OBJECTIVES: To explore the potential prognostic role of family history (FH) of prostate cancer and prostate cancer risk single nucleotide polymorphisms (SNPs) in patients undergoing active surveillance (AS) for prostate cancer. This is the first study to date, which has investigated the potential prognostic role of SNP profiles in an AS cohort PATIENTS AND METHODS: FH data were collected from patients in the Royal Marsden Hospital AS study. In all, 39 prostate cancer-risk SNPs identified from published genome wide association studies (GWAS) were genotyped using the Sequenom Platform and TaqMan™ assays from available DNA. The cumulative genetic-risk scores for each patient were then calculated using the weighted effect estimated from previous GWAS (log-additive model). FH status and the genetic-risk scores were assessed against adverse outcomes in AS, time to treatment and adverse histology on repeat biopsy, using univariable and multivariable Cox regression models to address time to treatment; and binary logistic regression to address biopsy upgrade. RESULTS: Of 471 patients, 55 (13.6%) had adverse histology on repeat biopsies and 145 (30.8%) had deferred treatment. On univariate analysis, there was no significant relationship between FH of prostate cancer in any degree of relation, and adverse histology or time to treatment. For risk score analyses, 386 patients' DNA was studied; and there was also no relationship found between the calculated genetic risk scores and adverse histology or time to treatment (P = 0.573 and P = 0.965, respectively). The retrospective study design and the few events were the main limitation of the study. CONCLUSIONS: There is currently insufficient data to support the use of FH status or prostate cancer SNP profile risk scores as prognostic factors in AS and these should not be used to influence management decisions. As more genetic variants are discovered this may change and should be reassessed in multicentre AS cohorts.
OBJECTIVES: To explore the potential prognostic role of family history (FH) of prostate cancer and prostate cancer risk single nucleotide polymorphisms (SNPs) in patients undergoing active surveillance (AS) for prostate cancer. This is the first study to date, which has investigated the potential prognostic role of SNP profiles in an AS cohort PATIENTS AND METHODS: FH data were collected from patients in the Royal Marsden Hospital AS study. In all, 39 prostate cancer-risk SNPs identified from published genome wide association studies (GWAS) were genotyped using the Sequenom Platform and TaqMan™ assays from available DNA. The cumulative genetic-risk scores for each patient were then calculated using the weighted effect estimated from previous GWAS (log-additive model). FH status and the genetic-risk scores were assessed against adverse outcomes in AS, time to treatment and adverse histology on repeat biopsy, using univariable and multivariable Cox regression models to address time to treatment; and binary logistic regression to address biopsy upgrade. RESULTS: Of 471 patients, 55 (13.6%) had adverse histology on repeat biopsies and 145 (30.8%) had deferred treatment. On univariate analysis, there was no significant relationship between FH of prostate cancer in any degree of relation, and adverse histology or time to treatment. For risk score analyses, 386 patients' DNA was studied; and there was also no relationship found between the calculated genetic risk scores and adverse histology or time to treatment (P = 0.573 and P = 0.965, respectively). The retrospective study design and the few events were the main limitation of the study. CONCLUSIONS: There is currently insufficient data to support the use of FH status or prostate cancer SNP profile risk scores as prognostic factors in AS and these should not be used to influence management decisions. As more genetic variants are discovered this may change and should be reassessed in multicentre AS cohorts.
Authors: Julius Gudmundsson; Patrick Sulem; Valgerdur Steinthorsdottir; Jon T Bergthorsson; Gudmar Thorleifsson; Andrei Manolescu; Thorunn Rafnar; Daniel Gudbjartsson; Bjarni A Agnarsson; Adam Baker; Asgeir Sigurdsson; Kristrun R Benediktsdottir; Margret Jakobsdottir; Thorarinn Blondal; Simon N Stacey; Agnar Helgason; Steinunn Gunnarsdottir; Adalheidur Olafsdottir; Kari T Kristinsson; Birgitta Birgisdottir; Shyamali Ghosh; Steinunn Thorlacius; Dana Magnusdottir; Gerdur Stefansdottir; Kristleifur Kristjansson; Yu Bagger; Robert L Wilensky; Muredach P Reilly; Andrew D Morris; Charlotte H Kimber; Adebowale Adeyemo; Yuanxiu Chen; Jie Zhou; Wing-Yee So; Peter C Y Tong; Maggie C Y Ng; Torben Hansen; Gitte Andersen; Knut Borch-Johnsen; Torben Jorgensen; Alejandro Tres; Fernando Fuertes; Manuel Ruiz-Echarri; Laura Asin; Berta Saez; Erica van Boven; Siem Klaver; Dorine W Swinkels; Katja K Aben; Theresa Graif; John Cashy; Brian K Suarez; Onco van Vierssen Trip; Michael L Frigge; Carole Ober; Marten H Hofker; Cisca Wijmenga; Claus Christiansen; Daniel J Rader; Colin N A Palmer; Charles Rotimi; Juliana C N Chan; Oluf Pedersen; Gunnar Sigurdsson; Rafn Benediktsson; Eirikur Jonsson; Gudmundur V Einarsson; Jose I Mayordomo; William J Catalona; Lambertus A Kiemeney; Rosa B Barkardottir; Jeffrey R Gulcher; Unnur Thorsteinsdottir; Augustine Kong; Kari Stefansson Journal: Nat Genet Date: 2007-07-01 Impact factor: 38.330
Authors: Julius Gudmundsson; Patrick Sulem; Thorunn Rafnar; Jon T Bergthorsson; Andrei Manolescu; Daniel Gudbjartsson; Bjarni A Agnarsson; Asgeir Sigurdsson; Kristrun R Benediktsdottir; Thorarinn Blondal; Margret Jakobsdottir; Simon N Stacey; Jelena Kostic; Kari T Kristinsson; Birgitta Birgisdottir; Shyamali Ghosh; Droplaug N Magnusdottir; Steinunn Thorlacius; Gudmar Thorleifsson; S Lilly Zheng; Jielin Sun; Bao-Li Chang; J Bradford Elmore; Joan P Breyer; Kate M McReynolds; Kevin M Bradley; Brian L Yaspan; Fredrik Wiklund; Par Stattin; Sara Lindström; Hans-Olov Adami; Shannon K McDonnell; Daniel J Schaid; Julie M Cunningham; Liang Wang; James R Cerhan; Jennifer L St Sauver; Sara D Isaacs; Kathleen E Wiley; Alan W Partin; Patrick C Walsh; Sonia Polo; Manuel Ruiz-Echarri; Sebastian Navarrete; Fernando Fuertes; Berta Saez; Javier Godino; Philip C Weijerman; Dorine W Swinkels; Katja K Aben; J Alfred Witjes; Brian K Suarez; Brian T Helfand; Michael L Frigge; Kristleifur Kristjansson; Carole Ober; Eirikur Jonsson; Gudmundur V Einarsson; Jianfeng Xu; Henrik Gronberg; Jeffrey R Smith; Stephen N Thibodeau; William B Isaacs; William J Catalona; Jose I Mayordomo; Lambertus A Kiemeney; Rosa B Barkardottir; Jeffrey R Gulcher; Unnur Thorsteinsdottir; Augustine Kong; Kari Stefansson Journal: Nat Genet Date: 2008-02-10 Impact factor: 38.330
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