Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

TP53 and liver carcinogenesis.

Frank Staib1, S Perwez Hussain, Lorne J Hofseth

  • 1Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-4255, USA.

Human Mutation
|March 6, 2003
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Panaxynol mitigates chemotherapy-induced intestinal mucositis by improving the colonic microenvironment in murine models.

American journal of physiology. Gastrointestinal and liver physiology·2026
Same author

The senescence-inhibitory p53 isoform Δ133p53α represses the proinflammatory chemokine CXCL10 in progeria model mice and naturally aged mice.

bioRxiv : the preprint server for biology·2026
Same author

Microplastics in Early Onset Carcinogenesis.

Carcinogenesis·2026
Same author

Senescence-inhibitory Δ133p53α counteracts accelerated ageing and mortality.

bioRxiv : the preprint server for biology·2026
Same author

Urinary pesticide profiles and liver disease risk in Thailand: a machine-learning risk-prediction model.

medRxiv : the preprint server for health sciences·2026
Same author

Urinary Metabolites and Survival in Malignant Mesothelioma.

medRxiv : the preprint server for health sciences·2025
Same journal

Diagnostic Yield of Genome Sequencing in an Iranian Exome-Negative Autosomal-Recessive Intellectual Disability Cohort.

Human mutation·2026
Same journal

Exploring the Functional Impact of Individual <i>DDX41</i> Variants With a Fast and Robust Cell-Based Method.

Human mutation·2026
Same journal

Modeling the Effects of Single Nucleotide Polymorphisms (SNPs) on the Structure and Function of the Human <i>RET</i> Gene: An In Silico Study.

Human mutation·2026
Same journal

Driver Mutation Subtypes Differentially Shape Immune Evasion Landscapes in Melanoma: An AI-Driven Inflammatory Pathway Model Implicating CCNE1.

Human mutation·2026
Same journal

Comment on "When the Outcome Contains the Exposure: Methodological Limits of a Genome-Wide Cross-Trait Analysis of Type 2 Diabetes and MASLD".

Human mutation·2026
Same journal

AI-Augmented Hematological Signatures for Equitable Detection of Hereditary Hemolytic Anemia Carriers: A Global Systematic Review and Meta-Analysis.

Human mutation·2026
See all related articles

Hepatocellular carcinoma (HCC) is a deadly cancer often caused by aflatoxin B1 (AFB1) or hepatitis B virus (HBV). These factors induce critical mutations, particularly in the p53 tumor suppressor gene, driving liver cancer development.

Area of Science:

  • Hepatology
  • Oncology
  • Molecular Biology

Background:

  • Primary hepatocellular carcinoma (HCC) is a leading cause of cancer mortality globally.
  • Major risk factors include chronic hepatitis B/C virus infections, aflatoxin B1 (AFB1) exposure, and alcohol consumption.
  • Geographic hotspots for HCC mortality correlate with high AFB1 exposure and hepatitis B virus (HBV) prevalence.

Purpose of the Study:

  • To elucidate the molecular pathogenesis of HCC, focusing on genetic and epigenetic alterations.
  • To investigate the role of environmental toxins and viral infections in HCC development.
  • To understand the impact of mutations in key tumor suppressor genes like p53.

Main Methods:

  • Review of recent studies on molecular mechanisms of HCC.

Related Experiment Videos

  • Analysis of genetic and epigenetic changes in HCC pathogenesis.
  • Examination of the effects of AFB1 and HBV on DNA and gene mutations.

    • Main Results:

    • AFB1 exposure is linked to specific G:C to T:A transversions in the TP53 gene.
    • Chronic hepatitis B and C infections, along with inflammatory conditions, generate reactive oxygen species that damage DNA.
    • Integrated hepatitis B virus X (HBx) gene mutations in HCC can impair p53-mediated apoptosis.
    • Alterations in ras, Wnt, p53, and Rb pathways are significant in liver carcinogenesis.

    Conclusions:

    • Both viral infections (HBV, HCV) and chemical exposures (AFB1) are critical in HCC etiology and molecular pathogenesis.
    • Mutations in the p53 tumor suppressor gene are a common molecular event in HCC development.
    • Dysregulation of signal-transduction pathways, including ras, Wnt, p53, and Rb, plays a crucial role in liver carcinogenesis.