Androgen receptors in ovarian tumors: correlation with oestrogen and progesterone receptors in an immunohistochemical and semiquantitative image analysis study.

The expression and distribution of androgen, estrogen and progesterone receptors was examined by immunohistochemical staining in 31 paraffin-embedded sections from ovarian tumors and the results were assessed by semiquantitative image analysis. Immunohistochemical staining showed heterogeneous patterns of steroid receptor distribution, with mainly nuclear immunoreactivity. Eighty-four percent of benign and malignant ovarian tumors expressed androgen receptors (AR), 74.19% estrogen receptors (ER) and 41.16% progesterone receptors (PR). All benign tumors showed immunoreactivity for the three steroid receptors. Malignant tumors expressed higher AR and ER histochemical scores (H-scores) than PR (82% vs 71% vs 39%). The incidence and expression levels of the steroid receptors varied widely in the different histological types of malignant tumors. Spearman rank analysis showed a positive significant (P < 0.05) correlation between AR- and ER and between ER- and PR-H-scores. In malignant ovarian tumors, neither AR, ER nor PR immunohistochemical scores correlated with tumor FIGO stage. Densitrometric analysis of immunostained steroid receptors is a valid method for assessing the steroid status, because it reduces subjective elements in scoring sections and increases the reliability of results. The high incidence of AR expression confirms the functional role of AR in ovarian tumors and suggests that the determination of AR content in ovarian cancer could have prognostic value.

Transforming growth factor-beta1 expression in human acoustic neuroma.

HYPOTHESIS: The differing clinical behavior of acoustic neuroma (AN) may be explained by the presence of specific biological features involved in tumorigenesis and growth. BACKGROUND: Transforming growth factor (TGF) beta1 is known to participate in the regulation of peripheral nerve tumors, modulating cell proliferation and differentiation with mechanisms different from those of glial growth factors (GGF) and fibroblastic growth factors (FGF), which are responsible for Schwann cells' mitogen activity. METHODS: Surgically removed human AN specimens were fixed in formalin and embedded in paraffin for immunohistochemistry studies. Expression and localization of TGF-beta1 in different tumor regions were assessed after incubation of paraffin sections with a mouse monoclonal anti-TGF beta1 antibody (DBA, Milan, Italy). Clinically, the time elapsed between the beginning of symptomatology and AN size as shown by preoperative computed tomography, magnetic resonance imaging, or both was calculated as rough value of growth rate, which enabled slow-growing and fast-growing ANs to be distinguished. RESULTS: Eighty-four percent of AN specimens expressed TGF-beta1 positivity at the level of the cytoplasm of the Schwann cells. TGF-beta1 reactivity was also shown in the blood vessel walls (96.15%) and the tumor capsule (80.86%). TGF-beta1 reaction appeared higher in Antoni A regions than in Antoni B regions. No significant relationship was found between TGF-beta1 positivity and AN growth rate in the two groups. CONCLUSIONS: TGF-beta1 could participate in the biological behavior of AN, particularly as an important factor of tumor growth prediction by allowing rapidly progressive or potentially recurrent tumors to be differentiated from slow-growing tumors that are unlikely to recur. The clinical course of patients with AN is currently still of little help in predicting the rate of AN growth.