Potential for targeted therapy in prostate cancers with ERG abnormalities

Williamson, Sean R.; Liu, Cheng

doi:10.1038/aja.2011.100

Cited by 1 publication

(1 citation statement)

References 21 publications

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“…Therefore, the current status of PCa subtypes, will be subsequently discussed, using TCGA study (17) as a reference for the majority of the comparisons, the prognostic involvement, and the therapies of inhibitors of target oncogenes associated with subtypes, such as EZH2 or ERG (Table I), which have been used or are currently in the experimental phase, in this way some treatments that apply to cases that are ETS(+) will not work for those that are ETS(-), such as blocking function of ERG regulating co-factors, such as PARP1 (25-27) (Table I). Table I summarizes the main clinical-pathological characteristics of the subtypes and treatments that have been investigated as a development of personalized medicine (13,17,(24)(25)(26).…”

Section: Molecular Heterogeneity Of Pcamentioning

confidence: 99%

Decoding the heterogeneous landscape in the development prostate cancer (Review)

et al. 2021

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Prostate cancer (PCa) is characterized as being histologically and molecularly heterogeneous; however, this is not only incorrect among individuals, but also at the multiple foci level, which originates in the prostate gland itself. The reasons for such heterogeneity have not been fully elucidated; however, understanding these may be crucial in determining the course of the disease. PCa is characterized by a complex network of chromosomal rearrangements, which simultaneously deregulate multiple genes; this could explain the appearance of exclusive events associated with molecular subtypes, which have been extensively investigated to establish clinical management and the development of therapies targeted to this type of cancer. From a clinical aspect, the prognosis of the patient has focused on the characteristics of the index lesion (the largest focus in PCa); however, a significant percentage of patients (11%) also exhibit an aggressive secondary foci, which may determine the prognosis of the disease, and could be the determining factor of why, in different studies, the classification of the subtypes does not have an association with prognosis. Due to the aforementioned reasons, the analysis of molecular subtypes in several foci, from the same individual could assist in determining the association between clinical evolution and management of patients with PCa. Castration-resistant PCa (CRPC) has the worst prognosis and develops following androgen ablation therapy. Currently, there are two models to explain the development of CRPC: i) The selection model and ii) the adaptation model; both of which, have been found to include alterations described in the molecular subtypes, such as Enhancer of zeste 2 polycomb repressive complex 2 subunit overexpression, isocitrate dehydrogenase (NAPD + )1 and forkhead box A1 mutations, suggesting that the presence of specific molecular alterations could predict the development of CRPC. This type of analysis could lead to a biological understanding of PCa, to develop personalized medicine strategies, which could improve the response to treatment thus, avoiding the development of resistance. Therefore, the present review discusses the primary molecular factors, to which variable heterogeneity in PCa progress has been attributed. Contents 1. Introduction 2. Molecular heterogeneity of PCa 3. Molecular progression to CRPC 4. Conclusions

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