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  Table of Contents  
Year : 2019  |  Volume : 56  |  Issue : 3  |  Page : 279-280

Papilloma virus infection in oral malignancies: An Italian experience

1 Department of Medicine (DIMED), Pathology and Cytopathology Unit, University of Padova, Italy
2 Department of Pathology, ULSS 6, Camposampiero Hospital, Italy
3 Department of Medicine (DIMED), Pathology and Cytopathology Unit, University of Padova; Veneto Cancer Registry, Veneto Region, Italy

Date of Web Publication19-Jul-2019

Correspondence Address:
Massimo Rugge
Department of Medicine (DIMED), Pathology and Cytopathology Unit, University of Padova; Veneto Cancer Registry, Veneto Region
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijc.IJC_373_18

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How to cite this article:
Cesaro S, Tsvetkova V, Traverso G, Cassaro M, Rugge M. Papilloma virus infection in oral malignancies: An Italian experience. Indian J Cancer 2019;56:279-80

How to cite this URL:
Cesaro S, Tsvetkova V, Traverso G, Cassaro M, Rugge M. Papilloma virus infection in oral malignancies: An Italian experience. Indian J Cancer [serial online] 2019 [cited 2022 Dec 7];56:279-80. Available from:

We have read with interest the paper by Rajesh et al.,[1] addressing the prevalence of human papilloma virus (HPV) in Indian patients harboring oral squamous cell cancer (OSCC).

Given our interest in HPV-associated squamous malignancies, we would like to report our experience on HPV status in a consecutive series of 46 Italian OSCC patients assessed histologically at our department in the years 2016–2017. HPV molecular testing was conducted on the microdissected neoplastic lesions obtained from the original (formalin-fixed paraffin-embedded [FFPE]) biopsy samples. Genomic DNA extraction (QIAamp DNA FFPE Tissue Kit; Qiagen, Hilden, Germany) and HPV testing procedures (AMPLIQUALITY HPV-TYPE EXPRESS v3.0; AB ANALITICA) were completed personally by the same expert technician [Sonia Cesaro], according to the manufacturers' recommendations. The method applied identifies 41 HPV genotypes, distinguishing between low-risk (HPV 6, 11, 40, 42, 43, 44, 54, 55, 61, 62, 69, 71, 72, 81, 83, 84, 87, 89, and 90) and high-risk (HPV 16, 18, 26, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 64, 66, 67, 68A, 68B, 70, 73, and 82) genotypes. In the final assessment, HPV-positive status was dichotomized as being due to low-risk versus high-risk genotypes (when high-and low-risk genotypes coexisted, the high-risk genotype was considered “dominant”).[2] Our 46 cases included 30 men and 16 women. Overall, HPV infection was identified in 16/46 (34.8%) cases. Among men, 11/30 OSCCs were HPV-positive (mean age 68 years, range 55–69; mean age of HPV-negative OSCCs 61 years, range 31–86). Among women, 5/16 OSCCs were HPV-positive (mean age 70 years, range 44–93; HPV-negative OSCCs: mean age 68 years, range 45–91). Among the 16/46 HPV-positive OSCCs, 13/16 (81.25%) were associated (or coexisted) with high-risk HPV genotypes (HPV 16, 31, and 66).

The above-mentioned results differ strongly from those reported by Rajesh et al.[1] A main difference concerns the epidemiological settings where patients were recruited:[3] the Indian patients usually came from rural areas and had a low socioeconomic status, while all the Italian patients lived in an industrialized region; and females prevailed significantly [male: female ratio (M:F) 15:45] in the Indian cohort, while males strongly predominated among the Italian patients (M:F 48:30). Another variable that might explain the differences between Indian and Italian OSCC patients' HPV status concerns the HPV testing procedures: in all Italian cases, genomic DNA was obtained for testing after the microscopic identification and manual microdissection of the cancer from the original FFPE tissue sample (a method that may exclude noncancerous tissue from the test procedure).

Even allowing for these differences, however, the surprising discrepancy in HPV status between Indian and Italian OSCC patients should fuel more extensive comparative etiopathogenic studies, which might significantly affect different choices of etiologically targeted prevention strategies.[4],[5],[6]

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There are no conflicts of interest.

  References Top

Rajesh D, Mohiyuddin SM, Kutty AV, Balakrishna S. Prevalence of human papillomavirus in oral squamous cell carcinoma: A rural teaching hospital-based cross-sectional study. Indian J Cancer 2017;54:498-501.  Back to cited text no. 1
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IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization International Agency for Research on Cancer. Vol. 90. Human Papillomaviruses; 2007.  Back to cited text no. 2
de Abreu PM, Có AC, Azevedo PL, do Valle IB, de Oliveira KG, Gouvea SA, et al. Frequency of HPV in oral cavity squamous cell carcinoma. BMC Cancer 2018;18:324.  Back to cited text no. 3
Thomas SJ, Penfold CM, Waylen A, Ness AR. The changing aetiology of head and neck squamous cell cancer: A tale of three cancers? Clin Otolaryngol 2018. DOI: 10.1111/coa.13144. [Epub ahead of print].  Back to cited text no. 4
Dalla Torre D, Burtscher D, Soelder E, Offermanns V, Rasse M, Puelacher W, et al. Human papillomavirus prevalence in a mid-European oral squamous cell cancer population: A cohort study. Oral Dis 2018;24:948-56.  Back to cited text no. 5
Wang C, Dickie J, Sutavani RV, Pointer C, Thomas GJ, Savelyeva N, et al. Targeting head and neck cancer by vaccination. Front Immunol 2018;9:830.  Back to cited text no. 6


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