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Related Concept Videos

Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

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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...
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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
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Skin Cancer01:30

Skin Cancer

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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.
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Cancer Prevention02:59

Cancer Prevention

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Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
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Mutagenicity and Carcinogenicity01:25

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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...
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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...
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Related Experiment Video

Updated: Mar 9, 2026

Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
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Virus and Host Events in Squamous Carcinogenesis.

Nicholas Coleman1

  • 1Department of Pathology, Cambridge University, Cambridge, United Kingdom.

The Keio Journal of Medicine
|December 28, 2016
PubMed
Summary

This study explores how high-risk human papillomavirus (HR-HPV) integration and oncostatin-M receptor (OSMR) signaling drive squamous cell carcinoma (SCC) progression, seeking new diagnostic and therapeutic targets for SCC. Findings may lead to novel epigenetic therapies.

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Squamous cell carcinomas (SCCs) are a significant health concern, with limited therapeutic options.
  • High-risk human papillomavirus (HR-HPV) infection is a known etiological factor in various SCCs.
  • The oncostatin-M receptor (OSMR) pathway is implicated in cancer progression and metastasis.

Purpose of the Study:

  • To investigate mechanisms of HR-HPV transcriptional deregulation and its role in SCC development.
  • To identify the role of the oncostatin-M receptor (OSMR) in SCC metastasis and therapeutic potential.
  • To explore new diagnostic and therapeutic strategies for SCC.

Main Methods:

  • Analyzing HPV16 integration into the host genome and its epigenetic regulation.

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  • Studying the effects of OSMR overexpression and its ligand OSM on SCC cells and the tumor microenvironment (TME).
  • Evaluating the efficacy of OSM:OSMR blockade in preclinical SCC models.

    • Main Results:

    • HPV16 integration does not always confer a growth advantage; epigenetic regulation is key to oncogene expression.
    • OSMR copy number gain and overexpression correlate with poor prognosis in SCC.
    • OSMR activation promotes epithelial-mesenchymal transition, metastasis, and influences the TME.

    Conclusions:

    • Epigenetic modifications of integrated HR-HPV are crucial for SCC progression and may offer therapeutic targets.
    • OSMR signaling is a promising therapeutic target for inhibiting SCC metastasis.
    • Understanding these pathways can lead to improved SCC diagnosis and treatment.