Prostatic carcinomas with neuroendocrine differentiation diagnosed in needle biopsies, a morphologic study of 7 cases among 465 sequential biopsies in a tertiary cancer center

Lima, Marcos Venício Alves; Nogueira, C; Oliveira, Joao; Neto, Francisco Júlio Muniz; Franco, Maria do Carmo Pinho; Tavora, Fabio

doi:10.1590/s1677-55382011000500005

Cited by 2 publications

(6 citation statements)

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“…The concept of neuroendocrine prostate cancer and neuroendocrine differentiation in the prostatic adenocarcinoma has recently attracted considerable attention as potentially significant entities with major prognostic and therapeutic ramifications. [1][2][3][4][5]7,9,10 Along with expertize in the diagnosis, grading, and staging, the pathologist plays a pivotal role in guiding subsequent tissue-based biomarker testing and their clinical utility. 5 Due to the highly aggressive nature of the neuroendocrine carcinoma, and its association with androgen resistance/independence and metastasis, rapid recognition of this entity is crucial.…”

Section: Discussionmentioning

confidence: 99%

“…[3][4][5] It is estimated that up to 10% of prostate cancer patients with the androgen-resistant disease following long-term androgen deprivation therapy (ADT), develop high-grade neuroendocrine carcinoma, mostly associated with acinar adenocarcinoma. [2][3][4][5] With the continual clinical and molecular data emerging from the study of prostate cancer treated with contemporary ADT, there has been a steady attempt to refine the terminology for neuroendocrine lesions in the prostate gland. 2,5,6 The WHO Classification 2016 is an excellent framework, classifying these entities into five distinct subgroups: neuroendocrine cells in the usual prostate cancer; adenocarcinoma with Paneth cell-like differentiation; well-differentiated neuroendocrine tumor; small cell neuroendocrine carcinoma; large cell neuroendocrine carcinoma.…”

Section: Introductionmentioning

confidence: 99%

“…Neuroendocrine differentiation in the prostate gland encompasses various entities, ranging from the presence of focal neuroendocrine cells in an otherwise conventional acinar adenocarcinoma to a small cell or large cell neuroendocrine carcinoma. [1][2][3][4][5] Neuroendocrine neoplasms of the prostate occur in two settings: de novo disease (in a treatment-naïve setting) or as a post-therapy transdifferentiated phenotype of a typical adenocarcinoma (Figure 1). Moreover, neuroendocrine neoplasm of the prostate gland represents a rare subtype of prostatic malignancies, [2][3][4][5] the most common by far being a small cell neuroendocrine carcinoma and mixed small cell and acinar adenocarcinoma.…”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3][4][5] Neuroendocrine neoplasms of the prostate occur in two settings: de novo disease (in a treatment-naïve setting) or as a post-therapy transdifferentiated phenotype of a typical adenocarcinoma (Figure 1). Moreover, neuroendocrine neoplasm of the prostate gland represents a rare subtype of prostatic malignancies, [2][3][4][5] the most common by far being a small cell neuroendocrine carcinoma and mixed small cell and acinar adenocarcinoma. [3][4][5] It is estimated that up to 10% of prostate cancer patients with the androgen-resistant disease following long-term androgen deprivation therapy (ADT), develop high-grade neuroendocrine carcinoma, mostly associated with acinar adenocarcinoma.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, neuroendocrine neoplasm of the prostate gland represents a rare subtype of prostatic malignancies, [2][3][4][5] the most common by far being a small cell neuroendocrine carcinoma and mixed small cell and acinar adenocarcinoma. [3][4][5] It is estimated that up to 10% of prostate cancer patients with the androgen-resistant disease following long-term androgen deprivation therapy (ADT), develop high-grade neuroendocrine carcinoma, mostly associated with acinar adenocarcinoma. [2][3][4][5] With the continual clinical and molecular data emerging from the study of prostate cancer treated with contemporary ADT, there has been a steady attempt to refine the terminology for neuroendocrine lesions in the prostate gland.…”

Section: Introductionmentioning

confidence: 99%

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Reporting Trends, Practices, and Resource Utilization in Neuroendocrine Tumors of the Prostate Gland: A Survey among Thirty-Nine Genitourinary Pathologists

Mohanty¹,

Lobo²,

Williamson

et al. 2022

Int J Surg Pathol

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Background: Neuroendocrine differentiation in the prostate gland ranges from clinically insignificant neuroendocrine differentiation detected with markers in an otherwise conventional prostatic adenocarcinoma to a lethal high-grade small/large cell neuroendocrine carcinoma. The concept of neuroendocrine differentiation in prostatic adenocarcinoma has gained considerable importance due to its prognostic and therapeutic ramifications and pathologists play a pivotal role in its recognition. However, its awareness, reporting, and resource utilization practice patterns among pathologists are largely unknown. Methods: Representative examples of different spectrums of neuroendocrine differentiation along with a detailed questionnaire were shared among 39 urologic pathologists using the survey monkey software. Participants were specifically questioned about the use and awareness of the 2016 WHO classification of neuroendocrine tumors of the prostate, understanding of the clinical significance of each entity, and use of different immunohistochemical (IHC) markers. De-identified respondent data were analyzed. Results: A vast majority (90%) of the participants utilize IHC markers to confirm the diagnosis of small cell neuroendocrine carcinoma. A majority (87%) of the respondents were in agreement regarding the utilization of type of IHC markers for small cell neuroendocrine carcinoma for which 85% of the pathologists agreed that determination of the site of origin of a high-grade neuroendocrine carcinoma is not critical, as these are treated similarly. In the setting of mixed carcinomas, 62% of respondents indicated that they provide quantification and grading of the acinar component. There were varied responses regarding the prognostic implication of focal neuroendocrine cells in an otherwise conventional acinar adenocarcinoma and for Paneth cell-like differentiation. The classification of large cell neuroendocrine carcinoma was highly varied, with only 38% agreement in the illustrated case. Finally, despite the recommendation not to perform neuroendocrine markers in the absence of morphologic evidence of neuroendocrine differentiation, 62% would routinely utilize IHC in the work-up of a Gleason score 5 + 5 = 10 acinar adenocarcinoma and its differentiation from high-grade neuroendocrine carcinoma. Conclusion: There is a disparity in the practice utilization patterns among the urologic pathologists with regard to diagnosing high-grade neuroendocrine carcinoma and in understanding the clinical significance of focal neuroendocrine cells in an otherwise conventional acinar adenocarcinoma and Paneth cell-like neuroendocrine differentiation. There seems to have a trend towards overutilization of IHC to determine neuroendocrine differentiation in the absence of neuroendocrine features on morphology. The survey results suggest a need for further refinement and development of standardized guidelines for the classification and reporting of neuroendocrine differentiation in the prostate gland.

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