Clinical impact of assay of XXXX receptor beta cx in @entity0 .

@entity172 @entity1 @entity1782 @entity0 @entity440 @entity5 @entity53 @entity1783 @entity969
Since 1996 when @entity172 receptor beta( @entity1783 ) was discovered, much effort has been devoted to the question of the value of @entity1783 as a prognostic and/or predictive factor in @entity0 and its potential as a novel target for pharmacological intervention. When @entity172 receptors are applied on @entity969 gradients and quantified by ligand binding, we found that in contrast to @entity1782 , which has a narrow tissue distribution, @entity1783 is expressed in many tissues including both normal and malignant breast tissue. Receptor protein levels in tissues can also be measured from the intensities of bands after Western blotting and can be quantified when purified and quantified receptor is used as a standard. With this technique, we found that there were some @entity5 which had over 600 fmol/mg of @entity1783 protein but no detectable @entity53 binding. In @entity5 , RT-PCR analysis revealed that @entity1783 cx is the only @entity1783 isoform present. @entity1783 cx is a splice variant which utilizes an alternative exon 8. This change in the C-terminus results in very poor binding to @entity53 (E2) and has a dominant negative effect on @entity1782 function. Immunohistochemical analysis with an @entity1783 cx specific antibody in 115 @entity1782 -positive @entity0 revealed that about half of the samples expressed @entity1783 cx protein. Initial analysis of samples from @entity1 with preoperative @entity440 treatment revealed that @entity1782 -positive @entity5 expressing @entity1783 cx and lacking PR seemed to be resistant to the anti- @entity172 . We conclude that, in order to better characterize @entity0 and design appropriate therapy for individual @entity1 , assays for @entity1783 cx must be made available to clinicians.
