Ovarian cancer is a group of diseases that originates in the ovaries, or in the related areas of the fallopian tubes and the peritoneum. Women have two ovaries that are located in the pelvis, one on each side of the uterus. The ovaries make female hormones and produce eggs. Women have two fallopian tubes that are a pair of long, slender tubes on each side of the uterus. Eggs pass from the ovaries through the fallopian tubes to the uterus. The peritoneum is the tissue lining that covers organs in the abdomen.
When ovarian cancer is found in its early stages, treatment works best. Ovarian cancer often causes signs and symptoms, so it is important to pay attention to your body and know what is normal for you. Symptoms may be caused by something other than cancer, but the only way to know is to see your doctor, nurse, or other health care professional.
Some mutations (changes in genes) can raise your risk for ovarian cancer. Mutations in the breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2), and those associated with Lynch syndrome, raise ovarian cancer risk.
Ovarian cancers come in a variety of different tumor types. The most common tumor type is high-grade serous carcinoma, occurring in about 70% of ovarian cancer cases.
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Pamiparib (BGB-290, BGB290) is a highly potent, selective and brain penetrant PARP1/2 inhibitor with potent anti-tumor activity.
Triapine (3-AP, PAN-811, OCX191, NSC 663249) is a potent ribonucleotide reductase inhibitor with broad spectrum antitumor activity.
Cridanimod sodium is a potent type I interferon (IFN) inducer that directly binds to STING and triggers a strong antiviral response through the TBK1/IRF3 route; displays extraordinary activity in phosphorylating IRF3 in the murine system; also increases progesterone receptor (PrR) expression in endometrial tissue.
Cridanimod (10-carboxymethyl-9-acridanone, 10-CMA, XBIO-101) is a potent type I interferon (IFN) inducer that directly binds to STING and triggers a strong antiviral response through the TBK1/IRF3 route; displays extraordinary activity in phosphorylating IRF3 in the murine system; also increases progesterone receptor (PrR) expression in endometrial tissue.
Fluzoparib (SHR-3162) is a novel, potent and orally available inhibitor of PARP; potently inhibited PARP1 enzyme activity and induced DNA double-strand breaks, G2/M arrest and apoptosis in homologous recombination repair (H)-deficient cells, Fluzoparib preferentially inhibited the proliferation of HR-deficient cells and sensitized both HR-deficient and HR-proficient cells to cytotoxic drugs; demonstrates superior anti-tumor activity in HR-deficient xenografts models, elicited significantly improved anti-tumor responses without extra toxicity in combination with apatinib or with apatinib plus paclitaxel.
ORIC-101 (ORIC101) is a highly potent, selective steroidal glucocorticoid receptor (GR) antagonist (IC50=5.6 nM) with reduced androgen receptor (AR) agonistic activity; dose-dependently reduces the expression levels of two established GR target genes, GILZ and FKBP5 with IC50 of 24.9 and 19.5 nM in human PBMCs; demonstrates in vivo antitumor activity by enhancing response to chemotherapy in the GR+ OVCAR5 ovarian cancer xenograft model.
Trabectedin (Ecteinascidin-743, ET-743, Ecteinascidin) is a marine alkaloid isolated from the Caribbean tunicate Ecteinascidia turbinata that shows remarkably anticancer activity in a variety of in vitro and in vivo systems; a DNA minor groove, guanine-specific alkylating agent; shows hign potency against ovarian carcinoma xenografts.
COTI-2 (COTI2) is an orally available thiosemicarbazone that may act on mutant forms of p53 and PI3K/AKT/mTOR pathway; induces apoptosis in a wide variety of human tumor cells in culture (IC50s<40 nM), inhibits the proliferation of colorectal cancer cell lines more effectively than cetuximab and erlotinib; shows superior activity against tumor, and is safe and well-tolerated in vivo.
A highly potent PARP inhibitor with IC50 of 3.8 nM/2.1 nM for PARP1/PARP2; inhibits PARP activity with EC50=4 nM in a whole cell assay, and inhibits proliferation of cancer cells with mutant BRCA-1 and BRCA-2 with CC50 in the 10−100 nM range; well tolerated in vivo and demonstrates efficacy as a single agent in a xenograft model of BRCA-1 deficient cancer.
A highly potent, orally bioavailable, pan-VEGFR inibitor with IC50 of 1, 5, 3 nM for VEGFR1, 2, 3, respectively; also inhibits c-Kit and PDGFRβ with IC50 of 2 and 5 nM, >36-fold selectivity over PDGFR-α, >1000-fold over Flt-3 and EGFR; inhibits VEGF-stimulated proliferation and KDR phosphorylation with IC50 of 0.4 and 0.5 nM in human umbilical vein endothelial cells; inhibits angiogenesis, neovascular survival and tumor growth in vivo.
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