Evidence map›Paper›PMID 25895919›Full record

ReviewCancer discovery2015

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

Aaron N Hata, Jeffrey A Engelman, Anthony C Faber

Abstract readReview
In one paragraph

Review in Cancer discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 324 papers.

0numbers the graph read from it
0cells of the map it votes in
324citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

324 citing papers in PubMed.

  1. Review
  2. Melatonin in lung cancer: integrating molecular mechanisms, tumor microenvironment regulation, apoptotic signaling, and therapeutic opportunities.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Antitumor Activity ofMarine drugs · 2025
    Article
  19. Article
  20. RSC advances · 2025
    Article

264 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Aaron N HataMassachusetts General Hospital Cancer Center, Charlestown, Massachusetts. Department of Medicine, Harvard Medical School, Boston, Massachusetts.
Jeffrey A EngelmanMassachusetts General Hospital Cancer Center, Charlestown, Massachusetts. Department of Medicine, Harvard Medical School, Boston, Massachusetts. jengelman@partners.org acfaber@vcu.edu.
Anthony C FaberVirginia Commonwealth University Philips Institute for Oral Health Research, School of Dentistry and Massey Cancer Center, Richmond, Virginia. jengelman@partners.org acfaber@vcu.edu.

Funding

Tissue and Pathology ResourcesP50CA127003 · NCI · DANA-FARBER CANCER INST · PI EL-BARDEESY, NABEEL, SELLERS, WILLIAM R · 2007 to 2023
$33.2M
The Activation of ERBB3 Signaling as a Resistance Mechanism to Targeted TherapiesR01CA137008 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI Aaron N Hata, ZOFIA PIOTROWSKA · 2009 to 2026
$5.7M
Overcoming Resistance Mechanisms to Anaplastic Lymphoma Kinase InhibitorsR01CA164273 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI Aaron N Hata, Jessica Jiyeong Lin · 2012 to 2026
$5.5M
Therapeutic strategies for specific subsets of KRAS mutant lung cancersR01CA140594 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WONG, KWOK KIN · 2009 to 2017
$4.5M
NCI NIH HHS 2P50CA127003NCI NIH HHS 2R01CA140594NCI NIH HHS P50 CA127003NCI NIH HHS R01 CA137008NCI NIH HHS R01CA137008NCI NIH HHS R01 CA140594NCI NIH HHS R01 CA164273NCI NIH HHS R01CA164273
6 · The paper itself

Abstract

unlabelledThe 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.

Indexed as

AnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11BiomarkersHumansMembrane ProteinsMolecular Targeted TherapyNeoplasmsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Signal TransductionAntineoplastic AgentsApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl-2-Like Protein 11BiomarkersMembrane ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID25895919
PMCPMC4727530

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.