UNASSIGNED: 4597 Background: @entity342 deprivation therapy (ADT) is the cornerstone of treatment for @entity263 . Our recent data demonstrates an integral role of luteinizing hormone (LH) signaling in @entity342 synthesis in @entity263 cells. We therefore hypothesized that genetic variation in the @entity10548 may impact the efficiency of signal transduction and influence the degree of castration, the duration of response to ADT and overall course. We now report the association between @entity10548 genotype and response to ADT. METHODS: Fifty eligible @entity1 had a histopathological diagnosis of @entity263 and had received ADT for @entity263 . The blood was collected from each @entity1 after obtaining informed consent. DNA was extracted from blood and genotypes for @entity10548 were assayed using the TaqMan method. The time to castration resistance and level of @entity251 suppression were obtained by linking to clinical records. Genotype groups were compared using ANOVA or Kruskal-Wallis tests. RESULTS: The median age at diagnosis was 59 (range 48-69). Of the 50 @entity1 enrolled, 29 were treated for primary @entity3 , 18 at biochemical recurrence (BCR) and 12 with BCR accompanied by radiographic metastases. The median PSA at initiation of ADT was 109.4 ng/ml for primary @entity3 and 9.8 ng/ml for recurrent disease. The median time to castration resistance was 12 months in the primary metastatic group and 32.4 months in the recurrent group. In the recurrent group, the presence of minor alleles in the @entity10548 genotype was associated with a shorter time to castration resistance with a median of 39 months in @entity1 with no minor alleles, 23 months in @entity1 with 1 minor allele and 16 months in @entity1 with 2 minor alleles (p<.05). Median @entity251 levels (T) during ADT were higher for @entity1 carrying any minor alleles. Median nadir T was 7 ng/dL for @entity1 with no minor alleles compared to 22.5 ng/dL for those with 1-2 minor alleles (p=0.07) with median peak T of 19 ng/dL vs. 43 ng/dL, respectively (p=0.01). CONCLUSIONS: Genetic variation in the @entity10548 was clearly linked with time to castration resistance and depth of castration and warrants further analysis to define its role as a prognostic and predictive marker.

@entity10548 polymorphisms and response to XXXX deprivation therapy in @entity263 .

@entity1 :: ('9606', 'Species') :: ['patients', 'patient', 'men'] @entity251 :: ('MESH:D013739', 'Chemical') :: ['testosterone'] @entity263 :: ('MESH:D011471', 'Disease') :: ['prostate cancer', 'advanced prostate cancer'] @entity342 :: ('CHEBI:50113', 'Chemical') :: ['androgen', 'Androgen'] @entity3 :: ('MESH:D009362', 'Disease') :: ['metastatic disease'] @entity10548 :: ('3973', 'Gene') :: ['LH receptor', 'LHR']
@entity342 :: (CHEBI:50113,Chemical) :: ['androgen']
