Evidence map›Paper›PMID 26567361›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2015

BCL-2 Antagonism to Target the Intrinsic Mitochondrial Pathway of Apoptosis.

Christopher J Gibson, Matthew S Davids

Abstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
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  11. Novel Withanolides fromMolecules (Basel, Switzerland) · 2024
    Article
  12. Review
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  15. Article
  16. Dual Targeting of Apoptotic and Signaling Pathways in T-Lineage Acute Lymphoblastic Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  17. Review
  18. Article
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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

2 authors at 1 institution in 1 country.

Christopher J GibsonDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Matthew S DavidsDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts. matthew_davids@dfci.harvard.edu.
Dana-Farber Cancer Institute · US

Funding

Training Program in Molecular HematologyT32HL116324 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI NANCY BERLINER · 2013 to 2026
$7.4M
NCI NIH HHS L30 CA162376NHLBI NIH HHS T32 HL116324NHLBI NIH HHS T32HL116324
6 · The paper itself

Abstract

Despite significant improvements in treatment, cure rates for many cancers remain suboptimal. The rise of cytotoxic chemotherapy has led to curative therapy for a subset of cancers, though intrinsic treatment resistance is difficult to predict for individual patients. The recent wave of molecularly targeted therapies has focused on druggable-activating mutations, and is thus limited to specific subsets of patients. The lessons learned from these two disparate approaches suggest the need for therapies that borrow aspects of both, targeting biologic properties of cancer that are at once distinct from normal cells and yet common enough to make the drugs widely applicable across a range of cancer subtypes. The intrinsic mitochondrial pathway of apoptosis represents one such promising target for new therapies, and successfully targeting this pathway has the potential to alter the therapeutic landscape of therapy for a variety of cancers. Here, we discuss the biology of the intrinsic pathway of apoptosis, an assay known as BH3 profiling that can interrogate this pathway, early attempts to target BCL-2 clinically, and the recent promising results with the BCL-2 antagonist venetoclax (ABT-199) in clinical trials in hematologic malignancies. See all articles in this CCR Focus section, "Cell Death and Cancer Therapy."

Indexed as

Molecular Targeted TherapyApoptosisBridged Bicyclo Compounds, HeterocyclicHematologic NeoplasmsHumansMitochondriaProto-Oncogene Proteins c-bcl-2Signal TransductionSulfonamidesBridged Bicyclo Compounds, HeterocyclicProto-Oncogene Proteins c-bcl-2Sulfonamidesvenetoclax

Identifiers

PMID26567361
PMCPMC4646729
OpenAlexW2269578998

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.