Clinical and Biological Features of Neuroendocrine Prostate Cancer

Yamada, Yasutaka; Beltran, Himisha

doi:10.1007/s11912-020-01003-9

Cited by 167 publications

(135 citation statements)

References 86 publications

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“…Like mentioned in an introductory part, CRPC often arises in a substantial subgroup of patients worsening the treatment options. Neuroendocrine prostate cancer (NEPC) is an aggressive subtype of prostate cancer with poor prognosis that most commonly arises in later stages of prostate cancer as a mechanism of treatment resistance [425]. Clinically distinct therapeutic strategies are considered against NEPC compared to the AR-driven adenocarcinomas.…”

Section: Therapeutic Potential Of Post-translational Modifications In Prostate Cancermentioning

confidence: 99%

Post-Translational Modifications That Drive Prostate Cancer Progression

Samaržija

2021

Biomolecules

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While a protein primary structure is determined by genetic code, its specific functional form is mostly achieved in a dynamic interplay that includes actions of many enzymes involved in post-translational modifications. This versatile repertoire is widely used by cells to direct their response to external stimuli, regulate transcription and protein localization and to keep proteostasis. Herein, post-translational modifications with evident potency to drive prostate cancer are explored. A comprehensive list of proteome-wide and single protein post-translational modifications and their involvement in phenotypic outcomes is presented. Specifically, the data on phosphorylation, glycosylation, ubiquitination, SUMOylation, acetylation, and lipidation in prostate cancer and the enzymes involved are collected. This type of knowledge is especially valuable in cases when cancer cells do not differ in the expression or mutational status of a protein, but its differential activity is regulated on the level of post-translational modifications. Since their driving roles in prostate cancer, post-translational modifications are widely studied in attempts to advance prostate cancer treatment. Current strategies that exploit the potential of post-translational modifications in prostate cancer therapy are presented.

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Section: Therapeutic Potential Of Post-translational Modifications In Prostate Cancermentioning

confidence: 99%

Post-Translational Modifications That Drive Prostate Cancer Progression

Samaržija

2021

Biomolecules

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“…Another justification for potentially targeting STAT3 in nonmetastatic CRPC is the fact that inhibition of STAT3 might prevent treatment-induced neuroendocrine-like prostate tumor phenotype, also termed as t-NEPC. Incidence of these type of tumors is expected to rise upon increased use of novel anti-AR agents [ 29 , 58 , 59 ]. These tumors alike classical NEPC tumors [ 59 ] are likely to be challenging to treat as they are resistant to anti-AR agents and are usually treated with platinum therapy subsequent to exhausting taxane therapy [ 56 , 59 , 60 , 61 ].…”

Section: Targeting Stat3 As Master Regulator In Nmcrpcmentioning

confidence: 99%

Novel Target Opportunities in Non-Metastatic Castrate Resistant Prostate Cancer

Gleicher

Porter

Nath

et al. 2021

Cancers

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Nearly one third of men will incur biochemical recurrence after treatment for localized prostate cancer. Androgen deprivation therapy (ADT) is the therapeutic mainstay; however, some patients will transition to a castrate resistant state (castrate resistant prostate cancer, CRPC). Subjects with CRPC may develop symptomatic metastatic disease (mCRPC) and incur mortality several years later. Prior to metastatic disease, however, men acquire non-metastatic CRPC (nmCRPC) which lends the unique opportunity for intervention to delay disease progression and symptoms. This review addresses current therapies for nmCRPC, as well as novel therapeutics and pathway strategies targeting men with nmCRPC.

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“…Generally, in addition to loss of AR signaling, t-NEPC is characterized by neuroendocrine (NE) markers neuron-specific enolase 2 (ENO2, NSE), 2 of 25 synaptophysin (SYP) and chromogranin A and B (CHGA and CHGB) [1][2][3]. In addition to t-NEPC, a less common de novo NEPC may also occur [4][5][6]. A recent analysis of 87 NEPC patients revealed that de novo NEPC has worse outcome than t-NEPC but no significant differences on the molecular features were identified between de novo NEPC and t-NEPC [6].…”

Section: Introductionmentioning

confidence: 99%

“…It has been suggested that the de novo NEPC drives from the human prostate luminal epithelial cells [7,8]. However, there are still significant clinical challenges in using NE markers for de novo or t-NEPC diagnosis due to wide variation in the pathologic and diagnostic features of the heterogenous tumors [4].…”

Section: Introductionmentioning

confidence: 99%

Molecular and Functional Links between Neurodevelopmental Processes and Treatment-Induced Neuroendocrine Plasticity in Prostate Cancer Progression

Kaarijärvi

Kaljunen

Ketola

2021

Cancers

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Neuroendocrine plasticity and treatment-induced neuroendocrine phenotypes have recently been proposed as important resistance mechanisms underlying prostate cancer progression. Treatment-induced neuroendocrine prostate cancer (t-NEPC) is highly aggressive subtype of castration-resistant prostate cancer which develops for one fifth of patients under prolonged androgen deprivation. In recent years, understanding of molecular features and phenotypic changes in neuroendocrine plasticity has been grown. However, there are still fundamental questions to be answered in this emerging research field, for example, why and how do the prostate cancer treatment-resistant cells acquire neuron-like phenotype. The advantages of the phenotypic change and the role of tumor microenvironment in controlling cellular plasticity and in the emergence of treatment-resistant aggressive forms of prostate cancer is mostly unknown. Here, we discuss the molecular and functional links between neurodevelopmental processes and treatment-induced neuroendocrine plasticity in prostate cancer progression and treatment resistance. We provide an overview of the emergence of neurite-like cells in neuroendocrine prostate cancer cells and whether the reported t-NEPC pathways and proteins relate to neurodevelopmental processes like neurogenesis and axonogenesis during the development of treatment resistance. We also discuss emerging novel therapeutic targets modulating neuroendocrine plasticity.

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Clinical and Biological Features of Neuroendocrine Prostate Cancer

Cited by 167 publications

References 86 publications

Post-Translational Modifications That Drive Prostate Cancer Progression

Post-Translational Modifications That Drive Prostate Cancer Progression

Novel Target Opportunities in Non-Metastatic Castrate Resistant Prostate Cancer

Molecular and Functional Links between Neurodevelopmental Processes and Treatment-Induced Neuroendocrine Plasticity in Prostate Cancer Progression

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