The presence of HPV was strongly correlated with non-melanoma skin cancers in a recent study published in the European Journal of Clinical Microbiology & Infectious Diseases.
“The public service announcement opportunity here is to remind us all that UVR [ultraviolet radiation], as well as immunosuppression, lead to skin cancer, and that chronically sun-exposed skin is more likely to have HPV,” said Sumaira Aasi, MD, a professor of dermatology and the director of Mohs and Dermatologic Surgery at Stanford Medicine, in Stanford, CA, in an exclusive interview with Cancer Network.
Baez et al found that 75% of tested non-melanoma skin cancer biopsies exhibited at least one of three viruses: HPV, Merkel cell polyomavirus, and Epstein-Barr virus. Only 38% of non-cancerous skin biopsies, however, were positive for these viruses (P = .02).
Importantly, HPV detection was common in non-melanoma skin cancers (43%; n = 83), but was nearly absent in non-cancerous biopsies (6.7%; n = 16; P = .007). Furthermore, Merkel cell polyomavirus was correlated with sites of increased exposure to ultraviolet radiation (P = .010), whereas Epstein-Barr virus was significantly linked to immunocompromise (P = .032).
Ultimately, HPV was strongly associated with non-melanoma skin cancer, while Epstein-Barr virus and Merkel cell polyomavirus were associated with other risk factors. Thus, the authors suggest that oncogenic viruses may play a role in non-melanoma skin cancers.
Aasi noted that other studies have found correlations between viruses and non-melanoma skin cancer, but this one is unique. “There have been multiple studies that have shown a correlation between viruses and non-melanoma skin cancer, particularly HPV, SCC [squamous cell carcinoma], and BCC [basal cell carcinoma],” she said.
“This is the first study that shows an association between Merkel cell polyomavirus with non-melanoma skin cancer. However, correlation still has not proven causation, and I do not think this data will change how we currently treat patients. We need further data to determine a causative role of viruses in non-melanoma skin cancer, and then we can move toward determining whether treating the virus would decrease incidence of skin cancer in patients,” Aasi said.
The investigators suggest that, once confirmed, the results of the study may help with non-melanoma skin cancer treatment and prevention. Because an HPV vaccine is available for the prevention of cervical cancer, this vaccine could possibly decrease non-melanoma skin cancer development in at-risk populations. Moreover, intratumoral treatment with the HPV vaccine could serve as an alternative to surgery, which is standard treatment, according to the authors.
The authors also reported the first association between Merkel cell polyomavirus detection and non-melanoma skin cancer in sun-exposed areas. This finding could support the co-carcinogen hypothesis. Alternatively, this higher incidence of Merkel cell polyomavirus in the elderly could be due to immune senescence, wherein increased levels of viral shedding from skin tissue is likely expected.
Aasi raised concerns about the design of the current study. “[There were] significantly fewer normal skin biopsies vs those with non-melanoma skin cancer—it would have been helpful to have equal numbers represented. Also, normal skin in those patients with non-melanoma skin cancer did not appear to have been tested. Do those patients have virus in the normal skin?” she questioned.
Finally, she noted, “Almost all the HPV found in skin biopsies were from UVR sites. No discussion about the presence or impact of HPV in skin cancers that develop in sun-protected sites [was presented].”