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181.
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182.
  • Zheng, S. Lilly, et al. (författare)
  • Genetic variants and family history predict prostate cancer similar to prostate-specific antigen
  • 2009
  • Ingår i: Clinical Cancer Research. - 1078-0432 .- 1557-3265. ; 15:3, s. 1105-1111
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>PURPOSE: Although prostate-specific antigen (PSA) is the best biomarker for predicting prostate cancer, its predictive performance needs to be improved. Results from the Prostate Cancer Prevention Trial revealed the overall performance measured by the areas under curve of the receiver operating characteristic at 0.68. The goal of the present study is to assess the ability of genetic variants as a PSA-independent method to predict prostate cancer risk. EXPERIMENTAL DESIGN: We systematically evaluated all prostate cancer risk variants that were identified from genome-wide association studies during the past year in a large population-based prostate cancer case-control study population in Sweden, including 2,893 prostate cancer patients and 1,781 men without prostate cancer. RESULTS: Twelve single nucleotide polymorphisms were independently associated with prostate cancer risk in this Swedish study population. Using a cutoff of any 11 risk alleles or family history, the sensitivity and specificity for predicting prostate cancer were 0.25 and 0.86, respectively. The overall predictive performance of prostate cancer using genetic variants, family history, and age, measured by areas under curve was 0.65 (95% confidence interval, 0.63-0.66), significantly improved over that of family history and age (0.61%; 95% confidence interval, 0.59-0.62; P = 2.3 x 10(-10)). CONCLUSION: The predictive performance for prostate cancer using genetic variants and family history is similar to that of PSA. The utility of genetic testing, alone and in combination with PSA levels, should be evaluated in large studies such as the European Randomized Study for Prostate Cancer trial and Prostate Cancer Prevention Trial.</p>
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183.
  • Zheng, S. Lilly, et al. (författare)
  • Genetic variants and family history predict prostate cancer similar to prostate-specific antigen
  • 2009
  • Ingår i: Clinical Cancer Research. - 1078-0432 .- 1557-3265. ; 15:3, s. 1105-1111
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>PURPOSE: Although prostate-specific antigen (PSA) is the best biomarker for predicting prostate cancer, its predictive performance needs to be improved. Results from the Prostate Cancer Prevention Trial revealed the overall performance measured by the areas under curve of the receiver operating characteristic at 0.68. The goal of the present study is to assess the ability of genetic variants as a PSA-independent method to predict prostate cancer risk. EXPERIMENTAL DESIGN: We systematically evaluated all prostate cancer risk variants that were identified from genome-wide association studies during the past year in a large population-based prostate cancer case-control study population in Sweden, including 2,893 prostate cancer patients and 1,781 men without prostate cancer. RESULTS: Twelve single nucleotide polymorphisms were independently associated with prostate cancer risk in this Swedish study population. Using a cutoff of any 11 risk alleles or family history, the sensitivity and specificity for predicting prostate cancer were 0.25 and 0.86, respectively. The overall predictive performance of prostate cancer using genetic variants, family history, and age, measured by areas under curve was 0.65 (95% confidence interval, 0.63-0.66), significantly improved over that of family history and age (0.61%; 95% confidence interval, 0.59-0.62; P = 2.3 x 10(-10)). CONCLUSION: The predictive performance for prostate cancer using genetic variants and family history is similar to that of PSA. The utility of genetic testing, alone and in combination with PSA levels, should be evaluated in large studies such as the European Randomized Study for Prostate Cancer trial and Prostate Cancer Prevention Trial.</p>
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184.
  •  
185.
  • Zheng, S. Lilly, et al. (författare)
  • Two independent prostate cancer risk-associated Loci at 11q13
  • 2009
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 18:6, s. 1815-1820
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Single nucleotide polymorphisms (SNP) at 11q13 were recently implicated in prostate cancer risk by two genome-wide association studies and were consistently replicated in multiple study populations. To explore prostate cancer association in the regions flanking these SNPs, we genotyped 31 tagging SNPs in a approximately 110 kb region at 11q13 in a Swedish case-control study (Cancer of the Prostate in Sweden), including 2,899 cases and 1,722 controls. We found evidence of prostate cancer association for the previously implicated SNPs including rs10896449, which we termed locus 1. In addition, multiple SNPs on the centromeric side of the region, including rs12418451, were also significantly associated with prostate cancer risk (termed locus 2). The two groups of SNPs were separated by a recombination hotspot. We then evaluated these two representative SNPs in an additional approximately 4,000 cases and approximately 3,000 controls from three study populations and confirmed both loci at 11q13. In the combined allelic test of all four populations, P = 4.0 x 10(-11) for rs10896449 at locus 1 and P = 1.2 x 10(-6) for rs12418451 at locus 2, and both remained significant after adjusting for the other locus and study population. The prostate cancer association at these two 11q13 loci was unlikely confounded by prostate-specific antigen (PSA) detection bias because neither SNP was associated with PSA levels in controls. Unlike locus 1, in which no known gene is located, several putative mRNAs are in close proximity to locus 2. Additional confirmation studies at locus 2 and functional studies for both loci are needed to advance our knowledge on the etiology of prostate cancer.</p>
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186.
  • Åström, Lennart (författare)
  • Dose Escalation with High Dose Rate Brachytherapy or Protons in Curative Radiotherapy of Prostate Cancer
  • 2018
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • <p>The aim of the thesis was to study the outcome and side effects after dose-escalated radiotherapy with high dose rate brachytherapy (HDR-BT) or proton beam therapy (PBT) boost in prostate cancer.</p><p>The first cohorts of men in Sweden treated with either HDR-BT or PBT in combination with conventional photon beam therapy (2 Gray (Gy) fractions to 50 Gy) were analysed. The HDR-BT was given with two 10 Gy fractions, and the PBT with four fractions of 5 Gy. The analyses included 823 men in two HDR-BT cohorts, and 265 men in the PBT cohort. A large proportion of the cohorts, from 38% to 53%, were classified as high risk. After a follow-up between four and eleven years, both combinations showed low risks for relapse. The overall 5-year risk for PSA relapse was 0% for men with low risk. After PBT, the 5-year PSA relapse risk for intermediate and high risk were 5% and 26% respectively. After HDR-BT the 10-year risks for PSA relapse were 0%, 21% and 33% for low, intermediate, and high risk, respectively.</p><p>The risk for early and late toxicity was low. Genitourinary (GU) toxicity was more frequent than gastrointestinal (GI) toxicity. GU toxicity may have a late onset and progress slowly with time after HDR-BT. The 5- and 10-year actuarial incidences of urethral stricture were 6% and 10% respectively after HDR-BT. With applied dose constraints to the urethra the 10-year risk was 5%. The actuarial prevalence of GI toxicity declined slowly with time after HDR-BT as well as after PBT.</p><p>A PSA bounce after HDR-BT was seen in 26% of the patients, more frequent with younger age and lower Gleason score, and followed by a low risk for relapse.</p><p>For dose-escalated radiotherapy with HDR-BT or PBT:</p><ul><li>long-term tumour control was achieved, not only for low- and intermediate risk, but also for the majority of high risk patients,</li></ul><ul><li>a PSA bounce after HDR-BT was folled by a good prognosis,</li></ul><ul><li>levels of late toxicity were low,</li></ul><ul><li>genitourinary toxicity was more frequent than gastrointestinal toxicity,</li></ul><ul><li>dose constraints to risk organs must be applied to minimise risks for late toxicity.</li></ul>
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