Relevant bibliographies by topics / Cancer neuroendocrine

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  2. Dissertations / Theses
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  5. Conference papers
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Academic literature on the topic 'Cancer neuroendocrine'

Author: Grafiati
Published: 11 January 2025

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Journal articles on the topic "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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Dissertations / Theses on the topic "Cancer neuroendocrine"

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Vias, Maria. "Neuroendocrine differentiation in hormone resistant prostate cancer cells." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612330.

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Hanna, Fahmy William Fahmy. "Calcitonin and related peptides in mammalian neuroendocrine tumours." Thesis, Queen's University Belfast, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295357.

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Bryant, Jennifer. "Neuroendocrine and epithelial markers of small cell lung cancer." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/neuroendocrine-and-epithelial-markers-of-small-cell-lung-cancer(c7c51e2c-6443-4021-b2ff-469966cd10b6).html.

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Small cell lung cancer (SCLC) is an extremely aggressive disease characterized by early metastasis and acquired resistance to therapy. SCLC is distinguished by its neuroendocrine (NE) component; the role of which is not fully understood in metastasis and response to therapy. Patients respond exceptionally well to first round chemotherapy; however, relapse with therapy-resistant tumours is virtually inevitable. Hypoxic regions within tumours can contribute towards metastasis and therapy resistance, highlighting hypoxia-targeted therapy as a novel approach for improving treatment for SCLC patients. Tumours are highly phenotypically heterogeneous, raising debate over the roles played by each cell type. Analysis of NE and epithelial markers in SCLC cell lines highlighted this inter-tumour heterogeneity. Further heterogeneity is displayed in SCLC xenograft tumours that show areas of dual epithelial and NE marker expression as well as regions negative for both markers. Irradiating xenograft tumours enhanced heterogeneity of the NE marker, pro-opiomelanocortin (POMC), which is ectopically secreted by a subset of SCLC tumours. Examining changes in marker expression post-therapy could provide vital information regarding transitions that can serve to guide therapy. SCLC is a highly metastatic disease. The role of the NE phenotype in human SCLC is not fully understood, but is considered essential for metastasis in murine models. Sub-cutaneous, intravenous and intra-splenic injection were carried out and resulted in no metastasis, spontaneous tumour generation and peripheral liver tumour growth, respectively. POMC expression was present and extremely heterogeneous within the liver, suggesting that NE properties are maintained in metastases; however, further work is necessary to develop a more consistent metastatic model that can be used to assess responses to therapy in a more clinically relevant setting. SCLC tumours proliferate rapidly and outgrow their nutrient and oxygen supplies, resulting in hypoxic conditions. Here, carbonic anhydrase IX (CA IX) becomes up-regulated in order to maintain pH levels suitable for survival. The specific CA IX inhibitor, S4, induces hypoxia-specific cell death in vitro and impairs tumour growth in vivo. This response is further accentuated by combining S4 with single or repeated cisplatin doses. Combination treatment reduced gene expression of S-phase kinase-associated protein (Skp2), associated with cisplatin resistance. CA IX inhibition combined with cisplatin chemotherapy therefore presents a novel treatment for SCLC tumours that could reduce therapy resistance. In summary, heterogeneity is extremely important when choosing treatment options for SCLC and must be considered when basing treatment on single biopsies. NE and epithelial markers are present within sub-cutaneous and liver tumours; however, a reliable multi-organ metastatic model is necessary to fully appreciate the role of these markers in the spread of SCLC. Hypoxic regions within sub-cutaneous xenograft tumours upregulate CA IX. Inhibition of this enzyme resulted in impaired tumour growth, particularly when used together with cisplatin. Combining CA IX inhibition with cisplatin presents a much-needed novel therapy for SCLC.
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Poiraudeau, Loïc. "Identification de nouvelles cibles thérapeutiques dans le cancer neuroendocrine de la prostate." Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASL143.

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Le cancer de la prostate est le cancer le plus fréquent chez l'homme et il constitue la deuxième cause de mortalité par cancer chez l'homme dans les pays industrialisés. Le traitement systémique de ces cancers repose sur une déprivation androgénique par castration chirurgicale ou pharmacologique. Le cancer de la prostate métastatique résistant à la castration (mCRPC) est traité par des inhibiteurs de la voie des androgènes (ARPI). Cependant, environ un tiers des patients ne sont pas sensibles à ces médicaments et les autres, sensibles initialement, développent malheureusement une résistance secondaire, acquise dans un délai d'environ 1 à 2 ans. Les mécanismes qui expliquent la résistance primaire et secondaire ne sont pas bien connus. Une différenciation neuroendocrine (NE) des constitue l'un de ces mécanismes. En effet, entre 15 et 20% des tumeurs évoluent vers un phénotype neuroendocrine de la prostate (NEPC). Le pronostic de ces patients est très mauvais car les mécanismes moléculaires précis impliqués dans la différenciation neuroendocrine ne sont pas clairement élucidés et il n'existe pas de solution thérapeutique adaptée à ces tumeurs. L'objectif de cette thèse était d'étudier la différenciation neuroendocrine afin d'identifier des nouvelles cibles thérapeutiques. Nous nous sommes appuyés sur l'étude MATCH-R visant à étudier les mécanismes de résistance aux thérapies ciblées (enzalutamide, abiraterone) dans le cancer de la prostate métastatique. Les biopsies de patients ont été caractérisées par des méthodes de séquençage à haut débit et d'immunohistochimie. Dans le cadre de cette étude le laboratoire a aussi développé et caractérisé des modèles précliniques de xénogreffes dérivées de patients (PDX). Nous montrons à partir du WES et RNAseq de biopsies de patients que la différenciation neuroendocrine résulte probablement d'altérations transcriptomiques et épigénétiques. Par ailleurs, nos PDX NEPC maintiennent les caractéristiques génétiques, moléculaires et pharmacologiques par rapport à leurs biopsies d'origine. L'analyse du RNAseq a permis d'identifier une protéine membranaire spécifiquement exprimée par les NEPC. L'expression de cette protéine est corrélée à l'expression de marqueurs NE tels que synaptophysine (SYP) et chromogranine A (CHGA) ainsi qu'à un plus mauvais pronostic. Le traitement de nos PDX NEPC exprimant cette protéine avec une unique injection intraveineuse d' un anticorps conjugué ciblant la protéine résulte en une diminution significative du volume tumoral dans le groupe de souris traitées par rapport au groupe de souris non traitées. Enfin, nous avons identifié un récepteur nucléaire orphelin NR0B2 surexprimé dans les NEPC qui pourrait être impliqué dans la résistance aux inhibiteurs de la voie du RA. Au final, la thèse a permis de confirmer la différenciation neuroendocrine comme mécanisme important de résistance aux thérapies ciblant la voie du récepteur aux androgènes, de développer de nouveaux modèles pertinents (PDX et organoïdes), d'identifier et valider une nouvelle cible thérapeutique et enfin de suggérer le rôle d'un facteur nucléaire orphelin comme acteur moléculaire dans la résistance des cancers neuroendocrines
Prostate cancer is the most common cancer in men and the second leading cause of cancer death in men in industrialized countries. The systemic treatment of these cancers is androgen deprivation therapy (ADT), which can be achieved through surgical or pharmacological castration. Metastatic castration-resistant prostate cancer (mCRPC) is treated with androgen receptor inhibitors (ARi). However, approximately one-third of patients are not responsive to these drugs and the others, who are initially responsive, unfortunately develop secondary resistance, which is acquired within approximately 1-2 years. The mechanisms that explain primary and secondary resistance are not well understood. Neuroendocrine differentiation (NE) of mCRPC is one of these mechanisms. In fact, between 15 and 20% of resistant tumors evolve into neuroendocrine prostate cancer (NEPC). The prognosis of these patients is very poor because the precise molecular mechanisms involved in neuroendocrine differentiation are not clearly elucidated and there is no therapeutic solution adapted to these tumors.The objective of this thesis was to study neuroendocrine differentiation in order to identify new therapeutic targets. We relied on the MATCH-R study, which aimed to study the mechanisms of resistance to targeted therapies (enzalutamide, abiraterone). Patient biopsies were characterized using high-throughput sequencing and immunohistochemistry methods. As part of this study, the laboratory also developed and characterized preclinical patient-derived xenograft (PDX) models. We show from WES and RNAseq performed on patient biopsies that neuroendocrine differentiation is likely the result of transcriptomic and epigenetic alterations. Moreover, our PDXs retain the genetic, molecular, and pharmacological characteristics of their original biopsies. RNAseq analysis identified a membrane protein, which is specifically expressed by NEPC. The expression of this protein is correlated with the expression of NE markers such as synaptophysin (SYP) and chromogranin A (CHGA), as well as a worse diagnosis. Treatment of our NEPC PDXs with a single intravenous injection of an antibody-drug conjugate targeting this protein, resulted in a significant decrease in tumor volume in the treated group compared to the untreated group. Finally, we identified an orphan nuclear receptor, NR0B2 that is overexpressed in NEPC and could be involved in resistance to ARi. NEPC are aggressive tumors with few therapeutic options. These tumors result from transcriptomic alterations and require the development of relevant models that recapitulate the complexity of the disease to identify potential targets for new targeted therapies. ADCs are promising therapies, especially in NEPC, and have shown anti-tumor efficacy in preclinical evaluation
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Гирявенко, Наталія Іванівна, Наталья Ивановна Гирявенко, Nataliia Ivanivna Hyriavenko, Микола Сергійович Линдін, Николай Сергеевич Лындин, Mykola Serhiiovych Lyndin, Владислав Володимирович Сікора, et al. "Synchronous case of the primary neuroendocrine cancer of fallopian tube and serous papillary cancer of ovary." Thesis, Springer, 2019. http://essuir.sumdu.edu.ua/handle/123456789/75206.

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Neuroendocrine tumours commonly occur in the gastrointestinal tract and lungs. They rarely were found in the genital organs. There are a few data about this neoplasia in the fallopian tubes, which is accidentally identified during the morphological study. The aim of our investigation was to demonstrate the case of the primary neuroendocrine cancer of the fallopian tube in combination with the serous papillary cancer of the ovary.
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Balabanova, Silviya. "The neuroendocrine-like phenotype of gastric myofibroblasts and its significance in cancer." Thesis, University of Liverpool, 2012. http://livrepository.liverpool.ac.uk/6453/.

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Cell-cell communication, and specifically epithelial-mesenchymal signalling, is a key factor determining normal tissue development and organisation in hollow organs such as gastrointestinal tract. Mechanisms governing normal epithelial-mesenchymal communication have been studied for many years, but the changes occurring during tissue damage, infection and inflammation, and in cancer, remain unclear. Myofibroblasts are recognised as key mesenchymal cells involved in this communication in health and in disease. Myofibroblasts produce and secrete many proteins responsible for the assembly of extracellular matrix (ECM), tissue organisation and morphogenesis. Initial studies from this laboratory suggested that myofibroblasts might exhibit regulated secretion. The aim of this project was to determine the secretory mechanisms of myofibroblasts from the upper gut of normal and cancer tissues, and to address their significance in cancer. Gastric myofibroblasts were shown to exhibit calcium-dependent secretion of the small ECM protein, Transforming growth factor-β inducible protein or TGFβig-h3, in response to acute stimulation (30 min) with insulin-like growth factor (IGF)s. Inhibitors of protein synthesis (actinomycin D and cycloheximide) and of protein transport from endoplasmic reticulum (ER) to Golgi (brefeldin A) inhibited basal, but not IGF-stimulated secretion, as seen from Western blot analyses of media. These observations support the idea that evoked secretion occurs from a pre-formed pool of vesicles. Myofibroblasts from the upper gut showed differences in their secretory phenotype; specifically normal myofibroblasts from stomach exhibited regulated secretion, but their counterparts from oesophagus did not. Moreover, gastric cancer-associated myofibroblasts (CAMs) from patients with poor survival tend not to exhibit regulated secretion. These findings suggest a role for the tissue microenvironment in determining the secretory phenotype of myofibroblasts. Secretome-wide analysis of myofibroblasts media collected after IGF stimulation revealed that about 85% of the secretome exhibits evoked release. The relevant proteins belonged to different classes including ECM proteins, ligands, binding proteins, carbohydrate-binding proteins, proteases and protease inhibitors. These data indicate that myofibroblasts may contribute to tissue organisation by rapid release of substances involved in re-modelling the tissue microenvironment. The regulated secretory phenotype of myofibroblasts was associated with the expression of the chromogranin-like protein, secretogranin II. Knock-down of secretogranin II inhibited regulated secretion, whereas over-expression in myofibroblasts that lacked regulated released - induced it. Expression of secretogranin II by myofibroblasts coincided with the expression of dense core secretory vesicles that were similar to those found in neuroendocrine cells. This work indicates that there is a neuroendocrine-like secretory phenotype in myofibroblasts, as illustrated by the expression of neuroendocrine cell protein secretogranin II and the presence of regulated secretion. However, not all normal myofibroblasts exhibit the regulated phenotype, and in gastric cancer the phenotype correlates with early stage of disease. These findings may be exploitable both in the development of novel therapies and in understanding cancer progression.
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Bari, Muhammad Furqan. "Biomarkers for the classification of high grade neuroendocrine lung cancers." Thesis, University of Warwick, 2012. http://wrap.warwick.ac.uk/56420/.

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In the management of lung cancer the most important step beyond establishing the presence a malignant tumour is identifying whether the tumour is small cell lung cancer (SCLC) or one of the variants of non-small cell carcinoma (NSCLC), which includes adenocarcinoma (AD), squamous (SCC), large cell carcinoma (LCC), large cell neuroendocrine carcinoma (LCNEC), typical carcinoids (TC) and atypical carcinoids (AT). SCLC is a high grade neuroendocrine tumour which usually presents as central mass. These tumours are not usually amenable to curative surgical resection and are treated primarily by chemotherapy resulting in a treatment dichotomy of SCLC and NSCLC. The diagnosis of the tumour subtypes is routinely established on cytology or histology samples and in case of AD, LCC and SCC, which are not neuroendocrine tumours, the diagnosis is aided by neuroendocrine markers. However for TC, AT and LCNEC which are neuroendocrine tumours, the diagnosis is based on morphological features alone, which in some cases overlap and result in difficulty in diagnosis. This inter-observer variability is common among the neuroendocrine lung tumours and is highest between SCLC and LCNEC followed by TC and AC. Currently no marker or ancillary stain are clinically in practice which can aid in classification of these neuroendocrine tumours. In an attempt to address this issue, this project evaluated the use of bioinformatics to analyze publicly available high through-put transcriptomic data to identify markers which would aid in the distinction of SCLC from LCNEC. However, the markers identified were found to have low specificity and sensitivity, leading to the conduction of a de novo gene expression study utilizing laser micro-dissection of pure tumour samples of SCLC and LCNEC. This experiment yielded a different set of top ranked discriminator genes of which validation at the protein level by immunocytochemistry supported CDX2, CD99 and CD44 as LCNEC specific markers and BAI3 as a SCLC specific marker.
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McWhinney, Sarah Renee. "Role of tumor suppressor genes in neuroendocrine neoplasias and cardiovascular disease." Columbus, Ohio : Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1133373765.

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Goodin, Jeremy Lee. "Characterization of Gene Expression During Adenosine 3':5'-Cyclic Monophosphate Induced Neuroendocrine Differentiation in Human Prostatic Adenocarcinoma." Diss., Virginia Tech, 2002. http://hdl.handle.net/10919/26791.

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The LNCaP cell line is a versatile and useful model that is suitable for the study of human prostate cancer in vitro. The elevation of LNCaP intracellular cAMP levels through the addition of membrane permeable cAMP analogues, phosphodiesterase inhibitors, adenylate cyclase activators, or components of the cAMP signal transduction pathway can induce reversible neuroendocrine differentiation. Elucidation of those genes that are differentially expressed between undifferentiated prostate cancer cells and prostate cancer cells that have been induced to differentiate may present new insights for the molecular mechanisms governing neuroendocrine differentiation, early detection of prostate cancer, and/or potential targets for gene therapy. In this study, differential display PCR was used to identify 226 differentially expressed PCR products. Twelve of the differential display PCR products were confirmed by Northern blot analysis and cloned. DNA sequencing and database comparisons were performed. Among the differentially expressed genes, the human ribosomal S3a gene was identified as down regulated in response to LNCaP differentiation. In order to better ascertain the mechanism by which HRS3a gene expression is decreased during differentiation, the promoter region for this gene was analyzed. Electrophoretic mobility shift assay, antibody supershift assays, site-directed mutagenesis, and luciferase reporter gene analysis were employed to authenticate the roles of several transcription factors in the regulation of the HRS3a gene. Two cyclic AMP response elements, a Sp1 element and a GA-binding protein element, were involved in the regulation of HRS3a gene expression. In order to ascertain the effect of HRS3a down regulation in LNCaP cells, antisense phosphorothioate oligonucleotides were designed to inhibit HRS3a gene expression. Treatment of LNCaP cells with antisense HRS3a oligonucleotides did not influence cAMP induced neuroendocrine differentiation but antisense treatment did result in a decrease in LNCaP cell growth. In addition, it was determined that morphological changes associated with cAMP induced differentiation of LNCaP cells from the epithelial to the neuroendocrine state may not require alterations in gene expression nor the expression of novel proteins.
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Chen, Ruiqi. "Implications of PI3K/AKT inhibition on REST protein stability and neuroendocrine prostate cancer." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/62099.

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Treatment-induced neuroendocrine (NE) prostate cancer (t-NEPC) is an aggressive subtype of prostate cancer (PCa) that can arise as a consequence of rigorous androgen receptor pathway inhibition (ARPI) therapies now used to treat castration resistant disease (CRPC). While the PI3K/AKT pathway has been investigated as a co-therapeutic target with ARPI for advanced prostate adenocarcinoma, whether this strategy has implications on t-NEPC progression remains unknown. Findings from this work indicate that PI3K/AKT inhibition alone reduces protein expression of the RE-1 silencing transcription factor (REST) and induces multiple NE markers in PCa cells. The loss of REST by PI3K/AKT inhibition is through protein degradation mediated by the E3-ubiquitin ligase β-TRCP and REST phosphorylations at the S1024, S1027, and S1030 sites. Since AR inhibition was previously reported to deplete REST, results from this project reveal that the combined inhibition of PI3K/AKT and AR further aggravates REST protein reduction. Upon profiling the transcriptomes of AKT inhibition, AR inhibition, and AKT/AR co-inhibition in the LNCaP cell model, Gene Set Enrichment Analysis (GSEA) shows that these transcriptomes are highly correlated with the REST-regulated gene signature. Co-targeting AKT and AR resulted in an even higher correlation comparing to those of single treatment. Comparing these transcriptomes to the RNA-seq gene signature of t-NEPC patients by GSEA, it was observed that adding AKT inhibition to AR blockade enhanced the expression of neurogenesis-related genes and resulted in a stronger and broader upregulation of REST-regulated genes specific to t-NEPC. Collectively, these results indicate that AKT pathway inhibition can induce NE transdifferentiation in PCa cells via REST protein degradation. It delineates a potential risk for the AR and PI3K/AKT co-targeting strategy as it may further facilitate t-NEPC development.
Medicine, Faculty of
Experimental Medicine, Division of
Medicine, Department of
Graduate
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Books on the topic "Cancer neuroendocrine"

1

Ito, Takaaki. Differentiation and proliferation of pulmonary neuroendocrine cells. Jena, Germany: Urban & Fischer, 1999.

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Khayat, Eric. Tumeurs neuroendocrines digestives et médecine nucléaire. Cachan: Editions médicales internationales, 2001.

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G, Maldonado Jonathon, and Cervantes Mikayla K, eds. Small cell carcinomas: Causes, diagnosis and treatment. Hauppauge, N.Y: Nova Science, 2009.

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Maldonado, Jonathon G. Small cell carcinomas: Causes, diagnosis and treatment. New York: Nova Biomedical Books, 2009.

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Maldonado, Jonathon G., and Mikayla K. Cervantes. Small cell carcinomas: Causes, diagnosis and treatment. New York: Nova Biomedical Books, 2009.

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Walsh, Bob. Good Looking Cancer: Neuroendocrine Cancer. Independently Published, 2018.

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Walsh, Bob. Neuroendocrine Cancer: What You Need to Know about This Deadly Cancer. Independently Published, 2018.

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Pisegna, Joseph R. Management of Pancreatic Neuroendocrine Tumors. Springer New York, 2016.

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Pisegna, Joseph R. Management of Pancreatic Neuroendocrine Tumors. Springer, 2014.

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Pisegna, Joseph R. Management of Pancreatic Neuroendocrine Tumors. Springer, 2014.

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Book chapters on the topic "Cancer neuroendocrine"

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Güler, E. Nilüfer, Murat Fani Bozkurt, Serdar Ozbas, and Suayib Yalcin. "Thyroid Cancer." In Neuroendocrine Tumours, 353–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45215-8_21.

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Hellman, Per, Olov Norlén, Peter Stålberg, and Kosmas Daskalakis. "Thyroid Cancer." In Neuroendocrine Tumours, 445–83. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-56968-5_22.

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Ciltas, Aydin, Yusuf Gunaydin, and Mustafa Benekli. "Medullary Thyroid Cancer." In Neuroendocrine Tumours, 389–401. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45215-8_22.

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Gall, Victor A., and Amanda M. Laird. "Medullary Thyroid Cancer." In Neuroendocrine Tumors, 223–36. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62241-1_14.

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Laçin, Şahin, and Suayib Yalcin. "Medullary Thyroid Cancer." In Neuroendocrine Tumours, 485–506. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-56968-5_23.

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Duran, Ignacio, and Lillian L. Siu. "Neuroendocrine Carcinoma." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_4029-4.

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Schmitt-Graeff, Annette. "Neuroendocrine Neoplasms." In Encyclopedia of Cancer, 1–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_4032-2.

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Duran, Ignacio, and Lillian L. Siu. "Neuroendocrine Carcinoma." In Encyclopedia of Cancer, 3052–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_4029.

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Schmitt-Graeff, Annette. "Neuroendocrine Neoplasms." In Encyclopedia of Cancer, 3057–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_4032.

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Duran, Ignacio, and Lillian L. Siu. "Neuroendocrine Carcinoma." In Encyclopedia of Cancer, 2482–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4029.

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Conference papers on the topic "Cancer neuroendocrine"

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Souto, Andreza Karine de Barros Almeida, Poliana Bergamaschine Giovani Blasi, Brenda Fabiola Delgado Taboada, Fernanda Teresa Lima, Bernardo Garicochea, and Cristiano Augusto Andrade de Resende. "NEUROENDOCRINE CARCINOMA OF THE BREAST AND ILEUM IN A PATIENT WITH BRCA2 PATHOGENIC VARIANT – ONCOLOGIC AND GENETIC CONSIDERATIONS DERIVED FROM A CASE REPORT." In Brazilian Breast Cancer Symposium 2022. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s2076.

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Background: Neuroendocrine neoplasms (NENs) are a heterogeneous group of neoplasms. Most frequently, they occur in the digestive system, and breast neuroendocrine tumors constitute less than 1% of all of them. Germline mutations can increase the risk of developing tumors and predispose to hereditary cancer syndromes. Some NENs are well-established components of common hereditary syndromes. Recently, whole genomic sequencing revealed that 17% of apparently sporadic pancreatic NENs carried germline mutations, including DNA repair genes, such as BRCAs. It is well known that this gene plays a role in hereditary breast cancer, but variations in these genes were not described in patients with breast/ ileum neuroendocrine tumors. We present a patient with a neuroendocrine tumor and a germline pathogenic variant in BRCA2. Case report: A 44-year-old female patient presented with a palpable lesion at the right breast, with 1.1×1.4 cm, and a biopsy confirmed an invasive ductal carcinoma, grade 2. Immunohistochemistry revealed a neuroendocrine breast carcinoma (ER10% PR5%, HER2 negative, Ki-67=8%). The regular staging examinations did not show any abnormalities, but a 68Ga PET/CT demonstrated an ileum wall thickening with a marked expression of somatostatin receptors compatible with primary disease, with mesenteric lymph nodes and hepatic lesions suggestive of metastasis, in addition to the right breast lesion that could be either a secondary implant or a primary synchronic tumor. A detailed family history did not reveal any important cancer cases in the family except for the father and a paternal uncle, both with prostate cancer at 72 and 85 years old, respectively. Germline genetic analysis confirmed the presence of a heterozygous pathogenic variant in BRCA2 (c.2167delA;p.Ser723Alafs*7). The patient is currently being treated with octreotide LAR with good tolerance and stable disease. Final comments: This case shows the importance of molecular germline investigation in patients with NENs. This patient adds knowledge to the association of the BRCA2 gene and neuroendocrine tumors.
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Aldanbara, H. "Cutan metastases of neuroendocrine cancer (NET)." In Abstract- und Posterband – 91. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Welche Qualität macht den Unterschied. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1710902.

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Puca, Loredana, Dong Gao, Myriam Kossai, Clarisse Marotz, Juan Miguel Mosquera, Theresa Y. MacDonald, Kyung Park, et al. "Abstract 3844: Targeting EZH2 in neuroendocrine prostate cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3844.

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Dardenne, Etienne, Himisha Beltran, Kaitlyn Gayvert, Matteo Benelli, Adeline Berger, Loredana Puca, Joanna Cyrta, et al. "Abstract 887: N-Myc drives neuroendocrine prostate cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-887.

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Marhold, Maximilian, Erwin Tomasich, Simon Udovica, Gerwin Heller, Corinna Altenberger, Andreas Spittler, Reinhard Horvat, Peter Horak, and Michael Krainer. "Abstract 2407: Neuroendocrine and luminal progenitors drive cancer progression in prostate cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2407.

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Ferguson, Alison M., Bhavneet Bhinder, Vincenza Conteduca, Michael Sigouros, Andrea Sboner, David Nanus, Scott Tagawa, David Rickman, Olivier Elemento, and Himisha Beltran. "Abstract 134: Immunogenomic landscape of neuroendocrine prostate cancer (NEPC)." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-134.

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Ferguson, Alison M., Bhavneet Bhinder, Vincenza Conteduca, Michael Sigouros, Andrea Sboner, David Nanus, Scott Tagawa, David Rickman, Olivier Elemento, and Himisha Beltran. "Abstract 134: Immunogenomic landscape of neuroendocrine prostate cancer (NEPC)." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-134.

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Sanders, Danielle N., Magdalena Grabowska, and Robert Matusik. "Abstract B23: Neuroendocrine differentiation in prostate cancer and development." In Abstracts: Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; November 13-16, 2015; Atlanta, Georgia. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7755.disp15-b23.

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Miller, M. A., A. J. Kumar, W. Shi, J. Karunamuni, G. Chen, and M. M. Fuster. "Spontaneous Regression of Neuroendocrine Lung Cancer: A Case Report." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a7479.

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Vieira, Juliana Sofia Silva, and Paula Karolyne Simões Mello. "Unresectable malignant gallbladder neoplasm." In V Seven International Multidisciplinary Congress. Seven Congress, 2024. http://dx.doi.org/10.56238/sevenvmulti2024-131.

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Gallbladder cancer often arises from somatic mutations in cells of the biliary epithelium, which can be precipitated by chronic inflammation (as in chronic cholelithiasis and cholecystitis), infections (e.g., by Salmonella spp. or Helicobacter spp.), and exposure to carcinogens. Adenocarcinomas represent more than 90% of gallbladder cancer cases, with other histological subtypes including squamous cell carcinomas, adenosquamous carcinomas, and neuroendocrine tumors.
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Reports on the topic "Cancer neuroendocrine"

1

Hu, Chang-Deng, Xuehong Deng, and Gyeon Oh. Targeting Neuroendocrine Differentiation for Prostate Cancer Radiosensitization. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613326.

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Evans, Christopher P. Castration Induced Neuroendocrine Mediated Progression of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2008. http://dx.doi.org/10.21236/ada492892.

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Evans, Christopher P. Castration-Induced Neuroendocrine Mediated Progression of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada446371.

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Huang, Jiaoti. The Function of Neuroendocrine Cells in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580194.

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Huang, Jiaoti. The Function of Neuroendocrine Cells in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada590965.

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Huang, Jiaoti. The Function of Neuroendocrine Cells in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2014. http://dx.doi.org/10.21236/ada604606.

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Huang, Jiaoti. The Function of Neuroendocrine Cells in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2015. http://dx.doi.org/10.21236/ada621366.

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Evans, Christopher P. Castration Induced Neuroendocrine Mediated Progression of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada476920.

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Huang, Jiaoti. Function of PTP1B in Neuroendocrine Differentiation of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2008. http://dx.doi.org/10.21236/ada481731.

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Kim, Isaac. Neuroendocrine Differentiation in Prostate Cancer: Role of Bone Morphogenetic Protein-6 and Macrophages. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada555480.

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