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Research Article | DOI: https://doi.org/10.31579/2692-9406/191
Medical Examiner Member (RC Path) London and Retired Urologist United Kingdom
*Corresponding Author: Anthony Kodzo-Grey Venyo. Medical Examiner Member (RC Path) London and Retired Urologist United Kingdom
Citation: Anthony Kodzo-Grey Venyo. (2024) Treatment Related Neuroendocrine Prostatic Carcinoma: Review and Update. Biomedical Research and Clinical Reviews, 9(3); Doi: 10.31579/2692-9406/191
Copyright: © 2024 Anthony Kodzo-Grey Venyo, This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Received: 12 December 2024 | Accepted: 20 December 2024 | Published: 25 December 2024
Keywords: treatment-related prostatic cancer; treatment-related prostate cancer; aggressive tumour; histopathology; immunohistochemistry.
Treatment-related neuroendocrine carcinoma of the prostate gland is stated to be a distinctive category of carcinoma of the prostate gland which tends to ensue intensive suppression of the androgen receptor by next-generation therapeutic inhibition of androgen receptor signalling. The biological processes which set in motion the series of events emanating in transformation of adenocarcinoma to neuroendocrine carcinoma has been iterated to include genomic (loss of tumour suppressors TP53 and RB1, amplification of oncogenes N-MYC and Aurora Kinase A, dysregulation of transcription factors SOX2, achaete-scute-homolog 1, and others) as well as epigenomic (DNA methylation, EZH2 overexpression, and others). Pathology examination diagnosis of specimens of the tumour has been iterated to be the key to effective treatment for this disease, and this is aided by localizing metastatic lesions for biopsy utilising radioligand imaging in the appropriate clinical context. As the understanding of biology of the tumour has evolved, there has been increased morphological examination recognition and characterization of tumour phenotypes which are present within this advanced post-treatment setting. New and promising biomarkers (delta-like ligand 3 and others) have been discovered, which has opened up novel treatment avenues including immunotherapy and antibody-drug conjugates for this lethal disease with currently limited treatment options. It is important for clinicians and patients all over the world to appreciate that treatment related neuroendocrine carcinoma of the prostate gland generally has tended to portend an aggressive clinical and biological behaviour that has tended to be associated with poor prognosis and early death of individuals afflicted by the tumour. There is the need for clinicians and research workers to undertake research work that would identify new treatment options that would help improve the outcome of the tumour by destroying the tumour cells effectively.
Prostate cancer (PCa) is stated to be the second most common malignancy among men worldwide. [1] [2] [3] The standard treatment for metastatic PCa is ADT; [4] nevertheless, eventually cancer cells do acquire resistance and castrate resistant prostate cancer (CRPC) develops. It is now widely understood that the majority of CRPCs are still dependent upon the androgen receptor (AR) signalling pathway, [5] [6] and novel AR pathway inhibitors, such as enzalutamide and abiraterone, have demonstrated efficacy against CRPC. [7] [8] [9] 10] treatment-related neuroendocrine prostate cancer (T-NEPC) is a rare AR-independent cancer subtype which develops at the later stage of CRPC treatment. [11] [12] Morphologically, it shows features of small cell carcinoma, and typically has low or absent AR expression. [13] Clinically, it overlaps with “anaplastic prostate carcinoma” or “AVPC,” which are characterized by extensive visceral metastases, short response duration to ADT, sensitivity to platinum-containing chemotherapy and poor prognosis. [14 [15] t-NEPC develops as a consequence of lineage plasticity, a phenomenon in which tumour cells acquire phenotypic characteristics of a cell lineage whose survival is no longer regulated by a certain drug target. [16] The incidence of t-NEPC has been rising rapidly as a result of the increasing use of potent AR pathway inhibitors, and it is now imperative to study the molecular characteristic of this aggressive subtype and identify specific molecular targets. Recent integrative genomic analysis and novel in vivo models of t-NEPC have identified several key molecular features of NEPC. In the present review, we discuss various clinical and molecular aspects of t-NEPC.
Aim: To review and update the literature on treatment-related neuroendocrine prostatic carcinoma.
Method
Internet data bases were searched including: Google; Google Scholar; Yahoo; and PUBMED. The search words that were used included: treatment related prostate carcer; treatment related carcinoma of prostate; treatment related prostatic carcinoma. Fifty-four (54) references were identified which were used to write the article which has been divided into two parts: (A) Overview, and (B) Miscellaneous narrations and discussions from some case reports, case series, and studies related to neuroendocrine prostatic carcinoma.
Results
[A] Overview
Definition / general statement
Essential features
The essential features of treatment-related prostatic carcinomas had been summated as follows: [17]
Epidemiology
The epidemiology of treatment-related prostatic carcinomas had been summated as follows: [17]
Sites
The sites of treatment-related prostatic carcinomas, had been summated to include the following: [17]
Pathophysiology
The pathophysiology of treatment-related prostatic carcinomas had been summated as follows: [17]
Aetiology
Clinical features
The clinical features of treatment-related prostatic carcinomas had been summated as follows: [17]
Diagnosis
The diagnosis of treatment-related prostatic carcinomas had been summated as follows: [17]
Laboratory tests
Laboratory tests that tend to be undertaken in cases of treatment-related prostatic carcinomas had been summated as follows: [17]
Radiology description
Prognostic factors
The prognostic factors associated with treatment-related prostatic carcinomas, had been summated as follows: [17]
Treatment
The treatment of treatment-related prostatic carcinomas had been summated as follows: [17]
Gross description
Macroscopy examination features of treatment-related prostatic carcinomas had been summated as follows: [17]
Microscopic (histologic) description
Microscopy examination features of treatment-related prostatic carcinomas had been summated as follows: [17]
Positive stains
Positive immunohistochemistry staining of treatment-related prostatic carcinomas had been summated as follows: [17]
Negative stains
Negative immunohistochemistry staining of treatment-related prostatic carcinomas had been summated as follows: [17]
Molecular / cytogenetics description
Molecular / cytogenetics description in treatment-related prostatic carcinomas had been summated as follows: [17]
Differential diagnoses
The differential diagnoses of treatment-related prostatic carcinomas had been summated as follows: [17]
[B] Miscellaneous Narrations and Discussions from some Case Reports, Case Series, and Studies Related to Treatment Effect Prostatic Carcinoma.
Akamatsu et al. [1] made the ensuing iterations:
Hirano et al. [11] evaluated the relationship between neuroendocrine differentiation (NED) status and hormone refractory prostate cancer (HRPC) following hormone therapy based upon immunohistochemical study. Hirano et al. [11] examined seventy-two prostate cancer specimens obtained at radical prostatectomy and 21 prostate cancer autopsy specimens from patients who died from HRPC after androgen deprivation therapy for NED status using an antibody against chromogranin A. They classified the specimens into 3 arms: 38 radical prostatectomy specimens from patients with no neoadjuvant hormone therapy (Group 1); 34 from patients with neoadjuvant hormone therapy for 3 months to 6 months (Group 2); and 21 autopsy specimens from patients with HRPC after androgen deprivation therapy for more than 1 year (Group 3). Hirano et al. [11] scored the staining of prostatic carcinoma as: 0 = no staining; 1 = staining cells <10 xss=removed>20%. Hirano et al. [11] compared the differences in scores among the groups using the Kruskal-Wallis rank test. Hirano et al. [11] performed multivariate analysis using a logistic regression model to examine whether NED status was associated with pathological stage (pT), grade and group. Hirano et al. [11] summarised the results as follows:
Hirano et al. [11] concluded that the results of this study demonstrated that NED status was significantly increased in patients with HRPC following long-term androgen deprivation therapy, but it could not be discriminate whether the increase of NED is attributable to condition of hormone refractoriness or long-term hormonal therapy. Bishop et al. [16] made the ensuing iterations.
Stock et al. [21] stated the following:
Conteduca et al. [22] made the ensuing iterations:
Conteduca et al. [22] reviewed baseline, treatment and outcome data of 87 patients with metastatic prostate cancer and tumour biopsy confirming NEPC histology. Forty-seven (54.0%) NEPC cases had presented de novo, and 40 (46.0%) were therapy-related (t-NEPC). Thirty-six (41.4%) were classified as pure small-cell carcinoma, and 51 (58.6%) demonstrated mixed features with both small-cell carcinoma and adenocarcinoma present. Genomic data were available for 47 patients. Conteduca et al. [22] summated the results as follows:
Conteduca et al. [22] concluded that they had described the clinical features of a cohort of patients with NEPC. These characteristics may inform future diagnostic strategies.
Tritschler et al. [23] made the ensuing iterations:
Tu et al. [25] stated that large cell neuroendocrine carcinoma (LCNEC) of the prostate is an extremely rare entity, and the clinicopathological course, potential effective treatment, and prognosis are yet to be elucidated. Tu et al. [25] undertook a systematic search in Pubmed, Embase, and Ovid from inception to January 2019. Tu et al. [25] reviewed each individual case of prostatic LCNEC and summarized specific features and outcomes for this rare pathologic entity. Tu et al. [25] summarised the results as follows:
Tu et al. [25] made the ensuing conclusions:
George et al. [27] made the ensuing iterations:
Yao et al. [28] made the ensuing iterations:
Yao et al. [28] undertook a study which was aimed to characterize the immunophenotype of histologically classic SCPC using a comprehensive panel of markers, to better understand its histogenesis, aid in its classification, and evaluate potential therapeutic targets. Yao et al. [28] using the World Health Organization morphologic criteria for SCLC, identified 18 SCPC cases and studied for the following tumour marker groups: prostate specific/related, neuroendocrine, sex steroid hormone receptors, and prognostic/treatment target-related. Yao et al. [28] used ten cases of UPC as controls. Yao et al. [28] summarised the results as follows:
Yao et al. [28] made the ensuing conclusions:
Nava Rodrigues et al. [29] stated the ensuing:
Nava Rodrigues et al. [29] used whole-genome sequencing (WGS) to investigate genomic heterogeneity in 21 previously treated CRPC metastases from 10 patients to investigate intrapatient molecular heterogeneity (IPMH). Nava Rodrigues et al. [29] performed WGS on topographically separate metastases from patients with advanced metastatic prostate cancer. IPMH of the RB1 gene was identified and further evaluated by FISH and IHC assays. Nava Rodrigues et al. [29] summarised the results as follows:
Nava Rodrigues et al. [29] made the ensuing conclusions:
Uehara et al. [30] stated that a new subtype of prostate cancer called treatment-related neuroendocrine prostate carcinoma (t-NEPC) was added to the revised World Health Organization classification of prostate cancer in 2022. t-NEPC cases are increasing, and there is no established standard treatment. Uehara et al. [30] reported a 49-year-old male patient, who was referred to their department for dysuria. He underwent a rectal examination and a prostate biopsy, which revealed stony hardness and prostate adenocarcinoma, respectively. He had radiology imaging studies which confirmed the presence of multiple bone and lymph node metastases. The patient was commenced upon upfront treatment with androgen deprivation therapy and an androgen receptor signalling inhibitor, that resulted in a significant (>90%) decrease in his serum prostate-specific antigen (PSA) levels. The patient experienced postrenal failure 6 months subsequently, which was attributable to local disease progression. Concurrently, there was an elevation in neuron-specific enolase (NSE) levels and an enlargement of pelvic lymph node metastases, without PSA progression. Uehara et al. [30] also reported the ensuing results:
Uehara et al. [30] made the ensuing conclusions:
Wang et al. [24] stated that an often-under-recognized late manifestation of prostate adenocarcinoma (PCa) is the development of treatment-related neuroendocrine prostate cancer (NEPC). Wang et al. [24] undertook a study in order to identify the risk factors related to survival after NEPC diagnosis (NEPCS) and time from initial diagnosis of PCa to development of NEPC (TTNEPC). Wang et al. [24] undertook a literature search on NEPC using databases such as MEDLINE and EMBASE. Wang et al. [24] iterated that the studies were eligible if outcomes data (NEPCS and/or TTNEPC) were reported in patients with a prior history of PCa and histopathologically confirmed NEPC. Wang et al. [24] evaluated NEPCS and TTNEPC using the Cox regression model with the robust sandwich estimates of the covariance matrix. Wang et al. [24] summarised the results as follows:
Wang et al. [24] made the ensuing conclusions:
Ikeda et al. [31] made the ensuing iterations:
Ikeda et al. [31] reported that in 2008, a 64‐year‐old man with a serum PSA level of 6.5 ng/mL and a family history of breast and prostate cancers was diagnosed as having cT3N0M0 prostate cancer. Pathology examination of his prostate biopsy specimen revealed adenocarcinoma with a Gleason score of 4 + 5 = 9. The patient underwent a prostatectomy 3 months after receiving neoadjuvant hormonal treatment. One year pursuant to his prostatectomy surgery, salvage ADT was introduced for biochemical recurrence, and the PSA level was <0>
Figure 1: Computed tomography image when the patient was diagnosed with t‐NEPC (a, b) and microscopic findings of the tumour (c–g). (c) Small, clustered cells with a high nuclear‐to‐cytoplasmic ratio and no glandular pattern are observed (hematoxylin and eosin staining: ×20). (d) There are frequent mitotic figures (hematoxylin and eosin staining: ×100). (e) The tumour cells are positive for synaptophysin, (f) CD56, and (g) chromogranin A, partially (×200). Reproduced from [31] under the Creative Commons Attribution License.
The clinical course pursuant to the NEPC diagnosis is shown in Figure 2. Four‐month chemotherapy with ETP and CBDCA resulted in a complete response. Nevertheless, in 2021, the pelvic floor tumour recurred again (see figure 3). Ikeda et al. [31] recommenced ETP and CBDCA chemotherapy, but the patient discontinued because he experienced delirium. At that time, the FoundationOne® genomic test on the biopsy specimen of the pelvic floor tumour diagnosed as NEPC revealed a BRCA2 gene mutation and some variants of uncertain significance. A single‐site analysis with peripheral blood was undertaken to confirm the pathogenic variant identified in FoundationOne®; the patient harboured a BRCA2 germline mutation. Therefore, olaparib was administered as a fifth‐line treatment for prostate cancer. The proGRP level decreased, and the tumour diminished in size, suggesting stable disease following the revised Response Evaluation Criteria in Solid Tumours version 1.1. [35] Nevertheless, the proGRP level gradually increased after 1 year of treatment with olaparib and 15 months after commencing olaparib, the pelvic floor tumour demonstrated regrowth, indicating progressive disease. The patient continued olaparib for 40 months after t‐NEPC diagnosis because of a slow increase in tumour size and minimal side effects.
Figure 2:The clinical course after the diagnosis of t‐NEPC. Olaparib resulted in decreased proGRP level and tumour reduction. Reproduced from [31] under the Creative Commons Attribution License.
Figure 3: Magnetic resonance imaging of recurrent pelvic floor tumour before olaparib administration. The tumours show faintly high signal intensity on T2‐weighted images and are diffusion‐weighted image‐positive. Reproduced from [31] under the Creative Commons Attribution License.
Ikeda et al. [31] made the ensuing educative discussions
Ikeda et al. [31] made the ensuing conclusions:
Nguyen et al. [49] stated the following:
Iwamoto et al. [50] stated that neuroendocrine prostate cancer (NEPC) is rare and has a poor prognosis; its clinical course and treatment outcomes are also unclear. Iwamoto et al. [50] undertook a study to investigate the clinical characteristics, clinical course, and treatment outcomes of patients with NEPC. Iwamoto et al. [50] undertook a retrospective study to investigate 14 patients, who were histologically diagnosed with NEPC at Kanazawa University Hospital between 2000 and 2019. Iwamoto et al. [50] reported that the overall survival (OS) and progression-free survival (PFS) were retrospectively analysed using the Kaplan–Meier method. Iwamoto et al. [50] additionally, used log-rank tests to compare survival distributions. Iwamoto et al. [50] summarised the results as follows:
Iwamoto et al. [50] made the ensuing conclusions:
Beltran and Demichelis [51] made the ensuing iterations:
Yamada and Beltran [52] made the ensuing iterations:
Yamada Y, Beltran [52] summarised recent findings as follows:
Yamada and Beltran [52] made the ensuing summating recommendation:
Apostolidis et al. [53] stated the following:
Apostolidis et al. [53] undertook a retrospective analysis of all patients with NEPCs including mixed differentiation with adenocarcinoma component and well differentiated neuroendocrine tumours (NETs, carcinoids) at two high-volume oncological centres between 12/2000 and 11/2017. Apostolidis et al. [53] summarised the results as follows:
Nill.
Acknowledgements to: IJU Case Reports, John Wiley and Sons and the Japanese Urological Association for granting permission for reproduction of figures and contents of their journal article under copyright © 2023 The Authors. IJU Case Reports published by John Wiley & Sons Australia, Ltd on behalf of Japanese Urological Association. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
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My experience publishing in International Journal of Clinical Case Reports and Reviews was exceptional. I Come forth to Provide a Testimonial Covering the Peer Review Process and the editorial office for the Professional and Impartial Evaluation of the Manuscript.
I would like to offer my testimony in the support. I have received through the peer review process and support the editorial office where they are to support young authors like me, encourage them to publish their work in your esteemed journals, and globalize and share knowledge globally. I really appreciate your journal, peer review, and editorial office.
Dear Agrippa Hilda- Editorial Coordinator of Journal of Neuroscience and Neurological Surgery, "The peer review process was very quick and of high quality, which can also be seen in the articles in the journal. The collaboration with the editorial office was very good."
I would like to express my sincere gratitude for the support and efficiency provided by the editorial office throughout the publication process of my article, “Delayed Vulvar Metastases from Rectal Carcinoma: A Case Report.” I greatly appreciate the assistance and guidance I received from your team, which made the entire process smooth and efficient. The peer review process was thorough and constructive, contributing to the overall quality of the final article. I am very grateful for the high level of professionalism and commitment shown by the editorial staff, and I look forward to maintaining a long-term collaboration with the International Journal of Clinical Case Reports and Reviews.
To Dear Erin Aust, I would like to express my heartfelt appreciation for the opportunity to have my work published in this esteemed journal. The entire publication process was smooth and well-organized, and I am extremely satisfied with the final result. The Editorial Team demonstrated the utmost professionalism, providing prompt and insightful feedback throughout the review process. Their clear communication and constructive suggestions were invaluable in enhancing my manuscript, and their meticulous attention to detail and dedication to quality are truly commendable. Additionally, the support from the Editorial Office was exceptional. From the initial submission to the final publication, I was guided through every step of the process with great care and professionalism. The team's responsiveness and assistance made the entire experience both easy and stress-free. I am also deeply impressed by the quality and reputation of the journal. It is an honor to have my research featured in such a respected publication, and I am confident that it will make a meaningful contribution to the field.
"I am grateful for the opportunity of contributing to [International Journal of Clinical Case Reports and Reviews] and for the rigorous review process that enhances the quality of research published in your esteemed journal. I sincerely appreciate the time and effort of your team who have dedicatedly helped me in improvising changes and modifying my manuscript. The insightful comments and constructive feedback provided have been invaluable in refining and strengthening my work".
I thank the ‘Journal of Clinical Research and Reports’ for accepting this article for publication. This is a rigorously peer reviewed journal which is on all major global scientific data bases. I note the review process was prompt, thorough and professionally critical. It gave us an insight into a number of important scientific/statistical issues. The review prompted us to review the relevant literature again and look at the limitations of the study. The peer reviewers were open, clear in the instructions and the editorial team was very prompt in their communication. This journal certainly publishes quality research articles. I would recommend the journal for any future publications.
Dear Jessica Magne, with gratitude for the joint work. Fast process of receiving and processing the submitted scientific materials in “Clinical Cardiology and Cardiovascular Interventions”. High level of competence of the editors with clear and correct recommendations and ideas for enriching the article.
We found the peer review process quick and positive in its input. The support from the editorial officer has been very agile, always with the intention of improving the article and taking into account our subsequent corrections.
