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Rous Sarcoma Virus (RSV) and Cancer01:03

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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.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
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Spontaneous Murine Model of Anaplastic Thyroid Cancer
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SARS-CoV-2 detection in primary thyroid sarcoma: coincidence or interaction?

M L Tanda1,2, S Ippolito3, D Gallo3

  • 1Department of Medicine and Surgery, University of Insubria, Varese, Italy. marialaura.tanda@uninsubria.it.

Journal of Endocrinological Investigation
|January 5, 2022
PubMed
Summary
This summary is machine-generated.

This study identified SARS-CoV-2 in a patient with thyroid sarcoma, suggesting a synergistic interaction between the virus and tumor growth. The findings indicate a potential link between viral persistence and cancer proliferation.

Keywords:
MDM2SARS-CoV-2SarcomaSubacute thyroiditisThyroid

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Area of Science:

  • Oncology
  • Virology
  • Endocrinology

Background:

  • Emerging evidence links SARS-CoV-2 infection with thyroid dysfunction.
  • This case study investigated a patient during the second COVID-19 wave with suspected subacute thyroiditis.

Observation:

  • SARS-CoV-2 was detected in fine-needle aspiration cytology samples.
  • Histological examination revealed a rare primary thyroid sarcoma with high MDM2 oncoprotein expression.
  • Viral particles were observed within cytoplasmic vacuoles in neoplastic cells.

Findings:

  • The study identified a co-occurrence of SARS-CoV-2 and thyroid sarcoma.
  • A potential synergistic interplay between the virus and tumor was hypothesized.
  • MDM2 overexpression in tumor cells may create a niche for SARS-CoV-2, while the virus might promote tumor growth via p53 downregulation.

Implications:

  • This interaction could favor both viral persistence and tumor proliferation.
  • Further functional studies are required to validate the proposed mechanism.
  • Understanding this interplay may inform future therapeutic strategies for co-infected patients.