Relevant bibliographies by topics / Pancreatic neuroendocrine tumour

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  2. Dissertations / Theses
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  4. Book chapters
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Academic literature on the topic 'Pancreatic neuroendocrine tumour'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Pancreatic neuroendocrine tumour"

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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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Dissertations / Theses on the topic "Pancreatic neuroendocrine tumour"

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Gill, Preetjote. "Studies In Patients With Surgically Resected Pancreatic Neuroendocrine Tumours - MicroRNA Expression And Clinical Correlation." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/18181.

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INTRODUCTION Pancreatic Neuroendocrine Tumours (PNETS) have increased in incidence over the past three decades. Treatment options currently include surgery, locoregional and systemic therapies, however the prognosis remains poor and biomarkers that accurately predict the clinical behavior of these tumours are lacking. Dysregulation of microRNAs (miRNAs) has recently been shown to play a role in the development of many cancers through post-transcriptional gene regulation, however, few studies have investigated the role of miRNAs as diagnostic or prognostic markers in PNETs. METHODS Patients undergoing resection of PNETs at our institutions between 1992 and 2014 were retrospectively included in this study. RNA was extracted from formalin-fixed, paraffin embedded PNET samples and microarray analysis performed and correlated with clinicopathological data. MicroRNAs with statistically significant differential expression between patients with locoregional disease only, versus those who developed metastases were subject to in-silico analysis using three target gene prediction databases. RESULTS 37 patients were included in the study. Patient subgroup DM had poorer overall survival (OS) as compared to subgroup L (p = 0.046). 506 miRNAs with differential expression between the ‘Distant metastasis’ group and ‘Locoregional’ group were identified. Of these, 265 miRNAs were downregulated, whilst 241 were upregulated. Four of these miRNAs were differentially expressed to statistical significance. These included miR-3653 which was upregulated and miR-4417, miR-574-3p and miR-664b-3p which were all downregulated. Only miRNA-3653 was identified by all three databases as having a potential PNET-related target; ATRX. CONCLUSION Higher expression of tumour miR-3653 was seen in the group of patients with metastatic disease compared to those with only locoregional disease. Several bioinformatic tools predicted transcriptional regulator ATRX as a possible target for miR-3653. Thus, it is possible that miR-3653 could be a biomarker for metastatic potential and consequently poorer prognosis in patients with PNETs. However, these conclusions cannot be made with certainty given the limitations of this study and further work beginning with validation is required.
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De, Cassan Chiara. "Elastography mean strain histogram value for the differential diagnosis of malignant pancreatic masses: a monocentric study." Doctoral thesis, Università degli studi di Padova, 2016. http://hdl.handle.net/11577/3424524.

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Introduction Endoscopic ultrasound (EUS) elastography is a recent ultrasound method used for the real-time visualization and evaluation of tissue elasticity. Qualitative and quantitative methods have been used, in particular in evaluation of pancreatic diseases and malignant lymph nodes, with interesting results regarding the accuracy and the differential diagnosis between malignant and benign masses. No consensus has been reached with regard to the superiority of different quantitative methods, but strain ratio and strain histogram (SH) remain the most used. SH corresponds to a graphical representation of the color distribution in a region of interest (ROI), and mean SH (mSH) value is a SH-derived quantitative measure of the global hardness in the evaluated ROI. Materials and methods The aim of the present study was to describe the different elastographic patterns of solid pancreatic masses (pancreatic adenocarcinoma, PA, and pancreatic neuroendocrine tumor, pNET) using the mSH value. A group of normal patients was enrolled to define the normal pancreatic elasticity. This is a prospective, observational, monocentric study. Experienced EUS examiners performed the endoscopic procedure and elastographic measures. Contrast enhancement was performed, and according to the European Federation Societies of Ultrasound in Medicine and Biology guidelines and recommendations, 2 phases were defined for CE-US and CEH-EUS of the pancreas: an early and/or arterial phase (starting from 10 to 30 seconds) and a late and/or venous phase (from 30 to 120 seconds). Enhancement was evaluated in arterial phase. When the lesion resulted hypovascular (hypo-enhanced), the aspect was defined as typical for adenocarcinoma while an hypervascular lesion (with strong arterial hyper-enhancement) was considered typical of neuroendocrine tumors. SH was calculated automatically by machine integrated software in a ROI manually selected by the operator. Four parameters were calculated using the histogram to quantify the elasticity of the pancreas: the mSH, the standard deviation of the histogram, the kurtosis and the skewness. Three different measures were performed by the same operator and the mean value of the previous described values was evaluated. After the elastographic measure a FNA was performed when a lesion was observed. We used the histology obtained by FNA or surgical specimens or the global assessment of cytology and imaging as reference standard for the diagnosis, except in case of normal examinations. Results A total of 88 patients were included: 9 normals, 45 PA, 9 pNET (5 grade 1, 4 grade2-3), 5 chronic pancreatitis, 20 others (IPMN, metastatic lesions, pancreatic cystoadenoma, etc). Only patients with normal pancreas, PA and pNET were included in the statistical analysis. Mean age was 64 (range: 19-88). All the patients presenting a pancreatic lesion, except one, received the contrast. All the patients with pNET presented a typical hypervascular enhancement. On the other hand, of patients with histological proven pancreatic adenocarcinoma, only 37 presented a typical hypoenhancement, while 5 presented an hypervascularisation and 2 patients an atypical enhancement (represented by a partial arterial enhancement). Regarding elastography, we obtained a statistically significant difference between the malignant lesions (p-Net grade 2/3 and adenocarcinoma) and normal pancreas, considering all the parameters evaluated (mSH, standard deviation, kurtosis and skewness). No differences were found in elastographic measurement between p-NET and adenocarcinoma, neither between p-NET grade 1 (that, considering the good prognosis and slow evolution, could be considered neither as benign neither as malign) and p-NET grade 2/3. At univariate analysis we found that all the elastographic parameters measured were capable to differentiate benign versus malign disease, with a cut-off calculated with ROC-curves of 43.250 for mSH, 44.63 for standard deviation, 1.5 for the skewness and 5 for kurtosis. At multivariate analysis only mSH resulted statistically significative to distinguish benign versus malign lesions. At a model constructed by logistic regression (9.8958 – 0.3170*moyenne + 0.2989*SD + 0.7935*kurtosis – 7.0642*skewness) a cut off of 0.57 was found to distinguish benign versus malign lesions. Conclusions Mean strain histogram seems able to differentiate pancreatic cancer from benign pancreas. EUS elastography could potentially be used in negative EUS–FNA cases, which represent up to 25% of patients with focal masses. The presence of a strong suspicion of pancreatic cancer is indicated when combining meanSH, standard deviation, skewness and kurtosis in a statistical model we obtain a cut-off>0.57.
Introduzione L’elastometria condotta tramite ecoendoscopia è una nuova tecnica utilizzata per la visualizzazione e la valutazione in real time dell’elasticità dei tessuti. È noto infatti che i tessuti patologici, quali ad esempio i tessuti tumorali, presentano un’elasticità diversa rispetto ai tessuti normali. Fino ad oggi sono state utilizzate tecniche di misurazione dell’elasticità sia di tipo qualitativo che di tipo quantitativo. Le misure qualitative sono però gravate da una scarsa riproducibilità. Per tale ragione esse sono state praticamente abbandonate afavore di misure quantitative. Non esiste un consenso circa la superiorità di un metodo quantitativo rispetto ad un altro, ma lo “strain ratio” (SR) e lo “strain histogram” restano le metodiche più utilizzate. Lo SH, utilizzato in questo studio, corrisponde a una rappresentazione grafica della distribuzione del colore in una determinata area di interesse, e il valore del mSH è una misura dell’elasticità globale in un’area di interesse prescelta, normalmente corrispondente alla lesione. L’accuratezza dell’elastometria è stata valutata nelle patologie pancreatiche e linfonodali, mostrando risulatati interessanti soprattutto nella diagnosi differenziale tra le masse benigne e le masse maligne. Materiali e metodi Lo scopo del nostro studio è la quantificazione del pattern elastografico nel pancreas normale, nell’adenocarcinoma pancreatico (AP) e nei tumori neuroendocrine (NET). Si tratta di uno studio prospettico, monocentrico e osservazionale. L’ecoendoscopia con contrasto è stata effettuata e, secondo le line guida della società Europea di ecografia, sono state individuate 2 fasi contrastografiche per lo studio del pancreas: la prima, dai 10 ai 30 secondi, denominata fase precoce o arteriosa e la seconda, tardiva o venosa, dai 30 ai 120 secondi. L’enhancement delle lesioni pancreatiche è stato valutato in fase arteriosa. All’ecoendoscopia con contrasto, l’aspetto tipico di AP è definito in presenza di ipo-enhancement, mentre l’aspetto tipèico in caso di NET è definite in presenza di iper-enhancement arterioso. Successivamente all’elastometria è stata eseguita un’elastografia. Lo SH è stato calcolato automaticamente da un software in un’area scelta manualmente dall’operatore. 4 parametri sono stati presi in considerazione: lo SH medio (Msh), la deviazione standard, la kurtosis e lo swekness. 3 misure differenti sono state effettuate dallo stesso operatore e il valore medio delle misure è stato preso in considerazione. Dopo la misura elastografica è stato eseguito il prelievo bioptico. Il risultato istologico ottenuto tramite biopsia è stato utilizzato come referenza per definire la natura della lesione, eccetto in caso di pancreas normale. Risultati Nello studio sono stati inclusi 88 pazienti: 9 pancreas normali, 9 NET, 45 AP, 5 pancreatiti croniche e 20 lesioni miste. Solo I pazienti con AP, NET e pancreas normale sono stati inclusi nell’analisi finale. Alla somministrazione di contrasto, i pazienti con NET hanno presentato un pattern ipervascolare dopo somministrazione di contrasto, mentre tra i pazienti con AP, solo 37 hanno presentato un pattern tipico ipovascolare, mentre 5 hanno presentato un pattern ipervascolare e 2 un enhancement atipico (arterioso parziale). Per ciò che riguarda l’elastografia, abbiamo ottenuto una differenza statisticamente significativa tra il pancreas normale e le lesioni maligne, per tutti i 4 parametri valutati (media, deviazione standard, kurtosis e skewness). Invece, non abbiamo trovato una differenza statisticamente significativa tra i NET e l’AP. All’analisi univariata abbiamo trovato che tutti i parametri erano in grado di differenziare il pancreas benigno dal pancreas maligno, con un cut-off calcolato mediante la curva ROC di 43.250 per mSH, 44.63 per la deviazione standard, 1.5 per lo skewness and 5 per la kurtosis. All’analisi multivariata, solo il mSH è risultato statisticamente significativo. Abbiamo costruito un modello statistico tramite regressione logistica (9.8958 – 0.3170*mSH + 0.2989*SD + 0.7935*kurtosis – 7.0642*skewness), individuando un cut off di 0.57 per distinguere il pancreas normale dale lesioni maligne. Conclusioni Il mSH sembra efficace nella differenziazione tra lesioni pancreatiche maligne e pancreas benigno. Proponiamo pertanto l’uso dell’elastometria, e del nostro modello statistico, per definire le lesioni da operare o da sorvegliare in caso di biopsia negativa. Riteniamo infatti che, pur in caso di biopsia negativa, un indice elastografico superiore a 0.57 sia indicativo di una lesione maligna e pertanto necessiti di una presa in carico chirurgica.
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Hanson, Matthew Richard. "Expression studies on PPARγ in pancreatic neuroendocrine tumours." Thesis, Queen Mary, University of London, 2010. http://qmro.qmul.ac.uk/xmlui/handle/123456789/710.

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Pancreatic NETs occur with an annual incidence of around 5 per 1,000,000 population per year, with survival rates of between 30 – 97% at 5 years depending on the tumour subtype. The PPARs (peroxisomal proliferator-activated receptors) are members of the nuclear receptor superfamily that includes receptors for thyroid, steroid and retinoid hormones. PPARγ protein is also thought to be expressed in human pancreatic islet cells and has been shown to be a negative regulator of islet β cell mass both in vivo and in vitro. Its emerging function in controlling cell proliferation, differentiation and apoptosis, both in vivo and in vitro, has suggested a putative role as a tumour suppressor gene. I postulated that PPARγ is expressed in pancreatic neuroendocrine tumours and that agonism with a thiazolidinedione will cause an anti-proliferative effect. Three different types of tissue/cells were available to me: frozen human pancreatic neuroendocrine tumours following surgical resection, paraffin-embedded samples held in the histopathology archives, and human neuroendocrine tumour cell lines CM, BON and QGP1 (insulinoma, carcinoid and somatostatinoma respectively). PPARγ RNA was shown to be present in the majority of frozen surgical samples. Immunohistochemistry for PPARγ protein on the paraffin-embedded samples, however, revealed a lack of positive staining. These samples were then subjected to further immunohistochemistry for detection of other potentially important proteins involved with cellular proliferation including p27, phospho-p27, JAB1, PTEN and phospho- AKT. In the tumour cell models, PPARγ RNA and protein was present in both BON and QGP1. Proliferation studies following treatment doses of PPARγ agonist 3 rosiglitazone show a significant anti-proliferative effect. Recovery of cells was shown following removal of treatment. However, inhibition of the effect was not achieved with the use of PPARγ antagonists raising the possibility that the anti-proliferative effects of thiazolidinediones may be independent of PPARγ.
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Bösch, Florian [Verfasser], and Markus [Akademischer Betreuer] Guba. "Single center experience in pancreatic neuroendocrine tumors / Florian Bösch. Betreuer: Markus Guba." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2015. http://d-nb.info/1081899859/34.

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Yamauchi, Yuki. "Rb and p53 Execute Distinct Roles in the Development of Pancreatic Neuroendocrine Tumors." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/264634.

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京都大学
新制・論文博士
博士(医学)
乙第13418号
論医博第2226号
新制||医||1052(附属図書館)
京都大学大学院医学研究科医学専攻
(主査)教授 羽賀 博典, 教授 長船 健二, 教授 伊藤 貴浩
学位規則第4条第2項該当
Doctor of Medical Science
Kyoto University
DFAM
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Körner, Jan Lennart [Verfasser], and Roland [Akademischer Betreuer] Kontermann. "Target identification and probe development for pancreatic neuroendocrine tumors / Jan Lennart Körner. Betreuer: Roland Kontermann." Stuttgart : Universitätsbibliothek der Universität Stuttgart, 2015. http://d-nb.info/1069290211/34.

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ANDREASI, VALENTINA. "ROLE OF CHROMOGRANIN A-DERIVED FRAGMENTS AND OTHER BIOMARKERS IN PANCREATIC NEOPLASMS: FOCUS ON NEUROENDOCRINE TUMORS." Doctoral thesis, Università Vita-Salute San Raffaele, 2021. http://hdl.handle.net/20.500.11768/121777.

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Introduction: The lack of valid biomarkers represents a major unmet clinical need in pancreatic neuroendocrine neoplasms (PanNENs). Chromogranin A (CgA) is the most commonly measured PanNEN biomarker, despite relevant limitations related to variable sensitivity, poor specificity and lack of assay standardization. Therefore, novel biomarkers are needed to improve diagnosis, detect disease recurrence and assess treatment response. In this project, the role of CgA-derived fragments as PanNEN biomarkers was investigated, focusing on the N-terminal peptide vasostatin-1 (VS-1). A multianalyte biomarker, NETest, was also assessed as PanNEN biomarker. Given the role of CgA-derived fragments in tumor vascular biology, their tissue expression was correlated with pathological features in PanNENs. Finally, the role of CgA-derived fragments was investigated in the setting of pancreatic ductal adenocarcinoma (PDAC). Methods: The project was developed according to different tasks: 1) CgA-derived fragments and total-CgA were measured in patients who underwent surgery for PanNENs; 2) NETest was evaluated as biomarker evaluate the efficacy of surgical resection in patients with PanNENs; 3) The site of CgA cleavage was investigated and CgA-derived fragments tissue expression was assessed; 4) The role of CgA fragmentation in terms of prognosis was assessed in patients with PDAC. Results: Aim 1. VS-1 is significantly correlated with tumor size, aggressiveness features and risk of disease relapse in patients with localized non-functioning (NF) PanNENs. VS-1 is not affected by proton pump inhibitors treatment. Aims 2-3. VS-1 is able to early assess surgical effectiveness in patients with NF-PanNETs, especially in those with aggressive tumors. Total-CgA, VS-2 and pancreastatin are not useful in this context. Aim 4. NETest seems able to provide a proper evaluation of the initial postoperative disease status in setting of PanNENs. Aim 5. CgA processing occurs within neuroendocrine tumor cells. VS-1 tissue expression is a marker of tumor differentiation. Aim 6. C-terminal CgA cleavage is enhanced in PDAC and it is associated with poorer survival outcomes. Conclusions: VS-1 has been identified as a promising biomarker for PanNENs. CgA C-terminal fragmentation is enhanced in PDAC, whereas N-terminal cleavage seems more relevant in PanNENs. Whether CgA fragmentation in PanNENs is just a disease epiphenomenon or plays a role in tumor vascular biology remains an open point.
Introduzione: La mancanza di biomarcatori validi rappresenta un'importante esigenza clinica nell’ambito delle neoplasie neuroendocrine pancreatiche (PanNEN). La cromogranina A (CgA) è il biomarcatore neuroendocrino più comunemente utilizzato, nonostante le rilevanti limitazioni legate alla sensibilità variabile, alla scarsa specificità ed alla mancanza di standardizzazione del suo dosaggio. Sono pertanto necessari nuovi biomarcatori al fine migliorare la diagnosi, predire la ricorrenza di malattia e valutare la risposta ai trattamenti. In questo progetto abbiamo studiato il ruolo dei frammenti derivati dalla CgA come biomarcatori nelle PanNEN, concentrandoci sul peptide N-terminale chiamato vasostatina-1 (VS-1). Anche un biomarcatore multianalita, NETest, è stato valutato nell’ambito delle PanNEN. Inoltre, considerato il ruolo dei frammenti derivati dalla CgA nella biologia vascolare dei tumori, la loro espressione tissutale è stata correlata con caratteristiche patologiche di aggressività in campioni di PanNEN. Infine, il ruolo dei frammenti della CgA è stato studiato anche nel contesto dell'adenocarcinoma duttale pancreatico (PDAC). Metodi: Il progetto è stato sviluppato secondo diverse attività: 1) I frammenti derivati dalla CgA e la CgA totale sono stati misurati in pazienti sottoposti ad intervento chirurgico per PanNEN; 2) Il NETest è stato valutato come biomarcatore per predire l'efficacia della resezione chirurgica in pazienti con PanNEN; 3) Il sito di clivaggio della CgA così come l'espressione tissutale dei frammenti derivati dalla CgA sono stati oggetto di studio; 4) Il ruolo prognostico della frammentazione della CgA è stato valutato in pazienti con PDAC. Risultati: Obiettivo 1. I livelli plasmatici di VS-1 sono significativamente correlati con le dimensioni del tumore, le caratteristiche di aggressività e il rischio di recidiva di malattia in pazienti con PanNEN localizzate non funzionanti (NF). La VS-1 non è influenzata dal trattamento con inibitori di pompa protonica. Obiettivi 2-3. La VS-1 è in grado di valutare precocemente l'efficacia chirurgica nei pazienti con NF-PanNET, specialmente in quelli con tumori aggressivi. La CgA totale, la vasostatina-2 e la pancreastatina non sono risultati utili in questo contesto. Obiettivo 4. Il NETest sembra in grado di fornire precocemente una corretta valutazione dello stato di malattia dopo resezione chirurgica in pazienti affetti da PanNEN. Obiettivo 5. Il clivaggio della CgA avviene all'interno delle cellule tumorali neuroendocrine. Una elevata espressione tissutale di VS-1 sembra essere un marker di differenziazione del tumore. Obiettivo 6. La scissione della CgA nella regione C-terminale è incrementata nel PDAC ed è associata a peggiore prognosi. Conclusioni: La VS-1 è stato identificata come un promettente biomarcatore per i pazienti affetti da PanNEN. La frammentazione C-terminale della CgA è incrementata nel PDAC, mentre la scissione N-terminale sembra essere più rilevante nelle PanNEN. Se la frammentazione della CgA sia solo un epifenomeno o svolga un ruolo nella biologia vascolare delle PanNEN resta un punto aperto.
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Örlefors, Håkan. "Positron Emission Tomography in the Management of Neuroendocrine Tumors." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3356.

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Neuroendocrine tumors (NET´s) are often characterized by overproduction of peptide hormones. In spite of pronounced clinical symptoms, the tumor lesions can be small and difficult to detect. The general aim of this thesis was to investigate, in vitro and in vivo, some of the potential monoamine pathways present in NET´s, using radiolabeled tracers for positron emission tomography (PET), with the intention to explore the value of PET-imaging in the management of NET´s.

We used the 11C-labeled serotonin precursor 5-hydroxy tryptophan (HTP) as the tracer for imaging of NET´s. More than 95% of the subjects displayed a high tracer uptake on PET and tumor detection rate with PET was higher in >50% of the patients compared both to computed tomography (CT) and somatostatin receptor scintigraphy (SRS). The primary tumor was imaged by PET in 84% (16/19), compared to 47% and 42% for SRS and CT, respectively. Tumor visibility was better with PET due to a higher tumor-to-background ratio and a better spatial resolution. There was a strong correlation (r = .907) between changes in urinary-5-hydroxy indole acetic acid and changes in transport rate of 11C-5-HTP during treatment, indicating the use of PET in treatment monitoring of NET´s.

Pretreatment with carbidopa decreased the urinary radioactivity concentration four-fold and significantly (p<0.001) increased the tumor tracer uptake. This greatly improved image interpretation and tumor lesion detection.

A screening for expression of monoamine pathways in NET´s revealed a high in vitro binding of the monoamineoxidase-A ligand harmine to tumor sections. PET examinations with 11C-harmine could visualize tumors in all patients, including non-functioning endocrine pancreatic tumors (EPT´s).

Finally, the in vitro turnover and in vivo distribution of the amino acids glutamate, glutamine and aspartate was investigated. Limited uptake in vivo indicates the lack of utility for these substances as PET-tracers for imaging and characterization of NET´s.

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Capodanno, Ylenia. "Identifying therapeutic implications of cancer stem cells in human and canine insulinoma." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31175.

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Pancreatic neuroendocrine tumours (PNETs) are the most common neuroendocrine tumours diagnosed in humans and dogs. Due to the highly heterogeneous nature of these tumours, definitive data are still lacking over the molecular mechanisms involved in their cancerous behaviour. This study focused on insulinoma (INS), as it is the most commonly diagnosed PNET in human and veterinary oncology. INS is an insulin-producing tumour that causes a hypoglycaemic syndrome related to the excessive insulin production. In humans, it is often a small benign neoplasm readily curable by surgical resection whereas, in dogs, INS is often malignant. Despite current treatment modalities, malignant canine and human INS have a poor prognosis as patients tend to develop metastases in liver and lymph nodes that do not respond to current therapies. From a comparative oncology perspective, the close resemblance of canine and human malignant INS makes canine INS an interesting study model for human INS. Cancer stem cells (CSCs) are critical for the engraftment and chemoresistance of many tumours. Although CSCs have been isolated from a range of solid tumours, a comprehensive characterisation of INS CSCs has not yet been reported. In this study, it was confirmed that INS CSCs can be enriched and are potential targets for novel INS therapies. Highly invasive and tumourigenic human and canine INS CSCs were successfully isolated and exhibited greater resistance to chemotherapy, which may play a significant role in the poor prognosis of this disease. To date, the mechanisms by which tumours spread and the clinical causes of chemoresistance remain only partially understood. Here, RNA-sequencing analysis was performed over a small set of canine INS tumour samples in order to identify mechanisms involved in INS carcinogenesis through different stages of the disease. Preliminary data showed that distinct gene profiles characterised early and late stage of canine INS. Interestingly, differential gene expression and gene pathways analysis, highlighted that sets of genes involved in pancreatic embryogenesis and insulin secretion were overexpressed in canine primary INS lesions compared with normal pancreas. The Notch pathway is fundamental in pancreatic embryogenesis and it has been previously associated with carcinogenesis of neuroendocrine tumours and with the CSC phenotype. Protein analysis showed that the Notch pathway is activated in both human and canine INS CSCs, particularly when treated with chemotherapy, indicating that the Notch pathway may be involved in chemoresistance. Additionally, it was demonstrated that inhibition of the Notch pathway decreased INS CSCs' survival and chemoresistance, both in vitro and in vivo. These findings provide preclinical evidence that anti-Notch therapy may improve outcomes for patients with malignant INS.
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Ekeblad, Sara. "Pancreatic Endocrine Tumors and GIST - Clinical Markers, Epidemiology and Treatment." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7937.

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Books on the topic "Pancreatic neuroendocrine tumour"

1

Pisegna, Joseph R., ed. Management of Pancreatic Neuroendocrine Tumors. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-1798-3.

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

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Bertram, Wiedenmann, ed. Molecular and cell biological aspects of gastroenteropancreatic neuroendocrine tumor disease. New York, N.Y: New York Academy of Sciences, 1994.

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

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Carton, James. Pancreatic pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0009.

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This chapter discusses pancreatic pathology and covers pancreatic malformations, acute pancreatitis, chronic pancreatitis, pancreatic ductal carcinoma, pancreatic neuroendocrine tumours, pancreatic cystic tumours, and acinar cell carcinoma.
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Pancreatic Cancer Cystic and Endocrine Neoplasm. John Wiley and Sons Ltd, 2014.

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(Editor), Bertram Wiedenmann, Gerhard M. Christofori (Editor), Michael Hocker (Editor), and Jean-Claude Reubi (Editor), eds. Gastroenteropancreatic Neuroendocrine Tumor Disease: Molecular and Cell Biological Aspects (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2004.

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Howe, James R. Management of GI and Pancreatic Neuroendocrine Tumors,an Issue of Surgical Oncology Clinics of North America. Elsevier, 2020.

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Book chapters on the topic "Pancreatic neuroendocrine tumour"

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Koumarianou, Anna, and Nicola Fazio. "Nonfunctioning Pancreatic Neuroendocrine Tumors." In Neuroendocrine Tumours, 275–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45215-8_18.

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Komminoth, Paul. "Somatostatin-Producing Tumor." In Pancreatic Neuroendocrine Neoplasms, 89–95. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17235-4_10.

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Uccella, Silvia, Roberta Maragliano, and Francesca Magnoli. "ACTH-Producing Tumor." In Pancreatic Neuroendocrine Neoplasms, 109–16. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17235-4_13.

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La Rosa, Stefano, Nora Sahnane, and Laura Cimetti. "Serotonin-Producing Tumor." In Pancreatic Neuroendocrine Neoplasms, 117–24. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17235-4_14.

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Chew, C., and G. K. Bonney. "Pancreatic Neuroendocrine Tumours." In Evidence-Based Endocrine Surgery, 467–76. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-1124-5_36.

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Tamburrino, Domenico, Stefano Partelli, and Massimo Falconi. "Pancreatic Neuroendocrine Tumours." In Surgical Diseases of the Pancreas and Biliary Tree, 333–43. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8755-4_13.

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Johnson, Paul R. V. "Pancreatic Neuroendocrine Tumours." In Endocrine Surgery in Children, 173–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-54256-9_13.

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Bennett, Sean Alexander, Calvin How Lim Law, Angela Assal, Sten Myrehaug, and Julie Hallet. "Functional Pancreatic Neuroendocrine Tumors." In Neuroendocrine Tumors, 137–56. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62241-1_9.

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Azadi, Javad, and Atif Zaheer. "Case 60: Neuroendocrine Tumor." In Pancreatic Imaging, 259–62. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52680-5_60.

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Horton, James, and Sajal Pokharel. "Case 81: Neuroendocrine Tumor." In Pancreatic Imaging, 349–52. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52680-5_81.

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Conference papers on the topic "Pancreatic neuroendocrine tumour"

1

Simon, T., S. Mamlouk, S. Khouja, M. Andrea, L. Dido, K. Detjen, M. Pavel, F. Rossner, J. Haybäck, and C. Sers. "PO-329 Genomic aberration in pancreatic neuroendocrine tumours (PNET)." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.359.

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Zhu, Zhuotun, Yongyi Lu, Wei Shen, Elliot K. Fishman, and Alan L. Yuille. "Segmentation for Classification of Screening Pancreatic Neuroendocrine Tumors." In 2021 IEEE/CVF International Conference on Computer Vision Workshops (ICCVW). IEEE, 2021. http://dx.doi.org/10.1109/iccvw54120.2021.00379.

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Mpilla, Gabriel B., Amro Aboukameel, Md Hafiz Uddin, Mohammed N. Al-Hallak, Bayan Al-Share, Yosef Landesman, Yiwei Li, et al. "Abstract 1122: Novel targets for therapy resistant pancreatic neuroendocrine tumors." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1122.

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Cazacu, IM, IF Cherciu Harbiyeli, A. Constantin, C. Copaescu, V. Tomulescu, N. Bejinariu, V. Surlin, C. Stroescu, C. Popescu, and A. Saftoiu. "Hypervascular Pancreatic Lesions on Contrast-Enhanced EUS: Beyond Neuroendocrine Tumors." In ESGE Days 2021. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1724433.

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Huang, Jingzhi, Xiaohua Xie, Manxia Lin, Ming Xu, Guangliang Huang, and Xiaoyan Xie. "IDDF2020-ABS-0041 Pancreatic neuroendocrine tumors: correlation between the sonographic features and the pathological tumor grade." In Abstracts of the International Digestive Disease Forum (IDDF), 22–23 November 2020, Hong Kong. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2020. http://dx.doi.org/10.1136/gutjnl-2020-iddf.49.

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Contractor, Tanupriya, Chang Chan, Shinta Kobayashi, Richard Clausen, Yvonne Sun, Edaise da Silva, Evan Vosburgh, Arnold J. Levine, Laura Tang, and Chris R. Harris. "Abstract 3185: Complement C5 promotes male bias of pancreatic neuroendocrine tumor metastasis." 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.am2015-3185.

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Maeng, Kyungah, Hye Seung Lee, Min Chen, and Maria Zajac-Kaye. "Abstract 3922: Deregulated thymidylate synthase promotes tumorigenecity in pancreatic neuroendocrine tumors." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3922.

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Balmaceda, Nicole, Sunil Abhyankar, Tyler Mouw, and Joaquina Baranda. "Abstract 599: Secondary malignancies in temozolomide-treated metastatic pancreatic neuroendocrine tumors." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-599.

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Saizu, A., G. Becheanu, M. Dumbrava, R. Costache, R. Iacob, and C. Gheorghe. "WHICH EUS FEATURE BEST PREDICT THE DIAGNOSIS OF PANCREATIC NEUROENDOCRINE TUMORS." In ESGE Days. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1705025.

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Ikezono, Yu, Hironori Koga, Jun Akiba, Mitsuhiko Abe, Fumitaka Wada, Toru Nakamura, Hideki Iwamoto, et al. "Abstract 1728: DCLK1 promotes tumor growth and invasion through Slug-mediated epithelial-mesenchymal transition in pancreatic neuroendocrine tumors." 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.am2016-1728.

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