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Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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Skin Cancer01:30

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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

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[Neuroendocrine prostate cancer].

S Tritschler1, R Erdelkamp2, C Stief3

  • 1Urologische Klinik und Poliklinik, Klinikum Großhadern, LMU München, Marchioninistr. 15, 81377, München, Deutschland. Stefan.Tritschler@med.uni-muenchen.de.

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|June 28, 2018
PubMed
Summary
This summary is machine-generated.

Neuroendocrine prostate cancer (NEPC) arises from androgen deprivation treatment. Suspect NEPC in aggressive metastatic castration-resistant prostate cancer (mCRPC) with low PSA and elevated neuroendocrine markers.

Keywords:
Androgen deprivation therapyChemotherapyChromogranin ANeuroendocrine carcinomaProstate

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Area of Science:

  • Oncology
  • Urology
  • Cancer Research

Background:

  • Neuroendocrine prostate cancer (NEPC) often emerges as a treatment-induced adaptation to androgen deprivation therapy (ADT).
  • NEPC is found in 30-40% of metastatic castration-resistant prostate cancer (mCRPC) cases, while primary small cell prostate cancer is rare (<1%).
  • Initial Gleason score is a significant predictor for developing NEPC.

Purpose of the Study:

  • To outline the clinical suspicion, diagnostic indicators, and treatment strategies for neuroendocrine prostate cancer (NEPC).

Main Methods:

  • Clinical suspicion based on aggressive mCRPC, low prostate-specific antigen (PSA), and elevated neuroendocrine markers (chromogranin A, neuron-specific enolase).
  • Correlation of initial Gleason score with NEPC development risk.
  • Treatment protocols mirroring those for small cell lung cancer.

Main Results:

  • Cisplatin and etoposide chemotherapy yields 30-60% response rates in NEPC patients with negative PSA.
  • Median survival is typically under 1 year with this regimen.
  • Carboplatin plus docetaxel is considered for NEPC patients with significantly elevated PSA levels.

Conclusions:

  • NEPC is a critical consideration in advanced prostate cancer, particularly under ADT pressure.
  • Early identification through specific clinical and biomarker profiles is essential.
  • Tailored chemotherapy regimens, based on PSA levels, are crucial for managing NEPC.