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Related Concept Videos

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...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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...

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RNAscope for In situ Detection of Transcriptionally Active Human Papillomavirus in Head and Neck Squamous Cell Carcinoma
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Human papillomavirus: E6 and E7 oncogenes.

Gaëlle Boulet1, Caroline Horvath, Davy Vanden Broeck

  • 1AMBIOR, Laboratory for Cell Biology & Histology, University of Antwerp, Groenenborgerlaan 171, BE-2020 Antwerp, Belgium.

The International Journal of Biochemistry & Cell Biology
|September 5, 2007
PubMed
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Human papillomaviruses (HPV) cause cancer through E6 and E7 oncoproteins targeting tumor suppressors. Understanding HPV oncogenesis is crucial for developing new cancer therapies and diagnostics.

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Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
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In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
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RNAscope for In situ Detection of Transcriptionally Active Human Papillomavirus in Head and Neck Squamous Cell Carcinoma
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Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
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In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells
09:20

In situ Subcellular Fractionation of Adherent and Non-adherent Mammalian Cells

Published on: July 23, 2010

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Human papillomaviruses (HPV) are recognized as a major cause of cancer, particularly cervical cancer.
  • The viral oncoproteins E6 and E7 are key mediators of HPV-induced carcinogenesis.
  • These oncoproteins interact with critical host-cell proteins, including tumor suppressors p53 and pRb.

Purpose of the Study:

  • To review the current understanding of HPV-induced carcinogenesis.
  • To highlight the role of E6 and E7 oncoproteins in cancer development.
  • To discuss the implications for diagnostics, therapeutics, and future research.

Main Methods:

  • Literature review of HPV research over the past 30 years.
  • Analysis of the molecular mechanisms of E6 and E7 oncoproteins.
  • Examination of current and emerging diagnostic and therapeutic strategies.

Main Results:

  • Established causal link between HPV and cancer, with E6 and E7 as primary drivers.
  • Demonstrated pleiotropic binding of E6/E7 to host proteins, disrupting tumor suppression.
  • Development of HPV detection methods and targeted therapies based on E6/E7.

Conclusions:

  • Continued research into HPV life cycle and oncogenesis is essential.
  • Further understanding is needed to address challenges in HPV-related cancer prevention and treatment.
  • Therapeutic vaccines and gene therapies targeting E6/E7 show promise.