Loading
High-grade serous ovarian carcinoma is the most common type of ovarian cancer and the one most often found late; it actually starts in the fallopian tube and almost always has a broken TP53 gene, and it is the type PARP inhibitors were built for.
The type behind about 70% of ovarian cancer deaths, and the one where maintenance therapy has changed the most. Near-universal TP53 mutation, ~50% homologous recombination deficiency (including ~20% BRCA1/2), extensive copy-number instability, few recurrent targetable mutations. Arises from serous tubal intraepithelial carcinoma, which is why opportunistic salpingectomy prevents it. PARP inhibitors, platinum, and FRα ADCs are the main therapeutic levers.
In plain words · TP53 is the 'guardian of the genome', broken in half of all cancers. Fixing it directly has so far defeated every attempt, so drugs exploit what its loss makes cancers depend on.
Showing the target this term concerns: TP53.
Shares Ovarian Cancer Research Alliance (OCRA), Ovarian cancer.
Shares Homologous recombination deficiency (HRD), BRCA1 / BRCA2 (HRD).
Shares Risk-reducing and opportunistic salpingectomy, BRCA1 / BRCA2 (HRD), Ovarian cancer.
Shares Homologous recombination deficiency (HRD), BRCA1 / BRCA2 (HRD), Ovarian cancer.
Shares Folate receptor alpha, Ovarian cancer.
Shares Folate receptor alpha, Ovarian cancer.
Shares Folate receptor alpha, BRCA1 / BRCA2 (HRD), Ovarian cancer.
Shares Folate receptor alpha, Ovarian cancer.