Prostate cancer

Gerhardt Attard, Chris Parker, Ros A. Eeles, Fritz Schröder, Scott A. Tomlins, Ian Tannock, Charles G. Drake, Johann S. De Bono

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)70-82
Number of pages13
JournalThe Lancet
Volume387
Issue number10013
DOIs
StatePublished - Jan 2 2016

Fingerprint

Prostatic Neoplasms
Castration
docetaxel
Therapeutics
Drug Costs
Translational Medical Research
Survival
Genome-Wide Association Study
Gene Fusion
Licensure
Prostate-Specific Antigen
Patient Selection
Androgens
Prostate
Alleles
Observation
Biopsy
Mutation
Mortality
Research

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Attard, G., Parker, C., Eeles, R. A., Schröder, F., Tomlins, S. A., Tannock, I., ... De Bono, J. S. (2016). Prostate cancer. The Lancet, 387(10013), 70-82. https://doi.org/10.1016/S0140-6736(14)61947-4

Prostate cancer. / Attard, Gerhardt; Parker, Chris; Eeles, Ros A.; Schröder, Fritz; Tomlins, Scott A.; Tannock, Ian; Drake, Charles G.; De Bono, Johann S.

In: The Lancet, Vol. 387, No. 10013, 02.01.2016, p. 70-82.

Research output: Contribution to journalArticle

Attard, G, Parker, C, Eeles, RA, Schröder, F, Tomlins, SA, Tannock, I, Drake, CG & De Bono, JS 2016, 'Prostate cancer', The Lancet, vol. 387, no. 10013, pp. 70-82. https://doi.org/10.1016/S0140-6736(14)61947-4
Attard G, Parker C, Eeles RA, Schröder F, Tomlins SA, Tannock I et al. Prostate cancer. The Lancet. 2016 Jan 2;387(10013):70-82. https://doi.org/10.1016/S0140-6736(14)61947-4
Attard, Gerhardt ; Parker, Chris ; Eeles, Ros A. ; Schröder, Fritz ; Tomlins, Scott A. ; Tannock, Ian ; Drake, Charles G. ; De Bono, Johann S. / Prostate cancer. In: The Lancet. 2016 ; Vol. 387, No. 10013. pp. 70-82.
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