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2020 Volume 7
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RESEARCH ARTICLE   Open Access    

Presence of JC Polyomavirus in Nonneoplastic Inflamed Colon Mucosa and Primary and Metastatic Colorectal Cancer

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  • Corresponding author: Farzin Sadeghi Cellular and Molecular Biology Research Center, Health Research Institute Babol University of Medical Sciences, Ganj-Afrooz Street Babol, Mazandaran 47176-47754 (Iran) E-Mail sadeghifarzin6@gmail.com
  • Background: Despite decades of epidemiologic and histopathologic investigations, the association between JC polyomavirus (JCPyV) infection and colorectal cancer (CRC) remains controversial.
    Objective: This study tested the presence of JCPyV sequences and determined the viral load in a series of colorectal samples from Iranian patients. In total, 223 formalin-fixed paraffin-embedded samples from patients diagnosed with primary and metastatic CRC as well as with nonneoplastic inflamed colon mucosa were analyzed by quantitative real-time PCR for the presence of JCPyV large tumor antigen (LT-Ag) sequences.
    Results: JCPyV LT-Ag sequences were detected in 18.6% of the CRC tissues and in 15.5% of the nonneoplastic control group. Viral LT-Ag was quantified in 18/100 primary colon adenocarcinomas, 2/10 metastatic adenocarcinomas, and 1/3 primary adenocarcinomas of the rectum. Two JCPyV-positive metastatic tumors presented a negative test result for JCPyV in the corresponding primary tumor. The median JCPyV LT-Ag copy number was 64 × 10–2 per cell and 14 × 10–2 per cell in the CRC cases and the nonneoplastic samples, respectively. There was no statistically significant difference between the two study groups regarding median LT-Ag DNA load (p = 0.059). Among the JCPyV-positive samples, the LT-Ag DNA load was higher in 2 metastatic tumors (from a patient with lung metastasis: 232 × 10–2 copies per cell; from a patient with liver metastasis: 121 × 10–2 copies per cell).
    Conclusions: The detection of JCPyV DNA at low copy numbers (lower than 1 viral copy per cell equivalent) and the absence of viral sequences in the corresponding primary tumors of the JCPyV-positive metastatic samples weaken the hypothesis of an etiological role of JCPyV in primary CRC induction.
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    Nadia Esmailzadeh, Mohammad Ranaee, Ahad Alizadeh, Aynaz Khademian, Saghar Saber Amoli, Farzin Sadeghi. 2020. Presence of JC Polyomavirus in Nonneoplastic Inflamed Colon Mucosa and Primary and Metastatic Colorectal Cancer. Gastrointestinal Tumors. 7:3 doi: 10.1159/000504293
    Nadia Esmailzadeh, Mohammad Ranaee, Ahad Alizadeh, Aynaz Khademian, Saghar Saber Amoli, Farzin Sadeghi. 2020. Presence of JC Polyomavirus in Nonneoplastic Inflamed Colon Mucosa and Primary and Metastatic Colorectal Cancer. Gastrointestinal Tumors. 7:3 doi: 10.1159/000504293

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Research Article   Open Access    

Presence of JC Polyomavirus in Nonneoplastic Inflamed Colon Mucosa and Primary and Metastatic Colorectal Cancer

  • Corresponding author: Farzin Sadeghi Cellular and Molecular Biology Research Center, Health Research Institute Babol University of Medical Sciences, Ganj-Afrooz Street Babol, Mazandaran 47176-47754 (Iran) E-Mail sadeghifarzin6@gmail.com
Gastrointestinal Tumors  7 Article number: 10.1159/000504293  (2020)  |  Cite this article

Abstract: 

Background: Despite decades of epidemiologic and histopathologic investigations, the association between JC polyomavirus (JCPyV) infection and colorectal cancer (CRC) remains controversial.
Objective: This study tested the presence of JCPyV sequences and determined the viral load in a series of colorectal samples from Iranian patients. In total, 223 formalin-fixed paraffin-embedded samples from patients diagnosed with primary and metastatic CRC as well as with nonneoplastic inflamed colon mucosa were analyzed by quantitative real-time PCR for the presence of JCPyV large tumor antigen (LT-Ag) sequences.
Results: JCPyV LT-Ag sequences were detected in 18.6% of the CRC tissues and in 15.5% of the nonneoplastic control group. Viral LT-Ag was quantified in 18/100 primary colon adenocarcinomas, 2/10 metastatic adenocarcinomas, and 1/3 primary adenocarcinomas of the rectum. Two JCPyV-positive metastatic tumors presented a negative test result for JCPyV in the corresponding primary tumor. The median JCPyV LT-Ag copy number was 64 × 10–2 per cell and 14 × 10–2 per cell in the CRC cases and the nonneoplastic samples, respectively. There was no statistically significant difference between the two study groups regarding median LT-Ag DNA load (p = 0.059). Among the JCPyV-positive samples, the LT-Ag DNA load was higher in 2 metastatic tumors (from a patient with lung metastasis: 232 × 10–2 copies per cell; from a patient with liver metastasis: 121 × 10–2 copies per cell).
Conclusions: The detection of JCPyV DNA at low copy numbers (lower than 1 viral copy per cell equivalent) and the absence of viral sequences in the corresponding primary tumors of the JCPyV-positive metastatic samples weaken the hypothesis of an etiological role of JCPyV in primary CRC induction.

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    Cite this article
    Nadia Esmailzadeh, Mohammad Ranaee, Ahad Alizadeh, Aynaz Khademian, Saghar Saber Amoli, Farzin Sadeghi. 2020. Presence of JC Polyomavirus in Nonneoplastic Inflamed Colon Mucosa and Primary and Metastatic Colorectal Cancer. Gastrointestinal Tumors. 7:3 doi: 10.1159/000504293
    Nadia Esmailzadeh, Mohammad Ranaee, Ahad Alizadeh, Aynaz Khademian, Saghar Saber Amoli, Farzin Sadeghi. 2020. Presence of JC Polyomavirus in Nonneoplastic Inflamed Colon Mucosa and Primary and Metastatic Colorectal Cancer. Gastrointestinal Tumors. 7:3 doi: 10.1159/000504293

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