Evidence map›Paper›PMID 21434856›Full record

ReviewAnti-cancer agents in medicinal chemistry2011

Manganese superoxide dismutase (Sod2) and redox-control of signaling events that drive metastasis.

Nadine Hempel, Pauline M Carrico, J Andres Melendez

Abstract readReview
In one paragraph

Review in Anti-cancer agents in medicinal chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

95 citing papers in PubMed, 163 citations in OpenAlex.

  1. Review
  2. Article
  3. The curious life of human mitochondrial SOD2.International journal of biological macromolecules · 2026
    Review
  4. Article
  5. Article
  6. Metal Ion Signaling in Biomedicine.Chemical reviews · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Molecules (Basel, Switzerland) · 2022
    Review

35 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.

Nadine HempelCenter for Immunology and Microbial Diseases, Albany Medical College, 47 New Scotland Avenue, Albany NY 12208, USA.
Pauline M Carrico
J Andres Melendez
Albany Medical Center Hospital · USEmpire State University · US

Funding

Redox-Control of MMP-1 and SenescenceR01AG031067 · NIA · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI MELENDEZ, JUAN ANDRES · 2008 to 2012
$1.8M
Mitochondrial Redox Control of MetastasisK99CA143229 · NCI · STATE UNIVERSITY OF NEW YORK AT ALBANY · PI HEMPEL, NADINE · 2010 to 2011
$228k
Regulation of Tumor Cell Migration by Mitochondrial Superoxide DismutaseF32CA134165 · NCI · ALBANY MEDICAL COLLEGE · PI HEMPEL, NADINE · 2008 to 2010
$114k
NCI NIH HHS F32 CA134165NCI NIH HHS F32CA13465NCI NIH HHS K99 CA143229NCI NIH HHS K99CA143229NIA NIH HHS NIH R01 AG031067NIA NIH HHS R01 AG031067
6 · The paper itself

Abstract

Manganese superoxide dismutase (Sod2) has emerged as a key enzyme with a dual role in tumorigenic progression. Early studies were primarily directed at defining the tumor suppressive function of Sod2 based on its low level expression in many tumor types. It is now commonly held that loss of Sod2 expression is likely an early event in tumor progression allowing for further propagation of the tumorigenic phenotype resulting from steady state increases in free radical production. Increases in free radical load have also been linked to defects in mitochondrial function and metastatic disease progression. It was initially believed that Sod2 loss may propagate metastatic disease progression, in reality both epidemiologic and experimental evidence indicate that Sod2 levels increase in many tumor types as they progress from early stage non-invasive disease to late stage metastatic disease. Sod2 overexpression in many instances enhances the metastatic phenotype that is reversed by efficient H(2)O(2) scavenging. This review evaluates the many sequelae associated with increases in Sod2 that impinge on the metastatic phenotype. The ability to use Sod2 to modulate the cellular redox-environment has allowed for the identification of redox-responsive signaling events that drive malignancy, such as invasion, migration and prolonged tumor cell survival. Further studies of these redox-driven events will help in the development of targeted therapeutic strategies to efficiently restrict redox-signaling essential for malignant progression.

Indexed as

Signal TransductionDisease ProgressionHumansNeoplasm MetastasisNeoplasmsOxidation-ReductionSuperoxide DismutaseSuperoxide Dismutase 2Superoxide DismutaseSuperoxide Dismutase 2

Identifiers

PMID21434856
PMCPMC3902825
OpenAlexW2138605089

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.