A case of neuroendocrine carcinoma of the prostate.
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背景:前立腺のまれな腫瘍である神経内分泌癌: Neuroendocrine carcinoma (以下NEC) を経験したので報告する.症例:患者は78歳, 男性, 頻尿を主訴に来院した. 前立腺針穿刺組織検査で高分化腺癌が認められた. 尿細胞診においても腺癌を疑う異型細胞がみられた. 治療を開始し経過観察を行った. その後尿細胞診では異型細胞の出現は認められなかったが, 3年5ヵ月後に排尿困難を訴えTURを施行, 組織学的に一部腺癌を含むNECが認められた. ほぼ同時に施行された尿細胞診では腺癌由来の細胞は認められなかったが, 小型でN/C比が高く, クロマチンの増量した裸核状異型細胞が小集塊, 孤立散在性, また一部ではインディアンファイル状配列を呈して認められ, NEC由来の腫瘍細胞と診断した. 免疫組織化学的にNECはneuron specific enolase (NSE), synaptophysin, chromogranin Aが陽性であり, 腺癌部分ではprostatic specific antigen (PSA), prostaticacid phosphatase (PAP) が陽性であった.結論:尿細胞診スクリーニングにあたっては腺癌の既往歴を有してもNEC細胞が出現する可能性のあることを考慮することが重要と思われた.Keywords:
Enolase
Chromogranin A
Synaptophysin
Neuroendocrine carcinoma
Prostatic acid phosphatase
Prostate carcinoma
Neuroendocrine differentiation
The aim of this study was to examine the level of neuroendocrine differentiation to determine its association with clinicopathological parameters.Twenty-five primary MCC samples were evaluated for neuroendocrine differentiation profiles by immunohistochemistry using antibodies to chromogranin-A, microtubule associated protein-2 and synaptophysin. The data were compared with clinical parameters to find out whether their expression correlates with prognosis.In general, MCC shows a high degree of neuroendocrine differentiation. A higher expression of chromogranin-A and synaptophysin associated with benign behaviour. Chromogranin-A appeared to be the most important one in predicting the course of disease.Low levels of neuroendocrine differentiation in MCC associates with poor prognosis. Chromogranin-A could be used to identify patients who might benefit from oncological treatments.
Chromogranin A
Synaptophysin
Neuroendocrine differentiation
Merkel cell
Neuroendocrine cell
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Background . Carcinomas of the breast with neuroendocrine features are incorporated in the World Health Organization classification since 2003 and include well-differentiated neuroendocrine tumors, poorly differentiated neuroendocrine carcinomas/small cell carcinomas, and invasive breast carcinomas with neuroendocrine differentiation. Neuroendocrine differentiation is known to be more common in certain low-grade histologic special types and has been shown to mainly cluster to the molecular (intrinsic) luminal A subtype. Methods . We analyzed the frequency of neuroendocrine differentiation in different molecular subtypes of breast carcinomas of no histologic special type using immunohistochemical stains with specific neuroendocrine markers (chromogranin A and synaptophysin). Results . We found neuroendocrine differentiation in 20% of luminal B-like carcinomas using current WHO criteria (at least 50% of tumor cells positive for synaptophysin or chromogranin A). In contrast, no neuroendocrine differentiation was seen in luminal A-like, HER2 amplified and triple-negative carcinomas. Breast carcinomas with neuroendocrine differentiation presented with advanced stage disease and showed aggressive behavior. Conclusions . We conclude that neuroendocrine differentiation is more common than assumed in poorly differentiated luminal B-like carcinomas. Use of specific neuroendocrine markers is thus encouraged in this subtype to enhance detection of neuroendocrine differentiation and hence characterize the biological and therapeutic relevance of this finding in future studies.
Neuroendocrine differentiation
Chromogranin A
Synaptophysin
Neuroendocrine cell
Breast carcinoma
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Neuroendocrine differentiation and prognosis in breast adenocarcinoma Aims : Neuroendocrine differentiation has been detected, and its prognostic value studied, in a number of common human carcinomas. To date there are few detailed studies examining its relevance in breast carcinoma. In this study we evaluate the frequency and prognostic importance of neuroendocrine differentiation in breast adenocarcinoma. Methods and results : The presence of neuroendocrine differentiation, defined as positive reactivity for three markers, neuron‐specific enolase (NSE), chromogranin A and/or synaptophysin, has been evaluated in 99 patients with primary operable breast cancer using standard immunocytochemical techniques. A consecutive cohort of patients were selected from the Nottingham/Tenovus series. Comprehensive patient and tumour records have been maintained, and patients were followed up according to a defined protocol. Eighteen cases were positive for NSE, 10 for chromogranin A and 13 for synaptophysin. Eleven percent were positive with more than one neuroendocrine marker. No significant association was found between neuroendocrine differentiation and tumour size, grade, stage or the prevalence of vascular invasion. There was no significant difference in either overall or disease‐free survival between patients with or without neuroendocrine differentiation. Conclusions : In this study we confirm that neuroendocrine differentiation can be identified in a subset (10–18%) of human breast carcinomas. This phenomenon appears to have no relationship to established prognostic factors or patient outcome.
Neuroendocrine differentiation
Chromogranin A
Synaptophysin
Enolase
Breast carcinoma
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Purpose of the study . Determine the frequency of MiNeN among pancreatic carcinomas and analyze the survival rate of patients depending on the percentage of cells with neuroendocrine differentiation in the tumor. Materials and methods . The current study included 31 patients with a pancreatic tumor who received surgical treatment at the Rostov Cancer Research Institute. An immunohistochemical study was conducted on biomarkers of chromogranin A, synaptophysin, and ki-67 for these patients. Based on the data obtained, 4 groups for neuroendocrine differentiation were identified. Results . The direct effect of neuroendocrine differentiation on the survival of patients with histologically confirmed pancreatic ductal adenocarcinoma has been proven. Among the sample of 31 patients, neuroendocrine differentiation was revealed in 24 cases (77%), of which 3 cases of MiNeN (10.3%) were detected. It is also proven relationship between neuroendocrine and patient survival, where an increase percent of positive cells in tumors (chromogranin A or synaptophysin) means a better prognosis. Chromogranin A is a more significant predictor of survival compared to synaptophysin. The largest difference in survival was between negative expression of chromogranin A and the presence of more than 1% positive cells in the tumor. Conclusion . We supposed that it is necessary to use neuroendocrine markers (chromogranin A and synaptophysin) in the diagnosis of ductal adenocarcinomas, even without histological signs of neuroendocrine differentiation. This will allow for a larger amount of data to determine their significance as prognostic markers.
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Abstract Background Neuroendocrine differentiation of prostatic carcinoma is a rare entity associated with metastatic castration-resistant disease. Among useful biomarkers of neuroendocrine differentiation, chromogranin A, serotonin, synaptophysin and neuron-specific enolase stand out, while total prostate-specific antigen (PSA) levels are often low or undetectable. Case presentation We report a case of prostatic adenocarcinoma recurrence after a 6-year disease-free follow-up, in which increased serum chromogranin A levels and undetectable total PSA provided a prompt indication of neuroendocrine transformation, confirmed through immunohistochemical evaluation. Conclusions Neuroendocrine differentiation is a relevant cause of prostatic adenocarcinoma recurrence, and awareness of this entity is crucial due to its underdiagnosis and adverse prognosis.
Chromogranin A
Neuroendocrine differentiation
Synaptophysin
Enolase
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Insulinoma-associated protein-1 (INSM1), a transcription factor encoded by the insulinoma associated-1 gene, is a second-generation biomarker of neuroendocrine differentiation. Its sensitivity and specificity in comparison with chromogranin-A and synaptophysin have been extensively validated in several organs, but evidence regarding its expression in mammary neoplasms is limited. In this study, INSM1 immunohistochemistry was validated in a cohort of 22 mammary neoplasms, enriched with special type breast carcinomas with known neuroendocrine differentiation as determined by immunohistochemistry for synaptophysin and chromogranin-A. Subsequently, INSM1 expression was evaluated in a consecutive series of 66 invasive breast cancer biopsies. In the validation cohort, 14 tumors were synaptophysin-positive, of which all but one showed INSM1 immunoreactivity. Eight tumors were synaptophysin-negative, of which 3 showed focal nuclear INSM1 expression. Six tumors were chromogranin-A-positive, of which one was INSM1-negative. When compared with synaptophysin, INSM1 seems more sensitive but less specific than chromogranin-A. In the biopsy cohort, only one invasive carcinoma of no special type showed substantial INSM1 immunoreactivity (ie, 25% of the tumor cells). Three more cases showed 1% nuclear INSM1 staining. We conclude that neuroendocrine differentiation in invasive breast carcinoma of no special type is a rare finding. Immunohistochemical biomarkers, comprising INSM1 as well as the first-generation biomarkers chromogranin-A and synaptophysin, are useful to distinguish neuroendocrine differentiation in breast neoplasms. The identification of neuroendocrine differentiation can be helpful to establish the diagnosis of special type breast carcinomas such as solid papillary carcinoma.
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Neuroendocrine differentiation
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Chromogranin A
Synaptophysin
Neuroendocrine differentiation
Large cell
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We describe a primary mixed adenocarcinoma-neuroendocrine carcinoma of the urinary bladder of probable urachal origin. Neuroendocrine differentiation was confirmed by ultrastructural (neurosecretory granules) and immunohistochemical studies (chromogranin and neuron-specific enolase). Two local recurrences and multiple metastases consisted exclusively of the neuroendocrine component. The patient died 30 months after diagnosis with widely metastatic neuroendocrine carcinoma.
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Neuroendocrine differentiation
Enolase
Synaptophysin
Neuroendocrine carcinoma
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Prostate cancer (PCa) is the most frequent neoplasic condition in males, but only 64-65% of the cases are sensitive to hormone therapy. The aim of this study was to investigate the neuroendocrine component of the prostatic carcinoma, in relation to the histopathological form and the degree of differentiation. Biopsies were obtained through transurethral resection, from 82 patients with prostate cancer. In order to assess the histopathological form and the Gleason score, one section from each case was stained with Hematoxylin-Eosin. Additional sections were stained with chromogranin A. We considered neuroendocrine cell hyperplasia to have a higher value than that observed in benign prostatic hyperplasia (BPH) and normal prostate (over three neuroendocrine cells÷gland). The quantification of neuroendocrine differentiation (NED) has been significant; the reaction was considered to be weak (2-10% neuroendocrine cells), moderate (10-20%) and intense (over 50%). Cells positive for chromogranin A have been identified in all the cases, but a larger number than that registered in normal tissue has been noted in 59 patients (71.95%). In most of the cases, the neuroendocrine cells have been distributed in small groups among the neoplasic cells, and rarely isolated. In two cases of small cell carcinoma most of the tumoral cells have been positive for chromogranin A. In conclusion, the study of neuroendocrine differentiation in patients with prostatic carcinoma revealed hyperplasia of positive chromogranin A cells, in 71.95% of cases. Neuroendocrine prostatic differentiation is correlated with the advanced stage of evolution and possibly with the resistance to hormonal treatment.
Chromogranin A
Neuroendocrine differentiation
Neuroendocrine cell
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Chromogranin A
Neuroendocrine differentiation
Immunostaining
Neuroendocrine cell
Clinical Significance
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