Đang chuẩn bị liên kết để tải về tài liệu:
Báo cáo khoa học: " Radiation-induced Akt activation modulates radioresistance in human glioblastoma cells"
Đang chuẩn bị nút TẢI XUỐNG, xin hãy chờ
Tải xuống
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Radiation Oncology cung cấp cho các bạn kiến thức về ngành y đề tài: " Radiation-induced Akt activation modulates radioresistance in human glioblastoma cells. | Radiation Oncology BioMed Central Research Radiation-induced Akt activation modulates radioresistance in human glioblastoma cells Hui-Fang Li Jung-Sik Kim and Todd Waldman Open Access Address Department of Oncology Lombardi Comprehensive Cancer Center Georgetown University School of Medicine Washington DC USA Email Hui-Fang Li - hl235@georgetown.edu Jung-Sik Kim - jk99@georgetown.edu Todd Waldman - waldmant@georgetown.edu Corresponding author Published 14 October 2009 Received 2 June 2009 Accepted 14 October 2009 Radiation Oncology 2009 4 43 doi l0.ll86 l748-7l 7X-4-43 This article is available from http www.ro-journal.com content 4 l 43 2009 Li et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Ionizing radiation IR therapy is a primary treatment for glioblastoma multiforme GBM a common and devastating brain tumor in humans. IR has been shown to induce PI3K-Akt activation in many cell types and activation of the PI3K-Akt signaling pathway has been correlated with radioresistance. Methods Initially the effects of IR on Akt activation were assessed in multiple human GBM cell lines. Next to evaluate a potential causative role of IR-induced Akt activation on radiosensitivity Akt activation was inhibited during IR with several complementary genetic and pharmacological approaches and radiosensitivity measured using clonogenic survival assays. Results Three of the eight cell lines tested demonstrated IR-induced Akt activation. Further studies revealed that IR-induced Akt activation was dependent upon the presence of a serum factor and could be inhibited by the EGFR inhibitor AG1478. Inhibition of PI3K activation with LY294002 or with inducible wild-type PTEN inhibition of EGFR as well as direct inhibition .