Evidence map›Paper›PMID 19823771›Full record

ReviewMolecular and cellular biochemistry2010

NF-kappaB and cancer: how intimate is this relationship.

Sahdeo Prasad, Jayaraj Ravindran, Bharat B Aggarwal

Abstract readReview
In one paragraph

Review in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
198citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 2% 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

198 citing papers in PubMed, 1 synthesis or guideline pooled it, 385 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Translational cancer research · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Interaction of NF-κB and FOSL1 drives glioma stemness.Cellular and molecular life sciences : CMLS · 2024
    Article
  15. Review
  16. Article
  17. Anticancer activities of natural abietic acid.Frontiers in pharmacology · 2024
    Review
  18. Review
  19. Article
  20. Article

138 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 1 institution in 1 country.

Sahdeo PrasadCytokine Research Laboratory, Department of Experimental Therapeutics, The University of Texas, M. D. Anderson Cancer Center, Houston, TX, 77030, USA.
Jayaraj Ravindran
Bharat B Aggarwal
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TARGETING NF-KB ACTIVATION IN REGULATION OF SYMPTOMS IN PATIENTS WITH MULTIPLEP01CA124787 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI REUBEN, JAMES MARTIN · 2008 to 2012
$10.6M
NCI NIH HHS CA-124787-01A2NCI NIH HHS P01 CA124787
6 · The paper itself

Abstract

NF-kappaB, a transcription factor first discovered in 1986, is now known to be closely connected to the process of tumorogenesis based on a multiplicity of evidence. (1) NF-kappaB is activated in response to tobacco, stress, dietary agents, obesity, alcohol, infectious agents, irradiation, and environmental stimuli that account for as much as 95% of all cancers. (2) The transcription factor has been linked with transformation of cells. (3) It is constitutively active in most tumor cells. (4) It has also been linked with the survival of cancer stem cells, an early progenitor cell that has acquired self-renewal potential. (5) NF-kappaB regulates the expression of most anti-apoptotic gene products associated with the survival of the tumor. (6) It also regulates the gene products linked with proliferation of tumors. (7) The transcription factor controls the expression of gene products linked with invasion, angiogenesis, and metastasis of cancer. (8) While most carcinogens activate NF-kappaB, most chemopreventive agents suppress its activation. These observations suggest that NF-kappaB is intimately intertwined with cancer growth and metastasis. The mechanism that leads to constitutive activation of NF-kappaB in hematological, gastrointestinal, genitourinary, gynecological, thoracic head and neck, breast, and skin cancers, and the ways NF-kappaB is activated are the topics of discussion in this review.

Indexed as

AnimalsAnticarcinogenic AgentsApoptosis Regulatory ProteinsCarcinogensCell ProliferationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticHumansInflammationNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsNeoplastic Stem CellsNeovascularization, PathologicNF-kappa BAnticarcinogenic AgentsApoptosis Regulatory ProteinsCarcinogensNF-kappa B

Identifiers

PMID19823771
PMCPMC3148942
OpenAlexW1997546288

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.