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Detection of alpha‐ and beta‐human papillomavirus (HPV) in cutaneous melanoma: a matched and controlled study using specific multiplex PCR combined with DNA microarray primer extension
Author(s) -
Ruer Jean Baptiste,
Pépin Line,
Gheit Tarik,
Vidal Chrystelle,
Kantelip Bernadette,
Tommasino Massimo,
Prétet Jean Luc,
Mougin Christiane,
Aubin François
Publication year - 2009
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2009.00866.x
Subject(s) - melanoma , medicine , multiplex , hpv infection , multiplex polymerase chain reaction , population , primer (cosmetics) , oncology , biology , polymerase chain reaction , cervical cancer , cancer research , cancer , bioinformatics , genetics , gene , chemistry , environmental health , organic chemistry
  There are few contradictory studies investigating the involvement of HPV in melanoma. We designed a controlled study to evaluate the HPV DNA prevalence in melanoma. One hundred patients with cutaneous malignant melanoma diagnosed between 2002 and 2006 were included. Complementary wide excision (healthy skin) was performed in 85 patients and was used as internal control. After DNA extraction, 68 different HPV types were studied using a multiplex PCR combined with microarray primer extension. We did not observe any statistical significant difference in terms of HPV DNA prevalence in melanoma (38.8%) and in healthy skin from wide excision (42.4%). Twenty‐one different HPV types were detected but only one type was present in the majority of our samples (80/85 melanoma vs 59/66 HS). The distribution of HPV genera and types was similar in melanoma and HS, and beta‐HPV was predominant (30.6% and 31.8%). Among alpha‐HPV (10.6%), high‐risk mucosal HPV16 was predominant. Among beta‐HPV, melanoma harboured significantly more type 22 than control normal skin from the same patients and significantly less type 21 than paired control normal skin. No correlation between clinical and pathological melanoma characteristics and HPV DNA prevalence was found. Our data do not support a role of HPV infection in melanocarcinogenesis, but confirm the previous data suggesting that HPV DNA is widely distributed among the population and that occult HPV infections are frequent. Furthermore, specific HPV types, such as a‐HPV16 and beta‐HPV species 2 may be involved in a sub‐group of melanoma.

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