Evidence map›Paper›PMID 11971194›Full record

ReviewOncogene2002

Genetic mechanisms of hepatocarcinogenesis.

Mark A Feitelson, Bill Sun, N Lale Satiroglu Tufan, Jie Liu, Jingbo Pan, Zhaorui Lian

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 1 pooled it
7.8field-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

106 citing papers in PubMed, 1 synthesis or guideline pooled it, 323 citations in OpenAlex.

  1. Pooled it
  2. Prognostic value of Wnt inhibitory factor-1 expression in hepatocellular carcinoma that is independent of gene methylation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011
    Trial
  3. Article
  4. Functional Role of COP1 Gene in Hepatocellular Carcinoma Lipid Metabolism and Stemness.Genes to cells : devoted to molecular & cellular mechanisms · 2026
    Article
  5. Article
  6. Review
  7. Hydrogen sulfide suppresses HMedical oncology (Northwood, London, England) · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Zeaxanthin Dipalmitate in the Treatment of Liver Disease.Evidence-based complementary and alternative medicine : eCAM · 2019
    Review
  17. Review
  18. Article
  19. Article
  20. Article

46 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

6 authors at 1 institution in 1 country.

Mark A FeitelsonDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, 1020 Locust Street, Philadelphia, PA 19107, USA. Mark.Feitelson@mail.tju.edu
Bill Sun
N Lale Satiroglu Tufan
Jie Liu
Jingbo Pan
Zhaorui Lian
Thomas Jefferson University · US

Funding

MECHANISMS OF HBV X MEDIATED HCCR01CA066971 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FEITELSON, MARK A · 1995 to 2004
$1.6M
TRANSGENIC MOUSE FOR HBV ASSOCIATED HCC RISK FACTORSR01CA079512 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FEITELSON, MARK A · 2000 to 2002
$1.0M
SENESCENCE AND APOPTOSIS IN HBV ASSOCIATED HCCR01CA048656 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FEITELSON, MARK A · 1994 to 2002
$727k
PRODUCTS OF THE X AND POLYMERASE GENES OF HEPADNAVIRUSESR29CA048656 · NCI · THOMAS JEFFERSON UNIVERSITY · PI FEITELSON, MARK A · 1988 to 1992
–
NCI NIH HHS CA 48656NCI NIH HHS CA 66971NCI NIH HHS CA 79512
6 · The paper itself

Abstract

The development of hepatocellular carcinoma (HCC) is a multistep process associated with changes in host gene expression, some of which correlate with the appearance and progression of tumor. Preneoplastic changes in gene expression result from altered DNA methylation, the actions of hepatitis B and C viruses, and point mutations or loss of heterozygosity (LOH) in selected cellular genes. Tumor progression is characterized by LOH involving tumor suppressor genes on many chromosomes and by gene amplification of selected oncogenes. The changes observed in different HCC nodules are often distinct, suggesting heterogeneity on the molecular level. These observations suggest that there are multiple, perhaps redundant negative growth regulatory pathways that protect cells against transformation. An understanding of the molecular pathogenesis of HCC may provide new markers for tumor staging, for assessment of the relative risk of tumor formation, and open new opportunities for therapeutic intervention.

Indexed as

Carcinoma, HepatocellularDisease ProgressionDNA MethylationForecastingGene Expression Regulation, NeoplasticHepatitisHumansLiver NeoplasmsLoss of HeterozygosityModels, GeneticNeoplasm MetastasisRisk Factors

Identifiers

PMID11971194
OpenAlexW1968038516

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.