Evidence map›Paper›PMID 17401425›Full record

ReviewOncogene2007

TP53 mutations and hepatocellular carcinoma: insights into the etiology and pathogenesis of liver cancer.

S P Hussain, J Schwank, F Staib, X W Wang, C C Harris

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 296 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
296citing papers in PubMed, 2 pooled it
16.1field-weighted citation impact, top 1% 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

296 citing papers in PubMed, 2 syntheses or guidelines pooled it, 613 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. RELA Ablation Contributes to Progression of Hepatocellular Carcinoma with TP53Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

236 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

5 authors at 3 institutions in 2 countries.

S P HussainLaboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892-4258, USA.
J Schwank
F Staib
X W Wang
C C Harris
Center for Cancer Research · USJohannes Gutenberg University Mainz · DENational Cancer Institute · US

Funding

Strategies for improving early detection, diagnosis and treatment of liver cancerZIABC010313 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, XIN WEI · 2009 to 2025
$18.1M
Molecular Epidemiology of Human Lung CancerZIABC005480 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 2009 to 2012
$3.0M
p53 Tumor Suppressor PathwayZIABC005795 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 2009 to 2012
$3.0M
Molecular Epidemiology of Human Lung CancerZ01BC005480 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 1996 to 2008
$2.3M
p53 Tumor Suppressor PathwayZ01BC005795 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 1996 to 2008
$2.3M
Molecular signatures for liver cancer diagnosis and treatment stratificationZ01BC010313 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, XIN WEI · 1999 to 2008
$1.8M
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and the major risk factors include chronic infections with the hepatitis B (HBV) or C (HCV) virus, and exposure to dietary aflatoxin B(1) (AFB(1)) or alcohol consumption. Multiple genetic and epigenetic changes are involved in the molecular pathogenesis of HCC, for example, somatic mutations in the p53 tumor suppressor gene (TP53) and the activation of the WNT signal transduction pathway. AFB(1) frequently induces G:C to T:A transversions at the third base in codon 249 of TP53 and cooperates with HBV in causing p53 mutations in HCC. The detection of TP53 mutant DNA in plasma is a biomarker of both AFB(1) exposure and HCC risk. Chronic infection with HBV and HCV viruses, and oxyradical disorders including hemochromatosis, also generate reactive oxygen/nitrogen species that can both damage DNA and mutate cancer-related genes such as TP53. Certain mutant p53 proteins may exhibit a 'gain of oncogenic function'. The p53 biological network is a key responder to this oxidative and nitrosative stress. Depending on the extent of the DNA damage, p53 regulates the transcription of protective antioxidant genes and with extensive DNA damage, transactivates pro-oxidant genes that contribute to apoptosis. The X gene of HBV (HBx) is the most common open reading frame integrated into the host genome in HCC and the integrated HBx is frequently mutated. Mutant HBx proteins still retain their ability to bind to p53, and attenuate DNA repair and p53-mediated apoptosis. In summary, both viruses and chemicals are implicated in the etiology of TP53 mutations during the molecular pathogenesis of HCC.

Indexed as

Genetic Predisposition to DiseaseAflatoxin B1Carcinoma, HepatocellularHepatitis, ChronicHepatitis VirusesHumansIncidenceLiver NeoplasmsMutagenesisMutationTumor Suppressor Protein p53Aflatoxin B1Tumor Suppressor Protein p53

Identifiers

PMID17401425
OpenAlexW2042753075

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.