Overview

This trial is active, not recruiting.

Condition prostate cancer
Treatment laboratory biomarker analysis
Sponsor Alliance for Clinical Trials in Oncology
Collaborator National Cancer Institute (NCI)
Start date December 2010
End date January 2100
Trial size 48 participants
Trial identifier NCT01275651, CALGB-151004, CDR0000688286, NCI-2011-02835

Summary

This research trial studies biomarkers in bone marrow and blood samples from patients with prostate cancer treated with ketoconazole. Studying samples of bone marrow and blood from patients with prostate cancer in the laboratory may help doctors learn more about changes that occur in deoxyribonucleic acid (DNA) and identify biomarkers related to cancer.

United States No locations recruiting
Other Countries No locations recruiting

Study Design

Observational model case-only
Time perspective retrospective
Arm
Previously collected bone marrow tissue and blood samples are analyzed for AR activity, AR splice variations, expression of androgen transport/synthesis/metabolism genes, AKR1C3 protein levels, and testosterone and dihydrotestosterone levels via RT-PCR, SNP microarrays, IHC, gene expression analysis, and mass spectrometry methods.
laboratory biomarker analysis
Correlative studies

Primary Outcomes

Measure
Progression-free survival (PFS)
time frame: Baseline

Secondary Outcomes

Measure
Equal to or greater than 30% decline in PSA
time frame: Baseline
Overall survival
time frame: Baseline

Eligibility Criteria

Male participants of any age.

Inclusioin Criteria: - Patients must have been registered to CALGB 9583 and CALGB 9663 - Adequate tissue specimen available for analysis

Additional Information

Official title Androgen Receptor (AR) Activity in Castration-Resistant Prostate Cancer (CRPC) and Response to Ketoconazole
Description PRIMARY OBJECTIVES: I. To determine whether pre-treatment androgen receptor (AR) activity correlates with progression-free survival (PFS) of men with castration-resistant prostate cancer (CRPC) treated with ketoconazole. SECONDARY OBJECTIVES: I. To determine if expression of androgen transport/synthesis/metabolism genes (including cytochrome P450, family 17, subfamily A, polypeptide 1 [CYP17A1], aldo-keto reductase family 1 [AKR1]C3, hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 2 [HSD3B2], hydroxysteroid [17-beta] dehydrogenase [HSD17B]3, HSD17B6, AKR1C2, AKR1C1, UGTB15, UGTB17, steroid-5-alpha-reductase, alpha polypeptide 1 [3-oxo-5 alpha-steroid delta 4-dehydrogenase alpha] [SRD5A]1, SRD5A2, SRD5A3, and solute carrier organic anion transporter family, member 2B1 [SLCO2B1]) correlate with detected AR activity, time to progression (progression free survival [PFS]) following treatment with ketoconazole, and overall survival. II. To determine if semi-quantitative immunohistochemical analysis of AR and AKR1C3 protein levels correlate with PFS following treatment with ketoconazole. III. To determine if specific AR splice variations correlate with PFS in response to ketoconazole. IV. To determine if detected activity of signaling pathways that interact with AR pathway activity (e.g., phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha [PI3K] and downstream effectors, SRC proto-oncogene, non-receptor tyrosine kinase [SRC], others) correlate with detected AR activity, PFS, and OS. V. To determine if AR gene amplification correlates with detected AR activity and PFS on ketoconazole. VI. To determine if levels of testosterone and dihydrotestosterone (DHT) from tumor tissue correlate with AR activity and PFS on ketoconazole. VII. To determine the presence of specific prostate cancer-associated gene translocations in each sample of CRPC. VIII. To provide an unbiased data set of gene expression in CRPC that will markedly expand the currently available public domain data. IX. To provide a library of amplified ribonucleic acid (RNA) and complementary (c)DNA for further analysis by other investigators. OUTLINE: Previously collected bone marrow, tissue, and blood samples are analyzed for AR activity, AR splice variations, expression of androgen transport/synthesis/metabolism genes, AKR1C3 protein levels, and testosterone and dihydrotestosterone levels via reverse transcription (RT)-polymerase chain reaction (PCR), single nucleotide polymorphisms (SNP) microarrays, immunohistochemistry (IHC), gene expression analysis, and mass spectrometry methods.
Trial information was received from ClinicalTrials.gov and was last updated in July 2016.
Information provided to ClinicalTrials.gov by Alliance for Clinical Trials in Oncology.