Abstract

Discriminating patients with a low risk of progression from those with lethal prostate cancer is one of the main challenges in prostate cancer management. Indeed, such discrimination is essential if we aim to avoid overtreatment in men with indolent disease and to improve survival in those men with lethal disease. We are reporting on the current literature on such prognostic tools that are now available, their clinical role and their limitations in individualizing care. There is an urgent need to incorporate such genomic tools into new platform-based clinical trial structures to further develop and validate prognostic and predictive biomarkers and provide prostate cancer patients with an effective and cost-efficient access to new drugs in the setting of personalized treatment.

Highlights

  • In Europe, over 417,000 men were diagnosed with prostate cancer in 2012

  • In Europe, more than 90,000 men die of prostate cancer every year, that is less than one out of five patients [1]

  • Many studies have focused on the molecular basis of prostate cancer and highlighted several alterations in well-characterized cancer pathways, the androgen/ androgen receptor (AR) signaling, gene fusions or mutations directly related to gene expression, and chromatin regulation

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Summary

Introduction

In Europe, over 417,000 men were diagnosed with prostate cancer in 2012. Some patients will have highly aggressive disease that might metastasize early and prove fatal. The majority of the patients will have slow growing relatively harmless tumors that will not threaten their health during lifetime and can be appropriately managed with active surveillance or local treatment For those developing lethal disease, there has been a major advance in treatment with the introduction of seven systemic treatments in addition to androgen deprivation therapy that has been the sole systemic treatment for the last 60 years. Initial evaluation and treatment allocation are based exclusively on the combination of PSA value, histological grading, and clinic-radiological TNM staging In this context, many studies have focused on the molecular basis of prostate cancer and highlighted several alterations in well-characterized cancer pathways, the androgen/ androgen receptor (AR) signaling, gene fusions or mutations directly related to gene expression, and chromatin regulation.

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