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 Concept Videos

Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

15.1K
Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
15.1K
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

7.1K
Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
7.1K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

6.2K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
6.2K
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

2.0K
Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
2.0K
Skin Cancer01:30

Skin Cancer

6.3K
Skin cancer is a type of cancer that occurs when there is an abnormal growth of skin cells, usually triggered by damage to the DNA within the skin cells. It is primarily caused by exposure to ultraviolet (UV) radiation from the sun or artificial sources like tanning beds. Skin cancer is the most common type of cancer worldwide, and its incidence continues to rise.
Basal Cell Carcinoma (BCC): BCC is the most common type of skin cancer, accounting for about 80% of cases. It typically develops in...
6.3K
Abnormal Proliferation02:23

Abnormal Proliferation

5.3K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.3K

You might also read

Related Articles

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

Sort by
Same author

Longitudinal analysis of high-risk HPV infections reveals within-host viral genome changes over time.

PLoS pathogens·2026
Same author

Oophorectomy-Corrected Ovarian Cancer Incidence, Survival, and Mortality by Subtype, Race, Ethnicity.

Cancer medicine·2026
Same author

Long-term outdoor air pollution and risk of ovarian and endometrial cancers in a large prospective cohort.

Journal of exposure science & environmental epidemiology·2026
Same author

HPV16 genetic variation provides evidence of positive natural selection driven by HLA class I.

Nature communications·2026
Same author

TriosCompass: a snakemake workflow for integrated detection of SNVs, indels, STRs, and structural de novo variants in parent-child trios.

Bioinformatics (Oxford, England)·2026
Same author

Individual and Geographical Factors Associated With Follow-Up Care After an Abnormal Cervical Cancer Screening Result.

Women's health issues : official publication of the Jacobs Institute of Women's Health·2026

Related Experiment Video

Updated: Feb 25, 2026

A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions
13:56

A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions

Published on: July 18, 2013

11.6K

Somatic Host Cell Alterations in HPV Carcinogenesis.

Tamara R Litwin1,2, Megan A Clarke3,4, Michael Dean5

  • 1Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, Rockville, MD 20850, USA. tamara.litwin@nih.gov.

Viruses
|August 4, 2017
PubMed
Summary

High-risk human papilloma virus (HPV) infections drive cancer by altering host cell DNA. Understanding these specific genetic mutations is key for developing early detection methods and improving patient treatment strategies.

Keywords:
APOBECHPVcervical cancerchromosomal instabilitycopy number variationhead and neck cancerintegrationsignificantly mutated genesomatic mutation

More Related Videos

Generation of Organotypic Raft Cultures from Primary Human Keratinocytes
07:26

Generation of Organotypic Raft Cultures from Primary Human Keratinocytes

Published on: February 22, 2012

19.8K
An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus
09:53

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus

Published on: August 25, 2017

9.4K

Related Experiment Videos

Last Updated: Feb 25, 2026

A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions
13:56

A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions

Published on: July 18, 2013

11.6K
Generation of Organotypic Raft Cultures from Primary Human Keratinocytes
07:26

Generation of Organotypic Raft Cultures from Primary Human Keratinocytes

Published on: February 22, 2012

19.8K
An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus
09:53

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus

Published on: August 25, 2017

9.4K

Area of Science:

  • Oncology
  • Virology
  • Genetics

Background:

  • High-risk human papilloma virus (HPV) infections are a primary cause of cervical and head and neck cancers.
  • Carcinogenesis involves viral oncoproteins (E6, E7) and critical host cell somatic events.
  • HPV-driven cancers exhibit characteristic APOBEC-driven mutations and genomic instability.

Purpose of the Study:

  • To elucidate the specific somatic events occurring in host cells following HPV infection.
  • To identify potential early detection biomarkers by characterizing mutations in precancerous lesions.
  • To understand how somatic mutations impact cancer prognosis and treatment decisions.

Main Methods:

  • Analysis of somatic mutations in HPV-associated cancers.
  • Characterization of genomic instability, including copy number variations and chromosomal rearrangements.
  • Identification of recurrent mutations in key cancer-related genes and pathways.

Main Results:

  • Recurrent mutations are observed in PIK3CA, PTEN, HLA-A/B, and TGFβ pathway genes.
  • TP53 and RB1 mutations are rare in HPV-associated cancers.
  • NOTCH1 mutations are predominantly found in head and neck cancers, indicating site-specific variations.

Conclusions:

  • Somatic events are crucial for malignant transformation in HPV-driven cancers.
  • Characterizing these mutations can lead to novel biomarkers for early cancer detection.
  • Understanding HPV-induced genetic alterations can inform therapeutic strategies and prognosis.