Evidence map›Paper›PMID 26293580›Full record

ReviewThe FEBS journal2016

Attacking cancer's Achilles heel: antagonism of anti-apoptotic BCL-2 family members.

Joseph T Opferman

Open access · bronzeAbstract readReview
In one paragraph

Review in The FEBS journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
7.7field-weighted citation impact, top 2% of its field
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

71 citing papers in PubMed, 114 citations in OpenAlex.

  1. Saga of MCL1 inhibitors in multiple myeloma.Biochemical pharmacology · 2026
    Review
  2. Review
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  4. Two Novel Compounds Isolated from the Marine Fungal Symbiont ofJournal of experimental pharmacology · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. COPB2: a transport protein with multifaceted roles in cancer development and progression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Review
  14. Article
  15. Alternative splicing ofOncology letters · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

11 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

1 author at 1 institution in 1 country.

Joseph T OpfermanDepartment of Cell and Molecular Biology, St Jude Children's Research Hospital, Memphis, TN, USA.
St. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Regulation of Cell Death and Mitochondrial Physiology by Anti-Apoptotic MCL-1R01HL102175 · NHLBI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI OPFERMAN, JOSEPH T. · 2010 to 2014
$2.1M
Pathway Specific Combinational Therapy in Poor Prognosis B-Lineage Acute Lymphoblastic LeukemiaR01CA201069 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI OPFERMAN, JOSEPH T. · 2016 to 2020
$2.0M
Regulation of Cardiac Death and Energy Metabolism by MCL-1R01HL123543 · NHLBI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI OPFERMAN, JOSEPH T. · 2015 to 2018
$1.8M
NCI NIH HHS P30 CA021765NCI NIH HHS R01 CA201069NHLBI NIH HHS R01 HL102175NHLBI NIH HHS R01 HL123543
6 · The paper itself

Abstract

Malignant cells routinely violate cellular checkpoints that should initiate cell death in normal cells by triggering pro-apoptotic members of the BCL-2 family of proteins. To escape such death inducing signals, cancer cells often select for upregulation of anti-apoptotic BCL-2 family members including BCL-2, BCL-XL , BFL-1, BCL-W and MCL-1. These family members prevent death by sequestering pro-apoptotic molecules. To counter this resistance mechanism, small molecule inhibitors of anti-apoptotic BCL-2 family members have been under development. These molecules have shown promise in pre-clinical and clinical testing to overcome apoptotic resistance, prompting cancer cells to undergo apoptosis. Alternatively, other strategies have taken advantage of the normal regulatory machinery controlling anti-apoptotic molecules and have used inhibitors of signaling pathways to down-modulate the expression of anti-apoptotic molecules, thus tilting the balance in cancer cells to cell death. This review explores recent developments and strategies aimed at antagonizing anti-apoptotic BCL-2 family member action to promote the induction of cell death in cancer therapy.

Indexed as

Aniline CompoundsAnimalsAntineoplastic AgentsApoptosisbcl-2-Associated X ProteinBridged Bicyclo Compounds, HeterocyclicDrug DesignHumansInhibitor of Apoptosis ProteinsModels, BiologicalMyeloid Cell Leukemia Sequence 1 ProteinNeoplasmsProto-Oncogene Proteins c-bcl-2Signal TransductionSulfonamidesAniline CompoundsAntineoplastic Agentsbcl-2-Associated X ProteinBridged Bicyclo Compounds, HeterocyclicInhibitor of Apoptosis ProteinsMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinnavitoclaxProto-Oncogene Proteins c-bcl-2SulfonamidesvenetoclaxapoptosisBCL-2 familyBH3-mimeticcancerMCL-1therapy

Identifiers

PMID26293580
PMCPMC4761532
OpenAlexW2142098498

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.