Статті в журналах: "Cancer neuroendocrine"

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Palomares Casasús, Sara, Marcos Rolando Adrianzén, Maria Luisa Spa, Octavio Burgués, Juan Miguel Cejalvo, Elvira Buch, and Gemma Bellver Lobato. "NEUROENDOCRINE BREAST TUMOUR: A CHALLENGING ENTITY." Annals of Mediterranean Surgery 5 (February 22, 2022): 27–32. http://dx.doi.org/10.22307/2603.8706.2022.01.005.

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NEUROENDOCRINE BREAST TUMOUR: A CHALLENGING ENTITY TUMOR NEUROENDOCRINO DE MAMA: UNA ENTIDAD DESAFIANTE Neuroendocrine breast carcinoma is a rare type of breast cancer with neuroendocrine differentiation which is found in around 2-5% of all invasive breast carcinomas. In most cases it is a challenge to get to the right diagnosis due to the sporadic number of cases and the need for special immunochemistry techniques, which are not routinely used. Due to the rare number of cases, it is difficult to update guidelines so that the correct diagnosis and treatment is decided. Our purpose is to present a clinical case in order to emphasize the importance of having this diagnosis in mind when breast cancer is found.

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Miura, Kentaro, Kimihiro Shimizu, Shogo Ide, Shuji Mishima, Shunichiro Matsuoka, Tetsu Takeda, Takashi Eguchi, Kazutoshi Hamanaka, and Takeshi Uehara. "A Novel Strategy for the Diagnosis of Pulmonary High-Grade Neuroendocrine Tumor." Diagnostics 11, no. 11 (October 20, 2021): 1945. http://dx.doi.org/10.3390/diagnostics11111945.

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Correctly diagnosing a histologic type of lung cancer is important for selecting the appropriate treatment because the aggressiveness, chemotherapy regimen, surgical approach, and prognosis vary significantly among histologic types. Pulmonary NETs, which are characterized by neuroendocrine morphologies, represent approximately 20% of all lung cancers. In particular, high-grade neuroendocrine tumors (small cell lung cancer and large cell neuroendocrine tumor) are highly proliferative cancers that have a poorer prognosis than other non-small cell lung cancers. The combination of hematoxylin and eosin staining, Ki-67, and immunostaining of classic neuroendocrine markers, such as chromogranin A, CD56, and synaptophysin, are normally used to diagnose high-grade neuroendocrine tumors; however, they are frequently heterogeneous. This article reviews the diagnostic methods of lung cancer diagnosis focused on immunostaining. In particular, we describe the usefulness of immunostaining by Stathmin-1, which is a cytosolic phosphoprotein and a key regulator of cell division due to its microtubule depolymerization in a phosphorylation-dependent manner, for the diagnosis of high-grade neuroendocrine tumors.

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Liu, Jin, Xiaohua Pan, Yan Sun, Tingting Dong, Xiao Hu, Huijuan Zhong, and Jianwei Lu. "Clinicopathological Features and Postoperative Survival Analysis of Gastric Carcinoma with Neuroendocrine Differentiation." Journal of Oncology 2022 (August 17, 2022): 1–9. http://dx.doi.org/10.1155/2022/4440098.

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Objectives. This study aims at investigating the differences of clinicopathological features and postoperative prognosis in three different types of neuroendocrine differentiation-related gastric cancers. Methods. From January 1, 2015 to September 30, 2016, 47 patients diagnosed with neuroendocrine differentiation-related gastric cancers were collected from 1095 patients with gastric cancer who underwent surgical treatment in the Department of Gastrointestinal Surgery, Jiangsu Cancer Hospital. Patients were followed up regularly, and the last follow-up time was October 25, 2021. A total of 38 cases met the inclusion criteria and completed follow-up. The clinicopathological characters and immunohistochemical results of these three special pathological types of gastric cancer (adenocarcinoma with neuroendocrine differentiation, mixed adenoneuroendocrine carcinoma, and neuroendocrine carcinoma of the stomach) patients were compared. Tissues from these patients were tested with immunohistochemical markers synaptophysin (Syn), chromogranin A (CgA), and Ki-67. The Kaplan–Meier method and log-rank test were used to analyze the effect of different histological types of gastric cancer on overall survival (OS). The differences in positive rates of chromogranin A (CgA) and Ki-67 were analyzed by univariate Cox regression analysis as independent risk factors that may affect the survival of gastric cancer patients. Results. Ki-67 and N staging were significantly correlated with OS in gastric cancer patients and were independent prognostic factors affecting the survival of gastric cancer patients. There was no statistical difference in OS between the two histopathological types (adenocarcinoma with neuroendocrine differentiation and mixed adenoneuroendocrine carcinoma) of gastric cancer patients. There were no significant differences in the positive rates of immunohistochemical markers Syn, CgA, and Ki-67 in gastric cancer patients with different histological types. Conclusion. The combined detection of Syn and CgA is of great value for the diagnosis of neuroendocrine differentiation-related gastric cancers, Ki-67 is of significance for the prognosis prediction of neuroendocrine differentiation-related gastric cancers, regional lymph node metastasis has a great impact on tumor prognosis, and the N staging determines the necessity of postoperative adjuvant chemotherapy for patients with neuroendocrine differentiation-related gastric cancer.

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Sheikh, Rabeeta, Irfan Haider, Muhammad Sohaib Nadeem, Jawad Latif, Kiran Inam, and Muhammad Fawad UL Qamar. "Neuroendocrine Breast Carcinoma: a Case Series." Pakistan Armed Forces Medical Journal 73, no. 5 (October 30, 2023): 1404–6. http://dx.doi.org/10.51253/pafmj.v73i5.9418.

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Neuroendocrine breast carcinoma (NEBC) is histologically a rare type of invasive breast cancer. It constitutes only 0.2–0.5% of all invasive breast cancers. In this case series, we are presenting five cases having primary neuroendocrine breast cancers that had been reported at a high-volume cancer centre in Pakistan. In this study, neuroendocrine breast cancer patients at Shaukat Khanum Memorial Cancer Hospital and Research Centre Peshawar were evaluated. We had retrospectively collected information on demographic characteristics of our patients, physical examination, radiological findings, surgical procedures with their outcomes, histopathological and immuno-histochemical characteristics, systemic adjuvant/neoadjuvant therapy and follow-up.

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Bajetta, Emilio, Laura Catena, Monika Ducceschi, Sara Pusceddu, Massimo Milione, Marco Maccauro, Roberto Bajetta, et al. "Pitfalls in the Diagnosis of Neuroendocrine Tumors: Atypical Clinical and Radiological Findings as Cause of Medical Mistakes." Tumori Journal 95, no. 4 (July 2009): 501–7. http://dx.doi.org/10.1177/030089160909500416.

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Aims and background Carcinoids are infrequent neoplasms arising from neuroendocrine cells. Due to blurred symptoms and the presence of equivocal diagnostic findings, these tumors are sometimes misdiagnosed. Therefore, increased rates of false neuroendocrine tumors represent an emerging problem in clinical practice. Our aim is to alert clinicians on this matter by supplying them with useful warnings. Methods In the specialized neuroendocrine tumor study Center Centro di Riferimento per lo Studio e la Cura dei Carcinoidi e dei Tumori Neuroendocrini (Ce.Ri.Ca), some patients highly suspected to have a neuroendocrine tumor have been recognized as having false neuroendocrine tumors. The related clinical and instrumental findings leading to a previous wrong neuroendocrine tumor diagnosis are reported. Results From July 2006 to December 2008, 88 consecutive cases of neuroendocrine tumors (Nets) were referred at Ce.Ri.Ca. In the former group, 8 cases of false Nets were discovered while in the remaining 80 cases a correct Net diagnosis was carried out. Watchful differential diagnoses and skill appraisal of laboratory investigations resulted in: chronic atrophic gastritis with enterochromaffin-like cell hyperplasia (4 cases), estrogen-deprivation syndrome (1), hypochondriac disorder (1), metabolic syndrome (1), and sarcoidosis (1). Conclusions Neuroendocrine tumors are still relatively known clinical entities. To discriminate false neuroendocrine tumors from neuroendocrine tumors requires a good expertise and a large daily practice with the disease. Good knowledge and skillfulness in identifying biochemical alterations and false radiological positive results could avoid both patient inconvenience and very expensive workup. The importance of a multidisciplinary approach in specialized centers is emphasized.

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Tsedenova, K. O., M. I. Komarov, V. B. Matveev, and A. D. Panakhov. "Neuroendocrine urethral cancer." Experimental and Сlinical Urology 11, no. 2 (July 29, 2019): 38–42. http://dx.doi.org/10.29188/2222-8543-2019-11-2-38-42.

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Graca, S., J. Esteves, S. Costa, S. Vale, and J. Maciel. "Neuroendocrine breast cancer." Case Reports 2012, aug09 1 (August 13, 2012): bcr1220115343. http://dx.doi.org/10.1136/bcr.12.2011.5343.

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Safina, S. Z., and A. Z. Isyangulova. "Neuroendocrine prostate cancer." Cancer Urology 19, no. 2 (August 12, 2023): 94–100. http://dx.doi.org/10.17650/1726-9776-2023-19-2-94-100.

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In Russia, prostate cancer is a common disease with fast increasing incidence. In the vast majority of prostate cancer patients receiving hormone therapy, on average 18–36 months after the start of treatment refractoriness to androgen ablation develops. In 15–20 % of patients, signs of neuroendocrine differentiation may develop.Neuroendocrine prostate cancer is an aggressive variant of castration-resistant prostate cancer with poor prognosis and low survival.Due to the rarity of these types of tumors, specific diagnostic and treatment algorithms have not been developed. As a rule, they are similar to the methods for other malignant forms of prostate cancer and neuroendocrine tumors.

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Siddeek, Rohik Anjum T., Amit Gupta, Krishna Bhukya Sai, Edem Sanketh, Deepak Rajput, Sweety Gupta, and Ravi Hari Phulware. "Mixed squamous – neuroendocrine carcinoma of the gallbladder: A case report of a rare pathological entity." Cancer Research, Statistics, and Treatment 7, no. 1 (2024): 121–25. http://dx.doi.org/10.4103/crst.crst_186_23.

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Gallbladder cancers are the most common biliary tract malignancies in the world. Adenocarcinoma constitutes the most common histology in gallbladder cancer. Neuroendocrine neoplasms of the gallbladder account for about 0.5% of all neuroendocrine neoplasms and 2.1% of all gallbladder tumors. They are rare tumors and present with non-specific symptoms such as abdominal pain, weight loss, anorexia, and obstructive jaundice, and, therefore, are often challenging to diagnose and treat. Mixed neuroendocrine-non-neuroendocrine neoplasm is a subtype of neuroendocrine neoplasm. To add to the literature, we report a rare case of a patient who presented with pain in the abdomen and non-bilious vomiting and was diagnosed with mixed neuroendocrine-non-neuroendocrine gallbladder cancer, identified by immunohistochemistry, and treated with palliative chemotherapy. Due to non-specific symptoms, patients may present at an advanced stage. Further, immunohistochemistry may assist in clinching the diagnosis.

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Hsu, En-Chi, Meghan A. Rice, Abel Bermudez, Fernando Jose Garcia Marques, Merve Aslan, Shiqin Liu, Ali Ghoochani, et al. "Trop2 is a driver of metastatic prostate cancer with neuroendocrine phenotype via PARP1." Proceedings of the National Academy of Sciences 117, no. 4 (January 13, 2020): 2032–42. http://dx.doi.org/10.1073/pnas.1905384117.

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Resistance to androgen deprivation therapy, or castration-resistant prostate cancer (CRPC), is often accompanied by metastasis and is currently the ultimate cause of prostate cancer-associated deaths in men. Recently, secondary hormonal therapies have led to an increase of neuroendocrine prostate cancer (NEPC), a highly aggressive variant of CRPC. Here, we identify that high levels of cell surface receptor Trop2 are predictive of recurrence of localized prostate cancer. Moreover, Trop2 is significantly elevated in CRPC and NEPC, drives prostate cancer growth, and induces neuroendocrine phenotype. Overexpression of Trop2 induces tumor growth and metastasis while loss of Trop2 suppresses these abilities in vivo. Trop2-driven NEPC displays a significant up-regulation of PARP1, and PARP inhibitors significantly delay tumor growth and metastatic colonization and reverse neuroendocrine features in Trop2-driven NEPC. Our findings establish Trop2 as a driver and therapeutic target for metastatic prostate cancer with neuroendocrine phenotype and suggest that high Trop2 levels could identify cancers that are sensitive to Trop2-targeting therapies and PARP1 inhibition.

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Saeed, Mirza Farad, Isam Mazin Juma, Roshan George Varkey, Keith Pappachen Mathew, and Maryam Abdollah Kamali. "Rare presentation of metastasized primary neuroendocrine breast carcinoma to the right colon and literature review of primary neuroendocrine breast carcinoma metastasized to other organs of the body: case report." International Surgery Journal 7, no. 12 (November 27, 2020): 4188. http://dx.doi.org/10.18203/2349-2902.isj20205381.

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Primary neuroendocrine breast tumors account for less than 0.1% of all breast cancers, hence, unique in nature. This paper aims to report a 56 years old female, known case of primary neuroendocrine breast cancer with a metastatic right colonic neuro-endocrine tumor. The article also aims to review and acclaim the literature regarding primary breast neuroendocrine tumors metastasized to other parts of the body. The patient presented complaining of a breast mass, ulceration, and discharge, which was rapidly progressing. Examination revealed a right breast mass with skin erythema and impending ulceration and right axillary lymph nodes fixed with palpable supra-clavicular lymph nodes. Ultrasound-guided biopsy of right breast mass and axilla disclosed a large cell neuroendocrine carcinoma. CT abdomen and chest revealed metastases to the ascending colon. The patient was treated with palliative radiotherapy along with multiple cycles of chemotherapy for the primary breast cancer. She also underwent a laparoscopic-assisted right hemicolectomy with complete mesocolic excision and primary anastomosis for the metastatic colon cancer. The paper compares the reported case to other similar cases using the framework of an analysis based on age of the patient, primary breast cancer location, method of detection, presence of neuroendocrine markers, primary cancer presentation, metastases symptoms, and location and treatment approach. In conclusion, metastasized primary neuroendocrine breast cancer is a very rare presentation. Incidence and prevalence maybe influenced by age, primary breast cancer location, and presence of neuroendocrine markers. Prognosis may also be a product of metastatic location, associated symptoms and treatment approaches.

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Sivanandhan, Dhanalakshmi, Sridharan Rajagopal, Chandru Gajendran, Naveen Sadhu, Mohd Zainuddin, Ramachandraiah Gosu, and Luca Rastelli. "Abstract B029: LSD1-HDAC6 dual inhibitor JBI-802 is an epigenetic modulating agent with a novel mechanism of action that target MYC amplification in multiple neuroendocrine tumor types." Cancer Research 82, no. 23_Supplement_2 (December 1, 2022): B029. http://dx.doi.org/10.1158/1538-7445.cancepi22-b029.

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Abstract MYC is considered a master regulator of human cancers by modulating the transcription of numerous cancer-related genes. MYC amplification is reported in about 15% of all human cancers and is generally associated with poor prognosis and resistance to treatments. Focal amplification of MYC together with mutation in RB1 and p53 is an important event in the metastatic process of neuroendocrine tumor development. While limited options are available for direct targeting, transcriptional modulation via epigenetic modulating agent could be an attractive and viable option to target neuroendocrine cancers. JBI-802 inhibits the transcriptional regulator coREST via its component LSD1/HDAC6 therefore blocking neuroendocrine transdifferentiation and inducing cell death resulting in activity against neuroendocrine tumors. At the same time, this molecule has shown a good safety profile in toxicological studies. We have now identified a novel aspect of JBI-802 mechanism of action, the ability to induce downregulation of MYC RNA and degradation of MYC protein both in vitro and in animal models of two neuroendocrine tumors, small cell lung cancer and neuroendocrine prostate cancer JBI-802 showed significant anti-proliferative activity (0.2 to 1 µM) against several cancer cell lines as shown by Alamar blue or CTG assays. Sensitive ones included small cell lung cancer (SCLC), gastric cancer, breast cancer cell lines with RB1 mutation. Interestingly, dual inhibitor JBI-802 was also active in cell lines with MYC over-expression, while LSD1 selective inhibitors have been reported to be inactive in these cell lines. JBI-802 also inhibited MYC at RNA as well as protein level in hematological and solid tumors as assessed by RT-qPCR at RNA level and by Western blotting at protein level, while single agent LSD1 and HDAC6 inhibitors did not show significant modulation. JBI-802 also showed strong tumor growth inhibition of these tumors in mouse xenograft models. MYC levels showed a dose dependent inhibition in these tumors when tested at the end of the study. Only dual inhibition of both LSD1/HDAC6 with JBI-802 as opposed to single target inhibition is able to effectively downregulate MYC level and achieve efficacy in MYC amplified models in vivo and in vitro. This novel mechanism increases the potential population of neuroendocrine patients that could be sensitive to this compound, going beyond the proof of principle already established preclinically and clinically by single target LSD1 inhibitors. Therefore, by targeting 2 major pathways in neuroendocrine tumor development, JBI-802 novel mechanism of action is uniquely suited for the treatment of high unmet neuroendocrine tumors like small cell lung cancer, neuroendocrine prostate cancer and advanced, MYC amplified tumors. Based on this rationale, JBI-802 is being tested in phase 1/2 clinical trial focus on this type of tumors. Citation Format: Dhanalakshmi Sivanandhan, Sridharan Rajagopal, Chandru Gajendran, Naveen Sadhu, Mohd Zainuddin, Ramachandraiah Gosu, Luca Rastelli. LSD1-HDAC6 dual inhibitor JBI-802 is an epigenetic modulating agent with a novel mechanism of action that target MYC amplification in multiple neuroendocrine tumor types. [abstract]. In: Proceedings of the AACR Special Conference: Cancer Epigenomics; 2022 Oct 6-8; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2022;82(23 Suppl_2):Abstract nr B029.

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Amin, Sapna Vinit, Aswathy Kumaran, Sunanda Bharatnur, Akhila Vasudeva, Kartik Udupa, Dinesh Bangalore Venkateshiah, and Shaila T. Bhat. "Neuroendocrine Cancer of Rectum Metastasizing to Ovary." Case Reports in Oncological Medicine 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/7149821.

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Neuroendocrine carcinomas (NECs) are rare malignancies that originate from the hormone-producing cells of the body’s neuroendocrine system. Rectal high grade NEC (HG-NEC) constituting less than 1% of colorectal cancers can cause large ovarian metastasis that may be the initial presenting complaint. Ovarian Krukenberg tumor from a primary rectal HG-NEC is a very unusual and exceedingly uncommon differential diagnosis for secondary ovarian malignancy. This case report describes one such extremely rare case of a woman who had presented to the gynecology department with features suggestive of ovarian malignancy and was ultimately diagnosed to have Krukenberg tumor originating from neuroendocrine cancer of rectum. We felt this is a good opportunity to spread more light on neuroendocrine neoplasms that are very rare in gynecological practice.

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Rinke, Anja, and Thomas M. Gress. "Neuroendocrine Cancer, Therapeutic Strategies in G3 Cancers." Digestion 95, no. 2 (2017): 109–14. http://dx.doi.org/10.1159/000454761.

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Popescu, Robert, Ovidiu Bratu, Dan Spînu, Dragos Marcu, Catalin Farcaș, Marius Dinu, and Dan Mischianu. "Neuroendocrine differentiation in prostate cancer – a review." Romanian Journal of Military Medicine 118, no. 3 (May 19, 2015): 16–19. http://dx.doi.org/10.55453/rjmm.2015.118.3.3.

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Objectives: This review aims to provide practicing clinicians with the most recent knowledge of the biological nature of prostate cancer especially the information regarding neuroendocrine differentiation. Methods: Review of the literature using PubMed search and scientific journal publications. Results: Much progress has been made towards an understanding of the development and progression of prostate cancer. The prostate is a male accessory sex gland which produces a fraction of seminal fluid. The normal human prostate is composed of a stromal compartment (which contains: nerves, fibroblast, smooth muscle cells, macrophages) surrounding glandular acins – epithelial cells. Neuroendocrine cells are one of the epithelial populations in the normal prostate and are believed to provide trophic signals trough the secretion of neuropeptides that diffuse and influence surrounding epithelial cells. Prostate cancer is the most frequently diagnosed malignancy in men. In prostate cancer, neuroendocrine cells can stimulate growth of surrounding prostate adenocarcinoma cells (proliferation of neighboring cancer cells in a paracrine manner by secretion of neuroendocrine products). Neuroendocrine prostate cancer is an aggressive variant of prostate cancer that commonly arises in later stages of castration resistant prostate cancer. The detection of neuroendocrine prostate cancer has clinical implications. These patients are often treated with platinum chemotherapy rather than with androgen receptor targeted therapies. Conclusion: This review shows the need to improve our knowledge regarding diagnostic and treatment methods of the Prostate Cancer, especially cancer cells with neuroendocrine phenotype.

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Evangelou, Georgios, Ioannis Vamvakaris, Anastasia Papafili, Maximilian Anagnostakis, and Melpomeni Peppa. "Lung NETs and GEPNETs: One Cancer with Different Origins or Two Distinct Cancers?" Cancers 16, no. 6 (March 17, 2024): 1177. http://dx.doi.org/10.3390/cancers16061177.

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Lung neuroendocrine tumors (LNETs) and gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are two distinct types of neuroendocrine tumors (NETs) that have traditionally been treated as a single entity despite originating from different sources. Although they share certain phenotypic characteristics and the expression of neuroendocrine markers, they exhibit differences in their microenvironment, molecular mutations, and responses to various therapeutic regimens. Recent research has explored the genetic alterations in these tumors, revealing dissimilarities in the frequently mutated genes, the role of EGFR in carcinogenesis, the presence of transcription factors, and the immunogenicity of the tumor and its microenvironment. Spread Through Air Spaces (STAS), a phenomenon unique to lung carcinomas, appears to play a crucial role in LNET prognosis. These distinctions are also evident in the cascade response of lung and GI tract neuroendocrine tumors to somatostatin analogs, Peptide Receptor Radionuclide Therapy (PRRT), chemotherapy, and immunotherapy. Identifying similarities and differences between the two groups may improve our understanding of the underlying mechanisms and facilitate the development of more effective treatment strategies.

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Adams, R. W., P. Dyson, and L. Barthelmes. "Neuroendocrine breast tumours: Breast cancer or neuroendocrine cancer presenting in the breast?" Breast 23, no. 2 (April 2014): 120–27. http://dx.doi.org/10.1016/j.breast.2013.11.005.

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Alami, Zenab, Sara Amrani Joutei, Samiya Mhirech, Amina Bouziane, M. Yessoufou, Wissal Hassani, Fatima Zahrae Farhane, and Touria Bouhafa. "LA PRISE EN CHARGE DES TUMEURS NEURO ENDOCRINES DU COL UTERIN : A PROPOS DUN CAS ET UNE REVUE DE LA LITTERATURE." International Journal of Advanced Research 9, no. 11 (November 30, 2020): 734–38. http://dx.doi.org/10.21474/ijar01/13797.

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Les tumeurs neuroendocrines sont une entite rare des tumeurs du tractus genital feminin, elles representent 1,4% de tous les cancers invasifs du col de luterus. Ce sont des tumeurs rares, de mauvais pronostic. Les options therapeutiques sont souvent extrapolees a partir du cancer du poumon a petites cellules et detudes retrospectives limitees. Le traitement prefere est une approche multimodale associant chirurgie, radiotherapie et traitement systemique. Nous rapportons le cas dune patiente traitee pour une tumeur neuroendocrine du col uterin au service de radiotherapie du Centre Hospitalier Universitaire Hassan II de FES.

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Wilson, Elizabeth M., Youngman Oh, Vivian Hwa, and Ron G. Rosenfeld. "Interaction of IGF-Binding Protein-Related Protein 1 with a Novel Protein, Neuroendocrine Differentiation Factor, Results in Neuroendocrine Differentiation of Prostate Cancer Cells." Journal of Clinical Endocrinology & Metabolism 86, no. 9 (September 1, 2001): 4504–11. http://dx.doi.org/10.1210/jcem.86.9.7845.

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Neuroendocrine cells have been implicated in many cancers, including small cell lung, cervical, breast, and prostate carcinomas. The increase in neuroendocrine cell number in prostate cancer has been reported to correlate with poor prognosis, progressive tumors, and androgen insensitivity. The mechanisms involved in this differentiation remain unknown. IGF-binding protein-related protein 1 is a member of the IGF-binding protein superfamily and has recently been shown to exhibit differentiation and tumor suppression activity in prostate cancer cell lines stably overexpressing IGF-binding protein-related protein 1. From a yeast two-hybrid screen, a novel IGF-binding protein-related protein 1-interacting protein was identified. Immunocytochemical techniques indicate that this protein, 25.1, and intracellular IGF-binding protein-related protein 1 colocalize in the nucleus. When 25.1 is transiently expressed in a stable prostate cancer cell line overexpressing IGF-binding protein-related protein 1, cells assume a neuritic-like morphology with long dendritic-like processes and express the neuroendocrine markers chromogranin A and neuron-specific enolase. We propose that 25.1 (neuroendocrine differentiation factor) together with IGF-binding protein-related protein 1 can induce neuroendocrine cell differentiation in prostate cancer cells.

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Ozsoy, Mehmet Sait, Hakan Baysal, Fatih Buyuker, Begumhan Baysal, Gozde Kir, and Orhan Alimoglu. "Neuroendocrine Carcinoma of the Breast: Report of A Case." Medical Science and Discovery 10, no. 5 (May 27, 2023): 357–60. http://dx.doi.org/10.36472/msd.v10i5.950.

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Objective: Breast cancer is the most prevalent malignant disease among women and ranks among the top three most common cancers globally, alongside lung and colon cancer. Various subtypes of breast cancer have been identified. Primary neuroendocrine breast cancer, a rare and distinct type of breast carcinoma, lacks specific radiological findings. The definitive diagnosis is achieved through the expression of Synaptophysin and Chromogranin A on tumor biopsy, and it necessitates the absence of tumor detection in other regions. Staging and treatment are recommended to follow a similar approach as that of conventional breast cancer. It is believed that the prognosis of neuroendocrine breast tumors is generally poorer compared to invasive cancers.

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Khanam, Razwana, Pranali Santhoshini Pachika, Payam Arya, Jason Bierenbaum, Kevin Kane, and Proshikha Saha. "“A Tale of 2 Demons”—Concomitant Presence of Hepatocellular Carcinoma and Primary Neuroendocrine Tumor of Liver: A Case Report and Review of Literatures." Journal of Investigative Medicine High Impact Case Reports 9 (January 2021): 232470962110433. http://dx.doi.org/10.1177/23247096211043397.

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Neuroendocrine tumors usually originate from the neuroendocrine cells of gastrointestinal tract and their presence in the liver is mostly in the form of metastases. A primary neuroendocrine tumor in the liver concomitantly with hepatocellular carcinoma is an infrequent phenomenon. We present a 66-year-old woman with a remote history of breast cancer coming with postprandial fullness, later found to have multiple liver masses. After a thorough investigation, she was found to have a combined type of hepatocellular and primary neuroendocrine tumor of liver with pulmonary metastases. She was not a surgical candidate due to distant metastases. She was treated with chemotherapy, immunotherapy, and targeted therapies but continued to deteriorate clinically, and finally succumbed to her illness. The presence of this combined type of tumor in our patient is unique in many different ways: It is extremely rare, she did not have any risk factors for liver cancer, no genetic mutation till date could tie all these cancers (breast cancer, neuroendocrine tumor, and hepatocellular carcinoma) together, and not a lot of literatures/studies performed on this illness.

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Wiesehöfer, Marc, Elena Dilara Czyrnik, Martin Spahn, Saskia Ting, Henning Reis, Jaroslaw Thomas Dankert, and Gunther Wennemuth. "Increased Expression of AKT3 in Neuroendocrine Differentiated Prostate Cancer Cells Alters the Response Towards Anti-Androgen Treatment." Cancers 13, no. 3 (February 2, 2021): 578. http://dx.doi.org/10.3390/cancers13030578.

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Patients with advanced prostate carcinoma are often treated with an androgen deprivation therapy but long-term treatment can result in a metastatic castration-resistant prostate cancer. This is a more aggressive, untreatable tumor recurrence often containing areas of neuroendocrine differentiated prostate cancer cells. Using an in vitro model of NE-like cancer cells, it could previously be shown that neuroendocrine differentiation of LNCaP cells leads to a strong deregulation of mRNA and miRNA expression. We observe elevated RNA and protein levels of AKT Serine/Threonine Kinase 3 (AKT3) in neuroendocrine-like LNCaP cells. We used prostate resections from patients with neuroendocrine prostate cancer to validate these results and detect a co-localization of neuroendocrine marker genes with AKT3. Analysis of downstream target genes FOXO3A and GSK3 strengthens the assumption AKT3 may play a role in neuroendocrine differentiation. Overexpression of AKT3 shows an increased survival rate of LNCaP cells after apoptosis induction, which in turn reflects the significance in vivo or for treatment. Furthermore, miR-17, −20b and −106b, which are decreased in neuroendocrine-like LNCaP cells, negatively regulate AKT3 biosynthesis. Our findings demonstrate AKT3 as a potential therapeutic target and diagnostic tool in advanced neuroendocrine prostate cancer and a new mRNA–miRNA interaction with a potential role in neuroendocrine differentiation of prostate cancer.

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Khakimov, G. A., G. G. Khakimova, S. F. Dallo, Sh G. Khakimova, and A. M. Khakimov. "Neuroendocrine prostate cancer (clinical case)." Medical alphabet, no. 27 (December 16, 2024): 55–59. https://doi.org/10.33667/2078-5631-2024-27-55-59.

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Neuroendocrine prostate cancer is a rare and aggressive cancer with a poor prognosis. This type of cancer is often diagnosed at an advanced stage and exhibits rapid resistance to standard therapeutic methods. Taking into account the low occurrence of this phenomenon, a description of poorly differentiated neuroendocrine (small cell) prostate cancer with extremely aggressive forms is given.

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Shimomura, Tatsuya, Takashi Kurauchi, Keigo Sakanaka, Takahiro Kimura, and Shin Egawa. "Clinical investigation of neuroendocrine differentiation in prostate cancer." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 138. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.138.

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138 Background: Neuroendocrine prostate cancer (NEPC) is a lethal disease subset with median overall survival of less than 1 year from time of detection. The treatment strategy against NEPC is not yet established and some clinical trials are ongoing now. Recently, clinical trial (RADIIANT4) showed that treatment with everolimus was associated with significant improvement in survival in patients with progressive lung or gastrointestinal neuroendocrine tumors. In this study we evaluated the neuroendocrine differentiation of prostate cancer and we tried to introduce everolimus against pathologically proven NEPC and investigated the clinical outcomes of this agent. Methods: Total of 193 prostate cancer cases were included in this study. We tested serum neuroendocrine markers, including (NSE and pro-GRP). And we evaluated positive rate of these markers. Eleven cases were pathologically proven neuroendocrine prostate cancer (NEPC) in this cohort. Seven out of eleven NEPC cases were introduced everolimus 10mg daily. We investigated the change of serum neuroendocrine markers (NSE and pro-GRP), radiologic examination and survival. Results: The positive rate of serum neuroendocrine markers (at least one of the markers increasing above normal limit) were 23.5% in hormone sensitive prostate cancer (HSPC), 59.5% in castration resistant prostate cancer (CRPC), and 100% in neuroendocrine prostate cancer (NEPC). There were significant differences in each other (HSPC vs. CRPC: p=0.0001, CRPC vs. NEPC: p=0.0109). We introduced everolimus in seven cases out of eleven NEPC cases. The median follow up period was 18 months. Neuroendocrine markers decreased in five of seven (71.4%) cases after introduction of everolimus. Median decreasing rate were 67.1% in NSE and 65.5% in pro GRP. 24M progression free survival rate was 57.1% and 24M overall survival rate was 57.1%. Conclusions: There is a possibility that the incidence of NEPC is higher than expected, and treatment against prostate adenocarcinoma accelerate neuroendocrine differentiation. Everolimus showed efficacy against NEPC. Although this study was retrospective and number of cases was limited, everolimus would be a one of the treatment options against NEPC.

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Sun, M. H. "Neuroendocrine Differentiation in Sporadic CRC and Hereditary Nonpolyosis Colorectal Cancer." Disease Markers 20, no. 4-5 (2004): 283–88. http://dx.doi.org/10.1155/2004/379053.

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Extent neuroendocrine differentiation can be encountered in many human neoplasm derived from different organs and systems using immunohistochemistry and ultrastructural techniques. The tumor cells' behaviors resemble those of neurons and neuroendocrine cells. The presence of neuroendocrine differentiation reputedly appears to be associated with a poorer prognosis than the adenocarcinoma counterparts in sporadic human neoplasm. In this review the neuroendocrine carcinoma and the adenocarcinoma with neuroendocrine differentiation of colon and rectum both in sporadic colorectal carcinoma and the hereditary nonpolyposis colorectal cancer, the relationship of neuroendocrine differentiation and some possible molecular pathways in tumorogenesis of colorectal cancer will be discussed. Possible treatment strategy will also be addressed.

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Gustafsson, Björn I., Mark Kidd, and Irvin M. Modlin. "Neuroendocrine tumors of the diffuse neuroendocrine system." Current Opinion in Oncology 20, no. 1 (January 2008): 1–12. http://dx.doi.org/10.1097/cco.0b013e3282f1c595.

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Kaarijärvi, Roosa, Heidi Kaljunen, and Kirsi Ketola. "Molecular and Functional Links between Neurodevelopmental Processes and Treatment-Induced Neuroendocrine Plasticity in Prostate Cancer Progression." Cancers 13, no. 4 (February 9, 2021): 692. http://dx.doi.org/10.3390/cancers13040692.

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Neuroendocrine plasticity and treatment-induced neuroendocrine phenotypes have recently been proposed as important resistance mechanisms underlying prostate cancer progression. Treatment-induced neuroendocrine prostate cancer (t-NEPC) is highly aggressive subtype of castration-resistant prostate cancer which develops for one fifth of patients under prolonged androgen deprivation. In recent years, understanding of molecular features and phenotypic changes in neuroendocrine plasticity has been grown. However, there are still fundamental questions to be answered in this emerging research field, for example, why and how do the prostate cancer treatment-resistant cells acquire neuron-like phenotype. The advantages of the phenotypic change and the role of tumor microenvironment in controlling cellular plasticity and in the emergence of treatment-resistant aggressive forms of prostate cancer is mostly unknown. Here, we discuss the molecular and functional links between neurodevelopmental processes and treatment-induced neuroendocrine plasticity in prostate cancer progression and treatment resistance. We provide an overview of the emergence of neurite-like cells in neuroendocrine prostate cancer cells and whether the reported t-NEPC pathways and proteins relate to neurodevelopmental processes like neurogenesis and axonogenesis during the development of treatment resistance. We also discuss emerging novel therapeutic targets modulating neuroendocrine plasticity.

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Fiorito, C., I. Lucca, M. Oderda, P. Mondino, G. Berta, E. A. Cattaneo, F. Valentino, A. Zitella, D. Pacchioni, and A. Tizzani. "Neuroendocrine bladder cancer: oncological emergency?" Urologia Journal 75, no. 1 (January 2008): 57–61. http://dx.doi.org/10.1177/039156030807500111.

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Neuroendocrine bladder cancer is extremely rare, with an estimated incidence of 0.5%- 0.7%. In bladder cancers there is no evident connection between the neuroendocrine phenotypic expression and the clinical history. However, prognosis is usually poor and the survival rate at 5 years does not exceed 8%, if untreated. Methods. We are here describing three case reports of bladder carcinoma with neuroendocrine differentiation, which is extremely aggressive and leads rapidly to death. At the present time, the local control of these tumors is achieved by radical cystectomy and radiotherapy; they can be both associated to chemotherapy. However, since these lesions are fairly rare, there is no gold standard therapy and there are no prospective studies on the management of these tumors. Conclusions. Considering the quick evolution and progression of any variant of the neuroendocrine tumors of the bladder, urologists and anesthetists should see them as real oncological emergencies. A prompt intervention through radical surgery with cystectomy and linfadenectomia, and the anathomo-pathologist's systematic investigation of the scraps could make the approach therapeutic and not only palliative. Prospective studies on neo-adjuvant chemotherapy as well as experimental studies about target therapies may yield new guidelines on the tumor management.

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Pankratjevaite, Lina, Mette Holmqvist, Amuras Samulionis, and Ute Hoyer. "Rare case of primary small-cell neuroendocrine breast carcinoma." BMJ Case Reports 14, no. 4 (April 2021): e237474. http://dx.doi.org/10.1136/bcr-2020-237474.

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Small-cell breast cancer is a very rare and aggressive type of neuroendocrine carcinoma. Histologically, it is indistinguishable from small-cell neuroendocrine lung cancer. Due to that, patients with small-cell neuroendocrine breast cancer should undergo examination of other areas of the body. Small-cell breast cancer may be treated with a combination of surgery, radiation therapy and chemotherapy. However, no standard treatment exists due to the small number of cases. We present a case of a 49-year-old woman with right breast primary small-cell neuroendocrine carcinoma.

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Abbasova, Daria V., Svetlana B. Polikarpova, Nikolai A. Kozlov, Madina P. Baranova, Irina P. Kovalenko, and Elena I. Ignatova. "Neuroendocrine carcinoma of the prostate (review of the literature)." Journal of Modern Oncology 21, no. 3 (September 15, 2019): 52–55. http://dx.doi.org/10.26442/18151434.2019.3.190673.

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Neuroendocrine neoplasia (NEC) of the prostate gland is a rather rare extrapulmonary neuroendocrine carcinoma and makes up only 0.5 to 1% of all malignant neoplasms of this localization. NEC of the prostate gland is a tumor of epithelial origin, histologically and immunohistochemically identical to analogues in the lungs and digestive system. When stained with hemotoxylin-eosin, neuroendocrine cells cannot always be visualized; they are best recognized by the immunohistochemical method of investigation using specific markers. Currently, a number of neuroendocrine markers are used, the expression of which may indicate a neuroendocrine nature. Androgen neuroendocrine cells themselves are independent and do not cause an increase in the concentration of prostate-specific antigen. Prostate NECs are represented by some histological forms according to WHO classification (2015): 1. Adenocarcinoma with focal neuroendocrine differentiation. 2. Well-differentiated neuroendocrine tumor. 3. Small cell neuroendocrine cancer is a high - grade tumor with high malignant potential. 4. Large cell neuroendocrine cancer is a high - grade tumor. Due to the rarity of NEC of the prostate, a specific algorithm for diagnosis and treatment has not been developed, as a rule, they are similar to methods of other malignant forms of prostate cancer and neuroendocrine tumors.

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Berman-Booty, Lisa D., and Karen E. Knudsen. "Models of neuroendocrine prostate cancer." Endocrine-Related Cancer 22, no. 1 (October 27, 2014): R33—R49. http://dx.doi.org/10.1530/erc-14-0393.

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Prostate cancer remains the second leading cause of cancer death in men in the USA and most western countries. Prostatic acinar adenocarcinoma is the most commonly diagnosed form of prostate cancer. Small-cell neuroendocrine carcinoma is less frequently identified at the time of initial diagnosis, but this highly aggressive form of prostate cancer is increasingly observed in patients who have failed first- and second-line hormone therapy. Thus, developing and exploring models of neuroendocrine prostate cancer (NePC) are of increasing importance. This review examines the relevant xenograft tumor and genetically engineered mouse models of NePC, with the aim of addressing salient features and clinical relevance.

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Wenzel, Mike, Claudia Collà Ruvolo, Christoph Würnschimmel, Luigi Nocera, Benedikt Hoeh, Zhe Tian, Fred Saad, et al. "Epidemiology of Unconventional Histological Subtypes of Urethral Cancer." Urologia Internationalis 107, no. 1 (July 26, 2022): 15–22. http://dx.doi.org/10.1159/000525673.

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Introduction: The aim of the study was to examine cancer-specific mortality (CSM) of unconventional urethral cancers. Methods: Within the SEER (2004–2016) database, we analyzed CSM of 165 patients with unconventional urethral-cancer histology. Kaplan-Meier plots were used to test the effect of unconventional histologies in urethral cancer on CSM. Results: Of 165 eligible patients, the Mullerian type accounted for 55 (33.3%) versus melanocytic (26.7%) versus neuroendocrine 25 (15.2%) versus lymphoma 22 (13.3%) versus mesenchymal/sarcoma 15 (9.1%) versus spindle cell 4 (2.1%) patients. Median age at diagnosis was 81 years in spindle cell, 75 in melanocytic, 74 in neuroendocrine and mesenchymal/sarcoma, 67 in lymphoma, and 62 years Mullerian type (p < 0.001). Of all, 116 (70.3%) were female. The Mullerian type exhibited the highest female ratio (96.4%) versus the lowest female ratio in neuroendocrine (24.0%). The Mullerian type was most frequent in African-American females. In Caucasian females, the melanocytic type was most frequent (49.1%). In African-American (38.9%) and Caucasian males (33.3%), neuroendocrine histology was most frequent. Three-year CSM was, respectively, 27.5%, 23.1% 22.3%, 20.5%, and 16.1% for melanocytic, mesenchymal/sarcoma, Mullerian type, neuroendocrine, and lymphoma histology. Median cancer-specific survival was 106 versus 10 months for combined nonmetastatic versus metastatic nonconventional histologies. Conclusion: Important age, sex, racial/ethnic group distribution, and survival differences exist between each unconventional urethral-cancer histological subtypes.

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Cristina G, Domingo, and Cornelio Gerardo H. "Mixed Neuroendocrine-Non-neuroendocrine Neoplasm (MiNEN) of the Esophagus: A Case Report." Asian Pacific Journal of Cancer Care 7, no. 4 (November 10, 2022): 755–56. http://dx.doi.org/10.31557/apjcc.2022.7.4.755-756.

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Esophageal cancer incidence rates have been increasing over the past years and survival rates remain low. According to the Global Cancer Observatory, 3.1% of new cancer cases consists of esophageal cancer and 5.5% of deaths was due to esophageal cancer. Histologic classification comprises of either squamous cell carcinoma (SCC) or Adenocarcinoma. Other types are reported to be uncommon. We present a case of 33-year old male admitted due to progressive dysphagia. He underwent esophagogastric resection and histopathologic studies revealed a mixed neuroendocrine- non-neuroendocrine tumor. He received adjuvant chemotherapy. On mid-cycle evaluation, the patient showed no evidence of disease recurrence.

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Samaan, Naguib A. "Neuroendocrine tumors." Current Opinion in ONCOLOGY 2, no. 1 (February 1990): 101–7. http://dx.doi.org/10.1097/00001622-199002000-00016.

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Granberg, Dan, and Kjell Öberg. "Neuroendocrine tumours." Update on Cancer Therapeutics 1, no. 1 (March 2006): 75–84. http://dx.doi.org/10.1016/j.uct.2006.04.007.

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Granberg, Dan, and Kjell Öberg. "Neuroendocrine tumours." Update on Cancer Therapeutics 2, no. 1 (March 2007): 41–52. http://dx.doi.org/10.1016/j.uct.2007.04.001.

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Laface, Carmelo, and Riccardo Memeo. "Clinical Updates for Gastrointestinal Malignancies." Journal of Personalized Medicine 13, no. 9 (September 21, 2023): 1424. http://dx.doi.org/10.3390/jpm13091424.

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Gastrointestinal (GI) cancers include hepatobiliary tumors, pancreatic cancer (PC), neuroendocrine tumors of the gastrointestinal tract, small bowel carcinomas, gastric cancer (GC), anal canal cancer, primary gastric and intestinal lymphomas, gastrointestinal stromal tumors (GISTs) and the most frequent colorectal cancer (CRC) [...]

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Katsetos, Christos D., George Kontogeorgos, Jennian F. Geddes, Mary M. Herman, Hera Tsimara-Papastamatiou, Yunxia Yu, Lazaros I. Sakkas та ін. "Differential Distribution of the Neuron-Associated Class III β-Tubulin in Neuroendocrine Lung Tumors". Archives of Pathology & Laboratory Medicine 124, № 4 (1 квітня 2000): 535–44. http://dx.doi.org/10.5858/2000-124-0535-ddotna.

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AbstractObjective.—To study the immunoreactivity profile of the neuron-associated class III β-tubulin isotype (β III) in epithelial lung tumors.Design.—One hundred four formalin-fixed, paraffin-embedded primary and metastatic lung cancer specimens were immunostained with an anti–β III mouse monoclonal antibody (TuJ1) and an anti–β III affinity-purified rabbit antiserum. Paraffin sections from fetal, infantile, and adult nonneoplastic lung tissues were also examined.Results.—In the fetal airway epithelium, β III staining is detected transiently in rare Kulchitsky-like cells from lung tissues corresponding to the pseudoglandular and canalicular but not the saccular or alveolar stages of development. β III is absent in healthy, hyperplastic, metaplastic, and dysplastic airway epithelium of the adult lung. In contrast, β III is highly expressed in small cell lung cancer, large cell neuroendocrine carcinoma, and in some non–small cell lung cancers, particularly adenocarcinomas. There is no correlation between expression of β III and generic neuroendocrine markers, such as chromogranin A and/or synaptophysin, in pulmonary adenocarcinomas. Also, focal β III staining is present in primary and metastatic adenocarcinomas (to the lung) originating in the colon, prostate, and ovary. β III is expressed to a much lesser extent in atypical carcinoids and is rarely detectable in typical carcinoids and squamous cell carcinomas of the lung. The distribution of β III in small cell lung cancer and adenocarcinoma metastases to regional lymph nodes and brain approaches 100% of tumor cells, which is substantially greater than in the primary tumors.Conclusions.—In the context of neuroendocrine lung tumors, β III immunoreactivity is a molecular signature of high-grade malignant neoplasms (small cell lung cancer and large cell neuroendocrine carcinoma) although its importance in atypical carcinoids must be evaluated further. In addition, β III may be a useful diagnostic marker in distinguishing between small cell lung cancers and certain non–small cell lung cancers (poorly differentiated squamous cell carcinomas), especially in small biopsy specimens. To our knowledge, β III is the only tumor biomarker that exhibits a substantially more widespread distribution in poorly differentiated than in better differentiated pulmonary neuroendocrine tumors. However, the significance of β III phenotypes in non–small cell lung cancer, particularly adenocarcinoma, with respect to neuroendocrine differentiation and prognostic value, requires further evaluation.

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Rindi, Guido, and Frediano Inzani. "Neuroendocrine neoplasm update: toward universal nomenclature." Endocrine-Related Cancer 27, no. 6 (June 2020): R211—R218. http://dx.doi.org/10.1530/erc-20-0036.

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Neuroendocrine neoplasia is described in almost every tissue, either in the pure endocrine organs, the nerve structures or in the so-called diffuse neuroendocrine system. The current nomenclature contains time-honored, widely accepted definitions; however, it is different according to anatomical sites. Diverse definitions may generate confusion and non-standard patient management. The International Agency for Research on Cancer – World Health Organization (IARC-WHO) proposed a framework for universal classification of neuroendocrine neoplasia. Evidence indicates that neuroendocrine cancer is composed by cells with a distinctive phenotype characterized by the expression of general and specific neuroendocrine markers. The neuroendocrine phenotype is indicated as descriptor of a unique cancer category, now recommended for all organs as neuroendocrine neoplasm. Evidence indicates that neuroendocrine neoplasia may be well or poorly differentiated, with diverse incidence and prevalence in different organs. It is proposed that the well-differentiated neoplasm is universally defined as neuroendocrine tumor (NET) and the poorly differentiated as neoplasm neuroendocrine carcinoma (NEC). Evidence indicates that a cancer grading tool based on a proliferation measure by mitotic count, Ki67 % and/or necrosis assessment is useful to predict NET patient behavior. It is proposed to utilize this tool for grading NET universally, with site-specific cut-offs to be defined. It is also acknowledged that significant biological site-specific differences exist. It is recommended that current pathology reports contain this classification together with the current traditional classifiers. This IARC-WHO common classification framework for neuroendocrine neoplasm aims at uniformizing nomenclature toward different organs and at fostering the definition of a similar site-specific gene signature.

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Tsunokake, Junichi, Fumiyoshi Fujishima, Hirofumi Watanabe, Ikuro Sato, Koh Miura, Kazuhiro Sakamoto, Hiroyoshi Suzuki, et al. "Tumor Microenvironment in Mixed Neuroendocrine Non-Neuroendocrine Neoplasms: Interaction between Tumors and Immune Cells, and Potential Effects of Neuroendocrine Differentiation on the Tumor Microenvironment." Cancers 14, no. 9 (April 26, 2022): 2152. http://dx.doi.org/10.3390/cancers14092152.

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The tumor microenvironment is considered to play a pivotal role in various human malignancies. Neuroendocrine and non-neuroendocrine neoplasms are considered to have different tumor microenvironments. However, owing to differences in the systemic and/or local immune statuses, tumor microenvironments in different patients may be difficult to compare. Mixed neuroendocrine non-neuroendocrine neoplasms (MiNENs), although rare, could be useful for exploring the effects of neuroendocrine differentiation on the tumor microenvironment, because both neuroendocrine and non-neuroendocrine components are present in the same tumor. Here, we examined 33 cases of histologically confirmed MiNENs and evaluated the influence of neuroendocrine differentiation on the tumor microenvironment by comparing tumor-infiltrating lymphocytes, tumor-associated macrophages, and other relevant factors in the two components the same tumor. The immunoreactivity of those examined above was evaluated quantitatively. The values of vasohibin-1-positive density (p < 0.0001) and immunoreactivity (p < 0.0001) (representing the neoangiogenesis status) were significantly higher in neuroendocrine as compared to non-neuroendocrine areas of the same tumors. In addition, the Foxp3/CD8 (p = 0.0717) and the PD-1/CD8 ratios (p = 0.0176) (representing tumor immunity suppression) tend to increase in neuroendocrine carcinomas. Immunoreactivity of CD163, a marker of M2-like macrophages, was also higher in the neuroendocrine areas. Our findings indicate that neuroendocrine and non-neuroendocrine tumors differ from each other with respect to the characteristics of both tumor cells and the tumor microenvironment.

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Tsunokake, Junichi, Fumiyoshi Fujishima, Hirofumi Watanabe, Ikuro Sato, Koh Miura, Kazuhiro Sakamoto, Hiroyoshi Suzuki, et al. "Tumor Microenvironment in Mixed Neuroendocrine Non-Neuroendocrine Neoplasms: Interaction between Tumors and Immune Cells, and Potential Effects of Neuroendocrine Differentiation on the Tumor Microenvironment." Cancers 14, no. 9 (April 26, 2022): 2152. http://dx.doi.org/10.3390/cancers14092152.

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Анотація:

The tumor microenvironment is considered to play a pivotal role in various human malignancies. Neuroendocrine and non-neuroendocrine neoplasms are considered to have different tumor microenvironments. However, owing to differences in the systemic and/or local immune statuses, tumor microenvironments in different patients may be difficult to compare. Mixed neuroendocrine non-neuroendocrine neoplasms (MiNENs), although rare, could be useful for exploring the effects of neuroendocrine differentiation on the tumor microenvironment, because both neuroendocrine and non-neuroendocrine components are present in the same tumor. Here, we examined 33 cases of histologically confirmed MiNENs and evaluated the influence of neuroendocrine differentiation on the tumor microenvironment by comparing tumor-infiltrating lymphocytes, tumor-associated macrophages, and other relevant factors in the two components the same tumor. The immunoreactivity of those examined above was evaluated quantitatively. The values of vasohibin-1-positive density (p < 0.0001) and immunoreactivity (p < 0.0001) (representing the neoangiogenesis status) were significantly higher in neuroendocrine as compared to non-neuroendocrine areas of the same tumors. In addition, the Foxp3/CD8 (p = 0.0717) and the PD-1/CD8 ratios (p = 0.0176) (representing tumor immunity suppression) tend to increase in neuroendocrine carcinomas. Immunoreactivity of CD163, a marker of M2-like macrophages, was also higher in the neuroendocrine areas. Our findings indicate that neuroendocrine and non-neuroendocrine tumors differ from each other with respect to the characteristics of both tumor cells and the tumor microenvironment.

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42

Tsunokake, Junichi, Fumiyoshi Fujishima, Hirofumi Watanabe, Ikuro Sato, Koh Miura, Kazuhiro Sakamoto, Hiroyoshi Suzuki, et al. "Tumor Microenvironment in Mixed Neuroendocrine Non-Neuroendocrine Neoplasms: Interaction between Tumors and Immune Cells, and Potential Effects of Neuroendocrine Differentiation on the Tumor Microenvironment." Cancers 14, no. 9 (April 26, 2022): 2152. http://dx.doi.org/10.3390/cancers14092152.

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Анотація:

The tumor microenvironment is considered to play a pivotal role in various human malignancies. Neuroendocrine and non-neuroendocrine neoplasms are considered to have different tumor microenvironments. However, owing to differences in the systemic and/or local immune statuses, tumor microenvironments in different patients may be difficult to compare. Mixed neuroendocrine non-neuroendocrine neoplasms (MiNENs), although rare, could be useful for exploring the effects of neuroendocrine differentiation on the tumor microenvironment, because both neuroendocrine and non-neuroendocrine components are present in the same tumor. Here, we examined 33 cases of histologically confirmed MiNENs and evaluated the influence of neuroendocrine differentiation on the tumor microenvironment by comparing tumor-infiltrating lymphocytes, tumor-associated macrophages, and other relevant factors in the two components the same tumor. The immunoreactivity of those examined above was evaluated quantitatively. The values of vasohibin-1-positive density (p < 0.0001) and immunoreactivity (p < 0.0001) (representing the neoangiogenesis status) were significantly higher in neuroendocrine as compared to non-neuroendocrine areas of the same tumors. In addition, the Foxp3/CD8 (p = 0.0717) and the PD-1/CD8 ratios (p = 0.0176) (representing tumor immunity suppression) tend to increase in neuroendocrine carcinomas. Immunoreactivity of CD163, a marker of M2-like macrophages, was also higher in the neuroendocrine areas. Our findings indicate that neuroendocrine and non-neuroendocrine tumors differ from each other with respect to the characteristics of both tumor cells and the tumor microenvironment.

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43

Pinto, Filipe, and Rui Manuel Reis. "Drivers of neuroendocrine prostate cancer." Translational Cancer Research 5, S3 (September 2016): S551—S553. http://dx.doi.org/10.21037/tcr.2016.09.26.

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44

Amorino, George P., and Sarah J. Parsons. "Neuroendocrine Cells in Prostate Cancer." Critical Reviews in Eukaryotic Gene Expression 14, no. 4 (2004): 14. http://dx.doi.org/10.1615/critreveukargeneexpr.v14.i4.40.

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45

Amorino, George P., and Sarah J. Parsons. "Neuroendocrine Cells in Prostate Cancer." Critical Reviews in Eukaryotic Gene Expression 14, no. 4 (2004): 287–300. http://dx.doi.org/10.1615/critreveukaryotgeneexpr.v14.i4.40.

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46

Cerovic, Snezana, Goran Brajuskovic, Vinka Maletic-Vukotic, and Sava Micic. "Neuroendocrine differentiation in prostate cancer." Vojnosanitetski pregled 61, no. 5 (2004): 513–18. http://dx.doi.org/10.2298/vsp0405513c.

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Background. In numerous recent studies attention has been focused to neuroendocrine differentiation (NED) in prostate cancer (PC). Focal NED is present in almost all PCs, but it is prominent in only 5-10% of the carcinomas. The prognostic significance of focal NED in PC is controversial, but current evidence suggests its influence on the onset and/or conversion of hormon resistant tumor phenotype. The aim of this study was to evaluate the relationship between NED status, based only on immunohistochemical use of neuroendocrine (NE) markers, with PC grade and stage, and preoperative serum levels of prostate-specific antigen (PSA). Methods. The study included the biopsy material of 73 untreated PC patients (pts.) obtained by transurethral resection (TUR) (37 pts.), and radical retropubic prostatectomy (RRP) (36 pts.). Two representative tissue samples (tipically the block containing the largest amount of neoplasm) were selected for immunohistochemical (IMM) staining. NE cells were identified using a panel of IMM markers: chromogranin A, neuron-specific enolase, and serotonin. The level of PC exocrine differentiation was detected by monoclonal antibodies against PSA. Results. Significant expression of NE cells was demonstrated in 26 (70.2%) pts. with PC after TUR. In this group, serum preoperative PSA values ranged from 0.1 to 9.6 ng/ml. The majority of pts. with NED had low differentiated PC with Gleason grade score (GGS) >7, and normal PSA values below 4 ng/ml (77%), in clinical stage D (54%). Statistically significant correlation (p<0.01) of positive NED with higher stage and grade and low PSA values was established. Among the pts. with localized PC in whom RRP was performed (n=36), significant expression of NE cells was found in 15 pts. (41.7%), 8 (53.3%) in pT2 stage, and 7 (46.7%) in pT3 stage. Significant correlation between NED with preoperative PSA values and stage of PC in pts. with RRP was not found. Conclusion. We demonstrated the significant NED in poorly differentiated PC in patients in the advanced stage of the disease. The expression of NED in organ-confined PC did not correlate with tumor stage, but it correlated with tumor grade (GGS?7).

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47

Shariff, Amir H., and M. Hammad Ather. "Neuroendocrine differentiation in prostate cancer." Urology 68, no. 1 (July 2006): 2–8. http://dx.doi.org/10.1016/j.urology.2006.02.002.

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48

Kránitz, Noémi, Zsolt Szepesváry, Károly Kocsis, and Tamás Kullmann. "Neuroendocrine Cancer of the Prostate." Pathology & Oncology Research 26, no. 3 (August 14, 2019): 1447–50. http://dx.doi.org/10.1007/s12253-019-00712-2.

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49

Armaiz-Pena, Guillermo N., Steve W. Cole, Susan K. Lutgendorf, and Anil K. Sood. "Neuroendocrine influences on cancer progression." Brain, Behavior, and Immunity 30 (March 2013): S19—S25. http://dx.doi.org/10.1016/j.bbi.2012.06.005.

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Thaker, Premal H., and Anil K. Sood. "Neuroendocrine influences on cancer biology." Seminars in Cancer Biology 18, no. 3 (June 2008): 164–70. http://dx.doi.org/10.1016/j.semcancer.2007.12.005.

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