Evidence map›Paper›PMID 30168803›Full record

ReviewThe Journal of clinical investigation2018

Emerging evidence for targeting mitochondrial metabolic dysfunction in cancer therapy.

Yueming Zhu, Angela Elizabeth Dean, Nobuo Horikoshi, Collin Heer, Douglas R Spitz, David Gius

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. CD320 Receptor and Vitamin B12 as Potential Targets for Anti-Cancer Therapy.International journal of molecular sciences · 2025
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Yueming ZhuDepartment of Radiation Oncology, Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Angela Elizabeth DeanDepartment of Radiation Oncology, Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Nobuo HorikoshiDepartment of Radiation Oncology, Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Collin HeerFree Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, University of Iowa, Iowa City, Iowa, USA.
Douglas R SpitzFree Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, University of Iowa, Iowa City, Iowa, USA.
David GiusDepartment of Radiation Oncology, Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Robert H. Lurie Comprehensive Cancer Center of Northwestern UniversityUniversity of Iowa · US

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Douglas Robert Spitz · 2000 to 2026
$70.0M
Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Brandi Janssen · 1990 to 2026
$40.5M
TRAINING PROGRAM IN FREE RADICAL AND RADIATION BIOLOGYT32CA078586 · NCI · UNIVERSITY OF IOWA · PI SPITZ, DOUGLAS ROBERT · 1999 to 2024
$5.7M
Loss of mtSIRT3, Decreased MnSOD Activity, and IR Induced Genomic InstabilityR01CA152601 · NCI · VANDERBILT UNIVERSITY · PI BONINI, MARCELO G. · 2010 to 2019
$3.5M
Dys-regulation of the MnSOD-Ac-ROS-HIF2a axis promotes IR / Cisplatin resistance phenotypeR01CA214025 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GIUS, DAVID · 2017 to 2021
$2.0M
ROS and HIFa as molecular targets for chemoprevention in Sirt3 -/- breast cancersR01CA168292 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GIUS, DAVID · 2012 to 2016
$1.9M
Enhancing Metabolic Oxidative Stress and Therapy Responses in Cancer Stem CellsR01CA182804 · NCI · UNIVERSITY OF IOWA · PI SPITZ, DOUGLAS ROBERT · 2014 to 2018
$1.7M
SIRT3 is a Mitochondrial Tumor Suppressor in ER/PR Positive Mammary TumorsR01CA152799 · NCI · VANDERBILT UNIVERSITY · PI GIUS, DAVID · 2011 to 2015
$1.6M
Selective targeting of tumor cell redox metabolism and DNA damage responses to enhance cancer therapyF99CA245722 · NCI · UNIVERSITY OF IOWA · PI HEER, COLLIN DAVID · 2019 to 2020
$65k
NCI NIH HHS F99 CA245722NCI NIH HHS R01 CA152601NCI NIH HHS R01 CA152799NCI NIH HHS R01 CA168292NCI NIH HHS R01 CA182804NCI NIH HHS R01 CA214025NCI NIH HHS T32 CA078586NIEHS NIH HHS P30 ES005605
6 · The paper itself

Abstract

Mammalian cells use a complex network of redox-dependent processes necessary to maintain cellular integrity during oxidative metabolism, as well as to protect against and/or adapt to stress. The disruption of these redox-dependent processes, including those in the mitochondria, creates a cellular environment permissive for progression to a malignant phenotype and the development of resistance to commonly used anticancer agents. An extension of this paradigm is that when these mitochondrial functions are altered by the events leading to transformation and ensuing downstream metabolic processes, they can be used as molecular biomarkers or targets in the development of new therapeutic interventions to selectively kill and/or sensitize cancer versus normal cells. In this Review we propose that mitochondrial oxidative metabolism is altered in tumor cells, and the central theme of this dysregulation is electron transport chain activity, folate metabolism, NADH/NADPH metabolism, thiol-mediated detoxification pathways, and redox-active metal ion metabolism. It is proposed that specific subgroups of human malignancies display distinct mitochondrial transformative and/or tumor signatures that may benefit from agents that target these pathways.

Indexed as

AnimalsFemaleGene ExpressionHumansMaleMitochondriaMitochondrial ProteinsModels, BiologicalNADNADPNeoplasmsOxidation-ReductionOxidative StressProtein TransportSignal TransductionSirtuinsMitochondrial ProteinsNADNADPSirtuins

Identifiers

PMID30168803
PMCPMC6118595
OpenAlexW2888838697

What OpenQuestion holds

Textmetadata
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.