Evidence map›Paper›PMID 26942674›Full record

ReviewMolecular cell2016

Mitochondria-Judges and Executioners of Cell Death Sentences.

Patrick D Bhola, Anthony Letai

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers.

0numbers the graph read from it
0cells of the map it votes in
169citing papers in PubMed
25.8field-weighted citation impact, top 1% 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

169 citing papers in PubMed, 319 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. The linker governs the organelle targeting of TPP⁺-modified zinc phthalocyanine photosensitizers.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

109 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

2 authors at 2 institutions in 1 country.

Patrick D BholaDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Anthony LetaiDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Electronic address: anthony_letai@dfci.harvard.edu.
Dana-Farber Cancer Institute · USHarvard University · US

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCOTT A ARMSTRONG · 1996 to 2026
$52.5M
Investigation of therapeutic modulators of apoptotic priming in pancreatic cancerR21CA188858 · NCI · DANA-FARBER CANCER INST · PI LETAI, ANTHONY G · 2014 to 2015
$414k
NCI NIH HHS 1R21CA188858-01NCI NIH HHS P01 CA066996NCI NIH HHS P01CA066996NCI NIH HHS R21 CA188858
6 · The paper itself

Abstract

Apoptosis is a form of programmed cell death that is critical for basic human development and physiology. One of the more important surprises in cell biology in the last two decades is the extent to which mitochondria represent a physical point of convergence for many apoptosis-inducing signals in mammalian cells. Mitochondria not only adjudicate the decision of whether or not to commit to cell death, but also release toxic proteins culminating in widespread proteolysis, nucleolysis, and cell engulfment. Interactions among BCL-2 family proteins at the mitochondrial outer membrane control the release of these toxic proteins and, by extension, control cellular commitment to apoptosis. This pathway is particularly relevant to cancer treatment, as most cancer chemotherapies trigger mitochondrial-mediated apoptosis. In this Review, we discuss recent advances in the BCL-2 family interactions, their control by upstream factors, and how the mitochondria itself alters these interactions. We also highlight recent clinical insights into mitochondrial-mediated apoptosis and novel cancer therapies that exploit this pathway.

Indexed as

ApoptosisSignal TransductionAnimalsAntineoplastic AgentsApoptosis Regulatory ProteinsHumansMitochondriaMitochondrial MembranesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMolecular Targeted TherapyNeoplasmsPermeabilityProtein BindingProtein Interaction Domains and MotifsProto-Oncogene Proteins c-bcl-2Antineoplastic AgentsApoptosis Regulatory ProteinsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreProto-Oncogene Proteins c-bcl-2

Identifiers

PMID26942674
PMCPMC4806554
OpenAlexW2289284908

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.