combined inactivation of myc and k-ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas结合k - ras基因失活myc和致癌基因逆转肿瘤发生在肺腺癌和淋巴瘤.pdfVIP

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combined inactivation of myc and k-ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas结合k - ras基因失活myc和致癌基因逆转肿瘤发生在肺腺癌和淋巴瘤.pdf

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combined inactivation of myc and k-ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas结合k - ras基因失活myc和致癌基因逆转肿瘤发生在肺腺癌和淋巴瘤

Combined Inactivation of MYC and K-Ras Oncogenes Reverses Tumorigenesis in Lung Adenocarcinomas and Lymphomas Phuoc T. Tran1,2,3., Alice C. Fan2,3., Pavan K. Bendapudi2,3., Shan Koh2,3, Kim Komatsubara2,3, Joy 2,3 2,3 2,3 4,5 2,3 6 Chen , George Horng , David I. Bellovin , Sylvie Giuriato , Craig S. Wang , Jeffrey A. Whitsett , Dean W. Felsher2,3* 1 Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, United States of America, 2 Division of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, California, United States of America, 3 Division of Oncology, Department of Pathology, Stanford University ´ ´ School of Medicine, Stanford, California, United States of America, 4 Institut National de la Sante et de la Recherche Medicale (INSERM) U563 Centre de physiopathologie ´ Toulouse Purpan, Toulouse, France, 5 Universite Paul-Sabatier, Toulouse, France, 6 Division of Pulmonary Biology, Cincinnati Children’s Hospital Medical Center and University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America Abstract Background: Conditional transgenic models have established that tumors require sustained oncogene activation for tumor maintenance, exhibiting the phenomenon known as ‘‘oncogene-addiction.’’ However, most cancers are caused by multiple genetic events making it difficult to determine which oncogenes or combination of oncogenes will be the most effective targets for their treatment. Methodology/Principal Findings: To examin