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

Carcinogenesis revisited.

W den Otter, J W Koten, D J Derkinderen

    Cancer Investigation
    |January 1, 1987
    PubMed
    Summary

    Cancer development likely requires multiple genetic mutations. A four-mutation model explains spontaneous tumor frequency and incidence patterns in humans, aligning with genetic and environmental factors in carcinogenesis.

    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

    Mathematical analysis of the cellular immune reaction against tumour cells.

    Immunology today·2014
    Same author

    Sponsorship of scientific work.

    Immunology today·2014
    Same author

    Local interleukin-2 therapy of bovine vulval papilloma and carcinoma complex.

    The Veterinary record·2011
    Same author

    Low-dose IL-2 therapy reduces HCV RNA and HBV DNA: case report.

    Anticancer research·2010
    Same author

    Treatment of ocular squamous cell carcinomas in cattle with interleukin-2.

    The Veterinary record·2006
    Same author

    Galectins as markers of aggressiveness of mouse mammary carcinoma: towards a lectin target therapy of human breast cancer.

    Breast cancer research and treatment·2005

    Area of Science:

    • Oncology
    • Genetics
    • Cancer Biology

    Background:

    • The precise role of genetic mutations in cancer development remains incompletely understood.
    • Establishing the number of mutations required for a cell to become cancerous is crucial for understanding carcinogenesis.
    • Simpler mutation theories have limitations in explaining cancer incidence and progression.

    Purpose of the Study:

    • To determine the number of genetic mutations necessary for a cell to initiate cancer.
    • To develop a quantitative model for spontaneous carcinogenesis in humans.

    Main Methods:

    • A multi-mutation model was proposed, specifically a four-mutation model.
    • Calculations were based on observed endogenous tumor frequencies (2% of the population).
    • Assumptions included a mean mutation rate per gene per generation and total cell production over a lifetime.

    Main Results:

    • A four-mutation model provides a better fit for human carcinogenesis than a one-mutation theory.
    • The model aligns observed endogenous tumor rates with spontaneous carcinogenesis frequency.
    • Calculations integrate mutation rates and total cell numbers across a lifetime.

    Conclusions:

    • A minimum of four genetic mutations are likely required for a cell to become cancerous.
    • The four-mutation model is consistent with cancer incidence peaks in childhood and hereditary factors.
    • This model supports the understanding of both hereditary and non-hereditary cancer mechanisms.

    Related Experiment Videos