+Mutations found in<unk>  subtypes Gene mutated Mutation type Subtype Prevalence AKT1 amplification 3% AKT2 amplification/mutation 6%, 20% ARID1A point mutation endometrioid and clear cell BECN1 deletion BRAF point mutation low-grade serous 0.5% BRCA1 nonsense mutation high-grade serous 5% BRCA2 frameshift mutation high-grade serous 3% CCND1 amplification 4% CCND2 upregulation 15% CCNE1 amplification 20% CDK12 high-grade serous CDKN2A downregulation (30%) and deletion (2%) 32% CTNNB1 clear cell DICER1 missense mutation (somatic) nonepithelial 29% DYNLRB1 (km23) mutation 42% EGFR amplification/overexpression 20% ERBB2 (Her2/neu) amplification/overexpression mucinous and low-grade serous 30% FMS coexpression with CSF-1 50% FOXL2 point mutation (402 C to G) adult granulosa cell ~100% JAG1 amplification 2% JAG2 amplification 3% KRAS amplification mucinous and low-grade serous 11% MAML1 amplification and point mutation 2% MAML2 amplification and point mutation 4% MAML3 amplification 2% MLH1 1% NF1 deletion (8%) and point mutation (4%) high-grade serous 12% NOTCH3 amplification and point mutation 11% NRAS low-grade serous PIK3C3 (PI3K3) amplification/mutation 12–20% PIK3CA amplification endometrioid and clear cell 18% PPP2R1A endometrioid and clear cell PTEN deletion endometrioid and clear cell 7% RB1 deletion (8%) and point mutation (2%) 10% TGF-β mutation/overexpression 12% TP53 mutation/overexpression high-grade serous 20–50% TβRI mutation 33% TβRII mutation 25% USP36 overexpression<unk>  forms when errors in normal<unk>  cell growth<unk> cur. Usually, when cells grow old or get damaged, they die, and new cells take their place. Cancer starts when new cells form unneeded, and old or damaged cells do not die as they should. The buildup of extra cells often forms a mass of tissue called an<unk>  tumor or growth. These abnormal cancer cells have many genetic abnormalities that cause them to grow excessively. When an ovary releases an egg, the egg follicle bursts open and becomes the corpus luteum. This structure needs to be repaired by dividing cells in the ovary. Continuous ovulation for a long time means more repair of the ovary by dividing cells, which can acquire mutations in each division. Overall, the most common gene mutations in<unk> <unk> cur in NF1, BRCA1, BRCA2, and CDK12. Type I<unk> s, which tend to be less aggressive, tend to have microsatellite instability in several genes, including both oncogenes (most notably BRAF and KRAS) and tumor suppressors (most notably PTEN). The most common mutations in Type I cancers are KRAS, BRAF, ERBB2, PTEN, PIK3CA, and ARID1A. Type II cancers, the more aggressive type, have different genes mutated, including p53, BRCA1, and BRCA2. Low-grade cancers tend to have mutations in KRAS, whereas cancers of any grade that develop from low malignant potential tumors tend to have mutations in p53. Type I cancers tend to develop from precursor lesions, whereas Type II cancers can develop from a serous tubal intraepithelial carcinoma. Serous cancers that have BRCA mutations also inevitably have p53 mutations, indicating that the removal of both functional genes is important for cancer to develop. In 50% of high-grade serous cancers, homologous recombination DNA repair is dysfunctional, as are the notch and FOXM1 signaling pathways. They also almost always have p53 mutations. Other than this, mutations in high-grade serous carcinoma are hard to characterize beyond their high degree of genomic instability. BRCA1 and BRCA2 are essential for homologous recombination DNA repair, and germline mutations in these genes are found in about 15% of women with<unk> . The most common mutations in BRCA1 and BRCA2 are the frameshift mutations that originated in a small founding population of Ashkenazi Jews. Almost 100% of rare mucinous carcinomas have mutations in KRAS and amplifications of ERBB2 (also known as Her2/neu). Overall, 20% of<unk> s have mutations in Her2/neu. Serous carcinomas may develop from serous tubal intraepithelial carcinoma, rather than developing spontaneously from<unk>  tissue. Other carcinomas develop from cortical inclusion cysts, which are groups of epithelial<unk>  cells inside the stroma.
Ovarian cancer
Uterine fibroid  s  1
Breast cancer
Uterine cancer
Cervical cancer
Endometrial cancer
Ovarian cyst
Fallopian tube cancer