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John Cunningham virus T-antigen expression in anal carcinoma
Sonia Ramamoorthy1, Bikash Devaraj, Katsumi Miyai
1Department of Surgery, University of California, San Diego, California; Moores Comprehensive Cancer Center, University of California, San Diego, California.
Background:
Anal carcinoma is thought to be driven by human papillomavirus (HPV) infection through interrupting function of cell regulatory proteins such as p53 and pRb. John Cunningham virus (JCV) expresses a T-antigen that causes malignant transformation through development of aneuploidy and interaction with some of the same regulatory proteins as HPV. JCV T-antigen is present in brain, gastric, and colon malignancies, but has not been evaluated in anal cancers. The authors examined a cohort of anal cancers for JCV T-antigen and correlated this with clinicopathologic data.
Methods:
Archived anal carcinomas were analyzed for JCV T-antigen expression. DNA from tumor and normal tissue was sequenced for JCV with viral copies determined by quantitative polymerase chain reaction and Southern blotting. HPV and microsatellite instability (MSI) status was correlated with JCV T-antigen expression.
Results:
Of 21 cases of anal cancer (mean age 49 years, 38% female), 12 (57%) were in human immunodeficiency virus (HIV)-positive individuals. All 21 cancers expressed JCV T-antigen, including 9 HPV-negative specimens. More JCV copies were present in cancer versus surrounding normal tissue (mean 32.54 copies/microg DNA vs 2.98 copies/microg DNA, P = .0267). There was no correlation between disease stage and viral copies, nor between viral copies and HIV-positive or -negative status (28.7 vs 36.34 copies/microg DNA, respectively, P = .7804). In subset analysis, no association was found between JCV T-antigen expression and HPV or MSI status.
Conclusions:
Anal carcinomas uniformly express JCV T-antigen and contain more viral copies compared with surrounding normal tissue. JCV and its T-antigen oncogenic protein, presumably through interruption of cell regulatory proteins, may play a role in anal cancer pathogenesis.
Insights
John Cunningham virus (JCV) T-antigen is uniformly present in anal cancers, with higher viral loads in tumors than normal tissue. This suggests JCV may contribute to the development of anal carcinoma.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Anal carcinoma is often linked to human papillomavirus (HPV) infection.
- John Cunningham virus (JCV) T-antigen is implicated in other cancers, but its role in anal cancer is unstudied.
- JCV T-antigen disrupts cell regulatory proteins, similar to HPV.
Purpose of the Study:
- To investigate the presence and role of JCV T-antigen in anal carcinoma.
- To correlate JCV T-antigen expression with clinicopathologic features of anal cancer.
Main Methods:
- Analysis of archived anal carcinoma samples for JCV T-antigen expression.
- DNA sequencing and quantitative PCR to determine JCV viral load.
- Correlation of JCV T-antigen status with HPV and microsatellite instability (MSI).
Main Results:
- All 21 anal cancer cases expressed JCV T-antigen.
- JCV viral load was significantly higher in tumor tissue than normal tissue.
- JCV T-antigen expression was independent of HPV status, MSI, disease stage, and HIV status.
Conclusions:
- Anal carcinomas consistently express JCV T-antigen.
- Elevated JCV viral copies in tumors suggest a potential role in anal cancer pathogenesis.
- JCV T-antigen may contribute to anal cancer development by interfering with cell regulatory proteins.
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