targeting egfr induced oxidative stress by parp1 inhibition in glioblastoma therapy针对parp1抑制表皮生长因子受体诱导氧化应激的胶质母细胞瘤的治疗.pdfVIP

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targeting egfr induced oxidative stress by parp1 inhibition in glioblastoma therapy针对parp1抑制表皮生长因子受体诱导氧化应激的胶质母细胞瘤的治疗.pdf

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targeting egfr induced oxidative stress by parp1 inhibition in glioblastoma therapy针对parp1抑制表皮生长因子受体诱导氧化应激的胶质母细胞瘤的治疗

Targeting EGFR Induced Oxidative Stress by PARP1 Inhibition in Glioblastoma Therapy 1. 1,2. 3 4 1 1 Masayuki Nitta , David Kozono , Richard Kennedy , Jayne Stommel , Kimberly Ng , Pascal O. Zinn , 1 5 6 7 4 Deepa Kushwaha , Santosh Kesari , Frank Furnari , Katherine A. Hoadley , Lynda Chin , Ronald A. 4 6 1 1,8 DePinho , Webster K. Cavenee , Alan D’Andrea , Clark C. Chen * 1 Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America, 2 Harvard Radiation Oncology Program, Boston, Massachusetts, United States of America, 3 Almac Diagnostics, Craigavon, Northern Ireland, United Kingdom, 4 Department of Medical Oncology, Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America, 5 Department of Neurology, Moores UCSD Cancer Center, University of California San Diego, La Jolla, California, United States of America, 6 San Diego Branch, Ludwig Institute for Cancer Research, La Jolla, California, United States of America, 7 Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America, 8 Division of Neurosurgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States of America Abstract Despite the critical role of Epidermal Growth Factor Receptor (EGFR) in glioblastoma pathogenesis [1,2], EGFR targeted therapies have achieved limited clinical eff