TY - JOUR
T1 - Erratum to
T2 - Association of a CYP17 Polymorphism With Overall Survival in Caucasian Patients With Androgen-independent Prostate Cancer (Urology (2007) 70(2) (217–220) (S0090429507017761) (10.1016/j.urology.2007.06.1097))
AU - Sissung, Tristan M.
AU - Venzon, David J.
AU - Figg, William D.
N1 - Funding Information:
Funding Support: This study was supported in part by the Intramural Research Program of the National Institutes of Health , National Cancer Institute, Bethesda, MD, USA.
Publisher Copyright:
© 2016
PY - 2016/9/1
Y1 - 2016/9/1
N2 - To determine if genetic variants in drug or hormone metabolizing enzymes and transporters are related to prostate cancer outcomes, we are currently evaluating ~235 genotypes included on the Drug Metabolizing Enzymes and Transporters Array (Affymetrix) in approximately 200 patients with prostate cancer. We included a subset of samples that had previously been reported in Hamada et al1 and determined that there were several miscalls of the CYP17 -34T>C that were most likely caused by error-prone RFLP technology used in the initial report. We therefore used direct sequencing to validate all of the findings of Hamada et al. Patient samples (n = 147) and controls (n = 40) were available for validation of genotype data, and we found that there were 30 genotype errors in patients with prostate cancer and 3 were detected in the control group (concordance rates are 80% and 93%, respectively). Overall survival differences were more statistically significant using the updated genotypes (P = .0050 vs P = .040; Fig. 1) whereas no associations were detected between genotype and risk or patient characteristics (P > .33; Tables 1 and 2). Therefore, the corrected data do not change the findings of Hamada et al, but alters the statistics slightly.
AB - To determine if genetic variants in drug or hormone metabolizing enzymes and transporters are related to prostate cancer outcomes, we are currently evaluating ~235 genotypes included on the Drug Metabolizing Enzymes and Transporters Array (Affymetrix) in approximately 200 patients with prostate cancer. We included a subset of samples that had previously been reported in Hamada et al1 and determined that there were several miscalls of the CYP17 -34T>C that were most likely caused by error-prone RFLP technology used in the initial report. We therefore used direct sequencing to validate all of the findings of Hamada et al. Patient samples (n = 147) and controls (n = 40) were available for validation of genotype data, and we found that there were 30 genotype errors in patients with prostate cancer and 3 were detected in the control group (concordance rates are 80% and 93%, respectively). Overall survival differences were more statistically significant using the updated genotypes (P = .0050 vs P = .040; Fig. 1) whereas no associations were detected between genotype and risk or patient characteristics (P > .33; Tables 1 and 2). Therefore, the corrected data do not change the findings of Hamada et al, but alters the statistics slightly.
UR - http://www.scopus.com/inward/record.url?scp=84979619112&partnerID=8YFLogxK
U2 - 10.1016/j.urology.2016.05.047
DO - 10.1016/j.urology.2016.05.047
M3 - Comment/debate
AN - SCOPUS:84979619112
SN - 0090-4295
VL - 95
SP - 225
JO - Urology
JF - Urology
ER -