Penile Cancer and Its Precursor Lesions 141 Penile Cancer and Adjacent Lesions

Penile cancers are thought to arise from the progression of precursor lesions and can be subdivided into HPV-positive and HPV-negative cases. The HPV prevalence differs significantly by histological subtype. Similar to vulvar and head and neck carcinomas, squamous cell carcinoma of the basaloid and warty type display the strongest association with hrHPV (ranging from 66% to 100%) and their etiological relationship with hrHPV infection is most plausible.4 19,32,33 The remaining penile squamous cell carcinomas demonstrate about 30% positivity for hrHPV DNA.4,7,17,18,34,35 Verrucous penile carcinoma seems to have a weaker association with HPV positivity, showing a prevalence of 22.4%.19 Despite the similarities between penile and vulvar cancer including the presence of HPV (mainly HPV-16) and their precursor lesions, the clear bimodal age distribution that is found for vulvar cancer is not clearly seen for penile cancer.36 Cubilla et al. observed a lower age for patients (average age 55 years) diagnosed with basaloid or warty types of cancer compared to other types of penile squamous cell carcinomas.33,37,38 However, in another study, no age difference was found between HPV-positive and -negative cases (i.e., average age 64 years).39

Cubilla et al.37 presented cross-sectional data of almost 300 cases of invasive penile cancers and studied the presence of associated epithelial lesions. Histological evaluation showed that histological hyperplastic epithelial alterations and low-grade penile intraepithelial neoplasia (PIN) were more commonly found in usual squamous, papillary, and verrucous squamous cell carcinomas than in cases with warty or basaloid carcinomas. Conversely, high-grade PIN was present in two thirds of the warty, basaloid, or mixed warty-basaloid tumor subtypes but absent in papillary and verrucous tumors. In fact, despite the lack of a clear identification of the clinical counterparts, corresponding histopathologic features between the precursor lesion and its associated tumor type were shown. Apparently, non-dysplastic or mildly dysplastic lesions may directly progress into invasive cancer in at least a substantial subset of the penile cancer cases. In conclusion, although there are several clear-cut differences between the subtypes of penile squamous cell carcinoma and their precursor lesions (i.e., histomorphological features and HPV status), their clinical distinction and the underlying molecular pathogenesis for progression into invasive cancer is not clear-cut and merits further investigation.

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