Neuroendocrine differentiation in the progression of prostate cancer

Komiya, Akira; Suzuki, Hiroyoshi; Igarashi, Takashi; Kamiya, Naoto; Nihei, Naoki; Naya, Yukio; Ichikawa, Tomohiko; Fuse, Hideki

doi:10.1111/j.1442-2042.2008.02175.x

Cited by 114 publications

(96 citation statements)

References 110 publications

(232 reference statements)

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“…Perhaps the most significant histological variant is neuroendocrine prostate cancer, which is generally classified as either small cell carcinoma or a carcinoid tumor, and represents <2% of prostate cancer cases (Grignon 2004). However, focal regions of neuroendocrine differentiation are more commonly observed in prostate adenocarcinoma, particularly following recurrence after prostatectomy and androgen deprivation therapy (Yuan et al 2007;Komiya et al 2009), and expression of the neuroendocrine marker chromogranin A is associated with the development of castration-resistant tumors and shortened time to disease recurrence (Kokubo et al 2005;Berruti et al 2007). This prevalence of neuroendocrine differentiation after recurrence may be due to the lack of AR expression by neuroendocrine cells, which are inherently castration-resistant.…”

Section: Subtypes Of Prostate Cancermentioning

confidence: 99%

Molecular genetics of prostate cancer: new prospects for old challenges

Shen¹,

2010

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Despite much recent progress, prostate cancer continues to represent a major cause of cancer-related mortality and morbidity in men. Since early studies on the role of the androgen receptor that led to the advent of androgen deprivation therapy in the 1940s, there has long been intensive interest in the basic mechanisms underlying prostate cancer initiation and progression, as well as the potential to target these processes for therapeutic intervention. Here, we present an overview of major themes in prostate cancer research, focusing on current knowledge of principal events in cancer initiation and progression. We discuss recent advances, including new insights into the mechanisms of castration resistance, identification of stem cells and tumor-initiating cells, and development of mouse models for preclinical evaluation of novel therapuetics. Overall, we highlight the tremendous research progress made in recent years, and underscore the challenges that lie ahead.

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Section: Subtypes Of Prostate Cancermentioning

confidence: 99%

Molecular genetics of prostate cancer: new prospects for old challenges

Shen¹,

2010

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“…The prostate NE cells affect the target cells in an AI manner. Therefore, the NE pathway is thought to be one of the most significant mechanisms for AIPC or CRPC (9). NE cells are detected by immunohistochemical staining (IHS) using antibodies against neuropeptides, of which CGA and NSE are the most thoroughly investigated and are believed to be the best markers for prostatic NED (9).…”

Section: Introductionmentioning

confidence: 99%

The prognostic significance of loss of the androgen receptor and neuroendocrine differentiation in prostate biopsy specimens among castration-resistant prostate cancer patients

Komiya

Yasuda

Watanabe

et al. 2013

Molecular and Clinical Oncology

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Abstract. Prostate cancer (PCa) is a leading cause of mortality, and despite good response to androgen ablation this response is eventually lost. In the present study, androgen receptor (AR) expression and neuroendocrine differentiation (NED) were evaluated in hormone-sensitive (HSPC) and castration-resistant prostate cancers (CRPC). Prostate tissues were obtained from 20 HSPC patients at diagnosis and 28 CRPC patients at castration-resistant progression. AR, chromogranin A (CGA) and neuron-specific enolase (NSE) were evaluated by immunohistochemical staining (IHS) in representative positive cores for PCa. IHS intensity was graded as negative, 0; positive, 1+ and strongly positive, 2+. The proportion of the 1+ and 2+ areas in PCa cells was determined. PCa was considered to be in NED if ≥50% of the tumor cells were 1+ or 2+ for CGA or NSE. The observed IHS intensity (0/1+/2+) for AR, CGA and NSE was 0/4/16, 5/11/4 and 11/4/5 in HSPC patients and 9/3/16, 5/8/15

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“…Therefore, cisplatin-based cytotoxic agents that are similar to those used for SCC of the lung are usually applied, such as irinotecan + cisplatin or etoposide + cisplatin (2,21,22). In the present patient, treatment with etoposide and cisplatin was effective in terms of the serum marker response; however, it was impossible to continue this therapy due to deterioration of the patient's general condition.…”

Section: Discussionmentioning

confidence: 73%

“…The identification of prostatic tumors with a neuroendocrine component has been reported to range from 10 to 100% by immunohistochemical studies (1,2). Neuroendocrine differentiation is characterized by the focal neuroendocrine cells commonly observed in conventional prostatic adenocarcinoma, but may also occur as rarer entities, including small cell carcinoma (SCC), carcinoid-like tumors and Paneth-like cells (3,4).…”

Section: Introductionmentioning

confidence: 99%

Small cell carcinoma of the prostate after high-dose-rate brachytherapy for low-risk prostatic adenocarcinoma

et al. 2012

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Abstract. In the present study, we describe an 80-year-old patient who developed prostatic small cell carcinoma (SCC) following high-dose-rate brachytherapy (HDR-BT) for low-risk prostatic adenocarcinoma. The patient received one implant of Ir-192 and 7 fractions of 6.5 Gy within 3.5 days, for a total prescribed dose of 45.5 Gy. A total of 27 months after HDR-BT, the patient complained of difficulty in urinating. His serum prostate-specific antigen (PSA) levels were 3.2 ng/ml. Systemic examination revealed an enlargement of the prostate, urethral stenosis, pelvic lymph node swelling and multiple lung and bone lesions. His serum neuron-specific enolase (NSE) levels were elevated to 120 ng/ml. A prostate needle biopsy was performed for pathological examination. Histologically, there were tumor cells with hyperchromatic nuclei and scant cytoplasm showing a solid or trabecular growth pattern. Immunohistochemically, they were positive for AE1/AE3, CD56 and synaptophysin, and negative for PSA, PAP and CD57. These findings are consistent with SCC of the prostate. A review of the prostate needle biopsy specimen prior to HDR-BT did not reveal any tumor cells positive for chromogranin A, nor synaptophysin. The final diagnosis was SCC of the prostate with local progression, with lung, lymph node and bone metastases. Three cycles of etoposide/cisplatin (EP) were administered. A greater than 50% decrease in the serum NSE levels was observed. However, there was no objective response. Due to the deterioration of the patient's general condition, EP was discontinued. One month later, his serum NSE showed a rapid increase to 210 ng/ml with aggressive local progression and the patient succumbed to the disease 5.5 months after the start of EP therapy.

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Neuroendocrine differentiation in the progression of prostate cancer

Cited by 114 publications

References 110 publications

Molecular genetics of prostate cancer: new prospects for old challenges

Molecular genetics of prostate cancer: new prospects for old challenges

The prognostic significance of loss of the androgen receptor and neuroendocrine differentiation in prostate biopsy specimens among castration-resistant prostate cancer patients

Small cell carcinoma of the prostate after high-dose-rate brachytherapy for low-risk prostatic adenocarcinoma

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