OVARIAN CANCER MODELS
Epithelial ovarian cancer (EOC) is the most common cause of gynecological cancer death in the United States. Most patients are diagnosed with advanced stage EOC and undergo surgical removal of the tumor and aggressive chemotherapy with DNA damaging agents and mitotic inhibitors (platinum, taxane). Tumor recurrence is high and more than 50% of patients succumb to disease in five years.
Novel therapeutic strategies are a very high priority for the treatment of ovarian cancers. Currently the most promising targets are the PIK3CA/PTEN and KRAS/BRAF signaling pathways.
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OVARIAN TUMOR TYPES AVAILABLE:
| Tumor Type | Mutations | Comments |
|---|---|---|
| Serous Adenocarcinoma | ||
| Papillary Serous Carcinoma | PIK3CA | Rapamycin sensitivity |
| Ovarian Carcinoma | ||
| Serous Carcinoma | TP53 | |
| Carcinosarcoma | KRAS, TP53 | |
| Invasive Mucinous Ovarian Carcinoma | ATM |
PIK3CA—phosphatidylinositol-4,5-bisphosphate 3-kinase: PIK3A mutations are associated with mTor inhibitor sensitivity.
TP53—tumor suppressor p53: Mutations in p53 lead to genomic instability and lower sensitivity to DNA damaging agents.
ATM—ataxia-telangiectasia mutated: Plays a central role in response to chemical and ionizing-radiation induced DNA damage. Mutations in ATM increase sensitivity to ionizing radiation.
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