Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 328

The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.

Role of autophagy in suppression of inflammation and cancer

Open access
White, Eileen, Karp, Cristina, Strohecker, Anne M, Guo, Yanxiang, Mathew, Robin·2010·Current Opinion in Cell Biology

Abstract

Autophagy is a crucial component of the cellular stress adaptation response that maintains mammalian homeostasis. Autophagy protects against neurodegenerative and inflammatory conditions, aging, and cancer. This is accomplished by the degradation and intracellular recycling of cellular components to maintain energy metabolism and by damage mitigation through the elimination of damaged proteins and organelles. How autophagy modulates oncogenesis is gradually emerging. Tumor cells induce autophagy in response to metabolic stress to promote survival, suggesting deployment of therapeutic strategies to block autophagy for cancer therapy. By contrast, defects in autophagy lead to cell death, chronic inflammation, and genetic instability. Thus, stimulating autophagy may be a powerful approach for chemoprevention. Analogous to infection or toxins that create persistent tissue damage and chronic inflammation that increases the incidence of cancer, defective autophagy represents a cell-intrinsic mechanism to create the damaging, inflammatory environment that predisposes to cancer. Thus, cellular damage mitigation through autophagy is a novel mechanism of tumor suppression.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.ceb.2009.12.008

Cites

20 of 20 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 20 references

Cited by

See all 328

Metadata

Authors
White, E., Karp, C., Strohecker, A. M., Guo, Y., & Mathew, R.
Venue
Current Opinion in Cell Biology
Publisher
Elsevier BV
Published
2010-04
Volume
22
Issue
2
Pages
212-217
ISSN
0955-0674 (ISSN-L)
OpenAlex
W1977841275
Cited by
328
References
20
FWCI
3.19
Type
journal article
Language
en
Open access
green

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: Role of autophagy in suppression of inflammation and cancer. https://app.cochat.ai/papers/10.1016/j.ceb.2009.12.008
The paper
White, E., Karp, C., Strohecker, A. M., Guo, Y., & Mathew, R. (2010). Role of autophagy in suppression of inflammation and cancer. Current Opinion in Cell Biology. https://doi.org/10.1016/j.ceb.2009.12.008

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.