Evidence map›Paper›PMID 26257067›Full record

ReviewOncogene2016

Targeting BCL-2 to enhance vulnerability to therapy in estrogen receptor-positive breast cancer.

D Merino, S W Lok, J E Visvader, G J Lindeman

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 3% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. The immunology of human breast cancer.Nature reviews. Immunology · 2026
    Review
  4. Targeting protein-protein interactions in the BCL-2 family: opportunities for precision oncology.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  5. Review
  6. Article
  7. A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Cell Death: Mechanisms and Potential Targets in Breast Cancer Therapy.International journal of molecular sciences · 2024
    Review
  16. Article
  17. Article
  18. PANoptosis: a potential new target for programmed cell death in breast cancer treatment and prognosis.Apoptosis : an international journal on programmed cell death · 2024
    Review
  19. Article
  20. Review

20 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

4 authors at 3 institutions in 1 country.

D MerinoStem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
S W LokStem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
J E VisvaderStem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
G J LindemanStem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.
University of Melbourne · AUThe Royal Melbourne Hospital · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The last three decades have seen significant progress in our understanding of the role of the pro-survival protein BCL-2 and its family members in apoptosis and cancer. BCL-2 and other pro-survival family members including Mcl-1 and BCL-XL have been shown to have a key role in keeping pro-apoptotic 'effector' proteins BAK and BAX in check. They also neutralize a group of 'sensor' proteins (such as BIM), which are triggered by cytotoxic stimuli such as chemotherapy. BCL-2 proteins therefore have a central role as guardians against apoptosis, helping cancer cells to evade cell death. More recently, an increasing number of BH3 mimetics, which bind and neutralize BCL-2 and/or its pro-survival relatives, have been developed. The utility of targeting BCL-2 in hematological malignancies has become evident in early-phase studies, with remarkable clinical responses seen in heavily pretreated patients. As BCL-2 is overexpressed in ~75% of breast cancer, there has been growing interest in determining whether this new class of drug could show similar promise in breast cancer. This review summarizes our current understanding of the role of BCL-2 and its family members in mammary gland development and breast cancer, recent progress in the development of new BH3 mimetics as well as their potential for targeting estrogen receptor-positive breast cancer.

Indexed as

EstrogensMolecular Targeted TherapyAniline CompoundsAnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsBiomarkers, TumorBreastBreast NeoplasmsBridged Bicyclo Compounds, HeterocyclicCarcinomaDrug DesignDrug SynergismFemaleGene Expression Regulation, NeoplasticAniline CompoundsAntineoplastic AgentsApoptosis Regulatory ProteinsBax protein (53-86)Biomarkers, TumorBridged Bicyclo Compounds, HeterocyclicEstrogensMTOR protein, humannavitoclaxNeoplasm ProteinsPeptide FragmentsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Receptors, EstrogenSulfonamidesTOR Serine-Threonine Kinasesvenetoclax

Identifiers

PMID26257067
OpenAlexW1917773519

What OpenQuestion holds

Textmetadata
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.