Altered androgen metabolism eventually leads XXXX to an impaired hormone responsiveness.

@entity1 @entity251 @entity96 @entity5 @entity53 @entity134 @entity230 @entity157 @entity3800
Sex @entity134 hormones are thought, among several other risk factors, to play a role in liver @entity5 . For example, from epidemiological studies in @entity157 ( @entity157 ), a clear disadvantage for male sex is evident. In addition, elevated levels of serum @entity251 (T) and increased T to @entity53 (E(2)) ratio have been reported to predict an increased risk of @entity157 for male cirrhotic @entity1 . On the other hand, palliative treatment of @entity96 patients with anti-hormones has been widely used in the past. However, the molecular mechanism(s) underlying sex @entity134 action on either normal or transformed liver cells, have not yet been fully clarified, nor endocrine discriminants have been satisfactorily assessed for an adequate characterization of @entity96 tissues. In this paper, we report studies on hormonal status of @entity1 liver tissues and cells, especially focusing on @entity3800 , to better define endocrine end-points of interest for @entity157 . A consistent evidence from ex vivo or in vitro systems strongly suggests that high affinity binding sites of @entity3800 are expressed at sufficient concentrations to induce a biological response in either normal or phenotipically transformed hepatocytes; in the latter, however, high heterogeneity and/or more scattering concentrations were encountered. Further, experimental data seem to suggest that lack of response to @entity3800 may be due to a rapid metabolic conversion of @entity230 by neoplastic tissues and cells. @entity5 hepatocytes privilege in fact 5beta more than 5alpha metabolic pathway of @entity3800 . This may eventually lead biologically active @entity3800 to be transformed into less active derivatives, as it occurs for T which is massively converted (>90% at 6 h) thus hindering the whole mechanism of action of @entity3800 .
