Related Experiment Video

Updated: Jul 6, 2026

Genome-wide RNAi Screening to Identify Host Factors That Modulate Oncolytic Virus Therapy
08:51

Genome-wide RNAi Screening to Identify Host Factors That Modulate Oncolytic Virus Therapy

Published on: April 3, 2018

Effect of transforming viruses on molecular mechanisms associated with cancer

Tajhal Dayaram1, Susan J Marriott

  • 1Interdepartmental Program in Cell and Molecular Biology, Department of Molecular Virology and Microbiology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.

Journal of Cellular Physiology
|March 28, 2008
PubMed

Insights

Oncogenic viruses cause about 20% of human tumors by encoding oncoproteins that disrupt cellular processes. Studying these viruses, like human papillomavirus, reveals cancer development mechanisms.

Area of Science:

  • Virology
  • Oncology
  • Molecular Biology

Background:

  • Viruses are implicated in approximately 20% of human tumors globally.
  • Transforming viruses encode oncoproteins that manipulate cellular proteins to boost viral replication and induce cell transformation.
  • Viral oncoproteins impact cellular pathways also dysregulated in cancers, offering insights into carcinogenesis.

Purpose of the Study:

  • To review cellular mechanisms targeted by oncogenic human viruses.
  • To elucidate how these viral effects contribute to cellular transformation and tumorigenesis.
  • To focus on human T-cell leukemia virus type-I, hepatitis B virus, and human papillomavirus as models.

Main Methods:

  • Review of existing literature on oncogenic viruses and their mechanisms of action.
  • Analysis of viral oncoproteins' roles in cell cycle regulation, DNA damage response, and apoptosis.
  • Examination of specific examples: human T-cell leukemia virus type-I, hepatitis B virus, and human papillomavirus.

Main Results:

  • Oncogenic viruses encode oncoproteins that promote cell cycle progression.
  • These viral oncoproteins inhibit DNA damage checkpoint responses, preventing necessary cellular repair.
  • Programmed cell death (apoptosis) is prevented by viral oncoproteins, aiding viral propagation and cell survival.

Conclusions:

  • Oncogenic viruses provide valuable models for studying cancer development.
  • Viral oncoproteins' effects on cell cycle, DNA repair, and apoptosis are key to understanding viral carcinogenesis.
  • Understanding these viral mechanisms enhances knowledge of the multistep process of tumorigenesis.

More Related Videos

Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo12:42

Paramyxoviruses for Tumor-targeted Immunomodulation: Design and Evaluation Ex Vivo

Published on: January 7, 2019

Related Concept Videos

Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

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...
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

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...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

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.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

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.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...