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-alpha and ER-beta, progesterone receptors PR-A and PR-B and the inhibin/activin subunits inhibin-alpha, -betaA and -betaB.
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 -betaB were not detected, while inhibin-betaA 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-alpha subunit suggests a tumor-suppressive function in adenosquamous endometrial tumors. The absence of the expression of the inhibin-betaB subunit, which is probably a marker of differentiation, points to the malignancy of these tumors. The other inhibin subunit, inhibin-betaA, was expressed in all adenosquamous tumors. It remains to be clarified if these parameters can be used as tumor markers.