The role of human oncoviruses in melanoma has been poorly investigated. The aim of this study was to investigate the association between oncoviruses and melanomas searching for human papillomavirus (HPV), Epstein Barr virus (EBV), and human herpesvirus 8DNA in melanoma specimens. Formalin‐fixed and paraffin‐embedded tissue specimens of cutaneous, mucosal, and ocular melanomas (OM) were selected from the Pathology Departments of the Galliera Hospital (Genoa) and the University Hospitals of Turin and Cagliari. Cutaneous and mucosal nevi have been collected as controls. The oncoviruses search has been performed with different polymerase chain reaction reagent kits. Fifty‐four melanomas (25 mucosal, 12 ocular, and 17 cutaneous) and 26 nevi (15 cutaneous and 11 mucosal) specimens were selected. The detection rate for one of the investigated oncoviruses was 17% in mucosal, 20% in ocular, and 0% in cutaneous melanomas (CMs). Despite the differences between groups seeming remarkable, there was no statistical significance ( p > 0.5). Our data do not support a primary role of oncoviruses in melanoma carcinogenesis; however, the finding of HPV and EBV DNA in a considerable fraction of mucosal and OMs suggests that these viruses may act as cofactors in the development of extra‐CMs.
Spontaneous regression (SR) of cancer is a rare but well‐documented biological phenomenon, which is even rarer in the context of metastatic breast carcinoma. Different mechanisms of SR are still under debate, including immune‐mediated response. We herein report a case of the SR of intralymphatic cutaneous metastases of a breast carcinoma with spontaneously‐induced T‐cell‐mediated cytotoxic response. An 86‐year‐old female was diagnosed with locally advanced right breast carcinoma and axillary lymph node metastases, without distant metastases The patient refused any therapy. Six months afterwards, she developed multiple, asymptomatic purpura‐like plaques with prominent teleangectasias on her right chest wall, continuous to the previous surgical scar and on her ipsilateral abdomen. Skin biopsy showed aggregates of atypical cells admixed with erythrocyte thrombi within dilated dermal lymphatic vessels. SR of the cutaneous lesions occurred within 6 months and persisted at the 15 months follow‐up in the absence of therapy, whilst no signs of internal relapse were observed. Immunohistochemically, the estrogen‐negative, CK7‐positive, C‐erb B2‐positive intralymphatic metastases were associated with extensive infiltration of CD8‐positive cytototoxic T lymphocytes. Factors that may have precluded the implantation of intralymphatic metastases leading to SR are discussed, with local immune surveillance being one major hypothesis.
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