Evidence map›Paper›PMID 37573235›Full record

ReviewTrends in cell biology2024

Sublethal engagement of apoptotic pathways in residual cancer.

Shane T Killarney, Stephen W G Tait, Douglas R Green, Kris C Wood

Abstract readReview
In one paragraph

Review in Trends in cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Article
  2. Review
  3. BCL-2/BCL-xL inhibitor pelcitoclax with osimertinib forJournal for immunotherapy of cancer · 2026
    Article
  4. Article
  5. Article
  6. A century of cell death research.Journal of cell science · 2026
    Review
  7. MTCH2 promotes BAX and BAK self-assembly and apoptotic pore growth.Nature structural & molecular biology · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Molecular Cell Biology of Apoptosis in Health and Disease.Advances in experimental medicine and biology · 2025
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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.

Shane T KillarneyDepartment of Pharmacology and Cancer Biology, Duke University, Durham, NC, USA.
Stephen W G TaitCancer Research UK Beatson Institute, Switchback Road, Glasgow G61 1BD, UK.
Douglas R GreenDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. Electronic address: douglas.green@stjude.org.
Kris C WoodDepartment of Pharmacology and Cancer Biology, Duke University, Durham, NC, USA. Electronic address: kris.wood@duke.edu.

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007171 · NIGMS · DUKE UNIVERSITY · PI KONTOS, CHRISTOPHER D · 1985 to 2021
$31.2M
MECHANISMS OF REGULATED CELL DEATHR35CA231620 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Douglas R. Green · 2018 to 2026
$9.2M
Screening for Cys-Reactive Ligands to Target PAX3-FOXO1U54CA231630 · NCI · DUKE UNIVERSITY · PI COUNTER, CHRISTOPHER M, LINARDIC, CORINNE MARY · 2019 to 2023
$6.5M
Survival Function of the Fadd-Caspase-8-Flip Complex - MERIT ExtensionR37AI044828 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Douglas R. Green · 2017 to 2026
$4.5M
Lineage-specific signaling and targeting of PI3K gamma in myeloid malignanciesR01CA266389 · NCI · DUKE UNIVERSITY · PI Kris C. Wood · 2022 to 2026
$2.0M
Mechanism-based targeting of unique survival signaling in residual tumorsR01CA263593 · NCI · DUKE UNIVERSITY · PI Kris C. Wood · 2022 to 2026
$1.7M
NCI NIH HHS R01 CA263593NCI NIH HHS R01 CA266389NCI NIH HHS R35 CA231620NCI NIH HHS U54 CA231630NIAID NIH HHS R37 AI044828NIGMS NIH HHS T32 GM007171
6 · The paper itself

Abstract

Cytotoxic chemo-, radio-, and targeted therapies frequently elicit apoptotic cancer cell death. Mitochondrial outer membrane permeabilization (MOMP) is a critical, regulated step in this apoptotic pathway. The residual cancer cells that survive treatment serve as the seeds of eventual relapse and are often functionally characterized by their transient tolerance of multiple therapeutic treatments. New studies suggest that, in these cells, a sublethal degree of MOMP, reflective of incomplete apoptotic commitment, is widely observed. Here, we review recent evidence that this sublethal MOMP drives the aggressive features of residual cancer cells while templating a host of unique vulnerabilities, highlighting how failed apoptosis may counterintuitively enable new therapeutic strategies to target residual disease (RD).

Indexed as

MitochondriaMitochondrial MembranesApoptosisHumansNeoplasm, ResidualDNA damage responsedrug-tolerant persistersintegrated stress responsesublethal MOMP

Identifiers

PMID37573235
PMCPMC10858294

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Registered trials

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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.