Evidence map›Paper›PMID 26942671›Full record

ReviewMolecular cell2016

Mitochondria and Cancer.

Wei-Xing Zong, Joshua D Rabinowitz, Eileen White

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 732 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
732citing papers in PubMed, 2 pooled it
43.7field-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

732 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,261 citations in OpenAlex.

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672 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 2 institutions in 1 country.

Wei-Xing ZongDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers University, 164 Frelinghuysen Road, Piscataway, NJ 08854, USA; Rutgers Cancer Institute of New Jersey, 195 Little Albany Street, New Brunswick, NJ 08903, USA.
Joshua D RabinowitzRutgers Cancer Institute of New Jersey, 195 Little Albany Street, New Brunswick, NJ 08903, USA; Lewis-Sigler Institute for Integrative Genomics and Department of Chemistry, Princeton University, Princeton, NJ 08544, USA.
Eileen WhiteRutgers Cancer Institute of New Jersey, 195 Little Albany Street, New Brunswick, NJ 08903, USA; Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854, USA. Electronic address: epwhite@cinj.rutgers.edu.
Rutgers Cancer Institute of New JerseyRutgers, The State University of New Jersey · US

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
Tumor cell metabolism in actionR01CA163591 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI JOSHUA D RABINOWITZ, Eileen P. White · 2012 to 2026
$7.0M
Protein and redox homeostasis in cancer development and therapyR01CA129536 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI ZONG, WEI-XING · 2008 to 2022
$4.8M
Role of Autophagy in CancerR01CA130893 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI WHITE, EILEEN P. · 2008 to 2017
$3.4M
Targeting Autophagy in Hereditary Breast CancerR01CA188096 · NCI · RBHS -CANCER INSTITUTE OF NEW JERSEY · PI WHITE, EILEEN P., XIA, BING · 2015 to 2019
$2.4M
Promoting Bim-driven apoptosis through MAPK inhibition: A therapeutic strategy in advanced melanomaR01CA193970 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI MEHNERT, JANICE M., SULLIVAN, RYAN J · 2016 to 2020
$2.3M
Phosphatidylinositol 3-kinases and AutophagyR01GM097355 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI ZONG, WEI-XING · 2012 to 2015
$1.5M
NCI NIH HHS P30 CA072720NCI NIH HHS P30CA72720NCI NIH HHS R01 CA129536NCI NIH HHS R01CA129536NCI NIH HHS R01 CA130893NCI NIH HHS R01CA130893NCI NIH HHS R01 CA163591NCI NIH HHS R01CA163591NCI NIH HHS R01 CA188096NCI NIH HHS R01CA188096NCI NIH HHS R01 CA193970NCI NIH HHS R01CA193970NIGMS NIH HHS R01 GM097355NIGMS NIH HHS R01GM97355
6 · The paper itself

Abstract

Decades ago, Otto Warburg observed that cancers ferment glucose in the presence of oxygen, suggesting that defects in mitochondrial respiration may be the underlying cause of cancer. We now know that the genetic events that drive aberrant cancer cell proliferation also alter biochemical metabolism, including promoting aerobic glycolysis, but do not typically impair mitochondrial function. Mitochondria supply energy; provide building blocks for new cells; and control redox homeostasis, oncogenic signaling, innate immunity, and apoptosis. Indeed, mitochondrial biogenesis and quality control are often upregulated in cancers. While some cancers have mutations in nuclear-encoded mitochondrial tricarboxylic acid (TCA) cycle enzymes that produce oncogenic metabolites, there is negative selection for pathogenic mitochondrial genome mutations. Eliminating mtDNA limits tumorigenesis, and rare human tumors with mutant mitochondrial genomes are relatively benign. Thus, mitochondria play a central and multifunctional role in malignant tumor progression, and targeting mitochondria provides therapeutic opportunities.

Indexed as

Energy MetabolismAnimalsAntineoplastic AgentsCell Transformation, NeoplasticDNA, MitochondrialGenetic Predisposition to DiseaseHumansMitochondriaMolecular Targeted TherapyMutationNeoplasmsSignal TransductionAntineoplastic AgentsDNA, Mitochondrial

Identifiers

PMID26942671
PMCPMC4779192
OpenAlexW2292613448

What OpenQuestion holds

Textmetadata
LicenceTDM
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.