Journal articles: 'Pancreatic neuroendocrine tumour'

1

Maslin, D., B. Challis, and H. Simpson. "Metastatic pancreatic neuroendocrine tumour." QJM 109, no. 5 (March 14, 2016): 355. http://dx.doi.org/10.1093/qjmed/hcw036.

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Ferrel, Benjamin, Jan Franko, and May C. Tee. "Rare case of pancreatic neuroendocrine tumour presenting as paraneoplastic hypercalcaemia." BMJ Case Reports 14, no. 4 (April 2021): e240786. http://dx.doi.org/10.1136/bcr-2020-240786.

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An asymptomatic 68-year-old woman who presented with an isolated hypercalcaemia was diagnosed with a rare, previously unsuspected parathyroid hormone-related peptide (PTHrP)-producing pancreatic neuroendocrine tumour. She underwent an extensive operation including vascular resection and reconstruction, resulting in successful removal of the tumour with negative margins. Medical and surgical management of pancreatic neuroendocrine tumours and PTHrP-mediated paraneoplastic hypercalcaemia is discussed.

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Weerasuriya, Scott, Kieran Palmer, Stephen Gregory, Benjamin C. Whitelaw, Elisa Gonzalez, and Rajaventhan Srirajaskanthan. "Mesenteric Variceal Haemorrhage and Ectopic Cushing’s Syndrome as Presenting Features of a Pancreatic Neuroendocrine Tumour Recurrence." Case Reports in Gastroenterology 15, no. 3 (October 11, 2021): 919–26. http://dx.doi.org/10.1159/000518021.

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Pancreatic neuroendocrine tumours can have varied and complex presentations. Whilst hormone hypersecretion often induces characteristic clinical syndromes, non-specific symptoms may arise due to localized tumour effects. Malignant invasion of local vasculature is an increasingly recognized complication of these neoplasms and can be associated with significant morbidity. Herein, we present the case of a 47-year-old male with a recurrence of a pancreatic neuroendocrine tumour who presented with unusual upper gastrointestinal bleeding. The tumour had recurred within the superior mesenteric vein, replacing the vessel and invading its branches. This resulted in porto-mesenteric hypertension and the formation of bleeding mesenteric varices. The patient subsequently developed progressive metabolic disturbances and was diagnosed with ectopic Cushing’s syndrome, despite his primary tumour having been non-functional. This case demonstrates not only a rare pattern of tumour recurrence but also the potential for pancreatic neuroendocrine tumours to de-differentiate and change from non-functional to hormone secreting, a phenomenon which may complicate diagnosis and management.

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Laccourreye, Ollivier, Eric Chabardes, Gregory Weinstein, Francoise Carnot, Daniel Brasnu, and Henri Laccourreye. "Synchronous arytenoid and pancreatic neuroendocrine carcinoma." Journal of Laryngology & Otology 105, no. 5 (May 1991): 373–75. http://dx.doi.org/10.1017/s0022215100116044.

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AbstractNeuroendocrine laryngeal carcinoid tumours are uncommon. The supraglottis is the main location of these tumours. Eighty-one cases have been reported in the world literature. We present the first case of a synchronous laryngeal and pancreatic neuroendocrine tumour.

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Lines, K. E., R. P. Vas Nunes, M. Frost, C. J. Yates, M. Stevenson, and R. V. Thakker. "A MEN1 pancreatic neuroendocrine tumour mouse model under temporal control." Endocrine Connections 6, no. 4 (May 2017): 232–42. http://dx.doi.org/10.1530/ec-17-0040.

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Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterised by occurrence of parathyroid tumours and neuroendocrine tumours (NETs) of the pancreatic islets and anterior pituitary. The MEN1 gene, encoding menin, is a tumour suppressor, but its precise role in initiating in vivo tumourigenesis remains to be elucidated. The availability of a temporally controlled conditional MEN1 mouse model would greatly facilitate the study of such early tumourigenic events, and overcome the limitations of other MEN1 knockout models, in which menin is lost from conception or tumour development occurs asynchronously. To generate a temporally controlled conditional mouse model, we crossbred mice with the MEN1 gene floxed by LoxP sites (Men1L/L), and mice expressing tamoxifen-inducible Cre recombinase under the control of the rat insulin promoter (RIP2-CreER), to establish a pancreatic β-cell-specific NET model under temporal control (Men1L/L/RIP2-CreER). Men1L/L/RIP2-CreER mice aged ~3 months were given tamoxifen in the diet for 5 days, and pancreata harvested 2–2.5, 2.9–3.5 and 4.5–5.5 months later. Control mice did not express Cre and did not receive tamoxifen. Immunostaining of pancreata from tamoxifen-treated Men1L/L/RIP2-CreER mice, compared to control mice, showed at all ages: loss of menin in all islets; increased islet area (>4.2-fold); increased proliferation of insulin immunostaining β-cells (>2.3-fold) and decreased proliferation of glucagon immunostaining α-cells (>1.7-fold). There were no gender and apoptotic or proliferation differences, and extra-pancreatic tumours were not detected. Thus, we have established a mouse model (Men1L/L/RIP2-CreER) to study early events in the development of pancreatic β-cell NETs.

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Venugopal, Abhirami, Agnes Michalczyk, Mustafa Khasraw, and M. Leigh Ackland. "EMT Molecular Signatures of Pancreatic Neuroendocrine Neoplasms." International Journal of Molecular Sciences 23, no. 21 (November 7, 2022): 13645. http://dx.doi.org/10.3390/ijms232113645.

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Neuroendocrine neoplasms (NENs) are relatively rare neoplasms occurring predominantly in the gastrointestinal tract and pancreas. Their heterogeneity poses challenges for diagnosis and treatment. There is a paucity of markers for characterisation of NEN tumours. For routine diagnosis, immunohistochemistry of the NEN-specific markers CgA and synaptophysin and the proliferation marker Ki-67 are used. These parameters, however, are qualitative and lack the capacity to fully define the tumour phenotype. Molecules of epithelial–mesenchymal transition (EMT) are potential candidates for improved tumour characterisation. Using qRT-PCR, we measured mRNA levels of 27 tumour markers, including 25 EMT-associated markers, in tumour tissue and matched non-tumour tissues for 13 patients with pancreatic NENs. Tissue from patients with three different grades of tumour had distinctly different mRNA profiles. Of the 25 EMT-associated markers analysed, 17 were higher in G3 tissue relative to matched non-tumour tissue, including CD14, CD24, CD31, CD44, CD45, CD56, CK6, CK7, CK13, CK20, NSE, CDX2, CgA, DAXX, PCNA, laminin and Ki-67. The differences in levels of seven EMT-associated markers, Ki-67, DAXX, CD24, CD44, vimentin, laminin and PDX1 plus CgA and NSE (neuroendocrine markers) enabled a distinct molecular signature for each tumour grade to be generated. EMT molecules differentially expressed in three tumour grades have potential for use in tumour stratification and prognostication and as therapeutic targets for treatment of neuroendocrine cancers, following validation with additional samples.

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Kann, P. H., E. Balakina, D. Ivan, D. K. Bartsch, S. Meyer, K.-J. Klose, Th Behr, and P. Langer. "Natural course of small, asymptomatic neuroendocrine pancreatic tumours in multiple endocrine neoplasia type 1: an endoscopic ultrasound imaging study." Endocrine-Related Cancer 13, no. 4 (December 2006): 1195–202. http://dx.doi.org/10.1677/erc.1.01220.

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Endoscopic ultrasound (EUS) enables detection and localization of pancreatic neuroendocrine tumours. Even small tumours down to a diameter of 1–2 mm can be visualized. Since such small tumours usually cannot be detected by computed tomography (ct), magnetic resonance imaging (mri) and somatostatin receptor scintigraphy (srs), and experience with EUS imaging is limited, there is no clear evidence for clinical management in multiple endocrine neoplasia type 1 (MEN1). Knowledge about the natural course of growth and metastatic distribution is mandatory to come to appropriate clinical decisions and guidelines. This prospective study was aimed to assess the natural course of small (<15 mm) neuroendocrine pancreatic tumours without clinical symptoms due to endocrine activity or mechanical problems and without clear indication for surgical therapy in MEN1 by EUS. A total of 82 asymptomatic tumours <15 mm (5.9 ± 3.2 mm diameter at baseline) in 20 patients with MEN1-disease (8 female/12 male, 43 ± 13 years) were studied over a period of 20 ± 12 months (33.8 patient years, 106.7 tumour years) by EUS. Change in largest diameter of each tumour and annual tumour incidence rate in the patients’ cohort were calculated. Increase of largest tumour diameter was found to be 1.3 ± 3.2% per month, annual tumour incidence rate 0.62 new tumours per patient year. In one patient, rapid progressive pancreatic manifestation of MEN1 was observed. There was no evidence in ct and/or srs and/or mri for metastatic disease in all patients. Only 4/84 (4.8%) pancreatic tumours could be visualized by computed tomography, 5/79 (6.3%) by somatostatin receptor imaging and 4/39 (10.3%) by magnetic resonance imaging. Small asymptomatic neuroendocrine pancreatic tumours in MEN1 usually seem to grow slowly. Annual tumour incidence rate is low. However, faster growing tumours and patients with rapidly progressive disease can be observed. Risk for obvious metastatic disease from asymptomatic neuroendocrine pancreatic tumours <15 mm in MEN1 seems to be low.

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Bertani, Helga, Alessandro Messerotti, Fabrizio Di Benedetto, Raffaele Manta, Milena Greco, Federica Casoni, Luisa Losi, and Rita Conigliaro. "Unusual Paraneoplastic Syndrome Accompanies Neuroendocrine Tumours of the Pancreas." Case Reports in Medicine 2011 (2011): 1–4. http://dx.doi.org/10.1155/2011/309149.

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Neuroendocrine tumours comprise a small percentage of pancreatic neoplasia (10%) (1). Diagnosis of neuroendocrine tumours is difficult, especially if the tumours are small and nonfunctional. CT scans, MRI, and nuclear scans are sufficiently sensitive assessment tools for tumours with diameters of at least 2 cm; otherwise, the sensitivity and specificity of these techniques is less than 50% (2). Myasthenia gravis (MG) is a heterogeneous neuromuscular junction disorder that is primarily caused when antibodies form against the acetylcholine receptors (Ab-AchR). MG can develop in conjunction with neoplasia, making MG a paraneoplastic disease. In those cases, MG is most commonly associated with thymomas and less frequently associated with extrathymic malignancies. The mechanism underlying this paraneoplastic syndrome has been hypothesized to involve an autoimmune response against the tumour cells (3). No published reports have linked malignant pancreatic diseases with MG. Here, we report the case of a young woman, negative for Ab-AchR, with a neuroendocrine tumour in the pancreatic head, who experienced a complete resolution of her MG-like syndrome after surgical enucleation of the tumour.

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Wang, C. Y., J. C. Lin, Y. F. Li, and C. W. Yang. "Alpha-fetoprotein producing pancreatic neuroendocrine tumour." QJM: An International Journal of Medicine 113, no. 8 (January 30, 2020): 565–66. http://dx.doi.org/10.1093/qjmed/hcaa018.

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Varshney, Bharti, Jyotsna Naresh Bharti, Vaibhav Kumar Varshney, and Taruna Yadav. "Mixed neuroendocrine-non-neuroendocrine neoplasms (MiNEN) of pancreas: a rare entity—worth to note." BMJ Case Reports 13, no. 4 (April 2020): e234855. http://dx.doi.org/10.1136/bcr-2020-234855.

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Mixed adenocarcinoma with neuroendocrine tumour of pancreas has been reported infrequently and consists of both epithelial and neuroendocrine component. We encountered an 81-year-old male patient who presented with clinical features of painful progressive jaundice for 1 month. Contrast-enhanced CT abdomen reported a mass in the pancreatic head with dilated common bile duct and pancreatic duct. He underwent pancreatoduodenectomy and histopathological examination revealed two different tumours: ductal adenocarcinoma admixed with neuroendocrine tumour of pancreas. He received adjuvant chemotherapy, and at the end of 1-year follow-up, he has no recurrence. Here, we reported this rare malignancy of pancreas for which pancreatoduodenectomy was done and diagnosed on histopathology with immunohistochemistry.

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Varshney, Vaibhav Kumar, Raghav Nayar, Taruna Yadav, and Sudeep Khera. "Duodenal gastrointestinal stromal tumour imitating as pancreatic head tumour." BMJ Case Reports 15, no. 3 (March 2022): e248828. http://dx.doi.org/10.1136/bcr-2022-248828.

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Duodenal gastrointestinal stromal tumours (D-GISTs) are a rare disease. It may arise commonly from the second or third part of the duodenum and can be erroneously diagnosed as a pancreatic head tumour due to proximity and morphology on imaging studies. We present a case of a 60-year-old woman who presented with abdominal pain and was diagnosed as a case of pancreatic neuroendocrine tumour on radiologic imaging and granulomatous lesion on aspiration cytology. A ~5×3 cm mass was noted in the pancreatic head on laparotomy, and pancreatoduodenectomy was performed. Histopathology reported an exophytic GIST arising from the second part of the duodenum. Hence, D-GIST can invade the pancreas and mimic pancreatic head tumours; therefore, these tumours should be kept in the differential diagnosis of an atypical pancreatic head mass.

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Rico, Karen, Suzann Duan, Ritu L. Pandey, Yuliang Chen, Jayati T. Chakrabarti, Julie Starr, Yana Zavros, et al. "Genome analysis identifies differences in the transcriptional targets of duodenal versus pancreatic neuroendocrine tumours." BMJ Open Gastroenterology 8, no. 1 (November 2021): e000765. http://dx.doi.org/10.1136/bmjgast-2021-000765.

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ObjectiveGastroenteropancreatic neuroendocrine tumours (GEP-NETs) encompass a diverse group of neoplasms that vary in their secretory products and in their location within the gastrointestinal tract. Their prevalence in the USA is increasing among all adult age groups.AimTo identify the possible derivation of GEP-NETs using genome-wide analyses to distinguish small intestinal neuroendocrine tumours, specifically duodenal gastrinomas (DGASTs), from pancreatic neuroendocrine tumours.DesignWhole exome sequencing and RNA-sequencing were performed on surgically resected GEP-NETs (discovery cohort). RNA transcript profiles available in the Gene Expression Omnibus were analysed using R integrated software (validation cohort). Digital spatial profiling (DSP) was used to analyse paraffin-embedded GEP-NETs. Human duodenal organoids were treated with 5 or 10 ng/mL of tumor necrosis factor alpha (TNFα) prior to qPCR and western blot analysis of neuroendocrine cell specification genes.ResultsBoth the discovery and validation cohorts of small intestinal neuroendocrine tumours induced expression of mesenchymal and calcium signalling pathways coincident with a decrease in intestine-specific genes. In particular, calcium-related, smooth muscle and cytoskeletal genes increased in DGASTs, but did not correlate with MEN1 mutation status. Interleukin 17 (IL-17) and tumor necrosis factor alpha (TNFα) signalling pathways were elevated in the DGAST RNA-sequencing. However, DSP analysis confirmed a paucity of immune cells in DGASTs compared with the adjacent tumour-associated Brunner’s glands. Immunofluorescent analysis showed production of these proinflammatory cytokines and phosphorylated signal transducer and activator of transcription 3 (pSTAT3) by the tumours and stroma. Human duodenal organoids treated with TNFα induced neuroendocrine tumour genes, SYP, CHGA and NKX6.3.ConclusionsStromal–epithelial interactions induce proinflammatory cytokines that promote Brunner’s gland reprogramming.

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Gunda, Deepika, Jack Naughton, Sean Gregory Stevens, and Marcos V. Perini. "Castleman’s disease masquerading as pancreatic neuroendocrine tumour." BMJ Case Reports 14, no. 6 (June 2021): e242597. http://dx.doi.org/10.1136/bcr-2021-242597.

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Castleman’s disease (CD) is a rare lymphoproliferative disorder. This case report, to the best of our knowledge, is the first report of CD simulating a pancreatic neuroendocrine tumour . The patient was a 58-year-old woman who initially presented with bilateral iritis and underwent investigation for possible systemic rheumatological disease. CT of the chest demonstrated an incidental finding of a well-demarcated retropancreatic mass. As the mass was found to enhance on DOTATATE (tetraazacyclododecanetetraacetic acid-DPhe1-Tyr3-octreotate) positron emission tomography, a diagnosis of pancreatic neuroendocrine tumour was made. The patient underwent an open distal pancreatectomy and splenectomy. Histopathological examination revealed the unexpected diagnosis of hyaline vascular CD of a lymph node posterior to the pancreas. After 2 years of follow-up, there is no evidence of disease recurrence.

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M, Sneha, Swarna Sri, and Anunayi J. "Pancreatic Neuroendocrine Tumour- An Interesting Case Report." Journal of Evolution of Medical and Dental Sciences 9, no. 19 (May 11, 2020): 1575–78. http://dx.doi.org/10.14260/jemds/2020/344.

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15

Bartz, C., C. Ziske, B. Wiedenmann, and K. Moelling. "p53 tumour suppressor gene expression in pancreatic neuroendocrine tumour cells." Gut 38, no. 3 (March 1, 1996): 403–9. http://dx.doi.org/10.1136/gut.38.3.403.

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Zierhut, B., K. Mechtler, W. Gartner, T. Daneva, W. Base, M. Weissel, B. Niederle, and L. Wagner. "Heat shock protein 70 (Hsp70) subtype expression in neuroendocrine tissue and identification of a neuroendocrine tumour-specific Hsp70 truncation." Endocrine-related cancer 11, no. 2 (June 2004): 377–89. http://dx.doi.org/10.1677/erc.0.0110377.

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In order to identify neuroendocrine tumour-specific protein expression, we generated monoclonal antibodies (mAbs) with a tumour-related reaction pattern using a human insulinoma as immunogen. One of the generated mAbs (mAb 1D4) exhibited striking immunoreactivity against various neuroendocrine tumours without staining pancreatic islets of Langerhans. Furthermore, mAb 1D4 immunostained a characteristic subtype of hypothalamic neurones. Using two-dimensional (2-D) gel electrophoresis, mAb 1D4 immunoblotting and mass spectrometry, heat shock protein 70 (Hsp70) isoforms were identified as the mAb 1D4-specific antigen. In hypothalamic tissue, the presence of two different Hsp70 isoforms (Hsp70-8 and Hsp70-1) was revealed by 2-D gel immunoblots and consecutive mass spectrometric peptide analysis. In contrast, insulinoma and other neuroendocrine tumours displayed solely Hsp70-8 expression. Moreover, the tumour-specific presence of an additional mAb 1D4 immunoreactive protein of 40 kDa was observed in eight out of eight tested neuroendocrine tumours. For this variant, exclusively, peptides derived from the C terminus excluding the 299 amino-terminal residues were detected. In cultured tumour-derived fibroblasts, expression of the truncated Hsp70-8 subtype was not present. In conclusion, we have demonstrated a neuroendocrine tumour-specific expression pattern of Hsp70 isoforms and identified an as yet unknown N-terminally truncated Hsp70-8 variant.

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Pardillos Tomé, Ana, Eduardo Bajador Andreu, Ana Comín Orce, and Francisco Marcilla Córdoba. "Familial adenomatous polyposis associated with pancreatic neuroendocrine tumour." Gastroenterología y Hepatología (English Edition) 44, no. 2 (February 2021): 130–31. http://dx.doi.org/10.1016/j.gastre.2020.05.013.

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Nowowiejska, Julia, Anna Baran, and Iwona Flisiak. "Folliculotropic mycosis fungoides coexisting with pancreatic neuroendocrine tumour." Dermatology Review 105, no. 6 (2018): 746–52. http://dx.doi.org/10.5114/dr.2018.80844.

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Halappanavar, Anup, and Rajeev Pakhetra. "An unusual presentation of pancreatic neuroendocrine tumour (PNET)." Clinical Medicine 19, Suppl 3 (June 2019): 7–8. http://dx.doi.org/10.7861/clinmedicine.19-3-s7.

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Halappanavar, Anup, and Rajeev Pakhetra. "An unusual presentation of pancreatic neuroendocrine tumour (PNET)." Clinical Medicine 19, Suppl 3 (June 2019): s7—s8. http://dx.doi.org/10.7861/clinmedicine.19-3s-s7.

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Ueno, Tatsuya, Masaki Munakata, and Masahiko Tomiyama. "Unilateral Ptosis Caused by Pancreatic Neuroendocrine Tumour Metastases." Internal Medicine 58, no. 1 (January 1, 2019): 151–52. http://dx.doi.org/10.2169/internalmedicine.1498-18.

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Zaborowski, Alexandra, Siun M. Walsh, Narayanasamy Ravi, and John V. Reynolds. "Pancreatic Aetiology for Massive Upper Gastrointestinal Haemorrhage in Pregnancy." Case Reports in Surgery 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/5491851.

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We present herein what we believe is the first reported case of massive upper gastrointestinal bleeding in pregnancy due to a pancreatic neuroendocrine tumour causing left sided portal hypertension. A 37-year-old 27-week pregnant female presented with massive haematemesis and melaena requiring transfusion of 10 units of red cell concentrate. Gastric varices were evident at endoscopy. An MRI revealed a large mass infiltrating the pancreatic tail and spleen with massive upper abdominal varix formation secondary to splenic vein invasion. A caesarean section was performed, followed by a radical en bloc partial pancreatectomy and splenectomy with resection of the fundus of the stomach and ligation of gastric and splenic varices. Her postoperative course was uncomplicated. Histology revealed a well differentiated grade 2 neuroendocrine tumour with final staging of T4N0. This case highlights an infrequently encountered cause of massive gastrointestinal bleeding. Diagnosis and management of pancreatic neuroendocrine tumours, due to their rarity and variable clinical presentation, can be challenging particularly in the setting of pregnancy where the wellbeing of a second patient must also be considered. A multidisciplinary approach with input from obstetricians and general surgeons is required when deciding optimum management, while also taking into account the patient’s preferences.

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Tremblay, Catherine, and Isabelle Marcil. "Necrolytic Migratory Erythema: A Forgotten Paraneoplastic Condition." Journal of Cutaneous Medicine and Surgery 21, no. 6 (June 29, 2017): 559–61. http://dx.doi.org/10.1177/1203475417719051.

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Background: Necrolytic migratory erythema (NME) is most commonly a paraneoplastic condition. It is the dermatologic manifestation classically associated with glucagonoma pancreatic neuroendocrine tumour. Glucagonoma syndrome has been defined by the constellation of secreting tumour associated with overproduction by the α-cells in the pancreatic islets of Langerhans, abnormally elevated blood level of glucagon, and skin findings of NME. Objective: Although rare, all dermatologists must know and recognise NME promptly to request useful investigations for the diagnosis of this characteristic neuroendocrine tumour. Methods and Results: We report a case of a middle-aged woman seen in our dermatology clinic with longstanding skin findings suggestive of NME revealing a glucagonoma. Surgical removal was associated with complete resolution of the cutaneous and systemic features. Conclusion: NME is often the first clinical finding of an occult neuroendocrine pancreatic neoplasia. Dermatologists must be aware of this condition since they can be the first physician to suspect it and allow multidisciplinary management, which influences the prognostic value. Surgical removal is the first-line therapy if early diagnosis is done before liver metastases occur.

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Clift, Ashley Kieran, Mark Kidd, Lisa Bodei, Christos Toumpanakis, Richard P. Baum, Kjell Oberg, Irvin M. Modlin, and Andrea Frilling. "Neuroendocrine Neoplasms of the Small Bowel and Pancreas." Neuroendocrinology 110, no. 6 (September 27, 2019): 444–76. http://dx.doi.org/10.1159/000503721.

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The traditionally promulgated perspectives of neuroendocrine neoplasms (NEN) as rare, indolent tumours are blunt and have been outdated for the last 2 decades. Clear increments in their incidence over the past decades render them increasingly clinically relevant, and at initial diagnosis many present with nodal and/or distant metastases (notably hepatic). The molecular pathogenesis of these tumours is increasingly yet incompletely understood. Those arising from the small bowel (SB) or pancreas typically occur sporadically; the latter may occur within the context of hereditary tumour predisposition syndromes. NENs can also be associated with endocrinopathy of hormonal hypersecretion. Tangible advances in the development of novel biomarkers, functional imaging modalities and therapy are especially applicable to this sub-set of tumours. The management of SB and pancreatic neuroendocrine tumours (NET) may be challenging, and often comprises a multidisciplinary approach wherein surgical, medical, interventional radiological and radiotherapeutic modalities are implemented. This review provides a comprehensive overview of the epidemiology, pathophysiology, diagnosis and treatment of SB and pancreatic NETs. Moreover, we provide an outlook of the future in these tumour types which will include the development of precision oncology frameworks for individualised therapy, multi-analyte predictive biomarkers, artificial intelligence-derived clinical decision support tools and elucidation of the role of the microbiome in NEN development and clinical behaviour.

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Krug, Sebastian, Julia Weissbach, Annika Blank, Aurel Perren, Johannes Haybaeck, Volker Fendrich, Anja Rinke, Thomas Mathias Gress, Jonas Rosendahl, and Patrick Michl. "CUX1—Transcriptional Master Regulator of Tumor Progression in Pancreatic Neuroendocrine Tumors." Cancers 12, no. 7 (July 19, 2020): 1957. http://dx.doi.org/10.3390/cancers12071957.

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Recently, we identified the homeodomain transcription factor Cut homeobox 1 (CUX1) as mediator of tumour de-differentiation and metastatic behaviour in human insulinoma patients. In insulinomas, CUX1 enhanced tumour progression by stimulating proliferation and angiogenesis in vitro and in vivo. In patients with non-functional pancreatic neuroendocrine tumours (PanNET), however, the impact of CUX1 remains to be elucidated. Here, we analysed CUX1 expression in two large independent cohorts (n = 43 and n = 141 tissues) of non-functional treatment-naïve and pre-treated PanNET patients, as well as in the RIP1Tag2 mouse model of pancreatic neuroendocrine tumours. To further assess the functional role of CUX1, expression profiling of DNA damage-, proliferation- and apoptosis-associated genes was performed in CUX1-overexpressing Bon-1 cells. Validation of differentially regulated genes was performed in Bon-1 and QGP1 cells with knock-down and overexpression strategies. CUX1 expression assessed by a predefined immunoreactivity score (IRS) was significantly associated with shorter progression-free survival (PFS) of pre-treated PanNET patients (23 vs. 8 months; p = 0.005). In treatment-naïve patients, CUX1 was negatively correlated with grading and recurrence-free survival (mRFS of 39 versus 8 months; p = 0.022). In both groups, high CUX1 levels indicated a metastatic phenotype. Functionally, CUX1 upregulated expression of caspases and death associated protein kinase 1 (DAPK1), known as mediators of tumour progression and resistance to cytotoxic drugs. This was also confirmed in both cell lines and human tissues. In the RIP1Tag2 mouse model, CUX1 expression was associated with advanced tumour stage and resistance to apoptosis. In summary, we identified the transcription factor CUX1 as mediator of tumour progression in non-functional PanNET in vitro and in vivo, indicating that the CUX1-dependent signalling network is a promising target for future therapeutic intervention.

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Lamarca, Clouston, Barriuso, McNamara, Frizziero, Mansoor, Hubner, Manoharan, O’Dwyer, and Valle. "Follow-Up Recommendations after Curative Resection of Well-Differentiated Neuroendocrine Tumours: Review of Current Evidence and Clinical Practice." Journal of Clinical Medicine 8, no. 10 (October 5, 2019): 1630. http://dx.doi.org/10.3390/jcm8101630.

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The incidence of neuroendocrine neoplasms (NENs) is increasing, especially for patients with early stages and grade 1 tumours. Current evidence also shows increased prevalence, probably reflecting earlier stage diagnosis and improvement of treatment options. Definition of adequate postsurgical follow-up for NENs is a current challenge. There are limited guidelines, and heterogeneity in adherence to those available is notable. Unfortunately, the population of patients at greatest risk of recurrence has not been defined clearly. Some studies support that for patients with pancreatic neuroendocrine tumours (PanNETs), factors such as primary tumour (T), stage, grade (Ki-67), tumour size, and lymph node metastases (N) are of relevance. For bronchial neuroendocrine tumours (LungNETs) and small intestinal neuroendocrine tumours (siNETs), similar factors have been identified. This review summarises the evidence supporting the rationale behind follow-up after curative resection in well-differentiated PanNETs, siNETs, and LungNETS. Published evidence informing relapse rate, disease-free survival, and relapse patterns are discussed, together with an overview of current guidelines informing postsurgical investigations and duration of follow-up.

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Ney, Alexander, Gabriele Canciani, J. Justin Hsuan, and Stephen P. Pereira. "Modelling Pancreatic Neuroendocrine Cancer: From Bench Side to Clinic." Cancers 12, no. 11 (October 28, 2020): 3170. http://dx.doi.org/10.3390/cancers12113170.

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Pancreatic neuroendocrine tumours (pNETs) are a heterogeneous group of epithelial tumours with neuroendocrine differentiation. Although rare (incidence of <1 in 100,000), they are the second most common group of pancreatic neoplasms after pancreatic ductal adenocarcinoma (PDAC). pNET incidence is however on the rise and patient outcomes, although variable, have been linked with 5-year survival rates as low as 40%. Improvement of diagnostic and treatment modalities strongly relies on disease models that reconstruct the disease ex vivo. A key constraint in pNET research, however, is the absence of human pNET models that accurately capture the original tumour phenotype. In attempts to more closely mimic the disease in its native environment, three-dimensional culture models as well as in vivo models, such as genetically engineered mouse models (GEMMs), have been developed. Despite adding significant contributions to our understanding of more complex biological processes associated with the development and progression of pNETs, factors such as ethical considerations and low rates of clinical translatability limit their use. Furthermore, a role for the site-specific extracellular matrix (ECM) in disease development and progression has become clear. Advances in tissue engineering have enabled the use of tissue constructs that are designed to establish disease ex vivo within a close to native ECM that can recapitulate tumour-associated tissue remodelling. Yet, such advanced models for studying pNETs remain underdeveloped. This review summarises the most clinically relevant disease models of pNETs currently used, as well as future directions for improved modelling of the disease.

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Jamieson, A., and J. M. C. Connell. "Neuroendocrine Pancreatic Cancer: An Unusual Case of Pancreatitis." Scottish Medical Journal 45, no. 2 (April 2000): 55–56. http://dx.doi.org/10.1177/003693300004500209.

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Yang, Zhizhou, Jorge G. Zarate Rodriguez, Haley Beck, Kathleen Byrnes, Nikolaos A. Trikalinos, and Chet W. Hammill. "Acinar cell carcinoma with PRKAR1A and PTEN alterations and paraneoplastic panniculitis." BMJ Case Reports 15, no. 12 (December 2022): e251400. http://dx.doi.org/10.1136/bcr-2022-251400.

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Pancreatic acinar cell carcinoma is a rare type of pancreatic malignancy, which can be confused with pancreatic neuroendocrine neoplasm. Here, we describe a woman in her 80s who presented with abdominal pain and bilateral lower extremity panniculitis. She underwent surgery for a presumed diagnosis of neuroendocrine tumour with PTEN and PRKAR1A alterations; 19 months, later, a recurrence of her pancreatic malignancy was discovered. The patient underwent repeat resection and this time immunohistochemical staining confirmed the diagnosis of acinar cell carcinoma. Staining for acinar cell carcinoma should be prompted based on clinical suspicion in context of PTEN or PRKAR1A mutation when appropriate.

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Gyorki, DE, NE Clarke, MW Hii, SW Banting, and RJ Cade. "Management of synchronous tumours of the oesophagus and pancreatic head: a novel approach." Annals of The Royal College of Surgeons of England 93, no. 6 (September 2011): e111-e113. http://dx.doi.org/10.1308/147870811x591675.

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Synchronous tumours of the oesophagus and pancreatic head are very rare. This report describes a unique case of an adenocarcinoma of the distal oesophagus and a neuroendocrine tumour of the pancreatic head diagnosed synchronously but successfully managed metachronously. Initially, the patient underwent an oesophagectomy, with a colonic reconstruction following some months later by pylorus-preserving pancreaticoduodenectomy. A staged resection was performed after a review of the literature suggested increased morbidity with synchronous major abdominal operations.

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Predescu, Dragoş. "Pancreatic Neuroendocrine Tumour in Pregnancy - Diagnosis and Treatment Management." Chirurgia 114, no. 5 (2019): 550. http://dx.doi.org/10.21614/chirurgia.114.5.550.

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Karanth, Jnanaprakash B., Vishwas Pai, and Kiran Maribashetti. "Pancreatic neuroendocrine tumour—insulinoma masquerading as a psychiatric illness." BMJ Case Reports 15, no. 6 (June 2022): e249698. http://dx.doi.org/10.1136/bcr-2022-249698.

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A female patient in her early sixties had problems of recurrent syncopal attacks and panic attacks over the last 5 years. She had been initially managed for an anxiety disorder with psychiatric medications. During one of those episodes, she was brought to our hospital in an unconscious state with a low blood sugar level of 43 mg/dL. She was suspected to have a neuroendocrine tumour and diagnosis was established by supervised fasting up to 72 hours and imaging. Her recorded blood sugar during fasting was 37 mg/dL. She underwent surgery and presently remains asymptomatic. Physicians should have a high suspicion of insulinoma in patients presenting with repeated episodes of hypoglycaemic symptoms in the absence of any cognizable cause.

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Cheuk, YY, WK Lo, SK Chan, and CW Wong. "Pancreatic Neuroendocrine Tumour Causing Chronic Diarrhoea: Radiological-Pathological Correlations." Hong Kong Journal of Radiology 17, no. 1 (March 28, 2014): 45–48. http://dx.doi.org/10.12809/hkjr1412150.

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Peixoto, Armando, Pedro Pereira, Susana Lopes, and Guilherme Macedo. "Pancreatic neuroendocrine tumour simulating an intraductal papillary mucinous neoplasm." Digestive and Liver Disease 47, no. 3 (March 2015): 256. http://dx.doi.org/10.1016/j.dld.2014.10.015.

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Rebours, Vinciane, Jacqueline Cordova, Anne Couvelard, Monique Fabre, Laurent Palazzo, Marie Pierre Vullierme, Olivia Hentic, et al. "Can pancreatic neuroendocrine tumour biopsy accurately determine pathological characteristics?" Digestive and Liver Disease 47, no. 11 (November 2015): 973–77. http://dx.doi.org/10.1016/j.dld.2015.06.005.

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Lin, Shaojian, Anke Zhang, Xun Zhang, and Zhe Bao Wu. "Treatment of Pituitary and Other Tumours with Cabergoline: New Mechanisms and Potential Broader Applications." Neuroendocrinology 110, no. 6 (October 10, 2019): 477–88. http://dx.doi.org/10.1159/000504000.

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Cabergoline is a dopamine agonist that has been used as the first-line treatment option for prolactin-secreting pituitary adenomas for several decades. It not only suppresses hormone production from these prolactinomas, but also causes tumour shrinkage. Recent studies revealed some novel mechanisms by which cabergoline suppresses tumour cell proliferation and induces cell death. In this article, we review the most recent findings in cabergoline studies, focusing on its anti-tumour function. These studies suggest the potential broader clinical use of cabergoline in the treatment of other tumours such as breast cancer, pancreatic neuroendocrine tumours, and lung cancer.

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Stridsberg, M., K. Öberg, Q. Li, U. Engström, and G. Lundqvist. "Measurements of chromogranin A, chromogranin B (secretogranin I), chromogranin C (secretogranin II) and pancreastatin in plasma and urine from patients with carcinoid tumours and endocrine pancreatic tumours." Journal of Endocrinology 144, no. 1 (January 1995): 49–59. http://dx.doi.org/10.1677/joe.0.1440049.

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Abstract Chromogranins and/or secretogranins constitute a family of water-soluble acidic glycoproteins that are present in almost all endocrine, neuroendocrine and neuronal tissue. Antibodies against chromogranins have been widely used for immunohistochemical staining of endocrine tissue and tumours of neuroendocrine origin. Furthermore, measurements of circulating chromogranin A have been used as a reliable marker for neuroendocrine tumour growth. In this study, we describe the development of specific antibodies against chromogranin A, chromogranin B (secretogranin I), chromogranin C (secretogranin II) and pancreastatin. The antibodies were used for immunohistochemical staining of normal and neoplastic neuroendocrine tissue and development of reliable radioimmunoassays for chromogranin A, chromogranin B, chromogranin C and pancreastatin. In 44 patients with carcinoid tumours, 17 patients with sporadic endocrine pancreatic tumours and 11 patients with endocrine pancreatic tumours and the multiple endocrine neoplasia 1 syndrome, plasma measurements revealed elevated chromogranin A levels in 99%, elevated chromogranin B in 88%, elevated chromogranin C in 6% and elevated pancreastatin in 46% of the patients. Urinary measurements revealed elevated levels in 39%, 15%, 14% and 33% of the patients respectively. Gel permeation chromatography of plasma and urine showed that circulating chromogranin A, and immunoreactive fragments of chromogranin A, had a higher molecular weight distribution than the chromogranin A fragments excreted to the urine. Furthermore, it was noted that most of the patients excreting chromogranin A fragments to the urine had previously been treated with streptozotocin, a cytotoxic agent known to induce renal tubular dysfunction. The antibodies raised proved useful for immunohistochemical staining and visualised endocrine cells in pancreatic islets, adrenal medulla and the small intestine as well as in endocrine pancreatic tumours, pheochromocytoma and midgut carcinoid tumours. In conclusion, the antibodies raised were useful for both immunohistochemical staining of normal tissue and endocrine tumours as well as development of specific radioimmunoassays for plasma measurements of the different chromogranins. Furthermore, we show that plasma measurements of chromogranin A and B were superior to measurements of chromogranin C and pancreastatin and plasma measurements of the different chromogranins were more reliable as markers for tumour growth than the corresponding urine measurements. Journal of Endocrinology (1995) 144, 49–59

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Alsadik, Shahad, Siraj Yusuf, and Adil AL-Nahhas. "Peptide Receptor Radionuclide Therapy for Pancreatic Neuroendocrine Tumours." Current Radiopharmaceuticals 12, no. 2 (July 16, 2019): 126–34. http://dx.doi.org/10.2174/1874471012666190201164132.

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Background: The incidence of pancreatic Neuroendocrine Tumours (pNETs) has increased considerably in the last few decades. The characteristic features of this tumour and the development of new investigative and therapeutic methods had a great impact on its management. Objective: The aim of this review is to investigate the outcome of Peptide Receptor Radionuclide Therapy (PRRT) in the treatment of pancreatic neuroendocrine tumours. Methods: A comprehensive literature search strategy was used based on two databases (SCOPUS, and PubMed). We considered all studies published in English, evaluating the use of PRRT (177Luteciuim- DOTA-conjugated peptides and 90Yetrium- DOTA- conjugated peptides) in the treatment of pancreatic neuroendocrine tumours as a standalone entity or as a subgroup within the wider category of Gastroenteropancreatic Neuroendocrine Tumours (GEP NETs). Results: PRRT was found to be an effective treatment modality as a monotherapy or in combination with other therapies in the treatment of non-operable and metastatic pNETs where other options are limited. Complete response was reported to be between 2-6% while partial response was achieved in up to 60% of cases. Survival analysis was also impressive. Progression Free Survival (PFS) reached a mean of 34 months and Overall Survival (OS) of 53 months. PRRT also proved to improve patients’ Quality of Life (QoL). Acute and sub-acute side effects like nephrotoxicity and haematotoxicity are usually mild and reversible. Conclusion: PRRT is well tolerated and effective treatment option for non-operable and/or metastatic pNETs. Side effects are usually mild and reversible. Larger randomized controlled trails need to be done to compare PRRT with other treatment modalities and to provide more detailed guidelines regarding patient selections, the choice of PRRT, follow up and response assessment to maximum potential benefit.

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Angelico, Roberta, Leandro Siragusa, Cristine Brooke Pathirannehalage Don, Bruno Sensi, Federica Billeci, Leonardo Vattermoli, Belen Padial, et al. "Pancreatic Adeno-MiNEN, a Rare Newly Defined Entity with Challenging Diagnosis and Treatment: A Case Report with Systematic Literature Review and Pooled Analysis." Journal of Clinical Medicine 11, no. 17 (August 26, 2022): 5021. http://dx.doi.org/10.3390/jcm11175021.

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Mixed neuroendocrine non-neuroendocrine neoplasms (MiNEN) are a peculiar entity that can occur throughout the whole gastrointestinal trait, and pancreatic localization is rare. Their main characteristic is the presence of at least a neuroendocrine and an epithelial component, each accounting for at least 30% of the tumour mass. The presence of epithelial ductal component defines adeno-MiNEN. We report a case of a 59-year-old woman affected by pancreatic adeno-MiNEN with challenging diagnosis and successfully treated. A systematic literature review and pooled analysis was also performed, aiming to define the management and outcomes of pancreatic adeno-MiNEN. Out of 190 identified records, 15 studies including 28 patients affected by pancreatic-adeno-MiNEN were included in the analysis. Pancreatic adeno-MiNEN occurred mainly in males (82.8%) and at a mean age of 61.7 (range: 24–82) years. Pre-operative diagnosis was possible only in 14.2% of cases. At presentation, the majority had already advanced disease (TNM stage III (53.8%) and stage IV 19.3%). Adjuvant therapy was performed in 55% of patients, and the tumour recurrence rate was in 30% of cases. Median disease-free survival (DFS) was 12 months (range: 0–216 months) with a 5-year DFS of 16.6%, while the median overall survival (OS) was 12 months (range: 0–288 months) with a 5-year OS of 23.5%. Pancreatic adeno-MiNENs are rare; as they have very heterogenous behaviour, they are rarely diagnosed preoperatively and have poor prognosis. Treatment of localised MiNEN still relies on radical surgical resection, which seems essential to achieve a good oncological prognosis. International registry on MiNEN is necessary to improve the knowledge on this rare tumour and to improve its outcomes.

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Krug, Sebastian, Benjamin Kühnemuth, Heidi Griesmann, Albrecht Neesse, Leonie Mühlberg, Michael Boch, Juliane Kortenhaus, et al. "CUX1: a modulator of tumour aggressiveness in pancreatic neuroendocrine neoplasms." Endocrine-Related Cancer 21, no. 6 (September 23, 2014): 879–90. http://dx.doi.org/10.1530/erc-14-0152.

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Pancreatic neuroendocrine neoplasms (PNENs) constitute a rare tumour entity, and prognosis and treatment options depend on tumour-mediating hallmarks such as angiogenesis, proliferation rate and resistance to apoptosis. The molecular pathways that determine the malignant phenotype are still insufficiently understood and this has limited the use of effective combination therapies in the past. In this study, we aimed to characterise the effect of the oncogenic transcription factor Cut homeobox 1 (CUX1) on proliferation, resistance to apoptosis and angiogenesis in murine and human PNENs. The expression and function ofCUX1were analysed using knockdown and overexpression strategies in Ins-1 and Bon-1 cells, xenograft models and a genetically engineered mouse model of insulinoma (RIP1Tag2). Regulation of angiogenesis was assessed using RNA profiling and functional tube-formation assays in HMEC-1 cells. Finally,CUX1expression was assessed in a tissue microarray of 59 human insulinomas and correlated with clinicopathological data.CUX1expression was upregulated during tumour progression in a time- and stage-dependent manner in the RIP1Tag2 model, and associated with pro-invasive and metastatic features of human insulinomas. Endogenous and recombinantCUX1expression increased tumour cell proliferation, tumour growth, resistance to apoptosis, and angiogenesisin vitroandin vivo. Mechanistically, the pro-angiogenic effect ofCUX1was mediated via upregulation of effectors such as HIF1α and MMP9.CUX1mediates an invasive pro-angiogenic phenotype and is associated with malignant behaviour in human insulinomas.

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Eren, Merve, and Feyzi Bostan. "Non- pancreatic neuroendocrine tumour presenting with hypoglycemia in an elderly patient." African Health Sciences 20, no. 4 (December 16, 2020): 1875–9. http://dx.doi.org/10.4314/ahs.v20i4.44.

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Background: Hypoglycemia is a common, symptom seen in individuals. Hypoglycemia in the elderly is both under-recog- nized and misdiagnosed due to nonspesific hypoglycemic symptoms and accompanying comorbidities in this population. In diabetic individuals, hypoglycemia is most commonly caused by administering insulin or sulphonylureas and insulin secretagogues. Other drugs, such as antibiotics or beta-blockers, have been reported to reduce blood glucose to abnormally low levels. Hypoglycemia in non-diabetic patients is considered a rare event, and the possible reasons may be reactive hypo- glycemia, insulin-secreting tumours and other malignancies, hypopituitarism, hypocortisolism, alcohol abuse, inappropriate insulin self-administration, malnutrition, renal failure and sepsis. Case: An 86- year- old male was admitted to the emergency department with hypoglycemia diagnosed with non-pancreatic neuroendocrine tumour (NET) on lung secreting insulin. No surgical intervention or chemotherapy was planned due to patients age and comorbidities so best supportive care was planned. We used prednisone for symptomatic treatment of hy- poglycemia and the patient has been followed up periodically. In this period he had no hypoglycemic attack. Conclusion: For patients with hypoglycemia who are unable/decline to receive any further treatment, low dose glucocorti- coid is a good choice to achieve normoglycemia. It seems to be more cost effective compared to other treatment options. Furthermore hospitalisation rates may decrease due to decreased hypogylcemic attacks. Keywords: Neuroendocrine tumour; hypoglycaemia; prednisone; non-islet cell tumour.

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Torres, Ulysses S., Daniel Nicoletti Cesar, and Giuseppe D’Ippolito. "Hypovascular Non-functional Neuroendocrine Pancreatic Tumour: An Unusual Presentation of a Rare Tumour." Cirugía Española (English Edition) 94, no. 3 (March 2016): 182–84. http://dx.doi.org/10.1016/j.cireng.2016.02.016.

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Gulpinar, Basak, Elif Peker, Cigdem Soydal, Mine Araz, and Atilla Halil Elhan. "Can we differentiate histologic subtypes of neuroendocrine tumour liver metastases at a single phase contrast-enhanced CT—correlation with Ga-68 DOTATATE PET/CT findings." British Journal of Radiology 93, no. 1106 (February 1, 2020): 20190735. http://dx.doi.org/10.1259/bjr.20190735.

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Objective: To assess the usefulness of a single-phase contrast-enhanced CT to differentiate subtypes of neuroendocrine tumour (NET) liver metastases and to evaluate the correlation between CT features and Ga-68 DOTATATE positron emission tomography/CT (PET/CT) findings. Methods: Between December 2017 and April 2019 patients with liver metastases of neuroendocrine tumours who underwent CT and Ga-68 DOTATATE PET/CT were enrolled in the study. All patients involved in the study had undergone a standardised single-phase contrast-enhanced CT. Whole body PET/CT images were obtained with a combined PET/CT scanner. All CT images were retrospectively analysed by two radiologists. Enhancement patterns of lesions were assessed. For quantitative examination; CT attenuation values of metastatic lesions, liver parenchyma and aorta were measured using a freehand ROI and tumour-to-liver ratio [T–L = (Tumour–Liver) / Liver] and tumour-to-aorta ratio [T–A = (Tumour–Aorta) / Aorta] were calculated. The lesion with the highest Ga-68 DOTATATE uptake in the liver was used for calculations. The metabolic tumour volume (MTV), maximum standardised uptake value (SUV max) and SUV mean were calculated for the target liver lesion. Results: A total of 137 NET liver metastases divided into in three groups: 49 (35.7%) pancreatic, 60 (44.5%) gastroenteric and 26 (18.9%) lung NET liver metastases were analysed. Gastroenteric NET metastases often showed heterogeneous enhancement which was significantly higher than in the pancreas and lung NET liver metastases (p < 0.001). 96.72% (n = 59) of the gastroenteric NET liver metastases were hypoattenuating whereas the most frequent presentation for the pancreatic group was hyperattenuation (63.26%,n = 31). The difference in enhancement patterns of the liver metastases was statistically significant (p < 0.001) with respect to the location of the primary tumour. For quantitative analysis; tumour CT values were significantly different between the groups (p < 0.001). The T–L ratio was statistically different between gastroenteric and pancreatic NET liver metastases and pancreatic and lung NET groups (p < 0.001). The T–A ratio was significantly higher in the pancreatic NET metastases (p < 0.001). SUVmax, SUVmean and MTV values, however, were not significantly different between the subgroups. There was a weak positive correlation between T–L ratio and SUV meanvalues. Conclusion: We noticed statistically significant differences in both qualitative and quantitative CT features between histologic subgroups of neuroendocrine tumour liver metastases at a single phase contrast-enhanced CT. Advances in knowledge: Our study will be the first in the literature which extensively focus on assessing the CT features of liver metastases of NETs at a single phase CT and Ga-68DOTATATE PET/CT. As the different histological subtypes of NET liver metastases exhibit different clinical outcomes, these features might help to identify the primary tumour to provide optimal treatment.

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Guidetti, Elena, Monica Cevenini, Maria Luigia Cipollini, Martina Ferrata, Paola Tomassetti, and Roberto Corinaldesi. "MEN1 syndrome: an anusual case." Clinical Management Issues 6, no. 1S (October 13, 2015): 23–28. http://dx.doi.org/10.7175/cmi.v6i1s.493.

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Multiple endocrine neoplasia type 1 (MEN1) is a rare autosomal dominant endocrine disorder and is characterised by the concurrent appearance of adenomas of the parathyroid glands, neuroendocrine-enteropancreatic tumours, and pituitary adenomas, as well as other types of less frequent tumours, such as adrenal cortical tumours, carcinoid tumours, lipomas, etc. Two different forms, familial and sporadic, have been described. The gene responsible, MEN1, consists of 10 exons encoding a 610-amino acid protein known as menin. The MEN1 syndrome is caused by inactivating mutations in MEN1 tumour suppressor gene. The combination of clinical and genetic investigation helps in the diagnosis. Genetic testing has been advocated to identify MEN1 carriers of the MEN1 families for the purpose of earlier detection of tumours. We present a patient with traditionally described manifestations of MEN1 (a parathyroid hyperplasia associated with a pancreatic neuroendocrine tumour and a gastrinoma), but with a negative genetic test for the MEN1 mutation.

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Yao, James, and Alexandria T. Phan. "Optimising Therapeutic Options for Patients with Advanced Pancreatic Neuroendocrine Tumours." European Oncology & Haematology 08, no. 04 (2012): 217. http://dx.doi.org/10.17925/eoh.2012.08.4.217.

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Pancreatic neuroendocrine tumours (pNETs) are a rare form of pancreatic cancer. Several therapeutic options exist for pNETS; however, there is no algorithm to determine the optimum sequence of therapies. Approved treatments for pNETs include somatostatin analogues (SSAs), streptozocin-based chemotherapy and targeted therapies such as everolimus and sunitinib. Unapproved therapies include systemic peptide receptor-targeted radiotherapy (PRRT), temozolomide-based chemotherapy, liver resection, liver transplantation, hepatic artery embolisation with or without chemotherapy and selective internal radiation therapy (SIRT). An individualised approach to the treatment of pNETs is described. Firstly, it is necessary to decide whether it is appropriate to treat at all. For those wi th symptoms, it is necessary to define the treatment goal: symptomatic or oncological control. Symptoms may direct treatment decisions; for example in patients with hypogycaemia, everolimus would be the most effective therapy. In high-volume disease where tumour reduction is the highest priority, streptozocin-based chemotherapy would be a more appropriate choice. For patients with disease progression and a moderate-to-high tumour volume, targeted therapy is the preferred choice. Following the failure of first-line therapies, second-line options include other targeted agents and cytotoxic chemotherapy. PRRT is recommended only after failure of prior therapy. Treatment decisions of pNETs should be made in a patient-oriented manner and on a case-by-case basis.

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Soni, S., S. Jabbar, A. Swami, and R. Nayar. "Synchronous Periampullary Adenocarcinoma with Pancreatic Neuroendocrine Tumour: A Rare Entity." HPB 24 (2022): S272. http://dx.doi.org/10.1016/j.hpb.2022.05.577.

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Shea, Y. f., W. y. J. Chiu, M. y. M. Mok, I. F. n. Hung, and C. c. T. Yau. "Sunitinib-induced hyperammonaemia in a patient with pancreatic neuroendocrine tumour." Journal of Clinical Pharmacy and Therapeutics 38, no. 4 (April 16, 2013): 327–29. http://dx.doi.org/10.1111/jcpt.12054.

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Shah, B., D. N. Rana, and M. Desai. "Cytomorphological and imunohistochemical evaluation of a cystic pancreatic neuroendocrine tumour." Cytopathology 18, no. 6 (December 2007): 395–96. http://dx.doi.org/10.1111/j.1365-2303.2007.00423.x.

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Kotoulas, Chr, J. Panayiotides, Chr Antiochos, D. Sambaziotis, G. Papadopoulos, and A. Karameris. "Huge non-functioning pancreatic cystic neuroendocrine tumour: A case report." European Journal of Surgical Oncology (EJSO) 24, no. 1 (February 1998): 74–76. http://dx.doi.org/10.1016/s0748-7983(98)80133-9.

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Mills, Logan, Panagiotis Drymousis, Yogesh Vashist, Christoph Burdelski, Andreas Prachalias, Parthi Srinivasan, Krishna Menon, et al. "Tumour diameter is not reliable for management of non-secreting pancreatic neuroendocrine tumours." Endocrine Connections 6, no. 8 (November 2017): 876–85. http://dx.doi.org/10.1530/ec-17-0293.

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Small non-functioning pancreatic NETs (pNETs) ≤2 cm can pose a management dilemma in terms of surveillance or resection. There is evidence to suggest that a surveillance approach can be considered since there are no significant radiological changes observed in lesions during long-term follow-up. However, other studies have suggested loco-regional spread can be present in ≤2 cm pNETs. The aim of this study was to characterise the prevalence of malignant features and identify any useful predictive variables in a surgically resected cohort of pNETs. 418 patients with pNETs were identified from 5 NET centres. Of these 227 were included for main analysis of tumour characteristics. Mean age of patients was 57 years, 47% were female. The median follow-up was 48.2 months. Malignant features were identified in 38% of ≤2 cm pNETs. ROC analysis showed that the current cut-off of 20 mm had a sensitivity of 84% for malignancy. The rate of malignant features is in keeping with other surgical series and challenges the belief that small pNETs have a low malignant potential. This study does not support a 20 mm size cut-off as being a solitary safe parameter to exclude malignancy in pNETs.

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Journal articles on the topic 'Pancreatic neuroendocrine tumour'

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