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Does the molecular classification of breast cancer point the way for biomarker identification in prostate cancer?

Does the molecular classification of breast cancer point the way for biomarker identification in prostate cancer?
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摘要 There is significant variation in clinical outcome between patients diagnosed with prostate cancer(Ca P). Although useful, statistical nomograms and risk stratification tools alone do not always accurately predict an individual's need for and response to treatment. The factors that determine this variation are not fully elucidated. In particular, cellular response to androgen ablation and subsequent paracrine/autocrine adaptation is poorly understood and despite best therapies, median survival in castrate resistant patients is only approximately 35 mo. We propose that one way of understanding this is to look for correlates in other comparable malignancies, such as breast cancer, where markers of at least 4 distinct gene clusters coding for 4 different phenotypic subtypes have been identified. These subtypes have been shown to demonstrate prognostic significance and successfully guide appropriate treatment regimens. In this paper we assess and review the evidence demonstrating parallels in the biology and treatment approach between breast and Ca P, and consider the feasibility of patients with Ca P being stratified into different molecular classes that could be used to complement prostate specific antigen and histological grading for clinical decision making. We show that there are significant correlations between the molecular classification of breast and Ca P and explain how techniques used successfully to predict response to treatment in breast cancer can be applied to the prostate. Molecular phenotyping is possible in Ca P and identification of distinct subtypes may allow personalised risk stratification way beyond that currently available. There is significant variation in clinical outcome between patients diagnosed with prostate cancer(Ca P). Although useful, statistical nomograms and risk stratification tools alone do not always accurately predict an individual's need for and response to treatment. The factors that determine this variation are not fully elucidated. In particular, cellular response to androgen ablation and subsequent paracrine/autocrine adaptation is poorly understood and despite best therapies, median survival in castrate resistant patients is only approximately 35 mo. We propose that one way of understanding this is to look for correlates in other comparable malignancies, such as breast cancer, where markers of at least 4 distinct gene clusters coding for 4 different phenotypic subtypes have been identified. These subtypes have been shown to demonstrate prognostic significance and successfully guide appropriate treatment regimens. In this paper we assess and review the evidence demonstrating parallels in the biology and treatment approach between breast and Ca P, and consider the feasibility of patients with Ca P being stratified into different molecular classes that could be used to complement prostate specific antigen and histological grading for clinical decision making. We show that there are significant correlations between the molecular classification of breast and Ca P and explain how techniques used successfully to predict response to treatment in breast cancer can be applied to the prostate. Molecular phenotyping is possible in Ca P and identification of distinct subtypes may allow personalised risk stratification way beyond that currently available.
出处 《World Journal of Clinical Urology》 2016年第2期80-89,共10页 世界临床泌尿杂志
关键词 PROSTATE CANCER Molecular classification BIOMARKER Breast CANCER PROGNOSTIC Prostate cancer Molecular classification Biomarker Breast cancer Prognostic
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  • 1FerlayJ, Shin HR, Bray F, Forman D, Mathers C etal. Estimatesofworldwide burden of cancer in 2008: GLOBOCAN 2008. IntJ Cancer 2010; 127: 2893-917.
  • 2Lee J, Demissie K, Lu SE, Rhoads GG. Cancer incidence among Korean-American immigrants in the United States and native Koreans in South Korea. Cancer Control 2007; 14: 78-85.
  • 3Jemal A, Bray F, Center MM, Ferlay J, Ward E etal. Global cancer statistics. CA Cancer J Clin 2011; 61: 69-90.
  • 4Carter BS, Beaty TH, Steinberg GD, Childs B, Walsh PC. Mendelian inheritance of familial prostate cancer. Proc Natl Acad Sci USA 1992; 89: 3367-71.
  • 5Eeles RA. Genetic predisposition to prostate cancer. Prostate Cancer Prostatic Dis 1999; 2: 9-15.
  • 6Edwards SM, Eeles RA. Unravelling the genetics of prostate cancer. Am J Med GenetC Semin Med Genet 2004; 129C: 65-73.
  • 7Lichtenstein P, Holm NV, Verkasalo PK, lIiadou A, Kaprio J et al. Environmental and heritable factors in the causation of cancer-analyses of cohorts of twins from Sweden, Denmark, and Finland. N Engl J Med 2000; 343: 78-85.
  • 8Yeager M, Orr N, Hayes RB, Jacobs KB, Kraft P et al. Genome-wide association study of prostate cancer identifies a second risk locus at 8q24. Nat Genet 2007; 39: 645-9.
  • 9AI Olama AA, Kote-Jarai Z, Giles GG, Guy M, Morrison Jet al. Multiple loci on 8q24 associated with prostate cancer susceptibility. Nat Genet 2009; 41: 1058-60.
  • 10Amundadottir LT, Sulem P, Gudmundsson J, Helgason A, Baker A et al. A common variant associated with prostate cancer in European and African populations. Nat Genet 2006; 38: 652-8.

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