EAU Guidelines on Prostate Cancer. Part II: Treatment of Advanced, Relapsing, and Castration-Resistant Prostate Cancer

Heidenreich, Axel; Bastian, Patrick J.; Bellmunt, Joaquim; Bolla, M.; Joniau, Steven; Kwast, Theodorus H. van der; Mason, Malcolm David; Матвеев, В. Б.; Wiegel, Thomas; Zattoni, Filiberto; Mottet, Nicolas

doi:10.1016/j.eururo.2013.11.002

Cited by 1,392 publications

(1,057 citation statements)

References 85 publications

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“…Observed changes in PSA and PGR expression in prostate and breast tumors as markers of AR and ERα signaling, respectively, reflected the natural tumor heterogeneity observed clinically for each tumor type examined (Arnedos et al ., 2013). Variation in PSA response to bicalutamide, the most common antagonist used in locally advanced disease (Heidenreich et al ., 2014), in prostate PDEs is consistent with outcomes of the TERRAIN and STRIVE clinical trials. As an AR antagonist, bicalutamide inhibits expression of AR‐regulated genes such as PSA , as well as genes involved in cellular proliferation, differentiation, and survival (Furr, 1996; Maucher and von Angerer, 1993).…”

Section: Discussionsupporting

confidence: 71%

A patient‐derived explant (PDE) model of hormone‐dependent cancer

et al. 2018

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Breast and prostate cancer research to date has largely been predicated on the use of cell lines in vitro or in vivo. These limitations have led to the development of more clinically relevant models, such as organoids or murine xenografts that utilize patient‐derived material; however, issues related to low take rate, long duration of establishment, and the associated costs constrain use of these models. This study demonstrates that ex vivo culture of freshly resected breast and prostate tumor specimens obtained from surgery, termed patient‐derived explants (PDEs), provides a high‐throughput and cost‐effective model that retains the native tissue architecture, microenvironment, cell viability, and key oncogenic drivers. The PDE model provides a unique approach for direct evaluation of drug responses on an individual patient's tumor, which is amenable to analysis using contemporary genomic technologies. The ability to rapidly evaluate drug efficacy in patient‐derived material has high potential to facilitate implementation of personalized medicine approaches.

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Section: Discussionsupporting

confidence: 71%

A patient‐derived explant (PDE) model of hormone‐dependent cancer

et al. 2018

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“…At first, these therapies include androgen deprivation therapy, radical prostatectomy and different radiation therapies [112][113][114]. Advanced, relapsing and castration-insensitive prostate cancers are largely treated with therapies that target the androgen signaling pathway and immune therapy (reviewed in [115,116]). In addition, more attempts to develop drugs that act on other prostate cancer targets, such as ETS-fusions, or the PI3K signaling pathway, or fatty acid metabolism, are reported [117,118].…”

Section: Prostate Cancer Facts and Current Treatmentmentioning

confidence: 99%

Organ-Specific Cancer Metabolism and Its Potential for Therapy

Elia

Schmieder

Christen

et al. 2015

Handbook of Experimental Pharmacology

101

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KEYWORDS:Cancer metabolism, metabolic therapy, tissue specific metabolism, genetic drivers, epigenetic drivers, microenvironment, Warburg effect, reverse Warburg effect, mixed Warburg effect, triple-negative breast cancer, estrogen receptor positive breast cancer; prostate cancer, liver cancer, gluconeogenesis, fatty acid metabolism, glucose metabolism, glutamine metabolism, serine metabolism, metabolic normalization, metabolic depletion ABSTRACTTargeting the metabolism of cancer cells has the potential to lead to major advances in tumor therapy. Numerous promising metabolic drug targets have been identified. Yet, it has emerged that there is no singular metabolism that defines the oncogenic state of the cell. Rather, the metabolism of cancer cells is a function of the requirements of a tumor. Hence, the tissue of origin, the (epi)genetic drivers, aberrant signaling, and the microenvironment all together define these metabolic requirements. In this chapter we discuss in light of (epi)genetic, signaling, and environmental factors the diversity in cancer metabolism based on triple-negative and estrogen receptor positive breast cancer, early and late stage prostate cancer, and liver cancer. These types of cancer all display distinct and partially opposing metabolic behaviors (e.g. Warburg versus reverse Warburg metabolism). Yet, for each of the cancers their distinct metabolism supports the oncogenic phenotype. Finally, we will assess the therapeutic potential of metabolism based on the concepts of metabolic normalization and metabolic depletion.

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“…Currently, the mainstay of therapy for metastatic prostate cancer is castration, which can be accomplished by either orchectomy or androgen-antagonistic agents. 4 However, although castration is initially effective and prolongs the period free of disease progression, PC eventually becomes castration resistant, resulting in disease relapse and less than 25 months of median survival. 5 Androgen receptor (AR) is a ligand-dependent transcription factor that plays important roles in both normal prostate development and prostate cancer.…”

Section: Introductionmentioning

confidence: 99%