HPV Typing in Brazilian Patients with Epidermodysplasia Verruciformis: High Prevalence of EV-HPV 25

Oliveira, Walmar Roncalli Pereira de; He, Qiaojun; Rády, Peter L.; Hughes, Thomas K.; Neto, Cyro Festa; Rivitti, Evandro A.; Tyring, Stephen K.

doi:10.1007/s10227-003-0100-6

Cited by 34 publications

(32 citation statements)

References 34 publications

(87 reference statements)

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“…Paraffin embedded skin biopsies from each case were subjected to HPV typing. [20][21][22] In the first patient's tissue sample, this procedure revealed the presence of HPVs 5 and 19, and HPV 5 was present in the second patient's tissue sample, confirming the diagnosis of EV in both cases.…”

Section: Histopathology and Ev-hpv Typingmentioning

confidence: 78%

Acquired epidermodysplasia verruciformis

Rogers¹,

MacGregor²,

Nord³

et al. 2009

Journal of the American Academy of Dermatology

115

121

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Section: Histopathology and Ev-hpv Typingmentioning

confidence: 78%

Acquired epidermodysplasia verruciformis

Rogers¹,

MacGregor²,

Nord³

et al. 2009

Journal of the American Academy of Dermatology

115

121

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“…23 Isolation, cloning and sequencing of putative HPV-PCR products were carried out as described earlier. 28 Briefly, the obtained putative HPV sequence information were aligned and compared to known HPV types available through the GenBank database using the BLAST program (National Center for Biotechnology Information, National Institutes of Health, Bethesda, MD). The PCR mixtures and products were analyzed on 2.0% agarose gel electrophoresis and visualized on a UV transilluminator.…”

Section: Resultsmentioning

confidence: 99%

Merkel Cell Polyomavirus and HPV-17 Associated With Cutaneous Squamous Cell Carcinoma Arising in a Patient With Melanoma Treated With the BRAF Inhibitor Dabrafenib

et al. 2013

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Background Approximately 10–25% of patients treated with BRAF inhibitors develop cutaneous squamous cell carcinoma (SCC), but the mechanism responsible has not yet been determined. We report the first case in which Merkel cell polyomavirus (MCPyV) and HPV-17 are associated with cutaneous SCC which developed during treatment with BRAF inhibitor GSK2118436. Observations A 62 year-old woman with V600E BRAF-mutant metastatic melanoma enrolled on a phase I trial of GSK2118436, a selective inhibitor of V600-mutant BRAF kinase. During the first six weeks of treatment, the patient developed multiple skin lesions, including a 6-mm crusted papule on the left eyebrow, which was resected and revealed SCC. DNA extracted from paraffin-embedded tissue was amplified by polymerase chain reaction (PCR) for detection of MCPyV and epidermodysplasia verruciformis HPV (EV-HPV) types. Analysis of the cloned and sequenced PCR products revealed the presence of MCPyV and HPV-17 DNA. Other EV-HPV subtypes were not detected. Conclusions To our knowledge, this is the first report demonstrating the co-existence of MCPyV and HPV-17 in cutaneous SCC. Because both viruses have known oncogenic potential, the role of these viruses in the etiology of BRAF inhibitor-related SCC merits further investigation.

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“…Isolation, cloning (TOPO TA cloning kit, Invitrogen Co. Carlsbad, CA) and sequencing of putative HPV-PCR products were carried out as described (34). HPV sequence data were aligned and identified to known HPV DNA sequences available through GenBank (National Center for Biotechnology Information, National Institutes of Health, Bethesda, MD) using the BLAST program (41). A minimum of 5 clones was sequenced from the above TOPO-cloning procedure for HPV genotyping per specimen.…”

Section: Methodsmentioning

confidence: 99%

Contribution of Beta-HPV Infection and UV Damage to Rapid-Onset Cutaneous Squamous Cell Carcinoma during BRAF-Inhibition Therapy

Cohen

Lawson

Shaver

et al. 2015

Clinical Cancer Research

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Purpose BRAF-inhibition (BRAFi) therapy for advanced melanoma carries a high rate of secondary cutaneous squamous cell carcinoma (cSCC) and risk of other cancers. Ultraviolet (UV) radiation and α-genus human papillomavirus (HPV) are highly associated with SCC, but a novel role for β-genus HPV is suspected in BRAFi-cSCC. Cutaneous β-HPV may act in concert with host and environmental factors in BRAFi-cSCC. Experimental Design Primary BRAFi-cSCC tissue DNA isolated from patients receiving vemurafenib (Vem) or dabrafenib from two cancer centers was analyzed for the presence of cutaneous oncogenic viruses and host genetic mutations. Diagnostic specimens underwent consensus dermatopathology review. Clinical parameters for UV exposure and disease course were statistically analyzed in conjunction with histopathology. Results Twenty-nine patients contributed 69 BRAFi-cSCC lesions. BRAFi-cSCC had wart-like features (BRAFi-cSCC-WF) in 22% of specimens. During Vem therapy, BRAFi-cSCC-WF arose 11.6 weeks more rapidly than conventional-cSCC when controlled for gender and UV-exposure (p-value=0.03). Among all BRAFi-cSCC, β-genus HPV-17, HPV-38, HPV-111 were most frequently isolated and novel β-HPV genotypes were discovered (CTR, CRT-11, CRT-22). Sequencing revealed 63% of evaluated BRAFi-cSCCs harbored RAS mutations with PIK3CA, CKIT, ALK and EGFR mutations also detected. Conclusions We examined clinical, histopathologic, viral and genetic parameters in BRAFi-cSCC demonstrating rapid onset; wart-like histomorphology; β-HPV-17, HPV-38, and HPV-111 infection; UV damage; and novel ALK and CKIT mutations. Discovered β-HPV genotypes expand the spectrum of tumor-associated viruses. These findings enhance our understanding of factors cooperating with BRAF inhibition that accelerate keratinocyte oncogenesis as well as broaden the knowledge base of multifactorial mediators of cancer in general.

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HPV Typing in Brazilian Patients with Epidermodysplasia Verruciformis: High Prevalence of EV-HPV 25

Abstract: EV-HPV 25 was the most prevalent in our study. The noteworthy association of EV-HPV type 14d with skin cancers suggests its possible oncogenic role in malignant transformation in this population.

Cited by 34 publications

References 34 publications

Acquired epidermodysplasia verruciformis

Acquired epidermodysplasia verruciformis

Merkel Cell Polyomavirus and HPV-17 Associated With Cutaneous Squamous Cell Carcinoma Arising in a Patient With Melanoma Treated With the BRAF Inhibitor Dabrafenib

Contribution of Beta-HPV Infection and UV Damage to Rapid-Onset Cutaneous Squamous Cell Carcinoma during BRAF-Inhibition Therapy

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