Evidence map›Paper›PMID 34532654›Full record

ArticleCancer drug resistance (Alhambra, Calif.)2021

P53-regulated autophagy and its impact on drug resistance and cell fate.

Daeun Shim, Lei Duan, Carl G Maki

Abstract read
In one paragraph

Article in Cancer drug resistance (Alhambra, Calif.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Autophagy in Ovarian Cancer, an Opportunity or an Additional Threat?International journal of molecular sciences · 2026
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Role of autophagy in angiogenic potential of vascular pericytes.Frontiers in cell and developmental biology · 2024
    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

3 authors.

Daeun ShimDepartment of Cell and Molecular Medicine, Rush University Medical Center, Chicago, IL 60612, USA.
Lei DuanDepartment of Cell and Molecular Medicine, Rush University Medical Center, Chicago, IL 60612, USA.
Carl G MakiDepartment of Cell and Molecular Medicine, Rush University Medical Center, Chicago, IL 60612, USA.

Funding

Targeting Prolyl Peptidases in Tamoxifen Resistant Breast CancerR01CA200232 · NCI · RUSH UNIVERSITY MEDICAL CENTER · PI MAKI, CARL G · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA200232
6 · The paper itself

Abstract

Wild-type p53 is a stress-responsive transcription factor and a potent tumor suppressor. P53 inhibits the growth of incipient cancer cells by blocking their proliferation or inducing their death through apoptosis. Autophagy is a self-eating process that plays a key role in response to stress. During autophagy, organelles and other intracellular components are degraded in autophagolysosomes and the autophagic breakdown products are recycled into metabolic and energy producing pathways needed for survival. P53 can promote or inhibit autophagy depending on its subcellular localization, mutation status, and the level of stress. Blocking autophagy has been reported in several studies to increase p53-mediated apoptosis, revealing that autophagy can influence cell-fate in response to activated p53 and is a potential target to increase p53-dependent tumor suppression.

Indexed as

Autophagyhistone methylationmetabolism

Identifiers

PMID34532654
PMCPMC8443158

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.