Treatment leaves behind damaged cells that stop dividing but do not die, and they release signals that help surviving cancer cells regrow. Removing them could reduce relapse.
Therapy-induced senescence produces a secretory phenotype that promotes proliferation, angiogenesis and immune suppression, and senescent tumour cells can re-enter the cell cycle. Senolytics such as navitoclax-class BCL-2 family inhibitors and dasatinib-quercetin combinations clear these cells in models, and a one-two sequence of pro-senescence therapy followed by a senolytic has shown benefit preclinically.
Shares Senolytics after cancer treatment, Intrinsic apoptosis (BCL-2 family), BCL-2.
Shares Intrinsic apoptosis (BCL-2 family), BCL-2.
Shares Intrinsic apoptosis (BCL-2 family), BCL-2.
Shares Intrinsic apoptosis (BCL-2 family), BCL-2.
Shares BCL-2, Cytotoxic chemotherapy.
Shares Intrinsic apoptosis (BCL-2 family), BCL-2.
Shares Intrinsic apoptosis (BCL-2 family), BCL-2.
Shares Intrinsic apoptosis (BCL-2 family), BCL-2.