Cited by 625Cell death mechanisms and regulationCancer-related Molecular PathwaysAutophagy in Disease and Therapy

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The BCL2 Family: Key Mediators of the Apoptotic Response to Targeted Anticancer Therapeutics

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Hata, Aaron N., Engelman, Jeffrey A., Faber, Anthony C.·2015·Cancer Discovery

DOI 10.1158/2159-8290.cd-15-0011PMC PMC4727530

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Abstract

The ability of cancer cells to suppress apoptosis is critical for carcinogenesis. The BCL2 family proteins comprise the sentinel network that regulates the mitochondrial or intrinsic apoptotic response. Recent advances in our understanding of apoptotic signaling pathways have enabled methods to identify cancers that are “primed” to undergo apoptosis, and have revealed potential biomarkers that may predict which cancers will undergo apoptosis in response to specific therapies. Complementary efforts have focused on developing novel drugs that directly target antiapoptotic BCL2 family proteins. In this review, we summarize the current knowledge of the role of BCL2 family members in cancer development and response to therapy, focusing on targeted therapeutics, recent progress in the development of apoptotic biomarkers, and therapeutic strategies designed to overcome deficiencies in apoptosis. Significance: Apoptosis, long known to be important for response to conventional cytotoxic chemotherapy, has more recently been shown to be essential for the efficacy of targeted therapies. Approaches that increase the likelihood of a cancer to undergo apoptosis following therapy may help improve targeted treatment strategies. Cancer Discov; 5(5); 475–87. ©2015 AACR.

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Authors: Hata, A. N., Engelman, J. A., & Faber, A. C.
Affiliations: Harvard University (US)
Virginia Commonwealth University (US)
Corresponding author: Engelman, Jeffrey A.
Faber, Anthony C.
ORCID: Hata, Aaron N.
Engelman, Jeffrey A.
Faber, Anthony C.
Venue: Cancer Discovery
Publisher: American Association for Cancer Research (AACR)
Published: 2015-05-01
Volume: 5
Issue: 5
Pages: 475-487
ISSN: 2159-8274 (ISSN-L)
2159-8290
DOI: 10.1158/2159-8290.cd-15-0011
PMC: PMC4727530
OpenAlex: W2067275727
Cited by: 619
References: 185
Citations by year: 2026: 19 · 2025: 48 · 2024: 46 · 2023: 42 · 2022: 69 · 2021: 79 · 2020: 83 · 2019: 79 · 2018: 73 · 2017: 45 · 2016: 29 · 2015: 6
FWCI: 4.94
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Cancer Discovery (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (P50CA127003, R01CA140594, R01CA164273, R01CA137008)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Keywords: Bcl-2 family proteins, apoptosis, targeted cancer therapy, mitochondrial apoptosis, cancer therapy response, carcinogenesis, apoptosis resistance
MeSH terms: Bcl-2-Like Protein 11, Animals, Antineoplastic Agents, Humans, Membrane Proteins, Neoplasms, Proto-Oncogene Proteins, Signal Transduction, Biomarkers, Apoptosis, Proto-Oncogene Proteins c-bcl-2, Apoptosis Regulatory Proteins, Molecular Targeted Therapy

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The BCL2 Family: Key Mediators of the Apoptotic Response to Targeted Anticancer Therapeutics

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