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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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MRI cannot distinguish between radiation necrosis and tumor progression; however, this distinction is critical in the assessment of tumor response to therapy. In this study, one delayed radiation necrosis model (dose, 40 Gy; radiation field, 10 × 10 mm2; n = 13) and two orthotopic glioma models in rats (9L gliosarcoma, n =8; human glioma xenografts, n = 5) were compared using multiple diffusion tensor imaging (DTI) indices. A visible isotropic apparent diffusion coefficient (ADC) pattern was observed in the lesion due to radiation necrosis, which consisted of a hypointense central zone and a hyperintense peripheral zone. There were significantly lower ADC, parallel diffusivity, and perpendicular diffusivity in the necrotic central zone than in the peripheral zone (all P \u003C 0.001). When radiation-induced necrosis was compared with viable tumor, radiation necrosis had significantly lower ADC than 9L gliosarcoma and human glioma xenografts (both P \u003C 0.01) in the central zone, and significantly lower fractional anisotropy than 9L gliosarcoma (P = 0.005) and human glioma xenografts (P = 0.012) in the peripheral zone. Histological analysis revealed parenchymal coagulative necrosis in the central zone, and damaged vessels and reactive astrogliosis in the peripheral zone. These data suggest that qualitative and quantitative analysis of the DTI maps can provide useful information by which to distinguish between radiation necrosis and viable glioma.",{"EN":1052},"Evaluation of radiation necrosis and malignant glioma in rat models using diffusion tensor MR imaging",{"VOID":1054},"Wen PY, Kesari S (2008) Malignant gliomas in adults. N Engl J Med 359:492–507\nStupp R, Mason WP, van den Bent MJ, Weller M, Fisher B, Taphoorn MJB, Belanger K, Brandes AA, Marosi C, Bogdahn U, Curschmann J, Janzer RC, Ludwin SK, Gorlia T, Allgeier A, Lacombe D, Cairncross JG, Eisenhauer E, Mirimanoff RO (2005) Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med 352:987–996\nMullins ME, Barest GD, Schaefer PW, Hochberg FH, Gonzalez RG, Lev MH (2005) Radiation necrosis versus glioma recurrence: conventional MR imaging clues to diagnosis. AJNR Am J Neuroradiol 26:1967–1972\nButowski NA, Sneed PK, Chang S (2006) Diagnosis and treatment of recurrent high-grade astrocytoma. J Clin Oncol 24:1273–1280\nJain R, Narang J, Sundgren PM, Hearshen D, Saksena S, Rock JP, Gutierrez J, Mikkelsen T (2010) Treatment induced necrosis versus recurrent\u002Fprogressing brain tumor: going beyond the boundaries of conventional morphologic imaging. J Neuro Oncol 100:17–29\nRogers LR, Gutierrez J, Scarpace L, Schultz L, Ryu S, Lord B, Movsas B, Honsowetz J, Jain R (2011) Morphologic magnetic resonance imaging features of therapy-induced cerebral necrosis. J Neuro Oncol 101:25–32\nGraves EE, Nelson SJ, Vigneron DB, Verhey L, McDermott M, Larson D, Chang S, Prados MD, Dillon WP (2001) Serial proton MR spectroscopic imaging of recurrent malignant gliomas after gamma knife radiosurgery. AJNR Am J Neuroradiol 22:613–624\nBarajas RF, Chang JS, Sneed PK, Segal MR, McDermott MW, Cha S (2009) Distinguishing recurrent intra-axial metastatic tumor from radiation necrosis following gamma knife radiosurgery using dynamic susceptibility-weighted contrast-enhanced perfusion MR imaging. AJNR Am J Neuroradiol 30:367–372\nMitsuya K, Nakasu Y, Horiguchi S, Harada H, Nishimura T, Bando E, Okawa H, Furukawa Y, Hirai T, Endo M (2010) Perfusion weighted magnetic resonance imaging to distinguish the recurrence of metastatic brain tumors from radiation necrosis after stereotactic radiosurgery. J Neuro Oncol 99:81–88\nZhou J, Tryggestad E, Wen Z, Lal B, Zhou T, Grossman R, Wang S, Yan K, Fu DX, Ford E, Tyler B, Blakeley J, Laterra J, van Zijl PC (2011) Differentiation between glioma and radiation necrosis using molecular magnetic resonance imaging of endogenous proteins and peptides. Nat Med 17:130–134\nArbab AS, Janic B, Jafari-Khouzani K, Iskander AS, Kumar S, Varma NR, Knight RA, Soltanian-Zadeh H, Brown SL, Frank JA (2010) Differentiation of glioma and radiation injury in rats using in vitro produce magnetically labeled cytotoxic T-cells and MRI. PLoS One 5:e9365\nSinha S, Bastin ME, Whittle IR, Wardlaw JM (2002) Diffusion tensor MR imaging of high-grade cerebral gliomas. AJNR Am J Neuroradiol 23:520–527\nMori S, Frederiksen K, van Zijl PC, Stieltjes B, Kraut MA, Solaiyappan M, Pomper MG (2002) Brain white matter anatomy of tumor patients evaluated with diffusion tensor imaging. Annu Neurol 51:377–380\nHuang H, Zhang J, Wakana S, Zhang W, Ren T, Richards LJ, Yarowsky P, Donohue P, Graham E, van Zijl PCM, Mori S (2006) White and gray matter development in human fetal, newborn and pediatric brains. Neuroimage 33:27–38\nWang SL, Wu EX, Qiu DQ, Leung LHT, Lau HF, Khong PL (2009) Longitudinal diffusion tensor magnetic resonance imaging study of radiation-induced white matter damage in a rat model. Cancer Res 69:1190–1198\nChan KC, Khong PL, Cheung MM, Wang SL, Cai KX, Wu EX (2009) MRI of late microstructural and metabolic alterations in radiation-induced brain injuries. J Magn Reson Imaging 29:1013–1020\nZhang J, van Zijl PCM, Laterra J, Salhotra A, Lal B, Mori S, Zhou J (2007) Unique patterns of diffusion directionality in rat brain tumors revealed by high-resolution diffusion tensor MRI. Magn Reson Med 58:454–462\nKim S, Pickup S, Hsu O, Poptani H (2008) Diffusion tensor MRI in rat models of invasion and well-demarcated brain tumors. NMR Biomed 21:208–216\nAsanuma T, Doblas S, Tesiram YA, Saunders D, Cranford R, Pearson J, Abbott A, Smith N, Towner RA (2008) Diffusion tensor imaging and fiber tractography of C6 rat glioma. J Magn Reson Imaging 28:566–573\nLope-Piedrafita S, Garcia-Martin ML, Galons J-P, Gillies RJ, Trouard TP (2008) Longitudinal diffusion tensor imaging in a rat brain glioma model. NMR Biomed 21:799–808\nSarkaria JN, Carlson BL, Schroeder MA, Grogan P, Brown PD, Giannini C, Ballman KV, Kitange GJ, Guha A, Pandita A, James CD (2006) Use of an orthotopic xenograft model for assessing the effect of epidermal growth factor receptor amplification on glioblastoma radiation response. Clin Cancer Res 12:2264–2271\nSalhotra A, Lal B, Laterra J, Sun PZ, van Zijl PCM, Zhou J (2008) Amide proton transfer imaging of 9L gliosarcoma and human glioblastoma xenografts. NMR Biomed 21:489–497\nWong J, Armour E, Kazanzides P, Iordachita U, Tryggestad E, Deng H, Matinfar M, Kennedy C, Liu Z, Chan T, Gray O, Verhaegen F, McNutt T, Ford E, DeWeese TL (2008) High-resolution, small animal radiation research platform with X-ray tomographic guidance capabilities. Int J Rad Oncol Biol Phys 71:1591–1599\nKennedy AS, Archambeau JO, Archambeau M-H, Holshouser B, Thompson J, Moyers M, Hinshaw D, Slater JM (1995) Magnetic resonance imaging as a monitor of changes in the irradiated rat brain. An aid in determining the time course of events in a histologic study. Invest Radiol 30:214–220\nJiang H, van Zijl PC, Kim J, Pearlson GD, Mori S (2006) DtiStudio: resource program for diffusion tensor computation and fiber bundle tracking. Comput Methods Programs Biomed 81:106–116\nBurger PC, Dubois PJ, Schold SCJ, Smith KRJ, Odom GL, Crafts DC, Giangaspero F (1983) Computerized tomographic and pathologic studies of the untreated, quiescent, and recurrent glioblastoma multiforme. J Neurosurg 58:159–169\nBeppu T, Inoue T, Shibata T, Kurose AHA, Ogasawara K, Ogawa A, Nakamura S, Kabasawa H (2003) Measurement of fractional anisotropy using diffusion tensor MRI in supratentorial astrocytic tumors. J Neuro Oncol 63:109–116\nBeppu T, Inoue T, Shibata Y, Yamada N, Kurose A, Ogasawara K, Ogawa A, Kabasawa H (2005) Fractional anisotropy value by diffusion tensor magnetic resonance imaging as a predictor of cell density and proliferation activity of glioblastomas. Surg Neurol 63:56–61\nKinoshita M, Hashimoto N, Goto T, Kagawa N, Kishima H, Izumoto S, Tanaka H, Fujita N, Yoshimine T (2008) Fractional anisotropy and tumor cell density of the tumor core show positive correlation in diffusion tensor magnetic resonance imaging of malignant brain tumors. Neuroimage 43:29–35\nYang I, Aghi MK (2009) New advances that enable identification of glioblastoma recurrence. Nat Rev Clin Oncol 6:648–657\nSundgren PC, Fan X, Weybright P, Welsh RC, Carlos RC, Petrou M, McKeever PE, Chenevert TL (2006) Differentiation of recurrent brain tumor versus radiation injury using diffusion tensor imaging in patients with new contrast-enhancing lesions. J Magn Reson Imaging 24:1131–1142\nWang SL, Wu EX, Tam CN, Lau HF, Cheung PT, Khong PL (2008) Characterization of white matter injury in a hypoxic-ischemic neonatal rat model by diffusion tensor MRI. Stroke 39:2348–2353\nHein PA, Eskey CJ, Dunn JF, Hug EB (2004) Diffusion-weighted imaging in the follow-up of treated high-grade gliomas: tumor recurrence versus radiation injury. AJNR Am J Neuroradiol 25:201–209\nAsao C, Korogi Y, Kitajima M, Hirai T, Baba Y, Makino K, Kochi M, Morishita S, Yamashita Y (2005) Diffusion-weighted imaging of radiation-induced brain injury for differentiation from tumor recurrence. AJNR Am J Neuroradiol 26:1455–1460\nKashimura H, Inoue T, Beppu T, Ogasawara K, Ogawa A (2007) Diffusion tensor imaging for differentiation of recurrent brain tumor and radiation necrosis after radiotherapy–three case reports. Clin Neurol Neurosurg 109:106–110\nChenevert TL, McKeever PE, Ross BD (1997) Monitoring early response of experimental brain tumors to therapy using diffusion magnetic resonance imaging. Clin Cancer Res 3:1457–1466\nInoue T, Ogasawara K, Beppu T, Ogawa A, Kabasawa H (2005) Diffusion tensor imaging for preoperative evaluation of tumor grade in gliomas. Clin Neurol Neurosurg 107:174–180\nWang YX, King AD, Zhou H, Leung SF, Abrigo J, Chan YL, Hu CW, Yeung DK, Ahuja AT (2010) Evolution of radiation-induced brain injury: MR imaging-based study. Radiology 254:210–218\nPoonawalla AH, Zhou XJ (2004) Analytical error propagation in diffusion anisotropy calculations. J Magn Reson Imaging 19:489–498\nNi H, Kavcic V, Zhu T, Ekholm S, Zhong J (2006) Effects of number of diffusion gradient directions on derived diffusion tensor imaging indices in human brain. AJNR Am J Neuroradiol 27:1776–1781\nGulani V, Weber T, Neuberger T (2005) Improved time efficiency and accuracy in diffusion tensor microimaging with multiple-echo acquisition. J Magn Reson 177:329–335\nNana R, Zhao T, Hu X (2008) Single-shot multiecho parallel echo-planar imaging (EPI) for diffusion tensor imaging (DTI) with improved signal-to-noise ratio (SNR) and reduced distortion. 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cyclin D1 (CCND1) in human glioblastoma correlates with poor clinical prognosis. In this study, the human glioblastoma cell lines SHG-44 and U251 were stably transfected with short hairpin RNA (shRNA) targeting cyclin D1 or with ectogenic cyclin D1 by lentivirus-mediated transfection. Glioblastoma cells overexpressing or underexpressing cyclin D1 were then examined by in vitro growth assays, apoptosis assays, cell cycle analysis, and invasion assays. Cyclin D1 knockdown in SHG-44 cells inhibited cell proliferation, induced apoptosis, and attenuated migration across Matrigel, a model of invasive capacity. Western blot analysis and quantitative reverse-transcription polymerase chain reaction (RT-PCR) revealed that cells underexpressing CCND1 exhibited decreased multidrug resistance protein 1 (MDR1) and B-cell lymphoma-2 (Bcl-2) expression, but enhanced apoptosis effector caspase-3 expression. In contrast, cyclin D1 overexpression promoted cell proliferation, attenuated apoptosis, and enhanced invasive capacity. Furthermore, cyclin D1 overexpression was associated with increased expression of MDR1 and Bcl-2, and decreased caspase-3 expression. Results using the U251 cell line confirmed the effects of CCND1-targeted shRNA and lentivirus-mediated overexpression on proliferation and apoptosis of glioblastoma cells. Overexpression of cyclin D1 enhanced the proliferation and invasive potential of human glioblastoma cells, while reducing apoptosis. The ability to suppress the malignant phenotype by downregulating cyclin D1 expression may provide a new gene therapy approach for patients with malignant glioma.",{"EN":1284},"Knockdown of cyclin D1 inhibits proliferation, induces apoptosis, and attenuates the invasive capacity of human glioblastoma cells",{"VOID":1286},"Pines J (1994) Protein kinases and cell cycle control. Semin Cell Biol 5:399–408\nTashiro E, Tsuchiya A, Imoto M (2007) Functions of cyclin D1 as an oncogene and regulation of cyclin D1 expression. Cancer Sci 98:629–635\nGrana X, Reddy EP (1995) Cell cycle control in mammalian cells: role of cyclins, cyclin dependent kinases (CDKs), growth suppressor genes and cyclin-dependent kinase inhibitors (CKIs). Oncogene 11:211–219\nCollecchi P, Santoni T, Gnesi E, Giuseppe Naccarato A, Passoni A, Rocchetta M, Danesi R, Bevilacqua G (2000) Cyclins of phases G1, S and G2\u002FM are overexpressed in aneuploid mammary carcinomas. Cytometry 42:254–260\nDraetta GF (1994) Mammalian G1 cyclins. Curr Opin Cell Biol 6:842–846\nSherr CJ (1994) G1 phase progression: cycling on cue. Cell 79:551–555\nPardee AB (1989) G1 events and regulation of cell proliferation. Science 246:603–608\nBernards R (1999) CDK-independent activities of D type cyclins. Biochim Biophys Acta 1424:M17–M22\nHui AB, Or YY, Takano H, Tsang RK, To KF, Guan XY, Sham JS, Hung KW, Lam CN, van Hasselt CA, Kuo WL, Gray JW, Huang DP, Lo KW (2005) Array-based comparative genomic hybridization analysis identified cyclin D1 as a target oncogene at 11q13.3 in nasopharyngeal carcinoma. Cancer Res 65:8125–8133\nOrmandy CJ, Musgrove EA, Hui R, Daly RJ, Sutherland RL (2003) Cyclin D1, EMS1 and 11q13 amplification in breast cancer. Breast Cancer Res Treat 78:323–335\nNishida N, Fukuda Y, Komeda T, Kita R, Sando T, Furukawa M, Amenomori M, Shibagaki I, Nakao K, Ikenaga M, Ishizaki K (1994) Amplification and overexpression of the cyclin D1 gene in aggressive human hepatocellular carcinoma. Cancer Res 54:3107–3110\nBuschges R, Weber RG, Actor B, Lichter P, Collins VP, Reifenberger G (1999) Amplification and expression of cyclin D genes (CCND1, CCND2 and CCND3) in human malignant gliomas. Brain Pathol 9:435–442 discussion 432–433\nHunter T, Pines J (1994) Cyclins and cancer. II: Cyclin D and CDK inhibitors come of age. Cell 79:573–582\nUmekita Y, Ohi Y, Sagara Y, Yoshida H (2002) Overexpression of cyclin D1 predicts for poor prognosis in estrogen receptor-negative breast cancer patients. Int J Cancer 98:415–418\nLiu B, Ren Z, Shi Y, Guan C, Pan Z, Zong Z (2008) Activation of signal transducers and activators of transcription 3 and overexpression of its target gene CyclinD1 in laryngeal carcinomas. Laryngoscope 118:1976–1980\nToyoda H, Nakamura T, Shinoda M, Suzuki T, Hatooka S, Kobayashi S, Ohashi K, Seto M, Shiku H, Nakamura S (2000) Cyclin D1 expression is useful as a prognostic indicator for advanced esophageal carcinomas, but not for superficial tumors. Dig Dis Sci 45:864–869\nGao P, Zhou GY, Liu Y, Li JS, Zhen JH, Yuan YP (2004) Alteration of cyclin D1 in gastric carcinoma and its clinicopathologic significance. World J Gastroenterol 10:2936–2939\nBahnassy AA, Zekri AR, El-Houssini S, El-Shehaby AM, Mahmoud MR, Abdallah S, El-Serafi M (1997) Cyclin A and cyclin D1 as significant prognostic markers in colorectal cancer patients. BMC Gastroenterol 4:22\nGansauge S, Gansauge F, Ramadani M, Stobbe H, Rau B, Harada N, Beger HG (1997) Overexpression of cyclin D1 in human pancreatic carcinoma is associated with poor prognosis. Cancer Res 57:1634–1637\nSallinen SL, Sallinen PK, Kononen JT, Syrjakoski KM, Nupponen NN, Rantala IS, Helen PT, Helin HJ, Haapasalo HK (1999) Cyclin D1 expression in astrocytomas is associated with cell proliferation activity and patient prognosis. J Pathol 188:289–293\nMalumbres M, Barbacid M (2006) Is Cyclin D1-CDK4 kinase a bona fide cancer target? Cancer Cell 9:2–4\nWang TC, Cardiff RD, Zukerberg L, Lees E, Arnold A, Schmidt EV (1994) Mammary hyperplasia and carcinoma in MMTV-cyclin D1 transgenic mice. Nature 369:669–671\nYu Q, Geng Y, Sicinski P (2001) Specific protection against breast cancers by cyclin D1 ablation. Nature 411:1017–1021\nZhou P, Jiang W, Zhang YJ, Kahn SM, Schieren I, Santella RM, Weinstein IB (1995) Antisense to cyclin D1 inhibits growth and reverses the transformed phenotype of human esophageal cancer cells. Oncogene 11:571–580\nArber N, Doki Y, Han EK, Sgambato A, Zhou P, Kim NH, Delohery T, Klein MG, Holt PR, Weinstein IB (1997) Antisense to cyclin D1 inhibits the growth and tumorigenicity of human colon cancer cells. Cancer Res 57:1569–1574\nSauter ER, Nesbit M, Litwin S, Klein-Szanto AJ, Cheffetz S, Herlyn M (1999) Antisense cyclin D1 induces apoptosis and tumor shrinkage in human squamous carcinomas. Cancer Res 59:4876–4881\nCarpentier AF (2005) Neuro–oncology: the growing role of chemotherapy in glioma. Lancet Neurol 4:4–5\nPrados MD, Levin V (2000) Biology and treatment of malignant glioma. Semin Oncol 27:1–10\nCavalla P, Dutto A, Piva R, Richiardi P, Grosso R, Schiffer D (1998) Cyclin D1 expression in gliomas. Acta Neuropathol 95:131–135\nPscherer A, Schliwka J, Wildenberger K, Mincheva A, Schwaenen C, Dohner H, Stilgenbauer S, Lichter P (2006) Antagonizing inactivated tumor suppressor genes and activated oncogenes by a versatile transgenesis system: application in mantle cell lymphoma. FASEB J 20:1188–1190\nChakrabarty A, Bridges LR, Gray S (1996) Cyclin D1 in astrocytic tumours: an immunohistochemical study. Neuropathol Appl Neurobiol 22:311–316\nKornmann M, Arber N, Korc M (1998) Inhibition of basal and mitogen-stimulated pancreatic cancer cell growth by cyclin D1 antisense is associated with loss of tumorigenicity and potentiation of cytotoxicity to cisplatinum. J Clin Invest 101:344–352\nLampert K, Machein U, Machein MR, Conca W, Peter HH, Volk B (1998) Expression of matrix metalloproteinases and their tissue inhibitors in human brain tumors. Am J Pathol 153:429–437\nForsyth PA, Wong H, Laing TD, Rewcastle NB, Morris DG, Muzik H, Leco KJ, Johnston RN, Brasher PM, Sutherland G, Edwards DR (1999) Gelatinase-A (MMP-2), gelatinase-B (MMP-9) and membrane type matrix metalloproteinase-1 (MT1-MMP) are involved in different aspects of the pathophysiology of malignant gliomas. Br J Cancer 79:1828–1835\nKargiotis O, Chetty C, Gondi CS, Tsung AJ, Dinh DH, Gujrati M, Lakka SS, Kyritsis AP, Rao JS (2008) Adenovirus-mediated transfer of siRNA against MMP-2 mRNA results in impaired invasion and tumor-induced angiogenesis, induces apoptosis in vitro and inhibits tumor growth in vivo in glioblastoma. Oncogene 27:4830–4840\nLakka SS, Gondi CS, Yanamandra N, Olivero WC, Dinh DH, Gujrati M, Rao JS (2004) Inhibition of cathepsin B and MMP-9 gene expression in glioblastoma cell line via RNA interference reduces tumor cell invasion, tumor growth and angiogenesis. Oncogene 23:4681–4689\nNoel EE, Yeste-Velasco M, Mao X, Perry J, Kudahetti SC, Li NF, Sharp S, Chaplin T, Xue L, McIntyre A, Shan L, Powles T, Oliver RT, Young BD, Shipley J, Berney DM, Joel SP, Lu YJ (2010) The association of CCND1 overexpression and cisplatin resistance in testicular germ cell tumors and other cancers. Am J Pathol 176:2607–2615\nBiliran H Jr, Wang Y, Banerjee S, Xu H, Heng H, Thakur A, Bollig A, Sarkar FH, Liao JD (2005) Overexpression of cyclin D1 promotes tumor cell growth and confers resistance to cisplatin-mediated apoptosis in an elastase-myc transgene-expressing pancreatic tumor cell line. Clin Cancer Res 11:6075–6086\nKornmann M, Danenberg KD, Arber N, Beger HG, Danenberg PV, Korc M (1999) Inhibition of cyclin D1 expression in human pancreatic cancer cells is associated with increased chemosensitivity and decreased expression of multiple chemoresistance genes. Cancer Res 59:3505–3511\nOchs K, Kaina B (2000) Apoptosis induced by DNA damage O6-methylguanine is Bcl-2 and caspase-9\u002F3 regulated and Fas\u002Fcaspase-8 independent. Cancer Res 60:5815–5824\nRoos WP, Batista LF, Naumann SC, Wick W, Weller M, Menck CF, Kaina B (2007) Apoptosis in malignant glioma cells triggered by the temozolomide-induced DNA lesion O6-methylguanine. Oncogene 26:186–197\nDemeule M, Shedid D, Beaulieu E, Del Maestro RF, Moghrabi A, Ghosn PB, Moumdjian R, Berthelet F, Beliveau R (2001) Expression of multidrug-resistance P-glycoprotein (MDR1) in human brain tumors. Int J Cancer 93:62–66\nToth K, Vaughan MM, Peress NS, Slocum HK, Rustum YM (1996) MDR1 P-glycoprotein is expressed by endothelial cells of newly formed capillaries in human gliomas but is not expressed in the neovasculature of other primary tumors. Am J Pathol 149:853–858\nBronger H, Konig J, Kopplow K, Steiner HH, Ahmadi R, Herold-Mende C, Keppler D (2005) Nies AT ABCC drug efflux pumps and organic anion uptake transporters in human gliomas and the blood-tumor barrier. Cancer Res 65:11419–11428\nSchaich M, Kestel L, Pfirrmann M, Robel K, Illmer T, Kramer M, Dill C, Ehninger G, Schackert G, Krex D (2009) A MDR1 (ABCB1) gene single nucleotide polymorphism predicts outcome of temozolomide treatment in glioblastoma patients. 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retrospectively analyze and assess the outcomes and prognostic factors in patients with anaplastic meningioma (AM) (WHO Grade III). Clinical data and outcome [overall (OS) and progression-free (PFS) survival] from 18 patients with Grade III meningioma (AM, based on World Health Organization 2016 definition) initially treated between March 2000 and June 2015 were analyzed. Eleven patients (61%) were male, median age at diagnosis was 63 (range 48–86), and 55% (10\u002F18 patients) had good performance status (KPS ≥ 80). Eight patients (45%) had lower grade disease (Grade I—n = 2; Grade II—n = 6) prior to being upgraded to AM. Ten patients had fractionated radiation after primary surgery, eight patients had salvage fractionated RT, stereotactic radiosurgery (SRS) boost along with primary RT in 1 patient, and salvage SRS to 18 separate areas in 14 patients. Salvage chemotherapy was mainly considered in third or fourth recurrences. 13 (72%) patients recurred and 10 (56%) have died. Median PFS was 14.5 months (95% CI 6.9–22.2). The 5-year survival rate was 40 ± 15% and median OS was 55.8 months (95% CI 27.7–80.3). Of all factors examined, only Karnofsky performance status (KPS) affected outcome (PFS p = 0.0003; OS p = 0.0003). With median OS of 55 months (4.6 years) our results are consistent with existing reports of the poor outcomes for AM patients. From the available data, surgical resection followed by RT and salvage radiosurgery and\u002For chemotherapy can lead to extended survival; however the benefit may decrease with successive treatments.",{"EN":1518},"Longitudinal experience with WHO Grade III (anaplastic) meningiomas at a single institution",{"VOID":1520},"Ostrom QT, Gittleman H, Fulop J, Liu M, Blanda R, Kromer C, Wolinsky Y, Kruchko C, Barnholtz-Sloan JS (2015) CBTRUS statistical report: primary brain and central nervous system tumors diagnosed in the United States in 2008–2012. Neurooncol 17:iv1–iv62\nDolecek TA, Dressler EV, Thakkar JP, Liu M, Al-Qaisi A, Villano JL (2015) Epidemiology of meningiomas post-Public Law 107–206: the Benign Brain Tumor Cancer Registries Amendment Act. Cancer 121:2400–2410. doi:10.1002\u002Fcncr.29379\nSEER Surveillance, Epidemiology, and End Results (SEER) Program (http:\u002F\u002Fwww.seer.cancer.gov) research data (1973–2012), National Cancer Institute, DCCPS, Surveillance Research Program, Surveillance Systems Branch, released April 2015, based on the November 2014 submission\nAmbekar S, Sharma M, Madhugiri VS, Nanda A (2013) Trends in intracranial meningioma surgery and outcome: a nationwide inpatient sample database analysis from 2001 to 2010. J Neurooncol 114:299–307. doi:10.1007\u002Fs11060-013-1183-6\nLouis DN, Perry A, Reifenberger G, von Deimling A, Figarella-Branger D, Cavenee WK, Ohgaki H, Wiestler OD, Kleihues P, Ellison DW (2016) The 2016 World Health Organization classification of tumors of the central nervous system: a summary. Acta Neuropathol (Berl) 131:803–820. doi:10.1007\u002Fs00401-016-1545-1\nClaus EB, Bondy ML, Schildkraut JM, Wiemels JL, Wrensch M, Black PM (2005) Epidemiology of intracranial meningioma. Neurosurgery 57:1088–1095\nAdeberg S, Hartmann C, Welzel T, Rieken S, Habermehl D, von Deimling A, Debus J, Combs SE (2012) Long-term outcome after radiotherapy in patients with atypical and malignant meningiomas–clinical results in 85 patients treated in a single institution leading to optimized guidelines for early radiation therapy. Int J Radiat Oncol Biol Phys 83:859–864. doi:10.1016\u002Fj.ijrobp.2011.08.010\nDurand A, Labrousse F, Jouvet A, Bauchet L, Kalamaridès M, Menei P, Deruty R, Moreau JJ, Fèvre-Montange M, Guyotat J (2009) WHO Grade II and III meningiomas: a study of prognostic factors. J Neurooncol 95:367–375\nEl-Khatib M, El Majdoub F, Hoevels M, Kocher M, Muller RP, Steiger HJ, Sturm V, Maarouf M (2011) Stereotactic LINAC radiosurgery for incompletely resected or recurrent atypical and anaplastic meningiomas. Acta Neurochir (Wien) 153:1761–1767. doi:10.1007\u002Fs00701-011-1073-7\nFerraro DJ, Funk RK, Blackett JW, Ju MR, DeWees TA, Chicoine MR, Dowling JL, Rich KM, Drzymala RE, Zoberi I, Simpson JR, Jaboin JJ (2014) A retrospective analysis of survival and prognostic factors after stereotactic radiosurgery for aggressive meningiomas. Rad Oncol (London, England) 9:38. doi:10.1186\u002F1748-717x-9-38\nMoliterno J, Cope WP, Vartanian ED, Reiner AS, Kellen R, Ogilvie SQ, Huse JT, Gutin PH (2015) Survival in patients treated for anaplastic meningioma. J Neurosurg 123:23–30. doi:10.3171\u002F2014.10.jns14502\nPollock BE, Stafford SL, Link MJ, Garces YI, Foote RL (2012) Stereotactic radiosurgery of World Health Organization Grade II and III intracranial meningiomas: treatment results on the basis of a 22-year experience. Cancer 118:1048–1054. doi:10.1002\u002Fcncr.26362\nRosenberg LA, Prayson RA, Lee J, Reddy C, Chao ST, Barnett GH, Vogelbaum MA, Suh JH (2009) Long-term experience with World Health Organization Grade III (malignant) meningiomas at a single institution. Int J Radiat Oncol Biol Phys 74:427–432. doi:10.1016\u002Fj.ijrobp.2008.08.018\nSughrue ME, Sanai N, Shangari G, Parsa AT, Berger MS, McDermott MW (2010) Outcome and survival following primary and repeat surgery for World Health Organization Grade III meningiomas. J Neurosurg 113:202–209. doi:10.3171\u002F2010.1.jns091114\nZhao P, Hu M, Zhao M, Ren X, Jiang Z (2015) Prognostic factors for patients with atypical or malignant meningiomas treated at a single center. Neurosurgical review 38: 101–107. doi:10.1007\u002Fs10143-014-0558-2(discussion 107)\nChoi Y, Lim DH, Jo K, Nam D-H, Seol HJ, Lee J-I (2014) Efficacy of postoperative radiotherapy for high grade meningiomas. J Neurooncol 119:405–412\nSughrue ME, Kane AJ, Shangari G, Rutkowski MJ, McDermott MW, Berger MS, Parsa AT (2010) The relevance of Simpson Grade I and II resection in modern neurosurgical treatment of World Health Organization Grade I meningiomas: clinical article. J Neurosurg 113:1029–1035\nSimpson D (1957) The recurrence of intracranial meningiomas after surgical treatment. J Neurol Neurosurg Psychiatry 20:22–39\nLouis DN, Ohgaki H, Wiestler OD, Cavenee WK, Burger PC, Jouvet A, Scheithauer BW, Kleihues P (2007) The 2007 WHO classification of tumours of the central nervous system. Acta Neuropathol (Berl) 114:97–109. doi:10.1007\u002Fs00401-007-0243-4\nRogers CL, Perry A, Pugh S, Vogelbaum MA, Brachman D, McMillan W, Jenrette J, Barani I, Shrieve D, Sloan A, Bovi J, Kwok Y, Burri SH, Chao ST, Spalding AC, Anscher MS, Bloom B, Mehta M (2016) Pathology concordance levels for meningioma classification and grading in NRG Oncology RTOG trial 0539. Neurooncol 18:565–574. doi:10.1093\u002Fneuonc\u002Fnov247\nRogers L, Barani I, Chamberlain M, Kaley TJ, McDermott M, Raizer J, Schiff D, Weber DC, Wen PY, Vogelbaum MA (2015) Meningiomas: knowledge base, treatment outcomes, and uncertainties. A RANO review. J Neurosurg 122: 4–23. doi:10.3171\u002F2014.7.jns131644\nSun SQ, Hawasli AH, Huang J, Chicoine MR, Kim AH (2015) An evidence-based treatment algorithm for the management of WHO Grade II and III meningiomas. Neurosurg Focus 38:E3. doi:10.3171\u002F2015.1.focus14757\nNanda A, Bir SC, Maiti TK, Konar SK, Missios S, Guthikonda B (2016) Relevance of Simpson grading system and recurrence-free survival after surgery for World Health Organization Grade I meningioma. J Neurosurg 1–11. doi:10.3171\u002F2016.1.jns151842\nNorden AD, Raizer JJ, Abrey LE, Lamborn KR, Lassman AB, Chang SM, Yung WK, Gilbert MR, Fine HA, Mehta M, Deangelis LM, Cloughesy TF, Robins HI, Aldape K, Dancey J, Prados MD, Lieberman F, Wen PY (2010) Phase II trials of erlotinib or gefitinib in patients with recurrent meningioma. J Neurooncol 96:211–217. doi:10.1007\u002Fs11060-009-9948-7\nNorden AD, Ligon KL, Hammond SN, Muzikansky A, Reardon DA, Kaley TJ, Batchelor TT, Plotkin SR, Raizer JJ, Wong ET, Drappatz J, Lesser GJ, Haidar S, Beroukhim R, Lee EQ, Doherty L, Lafrankie D, Gaffey SC, Gerard M, Smith KH, McCluskey C, Phuphanich S, Wen PY (2015) Phase II study of monthly pasireotide LAR (SOM230C) for recurrent or progressive meningioma. Neurology 84:280–286. doi:10.1212\u002Fwnl.0000000000001153\nSimo M, Argyriou AA, Macia M, Plans G, Majos C, Vidal N, Gil M, Bruna J (2014) Recurrent high-grade meningioma: a phase II trial with somatostatin analogue therapy. Cancer Chemother Pharmacol 73:919–923. doi:10.1007\u002Fs00280-014-2422-z\nChamberlain MC (2012) Hydroxyurea for recurrent surgery and radiation refractory high-grade meningioma. J Neurooncol 107:315–321. doi:10.1007\u002Fs11060-011-0741-z\nChamberlain MC, Johnston SK (2011) Hydroxyurea for recurrent surgery and radiation refractory meningioma: a retrospective case series. J Neurooncol 104:765–771. doi:10.1007\u002Fs11060-011-0541-5\nKaley TJ, Wen P, Schiff D, Ligon K, Haidar S, Karimi S, Lassman AB, Nolan CP, DeAngelis LM, Gavrilovic I, Norden A, Drappatz J, Lee EQ, Purow B, Plotkin SR, Batchelor T, Abrey LE, Omuro A (2015) Phase II trial of sunitinib for recurrent and progressive atypical and anaplastic meningioma. Neurooncol 17:116–121. doi:10.1093\u002Fneuonc\u002Fnou148\nRaizer JJ, Grimm SA, Rademaker A, Chandler JP, Muro K, Helenowski I, Rice L, McCarthy K, Johnston SK, Mrugala MM, Chamberlain M (2014) A phase II trial of PTK787\u002FZK 222584 in recurrent or progressive radiation and surgery refractory meningiomas. J Neurooncol 117:93–101. doi:10.1007\u002Fs11060-014-1358-9\nReardon DA, Norden AD, Desjardins A, Vredenburgh JJ, Herndon JE 2nd, Coan A, Sampson JH, Gururangan S, Peters KB, McLendon RE, Norfleet JA, Lipp ES, Drappatz J, Wen PY, Friedman HS (2012) Phase II study of Gleevec(R) plus hydroxyurea (HU) in adults with progressive or recurrent meningioma. J Neurooncol 106:409–415. doi:10.1007\u002Fs11060-011-0687-1\nWen PY, Yung WK, Lamborn KR, Norden AD, Cloughesy TF, Abrey LE, Fine HA, Chang SM, Robins HI, Fink K, Deangelis LM, Mehta M, Di Tomaso E, Drappatz J, Kesari S, Ligon KL, Aldape K, Jain RK, Stiles CD, Egorin MJ, Prados MD (2009) Phase II study of imatinib mesylate for recurrent meningiomas (North American Brain Tumor Consortium study 01–08). Neurooncol 11:853–860. doi:10.1215\u002F15228517-2009-010\nNayak L, Iwamoto FM, Rudnick JD, Norden AD, Lee EQ, Drappatz J, Omuro A, Kaley TJ (2012) Atypical and anaplastic meningiomas treated with bevacizumab. 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Furthermore, the extracellular pH of gliomas is relatively acidic suggesting that tumor selectivity could be further enhanced if nanoparticles can be designed to cationize in such an environment. With these motivating hypotheses the objective of this study was to determine whether nanoparticulate (20 nm) micelles could be designed to improve their deposition within gliomas in an animal model. To test this, we performed intra-arterial injection of micelles labeled with an optically quantifiable dye. We observed significantly greater deposition (end-tissue concentration) of cationizable micelles as compared to non-ionizable micelles in the ipsilateral hemisphere of normal brains. More importantly, we noted enhanced deposition of cationizable as compared to non-ionizable micelles in glioma tissue as judged by semiquantitative fluorescence analysis. Micelles were generally able to penetrate to the core of the gliomas tested. 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J Membr Biol 246(2):161–166. doi:10.1007\u002Fs00232-012-9516-5\nDobrzynska I, Szachowicz-Petelska B, Darewicz B, Figaszewski ZA (2015) Characterization of human bladder cell membrane during cancer transformation. J Membr Biol 248(2):301–307. doi:10.1007\u002Fs00232-015-9770-4\nJo DH, Kim JH, Lee TG, Kim JH (2015) Size, surface charge, and shape determine therapeutic effects of nanoparticles on brain and retinal diseases. Nanomed Nanotechnol Biol Med 11(7):1603–1611. doi:10.1016\u002Fj.nano.2015.04.015\nGarcia-Martin ML, Martinez GV, Raghunand N, Sherry AD, Zhang S, Gillies RJ (2006) High resolution pH(e) imaging of rat glioma using pH-dependent relaxivity. Magn Reson Med 55(2):309–315. doi:10.1002\u002Fmrm.20773\nJoshi S, Singh-Moon RP, Wang M, Chaudhuri DB, Holcomb M, Straubinger NL, Bruce JN, Bigio IJ, Straubinger RM (2014) Transient cerebral hypoperfusion assisted intraarterial cationic liposome delivery to brain tissue. J Neurooncol 118(1):73–82. doi:10.1007\u002Fs11060-014-1421-6\nJoshi S, Wang M, Etu JJ, Suckow RF, Cooper TB, Feinmark SJ, Bruce JN, Fine RL (2008) Transient cerebral hypoperfusion enhances intraarterial carmustine deposition into brain tissue. J Neurooncol 86(2):123–132. doi:10.1007\u002Fs11060-007-9450-z\nJoshi S, Singh-Moon RP, Ellis JA, Chaudhuri DB, Wang M, Reif R, Bruce JN, Bigio IJ, Straubinger RM (2015) Cerebral hypoperfusion-assisted intra-arterial deposition of liposomes in normal and glioma-bearing rats. Neurosurgery 76(1):92–100. doi:10.1227\u002FNEU.0000000000000552\nJoshi S, Singh-Moon R, Wang M, Chaudhuri DB, Ellis JA, Bruce JN, Bigio IJ, Straubinger RM (2014) Cationic surface charge enhances early regional deposition of liposomes after intracarotid injection. J Neurooncol 120(3):489–497. doi:10.1007\u002Fs11060-014-1584-1\nNguyen J, Sievers R, Motion JPM, Kivimae S, Fang QZ, Lee RJ (2015) Delivery of lipid micelles into infarcted myocardium using a lipid-linked matrix metalloproteinase targeting peptide. Mol Pharmaceut 12(4):1150–1157. doi:10.1021\u002Fmp500653y\nWalsh CL, Nguyen J, Szoka FC (2012) Synthesis and characterization of novel zwitterionic lipids with pH-responsive biophysical properties. Chem Commun 48(45):5575–5577. doi:10.1039\u002Fc2cc31710a\nBigio IJ, Bown SG (2004) Spectroscopic sensing of cancer and cancer therapy: current status of translational research. Cancer Biol Ther 3(3):259–267\nMourant JR, Johnson TM, Los G, Bigio IJ (1999) Non-invasive measurement of chemotherapy drug concentrations in tissue: preliminary demonstrations of in vivo measurements. 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J Neurooncol. doi:10.1007\u002Fs11060-014-1584-1\nJoshi S, Ellis JA, Ornstein E, Bruce JN (2015) Intraarterial drug delivery for glioblastoma mutiforme: will the phoenix rise again? J Neurooncol 124(3):333–343. doi:10.1007\u002Fs11060-015-1846-6\nHardebo JE, Nilsson B (1979) Estimation of cerebral extraction of circulating compounds by the brain uptake index method: influence of circulation time, volume injection, and cerebral blood flow. Acta Physiol Scand 107(2):153–159\nVaupel P, Kallinowski F, Okunieff P (1989) Blood flow, oxygen and nutrient supply, and metabolic microenvironment of human tumors: a review. Cancer Res 49(23):6449–6465\nKallinowski F, Vaupel P (1988) pH distributions in spontaneous and isotransplanted rat tumours. 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den-Disease-Report-of-a-Case-and-Review-of-the-Literature-for-the-Genetic-Relationship-between-the-Two-Diseases",{"abstract":2090,"title":2092,"references":2094,"doi":2096},{"EN":2091},"We report a case of dysplastic gangliocytoma of the cerebellum (Lhermitte-Duclos disease, LDD). The patient also had cutaneous and mucosal hamartomas, adenomatous goiter, bilateral breast tumors, and gastrointestinal polyposis, indicating the diagnosis of Cowden disease (CD), the familial hamartoma syndrome. This was a rare sporadic case without any family history of CD, though CD is considered to be an autosomal dominant hereditary disease. Based on a thorough review of the previously reported cases, it is reasonable to consider that CD is inherited in autosomal dominant fashion through a CD gene (PTEN) containing a germline mutation, and that the occurrence of LDD is predicated on an additional somatic hit on the remaining normal CD allele or another unknown gene.",{"EN":2093},"Dysplastic Gangliocytoma (Lhermitte-Duclos Disease) Associated with Cowden Disease: Report of a Case and Review of the Literature for the Genetic Relationship between the Two Diseases",{"VOID":2095},"Albrecht S, Haber RM, Goodman JC, Duvic M: Cowden syndrome and Lhermitte-Duclos disease. Cancer 70: 869-876, 1992\nAmbler M, Pogacar S, Sidman R: Lhermitte-Duclos disease (granule cell hypertrophy of the cerebellum). Pathological analysis of the first familial cases. J Neuropathol Exp Neurol 28: 622-647, 1969\nAwwad EE, Martin DS, Selhorst JB: CT and MR findings in Lhermitte-Duclos disease (abstr). In: Proceedings Book: American Society of Neuroradiology 1994. Chicago, III: American Society of Neuroradiology, 1994, pp 55-56\nCasteels I, Demaerel P, de Cock P, Casaer P, Spileers W, Wilms G: Leber congenital amaurosis and Lhermitte-Duclos syndrome: a previously unreported association. J Pediatr Ophthalmol Strabismus 32: 117-119, 1995\nEllis PK: Case report: Lhermitte-Duclos disease: enhancement following gadolinium-DTPA. Clin Radiol 51: 222-224, 1996\nEng C, Murday V, Seal S, Mohammad S, Hodgson SV, Chaudary MA, Fentiman IS, Ponder BAJ, Eeles RA: Cowden syndrome and Lhermitte-Duclos disease in a family: a single genetic syndrome with pleiotropy? J Med Genet 31: 458-461, 1994\nFerrer I, Isamat F, Lopez-Obarrio L, Conesa G, Rimbau J, Alcantara S, Espanol I, Zujar MJ: Paralbumin and calbindin D-28K immunoreactivity in central gangliocytoma and dysplastic gangliocytoma of the cerebellum. J Neurosurg 78: 133-137, 1993\nGrand S, Pasquier B, Le Bas JF, Chirossel JP: Case report: Mangetic resonance imaging in Lhermitte-Duclos disease. Br J Radiol 67: 902-905, 1994\nGrattan CEH, Hamburger J: Cowden's disease in two sisters, one showing partial expression. Clin Exp Dermatol 12: 360-363, 1987\nHair LS, Symmans F, Powers JM, Carmel P: Immunohistochemistry and proliferative activity in Lhermitte-Duclos disease. Acta Neuropathol 84: 570-573, 1992\nHashimoto M, Fujimoto K, Shinoda S, Masuzawa T: Magnetic resonance imaging of ganglion cell tumors. Neuroradiology 35: 181-184, 1993\nHulcelle P, Dooms G, Vermonden J: Lhermitte-Duclos disease. A case report. J Neuroradiol 21: 40-45, 1994\nKing MA, Coyne TJ, Spearritt DJ, Boyle RS: Lhermitte-Duclos disease and Cowden disease: a third case. Ann Neurol 32: 112-113, 1992\nLhermitte J, Duclos P: Sur un ganglioneuroma diffus du cortex du cervelet. Bull Assoc Fr Etude Cancer 9: 99-107, 1920\nLiawD, Marsh DJ, Li J, Dahia PL, Wang SI, Zheng Z, Bose S, Call KM, Tsou HC, Peacocke M, Eng C and Parsons R: Germline mutations of the PTEN gene in Cowden disease, an inherited breast and thyroid cancer syndrome. Nat Genet 16: 64-67, 1997\nLindboe CF, Helseth E, Myhr G: Lhermitte-Duclos disease and giant meningioma as manifestations of Cowden's disease. Clin Neuropathol 14: 327-330, 1995\nMarano SR, Johnson PC, Spetzler RF: Recurrent Lhermitte-Duclos disease in a child. J Neurosurg 69: 599-603, 1988\nMarcus CD, Galeon M, Peruzzi P, Bazin A, Bernard MH, Pluot M, Menanteau B: Lhermitte-Duclos disease associated with syringomyelia. Neuroradiology 38: 529-531, 1996\nMeltzer CC, Smirniotopoulos JG, JonesRV: The striated cerebellum: an MR imaging sign in Lhermitte-Duclos disease (dysplastic gangliocytoma). Radiology 194: 699-703, 1995\nNelen MR, Padberg GW, Peeters EAJ, Lin AY, van den Helm B, Frants RR, Coulon V, Goldstein AM, van Reen MMM, Easton DF, Eeles RA, Hodgson S, Mulvihill JJ, Murday VA, TuckerMA, MarimanECM, Starink TM, Ponder BAJ, Ropers HH, Kremer H, Longy M, Eng C: Localization of the gene for Cowden disease to chromosome 10q22-23. Nature Genetics 13: 114-116, 1996\nOrtiz O, Bloomfield S, Schochet S: Vascular contrast enhancement in Lhermitte-Duclos disease: case report. Neuroradiology 37: 545-548, 1995\nPadberg GW, Schot JDL, Vielvoye GJ, Bots GTAM, de Beer FC: Lhermitte-Duclos disease and Cowden disease: a single phakomatosis. Ann Neurol 29: 517-523, 1991\nRimbau J, Isamat F: Dysplastic gangliocytoma of the cerebellum (Lhermiitte-Duclos disease) and its relation to the multiple hamartoma syndrome (Cowden disease). J Neuro-Oncol 18: 191-198, 1994\nRussel Jones R, O'brien M, Wells RS: Cowden syndrome. Br J Dermatol 105: 57-58, 1981\nSalem OS, Steck WD: Cowden's disease (multiple hamartoma and neoplasia syndrome). J Am Acad Dermatol 8: 686-696, 1983\nShanley DJ, Vassallo CJ: Atyical presentation of Lhermitte-Duclos disease: preoperative diagnosis with MRI. Neuroradiology 34: 103-104, 1992\nSiddiqi SN, Fehlings MG: Lhermitte-Duclos disease mimicking adult-onset aqueductal stenosis. J Neurosurg 80: 1095-1098, 1994\nSonier CB, Feve JR, de Kersaint-Gilly A, Ruchoux MM, Rymer R, Auffray E: Lhermitte-Duclos disease. A rare cause of intracranial hypertension in adults. J Neuroradiol 19: 133-138, 1992\nStarink TM, Van Der Veen JPW, Arwert F, de Waal LP, de Lange GG, Gille JJP, Eriksson AW: The Cowden syndrome: a clinical and genetic study in 21 patiens. Clin Genet 29: 222-233, 1986\nVieco PT, del Carpio-O'Donovan R, Melanson D, Montes J, O'Gorman AM, Meagher-Villemure K: Dysplasticgangliocytoma (Lhermitte-Duclos disease): CT and MR imaging. Pediatr Radiol 22: 366-369, 1992\nVinchon M, Blond S, Lejeune JP, Krivosik I, Fossati P, Assaker R, Christiaens JL: Association of Lhermitte-Duclos and Cowden disease: report of a new case and review of the literature. J Neurol Neurosurg Psychiatry 57: 699-704, 1994\nVital A, Vital C, Martin-Negrier ML, McGrogan G, Bioulac P, Trojani M, Loiseau H, Rougier A: Lhermitte-Duclos type cerebellum hamartoma and Cowden disease. Clin Neuropathol 13: 229-231, 1994\nWells GB, Lasner TM, Yousem DM, Zager EL: Lhermitte-Duclos disease and Cowden's syndrome in an adolescent patient. J Neurosurg 81: 133-136, 1994\nWilliams DW, Elster AD, Ginsberg LE, Stanton C: Recurrent Lhermitte-Duclos disease: report of two cases and association with Cowden's disease. AJNR 13: 287-290, 1992\nWolansky LJ, Malantic GP, Heary R, Maniker AH, Lee HJ, Sharer LR, Patel UJ: Preoperative MRI diagnosis of Lherrnitte-Duclos disease: case report with associated enlarged vessel and syrinx. Surg Neurol 45: 470-476, 1996\nYuasa H, Motokishita T, Tokito S, Tokunaga M, Goto M: Lhermitte-Duclos disease associated with Cowden's disease. Case report. Neurol Med Chir (Tokyo) 37: 697-700, 1997",{"VOID":2097},"10.1023\u002FA:1006167421100","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FA:1006167421100",[2100,2124,2137,2150,2163,2176],{"id":2101,"sortIndex":32,"researcher":28,"roles":2102,"affiliations":2103,"properties":2121,"displayName":2123,"givenName":28,"familyName":28},"7c2f3eee-5280-4b60-a65b-78d0637415fd",[1064],[2104,2112],{"id":2105,"sortIndex":32,"affiliation":2106,"properties":28},"3020fe20-6f16-443f-943b-30f31acc4c3d",{"id":2105,"createTime":28,"updateTime":28,"relativeEntities":2107,"slug":28,"properties":2108,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2111,"statistic":28},[],{"title":2109},{"VI":2110},"Department of Neurosurgery, Hokkaido University School of Medicine, 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hibition-and-Apoptosis-in-Human-Glioblastomas",{"abstract":2260,"title":2262,"references":2264,"doi":2266},{"EN":2261},"High-grade gliomas are characterized by a rapid proliferation rate, invasiveness and angiogenesis. Our previous data indicated that the combination of ligands for peroxisome proliferator-activated receptor γ (PPARγ) and retinoic acid receptor (RAR) induces apoptosis of breast cancer cells in vitro and in a murine model. In this study, we have shown that 11 glioblastoma cell lines and nine fresh glioblastoma tissue samples from patients expressed high-levels of PPARγ. In contrast, glia from nine healthy human brains expressed very low levels of PPARγ. No mutations or polymorphisms of the PPARγ gene were observed in these cell lines. The effect of the PPARγ ligand Pioglitazone (PGZ) either in the absence or in the presence of a RAR ligand [all-trans retinoic acid (ATRA)] on the proliferation and apoptosis of glioblastoma cells was examined using two glioblastoma cell lines (N39 and DBTRG05MG). PGZ and\u002For ATRA inhibited significantly the proliferation of both cell lines. Flow cytometry analysis showed that G1 cell cycle arrest was induced by these ligands. In addition, apoptosis occurred in both cell lines treated with either PGZ or ATRA, which was associated with a downregulation of bcl-2 and an upregulation of bax proteins. An enhanced effect was observed when PGZ and ATRA were combined. Furthermore, treatment of fresh glioblastoma tissue from patients with PGZ, either alone or in combination with ATRA, induced a significant level of tumor cell apoptosis together with a downregulation of bcl-2 protein level as compared with untreated control brain tissue. Taken together, our data demonstrated that PGZ, either alone or in combination with ATRA, induced apoptosis and inhibited proliferation of glioblastoma cells, and more interestingly, induced apoptosis of fresh glioblastoma cells from patients. Therefore, we conclude that these ligands may possess adjuvant therapeutic potential for patients with glioblastoma.",{"EN":2263},"Ligands for PPARγ and RAR Cause Induction of Growth Inhibition and Apoptosis in Human Glioblastomas",{"VOID":2265},"Levin VA: Chemotherapy for brain tumors of astrocytic and oligodendroglial lineage: the past decade and where we are heading. Neuro-Oncology 1: 69–80, 1999\nHildebrand J, Dewitte O, Dietrich PY, de Tribolet N: Management of malignant brain tumors. Eur Neurol 38: 238–253, 1997\nShrieve DC, Alexander III, E, Black PM, Wen PY, Fine HA, Kooy HM, Loeffler JS: Treatment of patients with primary glioblastoma multiforme with standard postoperative radiotherapy and radiosurgical boost: prognostic factors and long-term outcome. J Neurosurg 90: 72–77, 1999\nChawla A, Schwarz EJ, Dimaculangan DD, Lazar MA: Peroxisome proliferator-activated receptor (PPAR) gamma: adipose-predominant expression and induction early in adipocyte differentiation. Endocrinology 135: 798–800, 1994\nTontonoz P, Graves RA, Budavari AI, Erdjument-Bromage H, Lui M, Hu E, Tempst P, Spiegelman BM: Adipocyte-specific transcription factor ARF6 is a heterodimeric complex of two nuclear hormone receptors, PPAR gamma and RXR alpha. Nucleic Acids Res 22: 5628–5634, 1994\nBrun RP, Kim JB, Hu E, Spiegelman BM: Peroxisome proliferator-activated receptor gamma and the control of adipogenesis. Curr Opin Lipidol 8: 212–218, 1997\nSpiegelman BM: PPAR-gamma: adipogenic regulator and thiazolidinedione receptor. Diabetes 47: 507–514, 1998\nDelerive P, Fruchart JC, Staels B: Peroxisome proliferatoractivated receptors in inflammation control. J Endocrinol 169: 453–459, 2001\nGelman L, Fruchart JC, Auwerx J: An update on the mechanisms of action of the peroxisome proliferator-activated receptors (PPARs) and their roles in inflammation and cancer. Cell Mol Life Sci 55: 932–943, 1999\nRoberts-Thomson SJ: Peroxisome proliferator-activated receptors in tumorigenesis: targets of tumour promotion and treatment. Immunol Cell Biol 78: 436–441, 2000\nGirnun GD, Smith WM, Drori S, Sarraf P, Mueller E, Eng C, Nambiar P, Rosenberg DW, Bronson RT, Edelmann W, Kucherlapati R, Gonzalez FJ, Spiegelman BM: APCdependent suppression of colon carcinogenesis by PPARgamma. Proc Natl Acad Sci USA 99: 13771–13776, 2002\nTontonoz P, Singer S, Forman BM, Sarraf P, Fletcher JA, Fletcher CD, Brun RP, Mueller E, Altiok S, Oppenheim H, Evans RM, Spiegelman BM: Terminal differentiation of human liposarcoma cells induced by ligands for peroxisome proliferator-activated receptor gamma and the retinoid X receptor. 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Carcinogenesis 22: 1379–1383, 2001\nElstner E, Mueller C, Koshizuka K, Williamson EA, Park D, Asou H, Shintaku P, Said JW, Heber D, Koeffler HP: Ligands for peroxisome proliferator-activated receptor gamma and retinoic acid receptor inhibit growth and induce apoptosis of human breast cancer cells in vitro and in BNX mice. Proc Natl Acad Sci USA 95: 8806–8811, 1998\nKilgore MW, Tate PL, Rai S, Sengoku E, Price TM: MCF-7 and T47D human breast cancer cells contain a functional peroxisomal response. Mol Cell Endocrinol 129: 229–235, 1997\nMueller E, Sarraf P, Tontonoz P, Evans RM, Martin KJ, Zhang M, Fletcher C, Singer S, Spiegelman BM: Terminal differentiation of human breast cancer through PPAR gamma. Mol Cell 1: 465–470, 1998\nTakahashi N, Okumura T, Motomura W, Fujimoto Y, Kawabata I, Kohgo Y: Activation of PPARgamma inhibits cell growth and induces apoptosis in human gastric cancer cells. FEBS Lett 455: 135–139, 1999\nSato H, Ishihara S, Kawashima K, Moriyama N, Suetsugu H, Kazumori H, Okuyama T, Rumi MA, Fukuda R, Nagasue N, Kinoshita Y: Expression of peroxisome proliferatoractivated receptor (PPAR)gamma in gastric cancer and inhibitory effects of PPARgamma agonists. Br J Cancer 83: 1394–1400, 2000\nChang TH, Szabo E: Induction of differentiation and apoptosis by ligands of peroxisome proliferator-activated receptor gamma in non-small cell lung cancer. Cancer Res 60: 1129–1138, 2000\nTsubouchi Y, Sano H, Kawahito Y, Mukai S, Yamada R, Kohno M, Inoue K, Hla T, Kondo M: Inhibition of human lung cancer cell growth by the peroxisome proliferatoractivated receptor-gamma agonists through induction of apoptosis. Biochem Biophys Res Commun 270: 400–405, 2000\nMotomura W, Okumura T, Takahashi N, Obara T, Kohgo Y: Activation of peroxisome proliferator-activated receptor gamma by troglitazone inhibits cell growth through the increase of p27KiP1 in human pancreatic carcinoma cells. Cancer Res 60: 5558–5564, 2000\nElnemr A, Ohta T, Iwata K, Ninomia I, Fushida S, Nishimura GI, Kitagawa H, Kayahara M, Yamamoto M, Terada T, Miwa K: PPARgamma ligand (thiazolidinedione) induces growth arrest and differentiation markers of human pancreatic cancer cells. Int J Oncol 17: 1157–1164, 2000\nAsou H, Verbeek W, Williamson E, Elstner E, Kubota T, Kamada N, Koeffler HP: Growth inhibition of myeloid leukemia cells by troglitazone, a ligand for peroxisome proliferator activated receptor gamma, and retinoids. Int J Oncol 15: 1027–1031, 1999\nBerger J, Bailey P, Biswas C, Cullinan CA, Doebber TW, Hayes NS, Saperstein R, Smith RG, Leibowitz MD: Thiazolidinediones produce a conformational change in peroxisomal proliferator-activated receptor-gamma: binding and activation correlate with antidiabetic actions in db\u002Fdb mice. Endocrinology 137: 4189–4195, 1996\nLehmann JM, Moore LB, Smith-Oliver TA, Wilkison WO, Willson TM, Kliewer SA: An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferatoractivated receptor gamma (PPARgamma). J Biol Chem 270: 12953–12956, 1995\nLambe KG, Tugwood JD: A human peroxisomeproliferator-activated receptor-gamma is activated by inducers of adipogenesis, including thiazolidinedione drugs. Eur J Biochem 239: 1–7, 1996\nForman BM, Tontonoz P, Chen J, Brun RP, Spiegelman BM, Evans RM: 15-Deoxy-delta 12,14-prostaglandin J2 is a ligand for the adipocyte determination factor PPAR gamma. Cell 83: 803–812, 1995\nElbrecht A, Chen Y, Cullinan CA, Hayes N, Leibowitz M, Moller DE, Berger J: Molecular cloning, expression and characterization of human peroxisome proliferator activated receptors gamma 1 and gamma 2. Biochem Biophys Res Commun 224: 431–437, 1996\nNwankwo JO, Robbins ME: Peroxisome proliferatoractivated receptor-gamma expression in human malignant and normal brain, breast and prostate-derived cells. Prostaglandins Leukot Essent Fatty Acids 64: 241–245, 2001\nPrasanna P, Thibault A, Liu L, Samid D: Lipid metabolism as a target for brain cancer therapy: synergistic activity of lovastatin and sodium phenylacetate against human glioma cells. J Neurochem 66: 710–716, 1996\nChattopadhyay N, Singh DP, Heese O, Godbole MM, Sinohara T, Black PM, Brown EM: Expression of peroxisome proliferator-activated receptors (PPARS) in human astrocytic cells: PPARgamma agonists as inducers of apoptosis. J Neurosci Res 61: 67–74, 2000\nZander T, Kraus JA, Grommes C, Schlegel U, Feinstein D, Klockgether T, Landreth G, Koenigsknecht J, Heneka MT: Induction of apoptosis in human and rat glioma by agonists of the nuclear receptor PPARgamma. J Neurochem 81: 1052–1060, 2002\nYung WK, Lotan R, Lee P, Lotan D, Steck PA: Modulation of growth and epidermal growth factor receptor activity by retinoic acid in human glioma cells. Cancer Res 49: 1014–1019, 1989\nHigashida H, Miki N, Ito M, Iwata T, Tsukida K: Cytotoxic action of retinoidal butenolides on mouse neuroblastoma and rat glioma cells. Int J Cancer 33: 677–681, 1984\nYung WK, Kyritsis AP, Gleason MJ, Levin VA: Treatment of recurrent malignant gliomas with high-dose 13-cis-retinoic acid. Clin Cancer Res 2: 1931–1935, 1996\nElstner E, Williamson EA, Zang C, Fritz J, Heber D, Fenner M, Possinger K, Koeffler HP: Novel therapeutic approach: ligands for PPARgamma and retinoid receptors induce apoptosis in bcl-2-positive human breast cancer cells. Breast Cancer Res Treat 74: 155–165, 2002\nGavrieli Y, Sherman Y, Ben Sasson SA: Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation. J Cell Biol 119: 493–501, 1992\nStadelmann C, Bruck W, Bancher C, Jellinger K, Lassmann H: Alzheimer disease: DNA fragmentation indicates increased neuronal vulnerability, but not apoptosis. J Neuropathol Exp Neurol 57: 456–464, 1998\nPE Biosystems: Relative quantitation of gene expression. ABI Prism 7700 Sequence Detection System, 1997\nDebril MB, Renaud JP, Fajas L, Auwerx J: The pleiotropic functions of peroxisome proliferator-activated receptor gamma. J Mol Med 79: 30–47, 2001\nKonopleva M, Andreeff M: Role of peroxisome proliferatoractivated receptor-gamma in hematologic malignancies. Curr Opin Hematol 9: 294–302, 2002.\nIkezoe T, Miller CW, Kawano S, Heaney A, Williamson EA, Hisatake J, Green E, Hofmann W, Taguchi H, Koeffler HP: Mutational analysis of the peroxisome proliferator-activated receptor gamma gene in human malignancies. Cancer Res 61: 5307–5310, 2001\nCullingford TE, Bhakoo K, Peuchen S, Dolphin CT, Patel R, Clark JB: Distribution of mRNAs encoding the peroxisome proliferator-activated receptor alpha, beta, and gamma and the retinoid X receptor alpha, beta, and gamma in rat central nervous system. J Neurochem 70: 1366–1375, 1998\nBouterfa H, Picht T, Kess D, Herbold C, Noll E, Black PM, Roosen K, Tonn JC: Retinoids inhibit human glioma cell proliferation and migration in primary cell cultures but not in established cell lines. Neurosurgery 46: 419–430, 2000 118\nToyota M, Miyazaki Y, Kitamura S, Nagasawa Y, Kiyohara T, Shinomura Y, Matsuzawa Y: Peroxisome proliferator-activated receptor gamma reduces the growth rate of pancreatic cancer cells through the reduction of cyclin D1. Life Sci 70: 1565–1575, 2002\nYin F, Wakino S, Liu Z, Kim S, Hsueh WA, Collins AR, Van Herle AJ, Law RE: Troglitazone inhibits growth of MCF-7 breast carcinoma cells by targeting G1 cell cycle regulators. Biochem Biophys Res Commun 286: 916–922, 2001\nGuan YF, Zhang YH, Breyer RM, Davis L, Breyer MD: Expression of peroxisome proliferator-activated receptor gamma (PPARgamma) in human transitional bladder cancer and its role in inducing cell death. Neoplasia 1: 330–339, 1999\nRumi MA, Sato H, Ishihara S, Kawashima K, Hamamoto S, Kazumori H, Okuyama T, Fukuda R, Nagasue N, Kinoshita Y: Peroxisome proliferator-activated receptor gamma ligand-induced growth inhibition of human hepatocellular carcinoma. Br J Cancer 84: 1640–1647, 2001\nCesi V, Tanno B, Vitali R, Mancini C, Giuffrida ML, Calabretta B, Raschella G: Cyclin D1-dependent regulation of B-myb activity in early stages of neuroblastoma differentiation. Cell Death Differ 9: 1232–1239, 2002\nSpinella MJ, Freemantle SJ, Sekula D, Chang JH, Christie AJ, Dmitrovsky E: Retinoic acid promotes ubiquitination and proteolysis of cyclin D1 during induced tumor cell differentiation. J Biol Chem 274: 22013–22018, 1999\nZhang D, Vuocolo S, Masciullo V, Sava T, Giordano A, Soprano DR, Soprano KJ: Cell cycle genes as targets of retinoid induced ovarian tumor cell growth suppression. Oncogene 20: 7935–7944, 2001\nZhu WY, Jones CS, Kiss A, Matsukuma K, Amin S, De Luca LM: Retinoic acid inhibition of cell cycle progression in MCF-7 human breast cancer cells. Exp Cell Res 234: 293–299, 1997\nNasi S, Ciarapica R, Jucker R, Rosati J, Soucek L: Making decisions through Myc. FEBS Lett 490: 153–162, 2001\nZajac-Kaye M: Myc oncogene: a key component in cell cycle regulation and its implication for lung cancer. Lung Cancer 34(Suppl. 2): S43–S46, 2001\nSears R, Ohtani K, Nevins JR: Identification of positively and negatively acting elements regulating expression of the E2F2 gene in response to cell growth signals. Mol Cell Biol 17: 5227–5235, 1997\nKing KL, Cidlowski JA: Cell cycle regulation and apoptosis. Annu Rev Physiol 60: 601–617, 1998\nChen GG, Lee JF, Wang SH, Chan UP, Ip PC, Lau WY: Apoptosis induced by activation of peroxisome-proliferator activated receptor-gamma is associated with Bcl-2 and NF-kappaB in human colon cancer. 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undergoing-surgery-assisted-by-5-aminolevulinic-acid-guided-resection-followed-by-BCNU-wafers-implantation-a-3-year-follow-up",{"abstract":2488,"title":2490,"references":2492,"doi":2494},{"EN":2489},"The purpose of the study was to evaluate the clinical outcome of the association of BCNU wafers implantation and 5-aminolevulinic acid (5-ALA) fluorescence in the treatment of patients with newly diagnosed glioblastoma (ndGBM). Clinical and surgical data from patients who underwent 5-ALA surgery followed by BCNU wafers implantation were retrospectively evaluated (20 patients, Group I) and compared with data of patients undergoing surgery with BCNU wafers alone (42 patients, Group II) and 5-ALA alone (59 patients, Group III). Patients undergoing 5-ALA assisted resection followed by BCNU wafers implantation (Group I) resulted long survivors (>3 years) in 15 % of cases and showed a median PFS and MS of 11 and 22 months, respectively. Patients treated with BCNU wafers presented a significantly higher survival when tumor was removed with the assistance of 5-ALA (22 months with vs 18 months without 5-ALA, p \u003C 0.0001); these data could be partially explained by the significantly higher CRET achieved in patients operated with 5-ALA assistance (80 % with vs 47 %% without 5-ALA). Moreover, patients of Group I showed a significant increased survival compared with Group III (5-ALA without BCNU) (22 months with vs 21 months without BCNU wafers, p = 0.0025) even with a comparable CRET (80 % vs 76 %, respectively). The occurrence of adverse events related to wafers did not significantly increase with 5-ALA (20 % with and 19 % without 5-ALA) and did not impact in survival outcome. In conclusion, our experience shows that on selected ndGBM patients 5-ALA technology and BCNU wafers implantation show a synergic action on patients’ outcome without increasing adverse events occurrence.",{"EN":2491},"Outcome of patients affected by newly diagnosed glioblastoma undergoing surgery assisted by 5-aminolevulinic acid guided resection followed by BCNU wafers implantation: a 3-year follow-up",{"VOID":2493},"Brem H, Piantadosi S, Burger PC, Walker M, Selker R, Vick NA, Black K, Sisti M, Brem S, Mohr G, Muller P, Morawetz R, Clifford Schold S (1995) Placebo-controlled trial of safety and efficacy of intraoperative controlled delivery by biodegradable polymers of chemotherapy for recurrent gliomas. The Polymer-brain Tumor Treatment Group. Lancet 345:1008–1012\nWestphal M, Hilt DC, Bortey E, Delavault P, Olivares R, Warnke PC, Whittle IR, Jääskeläinen J, Ram Z (2003) A Phase 3 trial of local chemotherapy with biodegradable carmustine (BCNU) wafers (Gliadel wafers) in patients with primary malignant glioma. Neuro-Oncology 5:79–88\nBarr JG, Grundy PL (2012) The effects of the NICE technology appraisal 121 (gliadel and temozolomide) on survival in high-grade glioma. Br J Neurosurg 26(6):818–822\nd’Avella D, Della Puppa A (2012) Safety and efficacy of Gliadel wafers for newly diagnosed and recurrent glioblastomas. Acta Neurochir 154(8):1379–1381\nHart MG, Grant R, Garside R, Rogers G, Somerville M, Stein K (2011) Chemotherapy wafers for high grade glioma. Cochrane Database Syst Rev 16(3):CD007294\nWatts C, Dunn L, Ashkan K, Jenkinson M, Smith P (2013) Establishing the efficacy of Gliadel wafers: progress towards a Phase III trial. Acta Neurochir (Wien) 155(1):61–62\nStummer W, Pichlmeier U, Meinel T, Wiestler OD, Zanella F, Reulen HJ; ALA-Glioma Study Group. (2006) Fluorescence-guided surgery with 5-aminolevulinic acid for resection of malignant glioma: a randomised controlled multicentre phase III trial. Lancet Oncol 7(5):392–401\nStummer W, Reulen HJ, Meinel T, Pichlmeier U, Schumacher W, Tonn JC, Rohde V, Oppel F, Turowski B, Woiciechowsky C, Franz K, Pietsch T; ALA-Glioma Study Group (2008) Extent of resection and survival in glioblastoma multiforme: identification of and adjustment for bias. Neurosurgery 62 (3): 564–576\nDella Puppa A, Gioffrè G, Gardiman MP, Frasson C, Cecchin D, Scienza R, Persano L (2014) Intra-operative 5-aminolevulinic acid (ALA)-induced fluorescence of medulloblastoma: phenotypic variability and CD133(+) expression according to different fluorescence patterns. Neurol Sci 35 (1):99–102\nDella Puppa A, Rustemi O, Gioffrè G, Troncon I, Lombardi G, Rolma G, Sergi M, Munari M, Cecchin D, Gardiman MP, Scienza R (2014) Predictive value of intraoperative 5-aminolevulinic acid-induced fluorescence for detecting bone invasion in meningioma surgery. J Neurosurg 120(4):840–845\nPrice SJ, Whittle IR, Ashkan K, Grundy P, Cruickshank G (2012) NICE guidance on the use of carmustine wafers in high grade gliomas: a national study on variation in practice. Br J Neurosurg 26:331–335\nStupp R, Mason WP, van den Bent MJ, Weller M, Fisher B, Taphoorn MJ, Belanger K, Brandes AA, Marosi C, Bogdahn U, Curschmann J, Janzer RC, Ludwin SK, Gorlia T, Allgeier A, Lacombe D, Cairncross JG, Eisenhauer E, Mirimanoff RO; European Organisation for Research and Treatment of Cancer Brain Tumor and Radiotherapy Groups; National Cancer Institute of Canada Clinical Trials Group (2005) Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. N Engl J Med 352:987–996\nLacroix M, Abi-Said D, Fourney DR, Gokaslan ZL, Shi W, DeMonte F, Lang FF, McCutcheon IE, Hassenbusch SJ, Holland E, Hess K, Michael C, Miller D, Sawaya R (2001) A multivariate analysis of 416 patients with glioblastoma multiforme: prognosis, extent of resection, and survival. J Neurosurg 95(2):190–198\nSawaya R, Hammoud M, Schoppa D, Hess KR, Wu SZ, Shi WM, Wildrick DM (1998) Neurosurgical outcomes in a modern series of 400 craniotomies for treatment of parenchymal tumors. Neurosurgery 42(5):1044–1055\nSchucht P, Beck J, Abu-Isa J, Andereggen L, Murek M, Seidel K, Stieglitz L, Raabe A (2012) Gross total resection rates in contemporary glioblastoma surgery: results of an institutional protocol combining 5-ALA intraoperative fluorescence imaging and brain mapping. Neurosurgery 71(5):927–935\nDella Puppa A, Ciccarino P, Lombardi G, Rolma G, Cecchin D, Rossetto M (2014) 5-Aminolevulinic acid fluorescence in high grade glioma surgery: surgical outcome, intraoperative findings, and fluorescence patterns. Biomed Res Int. doi:10.1155\u002F2014\u002F232561\nDella Puppa A, Rossetto M, Ciccarino P, Denaro L, Rotilio A, d’Avella D, Scienza R (2011) Carmustine wafer implantation when surgical cavity is communicating with cerebral ventricles: technical considerations on a clinical series. World Neurosurg 76(1–2):156–159\nDella Puppa A, De Pellegrin S, d’Avella E, Gioffrè G, Rossetto M, Gerardi A, Lombardi G, Manara R, Munari M, Saladini M, Scienza R (2013) 5-aminolevulinic acid (5-ALA) fluorescence guided surgery of high-grade gliomas in eloquent areas assisted by functional mapping. Our experience and review of the literature. Acta Neurochir 155(6):965–972\nBock HC, Puchner MJ, Lohmann F, Schütze M, Koll S, Ketter R, Buchalla R, Rainov N, Kantelhardt SR, Rohde V, Giese A (2010) First-line treatment of malignant glioma with carmustine implants followed by concomitant radiochemotherapy: a multicenter experience. Neurosurg Rev 33(4):441–449\nDuntze J, Litré CF, Eap C, Théret E, Debreuve A, Jovenin N, Lechapt-Zalcman E, Metellus P, Colin P, Guillamo JS, Emery E, Menei P, Rousseaux P, Peruzzi P (2013) Implanted carmustine wafers followed by concomitant radiochemotherapy to treat newly diagnosed malignant gliomas: prospective, observational, multicenter study on 92 cases. Ann Surg Oncol 20(6):2065–2072\nLechapt-Zalcman E, Levallet G, Dugué AE, Vital A, Diebold MD, Menei P, Colin P, Peruzzy P, Emery E, Bernaudin M, Chapon F, Guillamo JS (2012) O(6) -methylguanine-DNA methyltransferase (MGMT) promoter methylation and low MGMT-encoded protein expression as prognostic markers in glioblastoma patients treated with biodegradable carmustine wafer implants after initial surgery followed by radiotherapy with concomitant and adjuvant temozolomide. Cancer 118(18):4545–4554\nMcGirt MJ, Than KD, Weingart JD, Chaichana KL, Attenello FJ, Olivi A, Laterra J, Kleinberg LR, Grossman SA, Brem H, Quiñones-Hinojosa A (2009) Gliadel (BCNU) wafer plus concomitant temozolomide therapy after primary resection of glioblastoma multiforme. J Neurosurg 110(3):583–588\nMenei P, Metellus P, Parot-Schinkel E, Loiseau H, Capelle L, Jacquet G, Guyotat J (2010) Biodegradable carmustine wafers (Gliadel) alone or in combination with chemoradiotherapy: the French experience. Ann Surg Oncol 17(7):1740–1746\nDella Puppa A, Denaro L, Rossetto M, Ciccarino P, Manara R, Lombardi G, Del Moro G, Rotilio A, d’Avella D, Scienza R (2011) Postoperative seizure in high grade glioma patients treated with BCNU wafers. A mono-institutional experience. J Neurooncol 105(2):275–280\nChaichana KL, Kone L, Bettegowda C, Weingart JD, Olivi A, Lim M, Quinones-Hinojosa A, Gallia GL, Brem H (2015) Risk of surgical site infection in 401 consecutive patients with glioblastoma with and without carmustine wafer implantation. Neurol Res Aug;37(8):717–726\nDella Puppa A, Rossetto M, Ciccarino P, Del Moro G, Rotilio A, Manara R, Gardiman MP, Denaro L, d’Avella D, Scienza R (2010) The first 3 months after BCNU wafers implantation in high-grade glioma patients: clinical and radiological considerations on a clinical series. Acta Neurochir 152(11):1923–1931\nDíez Valle R, Slof J, Galván J, Arza C, Romariz C, Vidal C (2014) VISIONA study researchers. Observational, retrospective study of the effectiveness of 5-aminolevulinic acid in malignant glioma surgery in Spain (The VISIONA study). Neurologia 29(3):131–138\nJacquesson T, Ducray F, Maucort-Boulch D, Armoiry X, Louis-Tisserand G, Mbaye M, Pelissou-Guyotat I, Guyotat J (2013) Surgery of high-grade gliomas guided by fluorescence: a retrospective study of 22 patients. Neurochirurgie 59(1):9–16\nAldave G, Tejada S, Pay E, Marigil M, Bejarano B, Idoate MA, Díez-Valle R (2013) Prognostic value of residual fluorescent tissue in glioblastoma patients after gross total resection in 5-aminolevulinic acid-guided surgery. Neurosurgery 72(6):915–920\nStummer W, Nestler U, Stockhammer F, Krex D, Kern BC, Mehdorn HM, Vince GH, Pichlmeier U (2011) Favorable outcome in the elderly cohort treated by concomitant temozolomide radiochemotherapy in a multicentric phase II safety study of 5-ALA. J Neurooncol 103(2):361–370\nChaichana KL, Cabrera-Aldana EE, Jusue-Torres I, Wijesekera O, Olivi A, Rahman M, Quinones-Hinojosa A (2014) When gross total resection of a glioblastoma is possible, how much resection should be achieved? World Neurosurg 82(1–2). doi:10.1016\u002Fj.wneu.2014.01.019\nChaichana KL, Jusue-Torres I, Navarro-Ramirez R, Raza SM, Pascual-Gallego M, Ibrahim A, Hernandez-Hermann M, Gomez L, Ye X, Weingart JD, Olivi A, Blakeley J, Gallia GL, Lim M, Brem H, Quinones-Hinojosa A (2014) Establishing percent resection and residual volume thresholds affecting survival and recurrence for patients with newly diagnosed intracranial glioblastoma. Neurooncology 16(1):113–22. doi:10.1093\u002Fneuonc\u002Fnot137\nCoburger J, Hagel V, Wirtz CR, König R (2015) Surgery for glioblastoma: impact of the combined use of 5-aminolevulinic acid and intraoperative MRI on extent of resection and survival. PLoS One. doi:10.1371\u002Fjournal.pone.0131872\nSanai N, Polley MY, McDermott MW, Parsa AT, Berger MS (2011) An extent of resection threshold for newly diagnosed glioblastomas. J Neurosurg 115(1):3–8\nDas P, Puri T, Jha P, Pathak P, Joshi N, Suri V, Sharma MC, Sharma BS, Mahapatra AK, Suri A, Sarkar C (2011) A clinicopathological and molecular analysis of glioblastoma multiforme with long-term survival. J Clin Neurosci 18(1):66–70\nAmelot A, De Cremoux P, Quillien V, Polivka M, Adle-Biassette H, Lehmann-Che J, Françoise L, Carpentier AF, George B, Mandonnet E, Froelich S (2015) IDH-Mutation is a weak predictor of long-term survival in glioblastoma patients. PLoS One 9;10(7):e0130596. doi:10.1371\u002Fjournal.pone.0130596\nChaudhry NS, Shah AH, Ferraro N, Snelling BM, Bregy A, Madhavan K, Komotar RJ (2013) Predictors of long-term survival in patients with glioblastoma multiforme: advancements from the last quarter century. Cancer Invest 31(5):287–308\nMazaris P, Hong X, Altshuler D, Schultz L, Poisson LM, Jain R, Mikkelsen T, Rosenblum M, Kalkanis S (2014) Key determinants of short-term and long-term glioblastoma survival: a 14-year retrospective study of patients from the Hermelin Brain Tumor Center at Henry Ford Hospital. Clin Neurol Neurosurg 120:103–112\nStummer W, Tonn JC, Mehdorn HM, Nestler U, Franz K, Goetz C, Bink A, Pichlmeier U; ALA-Glioma Study Group (2011) Counterbalancing risks and gains from extended resections in malignant glioma surgery: a supplemental analysis from the randomized 5-aminolevulinic acid glioma resection study. Clinical article. 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investigated expression of macrophage inflammatory protein-1 (MIP-1) α and β in human astrocytoma cell lines and surgical specimens of astrocytic tumors. Enzyme-linked immunosorbent assay (ELISA) showed constitutive secretion of MIP-1α protein in only one and MIP-1β in none of 7 cell lines tested. However, MIP-1α production was increased in three cell lines by stimulation with lipopolysaccharide (LPS) and 5 cell lines by stimulation with phorbol-12myristate-13-acetate (PMA). Also, induction of MIP-1β production was observed in one cell line with LPS stimulation and in two cell lines with PMA stimulation. Reverse-transcription polymerase chain reaction (RT-PCR) showed the increase of MIP-1α and β mRNA expression in these cell lines. The increase of the mRNA with the stimuli was further confirmed by Northern blot analysis. In contrast, RT-PCR analysis revealed that the majority of the tested tumor specimens of high-grade astrocytomas expressed both MIP-1α and MIP-1β mRNAs. ELISA detected MIP-1β protein in 1 of 11 cerebrospinal fluid samples from patients with high-grade astrocytoma and in 8 of 9 tumor cyst fluid samples, whereas MIP-1α was detected in only 1 cyst fluid somple. Taken together, these results indicate that astrocytic tumor cells are capable of expressing and producing MIPs, and suggest that MIPs may participate in the inflammatory responses commonly seen in astrocytic tumors.",{"EN":2725},"Human astrocytoma cells are capable of producing macrophage inflammatory protein-1Β",{"VOID":2727},"Tada M, deTribolet N: Recent advances in immunobiology of brain tumors. J Neuro-Oncol 17: 261–271, 1993\nTada M, deTribolet N: Immunobiology of malignant gliomas. J Clin Neurosci 3: 102–113, 1996\nVanMeir EG: Cytokines and tumors of the central nervous system. Glia 15: 264–288, 1995\nBaggiolini M, Dahinden CA: CC chemokines in allergic inflammation. Immunol Today 15: 127–133, 1994\nRot A, Krieger M, Brunner T, Bischoff SC, Schall TJ, Dahinden CA: RANTES and macrophage inflammatory protein 1 alpha induce the migration and activation of normal human eosinophil granulocytes. J Exp Med 176: 1489– 1495, 1992\nSchall TJ, Bacon K, Camp RD, Kaspari JW, Goeddel DV: Human macrophage inflammatory protein alpha (MIP-1 alpha) and MIP-1 beta chemokines attract distinct population of lymphocytes. J Exp Med 177: 1821–1826, 1993\nTaub DD, Conlon K, Lloyd AR, Oppenheim JJ, Kelvin DJ: Preferential migration of activated CD4 ??and CD8 ??T cells in response to MIP-1 alpha and MIP-1 beta. Science 260: 355–358, 1993\nKoch AE, Kunkel SL, Harlow LA, Mazarakis DD, Haines GK, Burdick MD, Pope RM, Strieter RM: Macrophage inflammatory protein-1. A novel chemotactic cytokine for macrophages in rheumatoid arthritis. J Clin Invest 93: 921– 928, 1989\nWolpe SD, Cerami A: Macrophage inflammatory proteins 1 and 2: members of a novel superfamily of cytokine. FASEB J 3: 2565–2573, 1989\nFahey TJ3d, Tracey KJ, Tekamp-Olson P, Cousens LS, Jones WG, Shires GT, Cerami A, Sherry B: Macrophage inflammatory protein 1 modulates macrophage function. J Immunol 148: 2764–2769, 1992\nCook DN: The role of MIP-1 alpha in inflammation and hematopoiesis. J Leukocyte Biol 59: 61–66, 1996\nVanOtteren GM, Standiford TJ, Kunkel SL, Danforth JM, Burdick MD, Abruzzo LV, Strieter RM: Expression and regulation of macrophage inflammatory protein-1 alpha by murine alveolar and peritoneal macrophages. Am J Respir Cell Mol Biol 10: 8–15, 1994\nKasama T, Strieter RM, Standiford TJ, Burdick MD, Kunkel SL: Expression and regulatin of humanneutrophil-derived macrophage inflammatory protein 1 alpha.J ExpMed 178: 63–72, 1993\nRobinson E, Keystone EC, Schall TJ, Gillett N, Fish EN: Chemokine expression in rheumatoid arthritis (RA): evidence of RANTES and macrophage inflammatory protein (MIP)-1 beta production by synovial T cells. Clin Exp Immunol 101: 398–407, 1995\nLukacs NW, Chensue SW, Smith RE, Strieter RM, Warmington K, Wilke C, Kunkel SL: Production of monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 alpha by inflammatory granuloma fibroblasts. Am J Pathol 144: 711–718, 1994\nHeufler C, Topar G, Koch F, Trockenbacher B, Kampgen E, Romani N, Schuler G: Cytokine gene expression in murine epidermal cell suspensions: interleukin-1 beta and macrophage inflammatory protein 1 alpha are selectively expressed in Langerhans cells but are differentially regulated in culture. J Exp Med 176: 1221–1226, 1992\nMurphy GJ, Jia XC, Song Y, Ong E, Shrivastava R, Bocchini V, Lee YL, Eng LF: Macrophage inflammatory protein 1 alpha mRNA expression in an immortalized microglial cell line and cortical astrocyte cultures. 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Lab Invest 67: 635–642, 1992\nHunter CA, Roberts CW, Murray M, Alexander J: Detection of cytokine mRNA in the brains of mice with toxoplasmic encephalitis. Parasite Immunol 14: 405–413, 1992\nKim JS, Gautam SC, Chopp M, Zaloga C, Jones ML, Ward PA, Welch KM: Expression of monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 after focal cerebral ischemia in the rat. J Neuroimmunol 56: 127– 134, 1995\nMeek DW, Street AJ: Nuclear protein phosphorylation and growth control. Biochem J 287: 1–15, 1992\nBenzil DL, Finkelstein SD, Epstein MH, Finch PW: Expression pattern of ?-protein kinase C in human astrocytomas indicates a role in malignant progression. Cancer Res 52: 2951–2956, 1992\nRice NR, Ernst MK: In vivo control of NF-kB activation by IkBa. EMBO J 12: 4685–4695, 1993\nWidmer U, Manogue KR, Cerami A, Sherry B: Genomic cloning and promoter analysis of macrophage inflammatory protein (MIP)-2, MIP-1 alpha, and MIP-1 beta, members of the chemokine superfamily of proinflammatory cytokines. J Immunol 150: 4996–5012, 1993\nKhan S, Wigley C: Different effects of a macrophage cytokine on proliferation in astrocytes and Schwann cells. Neuroreport 5: 1381–1385, 1994\nHirose K, Hakozaki M, Nyunoya Y, Kobayashi Y, Matsuhita K, Takenouchi T, Mikata A, Mukaida N, Matsuhima K: Chemokine gene transfection into tumour cells reduced tumorigenicity in nude mice in association with neutrophilic infiltration. Br J Cancer 72: 708–714, 1995\nMantovani A: Tumor-associated macrophages in neoplastic progression: a paradigm for the in vivo function of chemokines. Lab Invest 71: 5–16, 1994",{"VOID":2729},"10.1023\u002FA:1005959719927","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FA:1005959719927",[2732,2747,2759,2772,2784,2797],{"id":2733,"sortIndex":32,"researcher":28,"roles":2734,"affiliations":2735,"properties":2744,"displayName":2746,"givenName":28,"familyName":28},"a6775702-3239-4d96-ada4-79588f0bb29f",[1064],[2736],{"id":2737,"sortIndex":32,"affiliation":2738,"properties":28},"a3f0ecc8-370c-43e2-98f3-925079d62979",{"id":2737,"createTime":28,"updateTime":28,"relativeEntities":2739,"slug":28,"properties":2740,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2743,"statistic":28},[],{"title":2741},{"VI":2742},"Department of Neurosurgery, University of Hokkaido, School of Medicine, Kita-ku, Sapporo, Japan",[],{"title":2745},{"VI":2746},"Nobuaki 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have been observed in the tumor environment for decades and have been demonstrated to play important roles in the pathogenesis and development of several different tumors. So far there is a clear lack of specific studies relating to the presence of bacteria in pituitary neuroendocrine tumors (PitNETs). In this study, we performed five region-based amplification and bacterial 16 S rRNA sequencing to identify the microbiome of PitNET tissues across four clinical phenotypes. Multiple filter procedures were performed to inhibit the risk of contamination with bacteria and bacterial DNA. Histological analysis was also conducted to validate the localization of bacteria in the intra-tumoral region. We identified common and diverse bacterial types across the four clinical phenotypes of PitNET. We also predicted the potential functions of these bacteria in tumor phenotypes and found that these functions were reported in certain previous mechanistic studies. Our data indicate that the pathogenesis and development of tumors may correlate with the behavior of intra-tumoral bacteria. Histological results, including lipopolysaccharide (LPS) staining and fluorescence in situ hybridization (FISH) for bacterial 16 S rRNA clearly demonstrated the localization of bacteria in the intra-tumoral region. Staining for Iba-1 suggested that the proportion of microglia was more abundant in FISH-positive regions than in FISH-negative regions. Furthermore, in FISH-positive regions, the microglia exhibited a longitudinally branched morphology that was different to the compact morphology observed in FISH-negative regions. In summary, we provide an evidence for the existence of intra-tumoral bacteria in PitNET.",{"EN":2879},"Evidence for an intra-tumoral microbiome in pituitary neuroendocrine tumors with different clinical phenotypes",{"VOID":2881},"Kostic AD, Chun E, Robertson L, Glickman JN, Gallini CA, Michaud M, Clancy TE, Chung DC, Lochhead P, Hold GL, El-Omar EM, Brenner D, Fuchs CS, Meyerson M, Garrett WS (2013) Fusobacterium nucleatum potentiates intestinal tumorigenesis and modulates the tumor-immune microenvironment. Cell Host Microbe 14:207–215. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.chom.2013.07.007\nBhandari S, Pandey RK, Dahal S, Shahreyar M, Dhakal B, Jha P, Venkatesan T, Saeian K (2018) Risk, outcomes, and predictors of Clostridium difficile infection in Lymphoma: a Nationwide Study. 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Front Endocrinol 9:678. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffendo.2018.00678\nSong J, Ma W, Gu X, Zhao L, Jiang J, Xu Y, Zhang L, Zhou M, Yang L (2019) Metabolomic signatures and microbial community profiling of depressive rat model induced by adrenocorticotrophic hormone. J Transl Med 17:224. https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs12967-019-1970-8\nHill MK, Macleod RM, Orcutt P (1976) Dibutyryl cyclic AMP, adenosine and guanosine blockade of the dopamine, ergocryptine and apomorphine inhibition of prolactin release in vitro. Endocrinology 99:1612–1617. https:\u002F\u002Fdoi.org\u002F10.1210\u002Fendo-99-6-1612\nFranco-Bocanegra DK, Gourari Y, McAuley C, Chatelet DS, Johnston DA, Nicoll JAR, Boche D (2021) Microglial morphology in Alzheimer’s disease and after Abeta immunotherapy. Sci Rep 11:15955. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41598-021-95535-0\nWalker FR, Beynon SB, Jones KA, Zhao Z, Kongsui R, Cairns M, Nilsson M (2014) Dynamic structural remodelling of microglia in health and disease: a review of the models, the signals and the mechanisms. Brain Behav Immunity 37:1–14. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.bbi.2013.12.010\nde Martel C, Ferlay J, Franceschi S, Vignat J, Bray F, Forman D, Plummer M (2012) Global burden of cancers attributable to infections in 2008: a review and synthetic analysis. 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lymphomas of the central nervous system (PCNSL) are highly aggressive tumors affecting exclusively the CNS, meninges, and eyes. PCNSL must be separated from secondary spread of systemic lymphoma to the CNS (SCNSL), which may occur at diagnosis or relapse of systemic lymphomas. At present, there are no valid methods to distinguish PCNSL from SCNSL based on tumor biopsy because of similar histological presentation. However, SCNSL and PCNSL are different in terms of prognosis and adequate therapy protocols. MicroRNA expression profiles of CSF samples collected from SCNSL and PCNSL patients were compared using microRNA arrays. MiR-30c revealed the largest differential expression and was selected for validation by RT-PCR on 61 CSF samples from patients with PCNSL and 14 samples from SCNSL. MiR-30c was significantly increased in patients with SCNSL compared to PCNSL (p \u003C 0.001). MiR-30c levels in CSF enabled the differentiation of patients with PCNSL from SCNSL with an area under the curve (AUC) of 0.86, with a sensitivity of 90.9% and a specificity of 85.5%. Our data suggest that miR-30c detected in the CSF can serve as biomarker for distinction between PCNSL and SCNSL. The validation in a larger cohort is needed. With respect to its function, miR-30c may facilitate lymphoma cells to engraft into CNS by interaction with CELSR3 gene that controls the function of ependymal cilia and, thus, affects the circulation of CSF.",{"EN":3077},"MicroRNA-30c as a novel diagnostic biomarker for primary and secondary B-cell lymphoma of the CNS",{"VOID":3079},"Ney DE, Deangelis LM (2010) Management of central nervous system lymphoma. In: Armitage JO, Mauch PM, Harris NL, Coiffier B, Dalla Favera R (eds) Non-Hodgkin lymphomas. Lippincott Willilams & Wilkins, Philadelphia, pp 527–539\nShenkier TN, Blay JY, O’Neill BP et al (2005) Primary CNS lymphoma of T-cell origin: a descriptive analysis from the international primary CNS lymphoma collaborative group. J Clin Oncol 23:2233–2239\nDeckert M, Paulus W, Kluin PM et al (2016) Lymphomas. In: World Health Organization histological classification of tumours of the central nervous system, 4th revised edn. pp 271–283\nFerreri AJ, Assanelli A, Crocchiolo R et al (2009) Central nervous system dissemination in immunocompetent patients with aggressive lymphomas: incidence, risk factors and therapeutic options. Hematol Oncol 27:61–70\nSchmitz N, Zeynalova S, Glass B et al (2012) CNS disease in younger patients with aggressive B-cell lymphoma: an analysis of patients treated on the Mabthera International Trial and trials of the German High-Grade Non-Hodgkin Lymphoma Study Group. Ann Oncol 23(5):1267–1273\nDoolittle ND, Abrey LE, Shenkier TN et al (2008) Brain parenchyma involvement as isolated central nervous system relapse of systemic non-Hodgkin lymphoma: an international primary CNS lymphoma collaborative group report. Blood 111(3):1085–1093\nAkkas BE, Vural GU (2013) The incidence of secondary central nervous system involvement in patients with non-Hodgkin’s lymphoma as detected by 18F-FDG PET\u002FCT. Nucl Med Commun 34(1):50–56\nKorfel A, Schlegel U (2013) Diagnosis and treatment of primary CNS lymphoma. Nat Rev Neurol 9(6):317–327\nKorfel A, Chamberlain M, Neuwelt E et al (2016) Therapy for secondary CNS involvement in malignant lymphomas: no standard yet! J Clin Oncol 34(15):1829–1830\nBaraniskin A, Kuhnhenn J, Schlegel U et al (2011) Identification of microRNAs in the cerebrospinal fluid as marker for primary diffuse large B-cell lymphoma of the central nervous system. Blood 117(11):3140–3146\nBaraniskin A, Kuhnhenn J, Schlegel U et al (2012) MicroRNAs in cerebrospinal fluid as biomarker for disease course monitoring in primary central nervous system lymphoma. J Neurooncol 109(2):239–244\nMarabita F, de Candia P, Torri A et al (2016) Normalization of circulating microRNA expression data obtained by quantitative real-time RT-PCR. Brief Bioinform 17(2):204–212\nCogswell JP, Ward J, Taylor IA et al (2008) Identification of miRNA changes in Alzheimer’s disease brain and CSF yields putative biomarkers and insights into disease pathways. J Alzheimers Dis 14(1):27–41\nBaraniskin A, Kuhnhenn J, Schlegel U et al (2012) Identification of microRNAs in the cerebrospinal fluid as biomarker for the diagnosis of glioma. Neuro Oncol 14(1):29–33\nFischer L, Hummel M, Korfel A et al (2011) Differential micro-RNA expression in primary CNS and nodal diffuse large B-cell lymphomas. Neuro Oncol 13(10):1090–1098\nBaraniskin A, Birkenkamp-Demtroder K, Maghnouj A et al (2012) MiR-30a-5p suppresses tumor growth in colon carcinoma by targeting DTL. Carcinogenesis 33(4):732–739\nChang TC, Yu D, Lee YS et al (2008) Widespread microRNA repression by Myc contributes to tumorigenesis. Nat Genet 40:43–50\nKong X, Xu X, Yan Y et al (2014) Estrogen regulates the tumour suppressor MiRNA-30c and its target gene, MTA-1, in endometrial cancer. PLoS ONE 9:e90810\nRodriguez-Gonzalez FG, Sieuwerts AM et al (2011) MicroRNA-30c expression level is an independent predictor of clinical benefit of endocrine therapy in advanced estrogen receptor positive breast cancer. Breast Cancer Res Treat 127:43–51\nWu F, Zhu S, Ding Y et al (2009) MicroRNA-mediated regulation of Ubc9 expression in cancer cells. Clin Cancer Res 15:1550–1557\nBudhu A, Jia HL, Forgues M et al (2008) Identification of metastasis-related microRNAs in hepatocellular carcinoma. Hepatology 47(3):897–907\nWang XJ, Zhang DL, Xu ZG et al (2014 Dec) Understanding cadherin EGF LAG seven-pass G-type receptors. J Neurochem 131(6):699–711\nTissir F, Qu Y, Montcouquiol M, Zhou L et al (2010) Lack of cadherins Celsr2 and Celsr3 impairs ependymal ciliogenesis, leading to fatal hydrocephalus. Nat Neurosci 13(6):700–707\nFletcher CD, Kahl B (2014) Central nervous system involvement in diffuse large B-cell lymphoma: An analysis of risks and prevention strategies in the post-rituximab era. Leuk Lymphoma 55:2228–2240\nSchmitz N, Zeynalova S, Nickelsen M et al (2016) CNS international prognostic index: a risk model for CNS relapse in patients with diffuse large B-cell lymphoma treated with R-CHOP. 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