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Merkel Cell Carcinomas Arising in Autoimmune Disease Affected Patients Treated with Biologic Drugs, Including

John Charles Rotondo1, Ilaria Bononi1, Andrea Puozzo1

  • 1Department of Morphology, Surgery and Experimental Medicine, School of Medicine, University of Ferrara, Ferrara, Italy.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|February 9, 2017
PubMed

Insights

Merkel cell carcinoma (MCC) in patients on biologic drugs may be linked to Merkel cell polyomavirus (MCPyV). MCC tumors showed MCPyV DNA and the viral large T oncoprotein, suggesting a possible drug-induced immune link.

Area of Science:

  • Oncology
  • Virology
  • Immunology

Background:

  • Merkel cell carcinoma (MCC) is a rare but aggressive skin cancer.
  • Patients with autoimmune diseases treated with biologic drugs, such as TNF inhibitors, have a higher risk of developing MCC.
  • The role of Merkel cell polyomavirus (MCPyV) in MCC pathogenesis is well-established, particularly the activity of its large T (LT) oncoprotein.

Purpose of the Study:

  • To investigate the presence and characteristics of MCPyV in MCC cases arising in patients with autoimmune diseases receiving biologic therapies.
  • To analyze the immune response against MCPyV antigens in these patients.
  • To explore the expression of MCPyV LT oncoprotein in MCC tumor tissues.

Main Methods:

  • Serum analysis for IgG antibodies against MCPyV large T (LT), small T (ST) oncoproteins, and viral capsid protein-1 (VP1) using indirect ELISA.
  • Detection of MCPyV DNA in MCC tissues and peripheral blood mononuclear cells (PBMCs) via PCR.
  • Immunohistochemical (IHC) analysis of MCC tissues for MCPyV LT oncoprotein expression.

Main Results:

  • MCPyV DNA with 100% homology to the European MKL-1 strain was found in MCC tissues, with viral loads ranging from 0.1 to 30 copies/cell.
  • Patients showed IgG antibodies against MCPyV VP1, and two out of three had antibodies against LT/ST oncoproteins.
  • MCC tissues were positive for MCPyV LT oncoprotein expression via IHC, with strong nuclear localization, while normal tissues were negative.

Conclusions:

  • The study identified MCC in patients with rheumatologic diseases treated with biologic drugs, suggesting a potential causal link between immunosuppressive therapy and MCC development.
  • The presence of MCPyV DNA and LT oncoprotein in MCC tumors supports the association between MCC and MCPyV LT oncoprotein activity.
  • Pharmacologic immunosuppression may facilitate MCC onset in genetically susceptible individuals or those exposed to MCPyV.

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