(1) Background: Human papillomavirus (HPV) E6 and E7 oncoproteins are vital for developing HPV induced penile carcinoma. The viral oncoproteins play a central role in oncogenesis by interacting with several cellular regulatory proteins, such as p16INK4a and p53. Many studies suggest that these proteins showed clinical utility in predicting nodal disease, cancer specific survival, overall survival and even tumor grade. Understanding the molecular mechanism involved in the carcinogenesis of penile cancer could offer biomarkers for disease progression, treatment response and potential targeted therapies; (2) Methods: This paper is a prospective study on a group of 100 patients who underwent prostate surgery during 2013 and 2014 in the Urology Clinic of “Carol Davila” Central Military Emergency University Hospital Bucharest. They were tested for HPV by PCR and IHC (p16) methods; (3) Results: 11 cases (22%) of HPV were found in the cluster of patients tested. PCR and P16 were the HPV diagnostic tests used. In order to determine the consistency of the 2 tests, the Cohen’s kappa coefficient was used at a p level < 0.05. The PCR method had a sensitivity of 81.8% and a specificity of 94.9%. The P16 method had a sensitivity of 63.6% and a specificity of 89.7%.
Melanoma outcome seems different between females and males, with a potential protective role of estrogen (E) through estrogen receptors (ER) expression into the tumor. In the study of ERs, both alfa (ERα) and beta (ERβ) is a well-known endocrine elements in non-melanoma tumors, like mammary and endometrial cancer. Immunohistochemistry (IHC) assessment of melanoma concerning ERs represents a path to explore the tumor profile to provide useful information concerning the prognostic and potential adjuvant treatment. Currently, this is not a routine practice, nor a mandatory step for deciding the medical therapy. Typically, IHCs are based on usual kits for mammary tumors regarding ERs configuration. Prior/concomitant use of oral contraceptives and hormonal replacement therapy is not correlated with a better prognostic in melanoma; neither have they represented a contraindication for survivors of melanoma; a subset of tumors might present a higher ER expression which is potentially targeted by the hormone-based treatment as SERMs (Selective Estrogen Receptors Modulator), for instance, tamoxifen. Experimental studies on melanoma cell lines confirmed the anti-tumor activity of ERβ which might function as a prognostic marker. G-protein-coupled estrogen receptors in melanocytes and keratinocytes might be involved, too. Additional crosstalk of TGF-β (Transforming Growth Factor β), respective IGF1 (Insulin-like Growth Factor), and ERα expression are involved in tumorigenic pathways. Recent preclinical studies showed the potential benefits of diarylpropionitrile, a selective agonist of ERβ; pyrazole derivates 21-23 can block ERs. Murine melanoma models showed the interference of anti-estrogenic medication (like molecule fulvestrant) to enhance immune checkpoint blockade, a modern approach to solid cancers. The proliferation of melanoma might be partially explained by ERs; whether this is generally applicable or there is a subgroup of tumors particularly related to E status is still debatable. The subject of E status in melanoma is far from clear at this point and further studies are necessary concerning this particular issue to implement it as a practical approach in the daily management of a disease that still has a very severe prognostic nowadays.
