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Published on: November 19, 2019
Targeting neuroendocrine prostate cancer: molecular and clinical perspectives
Panagiotis J Vlachostergios1, Christos N Papandreou2
1Department of Internal Medicine, Lutheran Medical Center , Brooklyn, NY , USA.
Abstract:
Neuroendocrine prostate carcinoma, either co-present with the local adenocarcinoma disease or as a result of transdifferentiation later in time, was described as one major process of emerging resistance to androgen deprivation therapies, and at the clinical level it is consistent with the development of rapidly progressive visceral disease, often in the absence of elevated serum prostate-specific antigen level. Until present, platinum-based chemotherapy has been the only treatment modality, able to produce a fair amount of responses but of short duration. Recently, several efforts for molecular characterization of this lethal phenotype have resulted in identification of novel signaling factors involved in microenvironment interactions, mitosis, and neural reprograming as potential therapeutic targets. Ongoing clinical testing of specific inhibitors of these targets, for example, Aurora kinase A inhibitors, in carefully selected patients and exploitation of expression changes of the target before and after manipulation is anticipated to increase the existing data and facilitate therapeutic decision making at this late stage of the disease when hormonal manipulations, even with the newest androgen-directed therapies are no longer feasible.
Insights
Neuroendocrine prostate cancer (NEPC) emerges as a resistance mechanism to androgen deprivation therapy, often presenting aggressively without elevated PSA. Novel molecular targets are being explored for this lethal prostate cancer subtype.
Area of Science:
- Oncology
- Molecular Biology
- Urology
Background:
- Neuroendocrine prostate carcinoma (NEPC) is a significant challenge, often arising from adenocarcinoma or co-presenting, leading to resistance against androgen deprivation therapies.
- Clinical manifestations include rapid visceral disease progression, frequently without elevated prostate-specific antigen (PSA) levels, complicating diagnosis and treatment.
- Current treatment options are limited, with platinum-based chemotherapy offering transient responses.
Purpose of the Study:
- To investigate novel molecular targets for the treatment of lethal neuroendocrine prostate carcinoma.
- To identify key signaling factors involved in NEPC's microenvironment interactions, mitosis, and neural reprogramming.
- To explore the potential of targeted therapies in advanced prostate cancer where hormonal treatments are no longer effective.
Main Methods:
- Molecular characterization of NEPC phenotype.
- Identification of signaling factors implicated in NEPC pathogenesis.
- Ongoing clinical trials evaluating targeted inhibitors, such as Aurora kinase A inhibitors.
- Analysis of target expression changes before and after therapeutic manipulation.
Main Results:
- Identification of novel signaling factors as potential therapeutic targets in NEPC.
- Emerging data on the efficacy of specific inhibitors in carefully selected patients.
- Understanding of NEPC's molecular underpinnings, including microenvironment, mitosis, and neural reprogramming pathways.
Conclusions:
- Targeted therapies, particularly inhibitors of identified signaling factors like Aurora kinase A, show promise for treating NEPC.
- Monitoring target expression changes can aid therapeutic decision-making in advanced prostate cancer.
- These advancements offer new hope for patients with lethal NEPC resistant to conventional therapies.
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