Evidence map›Paper›PMID 21486217›Full record

ReviewCurrent cancer drug targets2011

Targeting aldose reductase for the treatment of cancer.

Ravinder Tammali, Satish K Srivastava, Kota V Ramana

Abstract readReview
In one paragraph

Review in Current cancer drug targets, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

35 citing papers in PubMed, 89 citations in OpenAlex.

  1. Review
  2. Article
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  5. Article
  6. Review
  7. Article
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  9. Review
  10. Article
  11. Article
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  13. Article
  14. Metabolites · 2021
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
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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.

Ravinder TammaliDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Satish K Srivastava
Kota V Ramana
The University of Texas Medical Branch at Galveston · US

Funding

Role of Aldose Reductase in Diabetic ComplicationsR37DK036118 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI SRIVASTAVA, SATISH K · 2003 to 2013
$4.1M
Chemoprevention of Colorectal Cancer by Aldose Reductase InhibitionR01CA129383 · NCI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI RAMANA, KOTA VENKATA · 2008 to 2017
$3.1M
Aldose Reductase: A Regulator of Inflammatory SignalsR01GM071036 · NIGMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI RAMANA, KOTA VENKATA · 2005 to 2011
$1.8M
ALDOSE REDUCTASE AND DIABETIC COMPLICATIONSR01DK036118 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI SRIVASTAVA, SATISH K · 1987 to 2002
$626k
Structural Biology /Structural Genomics of TraffickingZ01DK036118 · NIDDK · DIABETES, DIGESTIVE, KIDNEY DISEASES · PI HURLEY, JAMES H · 1994 to 2006
–
Intramural NIH HHS Z01 DK036118NCI NIH HHS CA129383NCI NIH HHS R01 CA129383NIDDK NIH HHS R01 DK036118NIDDK NIH HHS R37 DK036118NIGMS NIH HHS GM71036NIGMS NIH HHS R01 GM071036
6 · The paper itself

Abstract

It is strongly established by numerous studies that oxidative stress-induced inflammation is one of the major causative agents in a variety of cancers. Various factors such as bacterial, viral, parasitic infections, chemical irritants, carcinogens are involved in the initiation of oxidative stress-mediated inflammation. Chronic and persistent inflammation promotes the formation of cancerous tumors. Recent investigations strongly suggest that aldose reductase [AR; AKR1B1], a member of aldo-keto reductase superfamily of proteins, is the mediator of inflammatory signals induced by growth factors, cytokines, chemokines, carcinogens etc. Further, AR reduced product(s) of lipid derived aldehydes and their metabolites such as glutathionyl 1,4-dihydroxynonanol (GS-DHN) have been shown to be involved in the activation of transcription factors such as NF-κB and AP-1 which transcribe the genes of inflammatory cytokines. The increased inflammatory cytokines and growth factors promote cell proliferation, a main feature involved in the tumorigenesis process. Inhibition of AR has been shown to prevent cancer cell growth in vitro and in vivo models. In this review, we have described the possible association between AR with oxidative stress- and inflammation- initiated carcinogenesis. A thorough understanding of the role of AR in the inflammation -associated cancers could lead to the use of AR inhibitors as novel chemotherapeutic agents against cancer.

Indexed as

Molecular Targeted TherapyAldehyde ReductaseAnimalsAnticarcinogenic AgentsAntineoplastic AgentsCachexiaDrug Resistance, NeoplasmEnzyme InhibitorsHumansInflammation MediatorsIsoenzymesNeoplasmsOxidative StressAKR1B1 protein, humanAldehyde ReductaseAnticarcinogenic AgentsAntineoplastic AgentsEnzyme InhibitorsInflammation MediatorsIsoenzymes

Identifiers

PMID21486217
PMCPMC3142792
OpenAlexW2162446904

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.