Evidence map›Paper›PMID 24350057›Full record

ReviewFrontiers in oncology2013

Mitochondrial dysfunction in cancer.

Michelle L Boland, Aparajita H Chourasia, Kay F Macleod

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 266 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
266citing papers in PubMed, 1 pooled it
17.9field-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

266 citing papers in PubMed, 1 synthesis or guideline pooled it, 509 citations in OpenAlex.

  1. Pooled it
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  14. Increasing autophagy activity suppressesAmerican journal of cancer research · 2026
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206 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

3 authors at 1 institution in 1 country.

Michelle L BolandThe Ben May Department for Cancer Research, The University of Chicago , Chicago, IL , USA ; Committee on Molecular Metabolism and Nutrition, The University of Chicago , Chicago, IL , USA.
Aparajita H ChourasiaThe Ben May Department for Cancer Research, The University of Chicago , Chicago, IL , USA ; Committee on Cancer Biology, The University of Chicago , Chicago, IL , USA.
Kay F MacleodThe Ben May Department for Cancer Research, The University of Chicago , Chicago, IL , USA ; Committee on Molecular Metabolism and Nutrition, The University of Chicago , Chicago, IL , USA ; Committee on Cancer Biology, The University of Chicago , Chicago, IL , USA.
University of Chicago · US

Funding

Multi-Disciplinary Training Grant in Cancer ResearchT32CA009594 · NCI · UNIVERSITY OF CHICAGO · PI KAY F MACLEOD, Scott A. Oakes · 1989 to 2026
$11.5M
Functions of BNIP3 in Mammary TumorigenesisR01CA131188 · NCI · UNIVERSITY OF CHICAGO · PI MACLEOD, KAY F · 2009 to 2013
$1.5M
An Interdisciplinary Molecular Metabolism Training ProgramT32DK087703 · NIDDK · UNIVERSITY OF CHICAGO · PI RHODES, CHRISTOPHER J · 2010 to 2014
$709k
NCI NIH HHS R01 CA131188NCI NIH HHS T32 CA009594NIDDK NIH HHS T32 DK087703
6 · The paper itself

Abstract

A mechanistic understanding of how mitochondrial dysfunction contributes to cell growth and tumorigenesis is emerging beyond Warburg as an area of research that is under-explored in terms of its significance for clinical management of cancer. Work discussed in this review focuses less on the Warburg effect and more on mitochondria and how dysfunctional mitochondria modulate cell cycle, gene expression, metabolism, cell viability, and other established aspects of cell growth and stress responses. There is increasing evidence that key oncogenes and tumor suppressors modulate mitochondrial dynamics through important signaling pathways and that mitochondrial mass and function vary between tumors and individuals but the significance of these events for cancer are not fully appreciated. We explore the interplay between key molecules involved in mitochondrial fission and fusion and in apoptosis, as well as in mitophagy, biogenesis, and spatial dynamics of mitochondria and consider how these distinct mechanisms are coordinated in response to physiological stresses such as hypoxia and nutrient deprivation. Importantly, we examine how deregulation of these processes in cancer has knock on effects for cell proliferation and growth. We define major forms of mitochondrial dysfunction and address the extent to which the functional consequences of such dysfunction can be determined and exploited for cancer diagnosis and treatment.

Indexed as

cancer metabolismcell cycle controlmitochondriamitochondrial biogenesismitochondrial fusion and fissionmitophagyoxidative phosphorylation

Identifiers

PMID24350057
PMCPMC3844930
OpenAlexW2153850374

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.