Expression of HPV, steroid receptors (ERα, ERβ, PR-A and PR-B) and inhibin/activin subunits (α, βA and βB) in adenosquamous endometrial carcinoma

Aim: The aim of the study was to determine possible pathogenetic factors and molecules which may be used as tumor markers of adenosquamous endometrial carcinoma. Materials and Methods: Eight adenosquamous endometrial carcinomas were immunohistochemically tested with specific monoclonal antibodies for HPV (polyclonal anti-HPV and monoclonal anti-HPV 18), estrogen receptors ER-a and ER-P, progesterone receptors PR-A and PR-B and the inhibin/activin subunits inhibin-alpha, -beta A and -beta B. Results: HPV 18 and the polyclonal HPV antibody was detected in all adenosquamous endometrial carcinomas, both in the endometrioid (n = 7/8) and squamous (n=8/8) parts of the tumor. Neither ER-alpha or ER-beta were detectable in any tumor, in contrast to PR-A and PR-B which were detected in about half of these tumors (PR-A: n=5/8 and PR-B: n=2/8). Inhibin-alpha and -beta B were not detected, while inhibin-beta A was expressed in all adenosquamous carcinomas. Conclusion: The carcinogenesis of adenosquamous endometrial carcinomas was associated with HPV infection. Adenosquamous endometrial carcinomas seem not to be controlled by estrogens. The absence of the expression of the inhibin-a subunit suggests a tumor-suppressive function in adenosquamous endometrial tumors. The absence of the expression of the inhibin-beta B subunit, which is probably a marker of differentiation, points to the malignancy of these tumors. The other inhibin subunit, inhibin-beta A, was expressed in all adenosquamous tumors. It remains to be clarified if these parameters can be used as tumor markers.