Evidence map›Paper›PMID 35689420›Full record

ReviewMolecular oncology2022

Autophagy at the intersection of aging, senescence, and cancer.

Liam D Cassidy, Masashi Narita

Open access · goldAbstract readReview
In one paragraph

Review in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
10.8field-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

58 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Terpenoids as modulators of autophagy-senescence crosstalk in lung cancer.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
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  8. The mechanism of the JNK signaling pathway in drug addiction : Author list.Journal of molecular medicine (Berlin, Germany) · 2026
    Review
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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 2 institutions in 3 countries.

Liam D CassidyCancer Research UK Cambridge Institute, University of Cambridge, UK.ORCID 0000-0002-9312-6256
Masashi NaritaCancer Research UK Cambridge Institute, University of Cambridge, UK.ORCID 0000-0001-7764-577X
Tokyo Institute of Technology · JPUniversity of Cambridge · GB

Funding

Biotechnology and Biological Sciences Research Council BB/T013486/1Cancer Research UK 24453Cancer Research UK C9545/A29580
6 · The paper itself

Abstract

Autophagy is an evolutionarily conserved cellular process in which macromolecules undergo lysosomal degradation. It fulfills essential roles in quality controlling cellular constituents and in energy homeostasis. Basal autophagy is also widely accepted to provide a protective role in aging and aging-related disorders, and its decline with age might precipitate the onset of a variety of diseases. In this review, we discuss the role of basal autophagy in maintaining homeostasis, in part through the maintenance of stem cell populations and the prevention of cellular senescence. We also consider how stress-induced senescence, for example, during oncogene activation and in premalignant disease, might rely on autophagy, and the possibility that the age-associated decline in autophagy might promote tumour development through a variety of mechanisms. Ultimately, evidence suggests that autophagy is required for malignant cancer progression in a number of settings. Thus, autophagy appears to be tumour-suppressive during the early stages of tumorigenesis and tumour-promoting at later stages.

Indexed as

AutophagyNeoplasmsAgingCellular SenescenceHumansLysosomesagingautophagycancersenescence

Identifiers

PMID35689420
PMCPMC9490138
OpenAlexW4282923268

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.