In tumoral cells, the modulation of the G1/S phases of cell cycle is destabilized by amplification and high expression of cyclin E (CCNE) or by mutation or loss of retinoblastoma 1 (RB1) gene. Cancer cells meeting these characteristics have been sown to be highly sensitive to cyclin-dependent kinase 2 (CDK2) depletion.
Poly (ADP-ribose) polymerase (PARP) inhibitors are used as maintenance therapy after completion of platinum-based chemotherapy in ovarian cancer. However, acquired or de novo resistance to PARP inhibitors is frequent and limits their application.
Wall Street wasn’t jumping up and down about Repare Therapeutics Inc.’s early data in gynecological cancers, though the findings look positive and the company has big plans for the combo therapy.
Gynecological cancers with amplifications in the CCNE1 gene, which encodes cyclin E1, usually exhibit resistance to standard therapies. Since cyclin-dependent kinase 2 (CDK2) is the primary partner of cyclin E, CDK2 inhibitors represent a potentially effective treatment strategy for these malignancies.
Eterna Therapeutics Inc. has announced plans to evaluate the ability of ERNA-101 to induce and modulate antitumor immunity in ovarian cancer and breast cancer models through a sponsored research agreement with The University of Texas MD Anderson Cancer Center.
Tumor cell survival is dependent on phosphate homeostasis, which requires high amounts of energy. Researchers have demonstrated that the silencing of xenotropic and polytropic retrovirus receptor 1 (XPR1) led to reduced tumor growth in an ovarian cancer cell line xenograft, and similar vulnerability was found in lung cancer.
The advantages of affibodies vs. antibodies are that they have a smaller size, better penetration and faster extravasation, can be produced both recombinantly and synthetically, and show robustness regarding protein scaffold.
