Glutathione S-transferase (GSTP) is an enzyme involved in the detoxification of several xenobiotics such as tobacco carcinogens or cisplatin drugs and is overexpressed in KRAS-mutant lung, colon and pancreatic cancer, among others. The upregulation of GSTP may partially contribute to chemotherapy and radiotherapy resistance.
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.
Researchers from Novacyte Therapeutics Co. Ltd. presented preclinical data for NC-18, a novel HER2-targeting antibody drug conjugate (ADC) being developed for the treatment of HER2-positive/expressing advanced solid tumors.
Cyclins and cyclin-dependent kinases (CDKs) regulate the activity of E2F and Rb to drive cell cycle progression. Disrupting this interaction has shown lethality in cancer cells harboring alterations that lead to higher expression of E2F1.
Claudin 18.2 (CLDN18.2) is a member of the claudin family and is overexpressed in gastric, gastroesophageal junction and pancreatic cancer, among others. Researchers from Elevation Oncology Inc. recently presented preclinical efficacy data on the combination of EO-3021, an antibody-drug conjugate (ADC) targeting CLDN18.2, with VEGFR-2 or PD-1 inhibitors in models of gastric adenocarcinoma.
Endocrine therapy against the estrogen receptor (ER) is widely used for the treatment of ER+ breast cancer. Selective estrogen receptor degraders (SERDs) compete directly with estrogen for ER binding and create an unstable protein complex that leads to proteasome-mediated ER protein degradation.
Cancer and autoimmunity are “often thought of as being at opposite ends of the immune response,” Ana Anderson told her audience at a joint meeting of the NIH’s Office of Autoimmune Disease Research and Office of Research in Women’s Health earlier this month. Cancer, that line of reasoning goes, arises when the immune system is not good enough at recognizing harmful autoantigens. Autoimmunity arises when it is hypervigilant, mistaking harmless autoantigens for problematic ones and going on the attack.
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