity of Ewing sarcoma cells in vitro.Proceedings of the National Academy of Sciences, U.S.A., 79, 4064–4068.\nStewart, W. E., Blalock, J. E., Burke, D. C., Chany, C., Dunnick, J. F., Falcoff, E., Friedman, R. M., Galasso, G. J., Joklik, W. K., Vilcek, J. T., Youngner, J. S., and Zoon, K. C., 1980, Interferon nomenclature.Nature, 286, 110.\nThorgeirsson, U. P., Liotta, L. A., Kalebic, T., Margulies, I. M., Thomas, K., Rios-Candelore, M., and Russo, R. G., 1982, Effect of natural protease inhibitors and a chemoattractant on tumor cell invasionin vitro.Journal of the National Cancer Institute, 69, 1049–1054.\nThorgeirsson, U. P., Turpeenniemi-Hujanen, T., Neckers, L. M., Johnson, D. W., and Liotta, L. A., 1984, Protein synthesis but not DNA synthesis is required for tumor cell invasionin vitro.Invasion Metastasis, 4, 73–83.\nWilliams, B. R. G., Golgher, R. R., and Kerr, I. 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M., 1978, Inhibition of protein synthesis by 2′–5′ linked adenine oligonucleotides in intact cells.Nature, 276, 88–89.",{"VOID":2778},"10.1007\u002FBF00117932","2025-02-05T18:20:59.658+00:00",[30],"http:\u002F\u002Flink.springer.com\u002F10.1007\u002FBF00117932",[2783,2798],{"id":2784,"sortIndex":32,"researcher":28,"roles":2785,"affiliations":2786,"properties":2795,"displayName":2797,"givenName":28,"familyName":28},"30b03bfe-491f-41ae-a49c-b012ffdacaaa",[1036],[2787],{"id":2788,"sortIndex":32,"affiliation":2789,"properties":28},"364fe91f-96a7-4567-ae2a-777c9e5ff12f",{"id":2788,"createTime":28,"updateTime":28,"relativeEntities":2790,"slug":28,"properties":2791,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2794,"statistic":28},[],{"title":2792},{"VI":2793},"Department of Biology, University of Akron, Akron, U.S.A.",[],{"title":2796},{"VI":2797},"Terrence J. Ravine",{"id":2799,"sortIndex":40,"researcher":28,"roles":2800,"affiliations":2801,"properties":2808,"displayName":2810,"givenName":28,"familyName":28},"5a460a0b-37ca-4cee-9865-c895eb1ae29c",[1036],[2802],{"id":2788,"sortIndex":32,"affiliation":2803,"properties":28},{"id":2788,"createTime":28,"updateTime":28,"relativeEntities":2804,"slug":28,"properties":2805,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2807,"statistic":28},[],{"title":2806},{"VI":2793},[],{"title":2809},{"VI":2810},"Nada Ledinko",{"url":2781,"publisher":2812,"properties":2862},{"id":868,"createTime":869,"updateTime":870,"relativeEntities":2813,"slug":872,"properties":2814,"entityType":25,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"subjectFields":2818,"manageAffiliations":2831,"indexDatabases":2842,"url":28,"thumbnailPath":28,"statistic":2857,"gsStatistic":28,"type":28,"analyzePriority":28},[],{"issn":2815,"title":2816,"eissn":2817},{"VOID":875},{"EN":877},{"VOID":879},[2819,2823,2827],{"id":883,"createTime":28,"updateTime":28,"relativeEntities":2820,"label":2821,"description":2822,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":886},{},{"id":889,"createTime":28,"updateTime":28,"relativeEntities":2824,"label":2825,"description":2826,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":892},{},{"id":895,"createTime":28,"updateTime":28,"relativeEntities":2828,"label":2829,"description":2830,"parentId":28,"standard":28,"scholarHubFieldId":28},[],{"EN":898},{},[2832,2837],{"id":902,"createTime":28,"updateTime":28,"relativeEntities":2833,"slug":28,"properties":2834,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2836,"statistic":28},[],{"title":2835},{"EN":906},[908],{"id":910,"createTime":28,"updateTime":28,"relativeEntities":2838,"slug":28,"properties":2839,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2841,"statistic":28},[],{"title":2840},{"EN":914},[],[2843,2850],{"id":918,"indexDatabase":2844,"url":924,"indexYears":925,"academicFieldIds":2849,"indexDatabaseRanking":930},{"id":775,"createTime":28,"updateTime":28,"relativeEntities":2845,"label":2846,"description":2847,"key":781,"publicationTags":2848,"standard":28},[],{"EN":778,"VI":778},{"EN":778,"VI":780},[783],[927,928,929],{"id":932,"indexDatabase":2851,"url":944,"indexYears":28,"academicFieldIds":2856,"indexDatabaseRanking":28},{"id":934,"createTime":28,"updateTime":28,"relativeEntities":2852,"label":2853,"description":2854,"key":941,"publicationTags":2855,"standard":28},[],{"EN":937,"VI":937},{"EN":939,"VI":940},[943,813],[946],{"impactFactor":32,"impactFactorByYear":2858,"i10Index":953,"i10IndexLast5Year":199,"totalPublication":954,"totalPublicationByYear":2859,"totalCitation":956,"totalCitationByYear":2860,"totalCitationPerPublication":977,"totalCitationPerPublicationByYear":2861,"hindexLast5Year":200,"hindex":200},{"2012":173,"2013":438,"2014":341,"2015":695,"2016":949,"2017":950,"2018":696,"2019":319,"2020":951,"2021":705,"2022":346,"2023":952},{"1983":147,"1984":134,"1985":128,"1986":135,"1987":130,"1988":139,"1989":142,"1990":202,"1991":133,"1992":281,"1993":141,"1994":148,"1995":150,"1996":516,"1997":139,"1998":280,"1999":564,"2000":325,"2002":689,"2003":207,"2004":137,"2005":50,"2006":278,"2007":162,"2008":560,"2009":434,"2010":196,"2011":206,"2012":332,"2013":436,"2014":149,"2015":206,"2016":142,"2017":131,"2018":206,"2019":196,"2020":141,"2021":149,"2022":201,"2023":202,"2024":135},{"1983":611,"1984":132,"1985":280,"1986":201,"1987":131,"1988":958,"1989":959,"1990":148,"1991":565,"1992":960,"1993":961,"1994":962,"1995":684,"1996":963,"1998":358,"2003":612,"2004":964,"2005":965,"2006":966,"2007":563,"2008":967,"2009":968,"2010":969,"2011":970,"2012":971,"2013":972,"2014":973,"2015":974,"2016":962,"2017":49,"2018":359,"2019":975,"2020":522,"2021":140,"2022":976,"2023":45},{"1983":979,"1984":980,"1985":981,"1986":185,"1987":982,"1988":983,"1989":984,"1990":985,"1991":986,"1992":987,"1993":988,"1994":989,"1995":990,"1996":991,"1998":442,"2003":992,"2004":993,"2005":994,"2006":995,"2007":996,"2008":997,"2009":998,"2010":999,"2011":1000,"2012":1001,"2013":1002,"2014":1003,"2015":1004,"2016":1005,"2017":320,"2018":1006,"2019":1007,"2020":1008,"2021":424,"2022":1009,"2023":104},{"pages":2863,"volume":2865},{"VOID":2864},"191-203",{"VOID":2866},"4","1986-07-01",1986,[943,930],{"id":2871,"createTime":2872,"updateTime":2872,"relativeEntities":2873,"slug":28,"properties":2874,"entityType":1028,"verifyStatus":880,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":32,"primaryUrl":2883,"fullTextUrl":28,"authors":2884,"publicationType":1064,"publisherRelationship":2913,"citationCount":28,"citationInfo":28,"publishDate":2969,"publishYear":2970,"citationAnalyzeStatus":880,"lastCitationAnalyze":28,"indexDatabases":2971,"openAccess":28,"references":28,"isForceReanalyzing":1126},"013067de-5f26-4389-b6a1-94e5189def19","2024-01-19T22:50:07.223+00:00",[],{"abstract":2875,"title":2877,"references":2879,"doi":2881},{"EN":2876},"Temporal and quantitative aspects of lymphogenous and hematogenous metastasis were examined using the rat MT-100-TC mammary carcinoma injected into the hind feet of syngeneic rats. Metastases first appeared in the draining popliteal nodes and then progressed in an invariable pattern to regional and then distal nodes: ‘skipped’ negative nodes within a chain of positive nodes were not observed. Metastatic progression in the lymphatic system occurred metachronously, with nodal metastases acting as ‘generalizing’ sites for ‘downstream’ nodes. Perturbation of lymph flow was apparent when nodes were involved with tumor, and resulted in retrograde seeding of contralateral nodes. Lung involvement was first observed by ectopic bioassay in 50 per cent of animals after 1 and 2 weeks of primary tumor growth; in contrast, all animals had popliteal involvement after 1 week. These results indicate that lymph nodes and lungs are not seeded synchronously, and the lungs are seeded after nodal metastases. Thus, a phase of metastasis has been identified, during which resection of the primary tumor and local nodes may well be curative in the 50 per cent of cases in which the disease is confined to these sites.",{"EN":2878},"The relationship between lymphogenous and hematogenous metastasis in rats bearing the MT-100-TC mammary carcinoma",{"VOID":2880},"Balch, C. M., 1988, The role of elective lymph node dissection in melanoma: rationale, results, and controversies.Journal of Clinical Oncology,6, 163–172.\nCarr, J., Carr, I., Dreher, B., andFranks, C. R., 1979, Lymphatic metastasis of tumour: persistent transport of cells.Experientia,35, 825–826.\nDixon, B., andBagnall, D. A., 1986, The pattern and timing of lymphatic metastasis of the rat carcinoma LMC.Clinical and Experimental Metastasis,4, 117–128.\nFinlay-Jones, J. J., Bartholomaeus, W. N., Fimmel, P. J., Keast, D., andStanley, N. F., 1980, Biologic and immunologic studies on a murine model of regional lymph node metastasis.Journal of National Cancer Institute,64, 1363–1372.\nGlaves, D., 1983, Correlation between circulating cancer cells and incidence of metastases.British Journal of Cancer,48, 665–673.\nGhosh, S., Roholt, O. A., andKim, U., 1983, Establishment of two nonmetastasizing and one metastasizing rat mammary carcinoma cell lines.In Vitro,19, 919–928.\nHaagensen, C. D., Feind, C. R., Herter, F. P., Slanetz, C. A., andWeinberg, J. A., 1972,The Lymphatics in Cancer (Philadelphia: W. B. Saunders), pp. 231–242.\nHewitt, H. B., andBlake, E. R., 1977, Further studies of the relationship between lymphatic dissemination and lymphnodal metastasis in non-immunogenic murine tumours.British Journal of Cancer,35, 415–419.\nKurokawa, Y., 1970, Experiments on lymph node metastasis by intralymphatic inoculation of rat ascites tumor cells, with special reference to lodgement, passage, and growth of tumor cells in lymph nodes.Gann,61, 461–471.\nNicolson, G. L., 1988, Organ specificity of tumor metastasis: role of preferential adhesion, invasion and growth of malignant cells at specific secondary sites.Cancer and Metastasis Reviews,7, 143–188.\nTsuruo, T., Naganuma, K., Yamori, T., Kawabata, H., Oh-Hara, T., Iida, H., Tsukagoshi, S., andSakurai, H. 1984, Spontaneous metastasis of highly metastatic variants of mouse tumors and the effect of drugs on the metastasis.Gann,75, 557–563.\nVeronesi, U., Rilke, F., Luini, A., Sacchini, V., Galimberti, V., Campa, T., Bei, E. D., Greco, M., Magni, A., Merson, M., andQuagiuolo, V., 1987, Distribution of axillary node metastases by level of invasion: an analysis of 539 cases.Cancer,59, 682–687.\nWeiss, L.,Principles of Metastasis (New York: Academic Press), pp. 163–199.\nWeiss, L. Gilbert, H. A., andBallon, S. C. (Editors), 1980,Lymphatic System Metastasis (Boston: G. K. Hall).\nWeiss, L., andWard, P. M., 1987, Lymphogenous and hematogenous metastasis of Lewis lung carcinoma in the mouse.International Journal of Cancer,40, 570–574.\nWeiss, L., Ward, P. M., Harlos, J. P., andHolmes, J. C., 1984, Target organ patterns of tumors in mice following the arterial dissemination of B16 melanoma cells.International Journal of Cancer,33, 825–830.\nWillis, R. A., 1952,The Spread of Tumours in the Human Body (London: Butterworth), pp. 169–170.\nWillis, R. A., 1952,The Spread of Tumours in the Human Body (London: Butterworth) pp. 24–26.\nZeidman, I., 1959, Experimental studies on the spread of cancer in the lymphatic system. IV. Retrograde spread.Cancer Research,19, 1114–1117.",{"VOID":2882},"10.1007\u002FBF01753678","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF01753678",[2885,2900],{"id":2886,"sortIndex":32,"researcher":28,"roles":2887,"affiliations":2888,"properties":2897,"displayName":2899,"givenName":28,"familyName":28},"6fbddbfb-44a7-42c9-b4be-1b9a5ee8dcdc",[1036],[2889],{"id":2890,"sortIndex":32,"affiliation":2891,"properties":28},"04671cb0-0b8d-4558-9c31-9967e89e7033",{"id":2890,"createTime":28,"updateTime":28,"relativeEntities":2892,"slug":28,"properties":2893,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2896,"statistic":28},[],{"title":2894},{"VI":2895},"Department of Experimental Pathology, Roswell Park Memorial Institute, Buffalo, USA",[],{"title":2898},{"VI":2899},"Pamela M. 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