作者: Moito Iijima , Kouji Banno , Ryuichiro Okawa , Megumi Yanokura , Miho Iida
DOI: 10.3892/OL.2017.5582
关键词: Gene 、 Microsatellite instability 、 Internal medicine 、 Breast cancer 、 Gene mutation 、 Cancer research 、 Ovarian cancer 、 Protein kinase B signaling 、 Epigenetics 、 Endometrial cancer 、 Oncology 、 Biology
摘要: Cancer typically develops due to genetic abnormalities, but a single gene abnormality cannot completely account for the onset of cancer. The Genome Atlas (CGA) project was conducted cross-sectional genome-wide analysis numerous abnormalities in various types This approach has facilitated identification novel AT-rich interaction domain 1A mutations ovarian clear cell carcinoma, frequent tumor protein 53 (TP53) high-grade serous and Kirsten rat sarcoma B-rapidly accelerated fibrosarcoma proto-oncogene, serine/threonine kinase low-grade carcinoma. Genome-wide endometrial cancers led establishment four subgroups: Polymerase ultramutated, microsatellite instability hypermutated, genome copy-number low high. These results may facilitate improvement prediction patient prognosis therapeutic sensitivity gynecologic enhanced use currently available agents development drugs be by classification cancer based on TP53 mutations, efficacy poly (ADP-ribose) polymerase inhibitors tumors with breast 1/2 effect phosphoinositide-3-kinase (PI3K)/mammalian target rapamycin PI3K/protein B signaling pathway. Important have been revealed analyses; however, pathogenic underlying mechanisms will require further studies multilateral evaluation using epigenetic, transcriptomic proteomic analyses, addition genomic analysis.