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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...
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...
Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...

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An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
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Telomerase reverse transcriptase expression elevated by avian leukosis virus integration in B cell lymphomas.

Feng Yang1, Rena R Xian, Yingying Li

  • 1Department of Biology, The Johns Hopkins University, 3400 North Charles Street, Baltimore, MD 21218, USA.

Proceedings of the National Academy of Sciences of the United States of America
|November 21, 2007
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Avian leukosis virus (ALV) insertional mutagenesis activates telomerase reverse transcriptase (TERT) in chicken lymphomas. This retroviral up-regulation of TERT by insertional activation promotes tumor progression.

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Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Retroviruses can cause tumors by integrating into host DNA, affecting oncogenes and tumor suppressor genes.
  • Understanding these integration sites reveals tumorigenesis mechanisms.

Purpose of the Study:

  • To identify avian leukosis virus (ALV) proviral integration sites in rapid-onset B cell lymphomas.
  • To investigate the role of these integrations in tumor development and gene expression.

Main Methods:

  • Inverse PCR was used to identify 28 unique viral integration sites in tumors.
  • Southern blots confirmed clonal integration events.
  • Real-time RT-PCR assessed TERT mRNA expression and telomerase activity.

Main Results:

  • Four tumors showed integration in the telomerase reverse transcriptase (TERT) promoter/enhancer region.
  • TERT mRNA and telomerase activity were significantly upregulated in tumors with TERT promoter integrations.
  • Viral LTR sequences directly enhanced TERT promoter-driven reporter gene expression.

Conclusions:

  • Retroviral insertional activation of the TERT promoter is a mechanism for up-regulating TERT in B cell lymphomas.
  • This up-regulation of TERT by ALV contributes to tumor initiation or progression.