| Literature DB >> 27372738 |
Hui Zhang1, Tao Liu2, Zhen Zhang1, Samuel H Payne2, Bai Zhang1, Jason E McDermott2, Jian-Ying Zhou1, Vladislav A Petyuk2, Li Chen1, Debjit Ray2, Shisheng Sun1, Feng Yang2, Lijun Chen1, Jing Wang3, Punit Shah1, Seong Won Cha4, Paul Aiyetan1, Sunghee Woo4, Yuan Tian1, Marina A Gritsenko2, Therese R Clauss2, Caitlin Choi1, Matthew E Monroe2, Stefani Thomas1, Song Nie2, Chaochao Wu2, Ronald J Moore2, Kun-Hsing Yu5, David L Tabb3, David Fenyö6, Vineet Bafna7, Yue Wang8, Henry Rodriguez9, Emily S Boja9, Tara Hiltke9, Robert C Rivers9, Lori Sokoll1, Heng Zhu1, Ie-Ming Shih10, Leslie Cope11, Akhilesh Pandey12, Bing Zhang3, Michael P Snyder13, Douglas A Levine14, Richard D Smith2, Daniel W Chan15, Karin D Rodland16.
Abstract
To provide a detailed analysis of the molecular components and underlying mechanisms associated with ovarian cancer, we performed a comprehensive mass-spectrometry-based proteomic characterization of 174 ovarian tumors previously analyzed by The Cancer Genome Atlas (TCGA), of which 169 were high-grade serous carcinomas (HGSCs). Integrating our proteomic measurements with the genomic data yielded a number of insights into disease, such as how different copy-number alternations influence the proteome, the proteins associated with chromosomal instability, the sets of signaling pathways that diverse genome rearrangements converge on, and the ones most associated with short overall survival. Specific protein acetylations associated with homologous recombination deficiency suggest a potential means for stratifying patients for therapy. In addition to providing a valuable resource, these findings provide a view of how the somatic genome drives the cancer proteome and associations between protein and post-translational modification levels and clinical outcomes in HGSC. VIDEO ABSTRACT.Entities:
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Year: 2016 PMID： 27372738 PMCID： PMC4967013 DOI： 10.1016/j.cell.2016.05.069
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582