2026-04-17T05:35:53Zhttps://recercat.cat/oai/requestoai:recercat.cat:2445/1863242025-12-05T14:18:26Zcom_2072_1057col_2072_478902col_2072_478917
RECERCAT
author
Montero Boronat, Juan José
author
Haq, Rizwan
2022-06-07T08:33:05Z2022-06-07T08:33:05Z2022-05-012022-06-03T07:09:04Z
A hallmark of cancer is cell death evasion, underlying suboptimal responses to chemotherapy, targeted agents, and immunotherapies. The approval of the anti apoptotic BCL2 antagonist venetoclax has fi nally validated the potential of targeting apoptotic pathways in patients with cancer. Nevertheless, pharmacologic modulators of cell death have shown markedly varied responses in preclinical and clinical studies. Here, we review emerging concepts in the use of this class of therapies. Building on these observations, we propose that treatment-induced changes in apoptotic dependency, rather than pretreatment dependencies, will need to be recognized and targeted to realize the precise deployment of these new pharmacologic agents. Signifi cance: Targeting antiapoptotic family members has proven effi cacious and tolerable in some cancers, but responses are infrequent, particularly for patients with solid tumors. Biomarkers to aid patient selection have been lacking. Precision functional approaches that overcome adaptive resistance to these compounds could drive durable responses to chemotherapy, targeted therapy, and immunotherapies.
cc by-nc-nd (c) Montero Boronat, Juan José et al, 2022 http://creativecommons.org/licenses/by-nc-nd/3.0/es/ info:eu-repo/semantics/openAccess
Apoptosi
Terapèutica
Apoptosis
Therapeutics
Adapted to Survive: Targeting Cancer Cells with BH3 Mimetics
info:eu-repo/semantics/other info:eu-repo/semantics/publishedVersion