Evidence map›Paper›PMID 21605374›Full record

ArticleBMC medicine2011

Mitochondrial oxidative stress drives tumor progression and metastasis: should we use antioxidants as a key component of cancer treatment and prevention?

Federica Sotgia, Ubaldo E Martinez-Outschoorn, Michael P Lisanti

Open access · goldAbstract readComment
In one paragraph

Article in BMC medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 139 citations in OpenAlex.

  1. Article
  2. Associations between Diabetes Mellitus and Selected Cancers.International journal of molecular sciences · 2024
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  4. Insulin Resistance: The Increased Risk of Cancers.Current oncology (Toronto, Ont.) · 2024
    Review
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  9. Mitochondrial Signaling Pathways Associated with DNA Damage Responses.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Review
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  14. Review
  15. Article
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  17. Article
  18. Article
  19. Review
  20. Article

7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Federica SotgiaThe Jefferson Stem Cell Biology and Regenerative Medicine Center, Philadelphia, PA, USA.
Ubaldo E Martinez-Outschoorn
Michael P Lisanti
Breast Cancer Research Foundation · USThomas Jefferson University · US

Funding

CAV-1, Stat5a Signaling, and Estrogen-Dependent Breast CancerR01CA098779 · NCI · YESHIVA UNIVERSITY · PI FRANK, PHILIPPE G. · 2003 to 2012
$3.5M
SIGNALING AND CELL TRANSFORMATIONR01CA080250 · NCI · YESHIVA UNIVERSITY · PI LISANTI, MICHAEL P · 1999 to 2008
$3.4M
Role of Caveolin in Scleroderma Tissue Fibrosis and VasculopathyR01AR055660 · NIAMS · THOMAS JEFFERSON UNIVERSITY · PI JIMENEZ, SERGIO A · 2008 to 2012
$1.7M
CAV-1 Epithelial-Stromal Interactions and Breast CancerR01CA120876 · NCI · THOMAS JEFFERSON UNIVERSITY · PI LISANTI, MICHAEL P · 2007 to 2011
$1.5M
NCI NIH HHS R01-CA-080250NCI NIH HHS R01-CA-098779NCI NIH HHS R01-CA-120876NIAMS NIH HHS R01-AR-055660
6 · The paper itself

Abstract

The functional role of oxidative stress in cancer pathogenesis has long been a hotly debated topic. A study published this month in BMC Cancer by Goh et al., directly addresses this issue by using a molecular genetic approach, via an established mouse animal model of human breast cancer. More specifically, alleviation of mitochondrial oxidative stress, via transgenic over-expression of catalase (an anti-oxidant enzyme) targeted to mitochondria, was sufficient to lower tumor grade (from high-to-low) and to dramatically reduce metastatic tumor burden by >12-fold. Here, we discuss these new findings and place them in the context of several other recent studies showing that oxidative stress directly contributes to tumor progression and metastasis. These results have important clinical and translational significance, as most current chemo-therapeutic agents and radiation therapy increase oxidative stress, and, therefore, could help drive tumor recurrence and metastasis. Similarly, chemo- and radiation-therapy both increase the risk for developing a secondary malignancy, such as leukemia and/or lymphoma. To effectively reduce mitochondrial oxidative stress, medical oncologists should now re-consider the use of powerful anti-oxidants as a key component of patient therapy and cancer prevention. Please see related research article: http://www.biomedcentral.com/1471-2407/11/191.

Indexed as

Oxidative StressAnimalsAntineoplastic AgentsAntioxidantsBreast NeoplasmsCatalaseDisease Models, AnimalFemaleGene ExpressionHumansMiceMitochondriaNeoplasm MetastasisNeoplasmsProtein TransportRodent DiseasesAntineoplastic AgentsAntioxidantsCatalase

Identifiers

PMID21605374
PMCPMC3123229
OpenAlexW2040264938

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.