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