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Lancet. 2016 Jan 2;387(10013):70-82. doi: 10.1016/S0140-6736(14)61947-4. Epub 2015 Jun 11.

Prostate cancer.

Author information

1
Division of Clinical Studies, The Institute of Cancer Research, London, UK; Prostate Cancer Targeted Therapy Group, Royal Marsden NHS Foundation Trust, Sutton, Surrey, UK.
2
Academic Urology Unit, Royal Marsden NHS Foundation Trust, Sutton, Surrey, UK.
3
Clinical Academic Cancer Genetics Unit, Royal Marsden NHS Foundation Trust, Sutton, Surrey, UK; Oncogenetics Team, Division of Cancer Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
4
Erasmus University Medical Center, Rotterdam, Netherlands.
5
Departments of Pathology Urology, Comprehensive Cancer Center and Michigan Center for Translational Pathology, University of Michigan Medical School, Ann Arbor, MI, USA.
6
Princess Margaret Cancer Centre and University of Toronto, Toronto, ON, Canada.
7
Division of Medical Oncology, Johns Hopkins Hospital, Baltimore, MA, USA.
8
Division of Clinical Studies, The Institute of Cancer Research, London, UK; Prostate Cancer Targeted Therapy Group, Royal Marsden NHS Foundation Trust, Sutton, Surrey, UK. Electronic address: jdebono@icr.ac.uk.

Abstract

Much progress has been made in research for prostate cancer in the past decade. There is now greater understanding for the genetic basis of familial prostate cancer with identification of rare but high-risk mutations (eg, BRCA2, HOXB13) and low-risk but common alleles (77 identified so far by genome-wide association studies) that could lead to targeted screening of patients at risk. This is especially important because screening for prostate cancer based on prostate-specific antigen remains controversial due to the high rate of overdiagnosis and unnecessary prostate biopsies, despite evidence that it reduces mortality. Classification of prostate cancer into distinct molecular subtypes, including mutually exclusive ETS-gene-fusion-positive and SPINK1-overexpressing, CHD1-loss cancers, could allow stratification of patients for different management strategies. Presently, men with localised disease can have very different prognoses and treatment options, ranging from observation alone through to radical surgery, with few good-quality randomised trials to inform on the best approach for an individual patient. The survival of patients with metastatic prostate cancer progressing on androgen-deprivation therapy (castration-resistant prostate cancer) has improved substantially. In addition to docetaxel, which has been used for more than a decade, in the past 4 years five new drugs have shown efficacy with improvements in overall survival leading to licensing for the treatment of metastatic castration-resistant prostate cancer. Because of this rapid change in the therapeutic landscape, no robust data exist to inform on the selection of patients for a specific treatment for castration-resistant prostate cancer or the best sequence of administration. Moreover, the high cost of the newer drugs limits their widespread use in several countries. Data from continuing clinical and translational research are urgently needed to improve, and, crucially, to personalise management.

PMID:
26074382
DOI:
10.1016/S0140-6736(14)61947-4
[Indexed for MEDLINE]

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