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Добірка наукової літератури з теми "Pancreatic neuroendocrine tumor"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "Pancreatic neuroendocrine tumor"

D’Onofrio, M., G. Mansueto, M. Falconi, and C. Procacci. "Neuroendocrine pancreatic tumor." Abdominal Imaging 29, no. 2 (January 28, 2004): 246–58. http://dx.doi.org/10.1007/s00261-003-0097-8.

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Abbasi, Arezou, Kristina M. Wakeman, and Venu G. Pillarisetty. "Pancreatic paraganglioma mimicking pancreatic neuroendocrine tumor." Rare Tumors 12 (January 2020): 203636132098279. http://dx.doi.org/10.1177/2036361320982799.

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Extra-adrenal paragangliomas are rare tumors arising from the chromaffin cells of the autonomic nervous system. Retroperitoneal paragangliomas may present as a pancreatic mass. We present a case of a 61-year-old woman with an incidentally found pancreatic mass (7.2 × 6.5 cm) in the CT scan. EUS- guided FNA result was compatible with pancreatic neuroendocrine tumor. Patient underwent pancreaticoduodenectomy and histopathologic assessment revealed the mass was an extra-adrenal paraganglioma. Preoperative diagnosis of pancreatic paragangliomas can be challenging due to imaging and histopathologic similarities with pancreatic neuroendocrine tumors.

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Manuel Vázquez, A., A. Valle Rubio, R. Latorre Fragua, L. Gijón de la Santa, and JM Ramia. "Pancreatic neuroendocrine tumor and chronic pancreatitis: chance or causality?" Cirugía Andaluza 32, no. 1 (February 5, 2021): 60–62. http://dx.doi.org/10.37351/2021321.11.

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Resumen Los tumores neuroendocrinos pancreáticos representan menos del 3% de neoplasias pancreáticas. Su asociación con pancreatitis puede ser causal por obstrucción ductal tumoral, pero puede ser casual por coexistencia de ambas entidades. Presentamos un caso de asociación casual de pancreatitis crónica y tumor neuroendocrino pancreático y realizamos una revisión sistemática. Se obtuvieron 325 artículos y se seleccionaron 6, todos casos clínicos, donde esta relación no estaba justificada por obstrucción tumoral. En conclusión, la coexistencia pancreatitis crónica-tumor neuroendocrino pancreático en ausencia de causa obstructiva tumoral es un hallazgo excepcional cuya fisiopatología está por esclarecer. Marcadores inmunohistoquímicos y moleculares podrían ayudar a definirla.

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Chetty, Runjan, and Ihab El-Shinnawy. "Intraductal Pancreatic Neuroendocrine Tumor." Endocrine Pathology 20, no. 4 (September 18, 2009): 262–66. http://dx.doi.org/10.1007/s12022-009-9093-z.

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Diehl, David L., Joseph Blansfield, and Jinhong Li. "Cystic pancreatic neuroendocrine tumor." Gastrointestinal Endoscopy 71, no. 6 (May 2010): 1064–65. http://dx.doi.org/10.1016/j.gie.2009.12.016.

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Yadav, Randhir Sagar, Ashik Pokharel, Shumneva Shrestha, Ashbita Pokharel, Deepshikha Gaire, Sumita Pradhan, and Prasan Bir Singh Kansakar. "Pancreatic Neuroendocrine Tumor with Benign Serous Cystadenoma: A Rare Entity." Case Reports in Oncological Medicine 2021 (August 4, 2021): 1–5. http://dx.doi.org/10.1155/2021/9979998.

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Mixed serous-neuroendocrine neoplasm constitutes pancreatic serous cystic neoplasms and pancreatic neuroendocrine tumor, two tumor components with different underlying pathologies. The differentiation of these tumors is important as the management and prognosis depend on the pancreatic neuroendocrine tumor component. We report a case of mixed serous-neuroendocrine neoplasm in a 47-year-old female who presented with epigastric pain abdomen for two years. Imaging studies, tumor markers, thorough systemic evaluation, surgical resection, histopathological examination, and timely follow-up constituted our management approach. A 4 cm × 4 cm mass in the distal pancreas with multiple cysts in the pancreatic parenchyma containing serous fluid on distal pancreatectomy and splenectomy was found. The histopathological examination revealed combined benign serous cystadenoma and neuroendocrine tumor. She did not have any recurrence or metastasis by four years of follow-up.

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Kim, Hanbaro, Ki Byung Song, Dae Wook Hwang, Jae Hoon Lee, Shadi Alshammary, and Song Cheol Kim. "Time-trend and recurrence analysis of pancreatic neuroendocrine tumors." Endocrine Connections 8, no. 7 (July 2019): 1052–60. http://dx.doi.org/10.1530/ec-19-0282.

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This study aimed to evaluate the evolving trends in clinicopathological features of pancreatic neuroendocrine tumors and to analyze the predictors of recurrence after curative resection. Data collected retrospectively from a single center between January 1990 and December 2017 were analyzed. Patients were categorized chronologically into three groups for evolving time-trend analysis. Overall, 542 patients (300 female, 55.4%) underwent surgical resection for pancreatic neuroendocrine tumors, including 435 (80.3%) with non-functional tumors. Time-trend analysis revealed that the surgically resected pancreatic neuroendocrine tumor number increased consistently; however, the incidental non-functional pancreatic neuroendocrine tumor number also increased over time (P < 0.001). The 5- and 10-year disease-free survival rates were 86.4 and 81.3%, respectively. The overall recurrence rate was 13.7%, and the most common site of recurrence was the liver. The median time to recurrence after primary surgery was 19.0 (range 0.8–236.3) months, and the median survival time after recurrence was 22.6 (range 0.4–126.9) months. On multivariate analysis, grade G3 pancreatic neuroendocrine tumors (hazard ratio 4.51; P < 0.001), lymph node metastasis (hazard ratio 2.46; P = 0.009), lymphovascular invasion (hazard ratio 3.62; P = 0.004), perineural invasion (hazard ratio 2.61; P = 0.004) and resection margin (hazard ratio 4.20; P = 0.003) were independent prognostic factors of disease-free survival. The surgically resected pancreatic neuroendocrine tumor number increased over time mainly because of an increase in incidentally discovered non-functional pancreatic neuroendocrine tumors. Grade G3 pancreatic neuroendocrine tumors, lymph node metastasis, lymphovascular invasion, perineural invasion and a positive resection margin were significant predictors of worse disease-free survival in patients with surgically resected pancreatic neuroendocrine tumors.

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Kulke, Matthew H., Heinz-Josef Lenz, Neal J. Meropol, James Posey, David P. Ryan, Joel Picus, Emily Bergsland, et al. "Activity of Sunitinib in Patients With Advanced Neuroendocrine Tumors." Journal of Clinical Oncology 26, no. 20 (July 10, 2008): 3403–10. http://dx.doi.org/10.1200/jco.2007.15.9020.

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Purpose Standard cytotoxic chemotherapy has limited efficacy in metastatic neuroendocrine tumor patients. Neuroendocrine tumors express vascular endothelial growth factor (VEGF) and its receptor (VEGFR). Sunitinib malate, an oral tyrosine kinase inhibitor, has activity against VEGFRs as well as platelet-derived growth factor receptors, stem-cell factor receptor, glial cell line–derived neurotrophic factor, and FMS-like tyrosine kinase-3. We evaluated the efficacy of sunitinib in a two-cohort, phase II study of advanced carcinoid and pancreatic neuroendocrine tumor patients. Patients and Methods Patients were treated with repeated 6-week cycles of oral sunitinib (50 mg/d for 4 weeks, followed by 2 weeks off treatment). Patients were observed for response, survival, and adverse events. Patient-reported outcomes were assessed. Results Among 109 enrolled patients, 107 received sunitinib (carcinoid, n = 41; pancreatic endocrine tumor, n = 66). Overall objective response rate (ORR) in pancreatic endocrine tumor patients was 16.7% (11 of 66 patients), and 68% (45 of 66 patients) had stable disease (SD). Among carcinoid patients, ORR was 2.4% (one of 41 patients), and 83% (34 of 41 patients) had SD. Median time to tumor progression was 7.7 months in pancreatic neuroendocrine tumor patients and 10.2 months in carcinoid patients. One-year survival rate was 81.1% in pancreatic neuroendocrine tumor patients and 83.4% in carcinoid patients. No significant differences from baseline in patient-reported quality of life or fatigue were observed during treatment. Conclusion Sunitinib has antitumor activity in pancreatic neuroendocrine tumors; its activity against carcinoid tumors could not be definitively determined in this nonrandomized study. Randomized trials of sunitinib in patients with neuroendocrine tumors are warranted.

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Ogbonna, Onyekachi Henry, Marie Carmel Garcon, Kostas N. Syrigos, and Muhammad Wasif Saif. "Mixed Acinar-Neuroendocrine Carcinoma of the Pancreas with Neuroendocrine Predominance." Case Reports in Medicine 2013 (2013): 1–3. http://dx.doi.org/10.1155/2013/705092.

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Background. Pancreatic tumors are rare and could arise from either the exocrine (ductal and acinar cells) or the endocrine (neuroendocrine cells) components of the pancreas. In some instances, the occurrence of pancreatic tumors comprising both acinar cells and neuroendocrine cells, with neuroendocrine cells making up more than 30% of the tumor, has been identified. This unique entity has been referred to as mixed acinar-neuroendocrine carcinoma (MANEC). Only about 20 such cases have been reported in the literature.Case Report. We report an interesting case of MANEC with neuroendocrine cell predominance in a woman presenting with epigastric pain secondary to a pancreatic mass with acinar and endocrine differentiation. She underwent surgical resection of the tumor and was offered adjuvant treatment chemotherapy with carboplatin, etoposide, and radiotherapy for positive tumor resection margins.Conclusions. Given the paucity of the cases of MANEC, continuous reporting of these cases when identified should be encouraged to aid oncologists in understanding the disease and help establish standardized management.

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Cheema, A., L. K. Kvols, and J. R. Strosberg. "Incidental diagnosis of pancreatic neuroendocrine tumors." Journal of Clinical Oncology 29, no. 4_suppl (February 1, 2011): 190. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.190.

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190 Background: Pancreatic neuroendocrine tumors are often discovered incidentally during radiologic or endoscopic examinations. The incidence of incidental detection is unknown. It is also unclear whether patients with incidentally discovered, asymptomatic tumors should be treated similarly to patients who present with tumor-related symptoms. Methods: A database of 425 patients with pancreatic neuroendocrine tumors treated at the H. Lee Moffitt Cancer Center was developed. Patient charts were reviewed to assess whether their diagnosis was incidental or prompted by tumor-related symptoms such as pain, jaundice, or neuroendocrine hormone secretion. The frequency of “incidentalomas” was categorized by TNM stage (AJCC, 7th edition). Overall survival was stratified by “incidental” versus “symptomatic” diagnosis. Results: Among 425 patients with histologically proven pancreatic neuroendocrine tumors, 112 patients (26%) had tumors that were discovered incidentally. The majority of stage I tumors (55%) were incidentally discovered. Among patients with stage IV tumors, 20% were detected incidentally (Table). Median survival of patients with incidentally discovered tumors was 103 months versus 84 months in patients who were symptomatic at diagnosis. Conclusions: A sizeable fraction of patients with pancreatic neuroendocrine tumors are diagnosed incidentally during evaluations for other conditions or unrelated symptoms. The majority of patients with stage I tumors are incidentally diagnosed. The increased incidence of pancreatic neuroendocrine “incidentaloms” may be contributing to improving survival rates in this disease. This study highlights the necessity of developing guidelines for management of patients with incidentally discovered, early-stage tumors. [Table: see text] No significant financial relationships to disclose.

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Більше джерел

Дисертації з теми "Pancreatic neuroendocrine tumor"

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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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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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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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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Behrang, Yasmin [Verfasser]. "Etablierung und Charakterisierung eines neuen humanen, hochdifferenzierten und funktionell-aktiven Tumormodells eines pankreatischen neuroendokrinen Tumors : Establishment and Characterization of a Novel Well-differentiated and Functionally Active Human Pancreatic Neuroendocrine Tumor Model / Yasmin Behrang." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2020. http://d-nb.info/1221084143/34.

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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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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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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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BERSANI, Samantha. "Molecular characterization of Pancreatic NeuroEndocrine Tumors (PanNETs)." Doctoral thesis, 2014. http://hdl.handle.net/11562/706564.

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Scopo: identificare le alterazioni molecolari clinicamente rilevanti associate ai tumori neuroendocrini del pancreas (PanNETs). Materiali e Metodi: 204 pazienti sono stati studiati per la ricerca mutazionale in 8 geni frequentemente alterati in PanNETs utilizzando Tecnologia Ion Torrent. Tali geni si dividono tra MEN1, ATRX e DAXX coinvolti nel rimodellamento della cromatina, PIK3CA,TSC2,PTEN,MTOR implicati nel mTOR pathway e infine ATM presente come ruolo centrale nel mantenimento della stabilità e riparazione del DNA. Inoltre sono stati valutati: i) le variazioni del numero di copie (CNV) tramite dati CGH array disponibili in 90 casi, ii) l’allungamento alternativo dei telomeri (ALT) tramite FISH in un numero selezionato di casi iii) l’espressione proteica tramite immunoistochimica per Menina, ATRX, Daxx, Atm e Pten in 171PanNETs. Risultati: l’analisi mutazionale mirata tramite next generation sequencing di 204 PanNETs ha dimostrato la presenza di mutazioni in 112/204 (55%), mentre in 92 (45%) risultano non alterati. E’ stato inoltre rilevato i) le mutazioni a carico dei geni Daxx e ATRX risultano essere mutuamente esclusive e più frequentemente presenti pari a 53/204 (26%) e associate con mutazioni di MEN1 o ATM a loro volta mutuamente esclusive; ii) mutazioni DAXX/ATRX sono associate a un sottoinsieme di PanNETs che presentano perdite cromosomiche ; iii ) le mutazioni PTEN e TSC2 si escludono a vicenda e sono state trovate in 31/204 (15%), mentre l'attivazione mTOR è associato con una migliore sopravvivenza libera da malattia. Conclusioni : in questo studio abbiamo dimostrato che i PanNETs possono essere suddivisi tra due principali sottogruppi molecolari. Un primo gruppo mostra una simultanea perdita cromosomica nelle neoplasie con mutazioni a carico di MEN1 e la contemporanea alterazione nei geni DAXX , ATRX , PTEN e TSC2 . Il secondo gruppo di casi presenta mutazioni di MEN1 senza alterazioni cromosomiche rincorrenti il cui significato deve essere ancora scoperto.
Purpose: To identify clinically relevant molecular alterations associated to pancreatic endocrine tumors (PanNETs) discovered by recent exome sequencing data. Patients and Methods: A series of 204 PanNETs were explored for intragenic mutations in 8 genes reported as recurrently altered in PanNETs using Ion Torrent technology. The 8 genes were MEN1, ATM, ATRX, DAXX, PIK3CA, TSC2, PTEN, MTOR. Their relation with chromosomal copy number aberrations were assessed in 90 cases having CGH array data available, and in a selected number of cases alternative lengthening of telomeres (ALT) was investigated by FISH. A total of 171 PanNETs were also investigated by immunohistochemistry for Menin, Atrx, Daxx, Atm and Pten. Results: Our targetted next-generation mutational analysis of 204 PanNETs for three chromatin remodelling genes (MEN1, ATRX, DAXX), MTOR pathway genes (PTEN, TSC2, PIK3CA, MTOR) and the ATM DNA repair gene assessed that 112/204 (55%) PanNETS had mutations, while 92 (45%) lacked mutations, and: i) the mutually exclusive mutations in DAXX and ATRX chromatin remodelling genes were the most frequent, accounting for 53/204 (26%) cases, and were associated with MEN1 or ATM mutations that were in turn mutually exclusive; ii) DAXX/ATRX mutations are associated with a subset of PanNETS showing a peculiar pattern of recurrent chromosomal losses; iii) the mutually exclusive mutations in genes belonging to mTOR pathways were found in 31/204 (15%), and mTOR pathway activation is associated with shorter disease-free survival. Conclusions: We report that PanNET can be subdived into two main molecular subgroups. The first showing the peculiar simultaneous loss of twelve chromosomes, which includes the vast majority of neoplasms showing MEN1 mutations and concurrent mutations in DAXX, ATRX, PTEN and TSC2. The second group, where only a small number of cases shows MEN1 mutations, lacks recurrent chromosomal anomalies and the gene alterations responsible for their development remain to be discovered.

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Книги з теми "Pancreatic neuroendocrine tumor"

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., 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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(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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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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Pancreatic Cancer Cystic and Endocrine Neoplasm. John Wiley and Sons Ltd, 2014.

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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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Частини книг з теми "Pancreatic neuroendocrine tumor"

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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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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Ali, Sumera, and Atif Zaheer. "Case 57: Cystic Neuroendocrine Tumor." In Pancreatic Imaging, 243–48. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52680-5_57.

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Johnson, Stephen I. "Case 24: Serotonin-Producing Neuroendocrine Tumor." In Pancreatic Imaging, 97–99. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52680-5_24.

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Wang, Jessica, and Martha Bishop Pitman. "Pancreatic Neuroendocrine Tumor, Cytological Findings." In Encyclopedia of Pathology, 363–68. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33286-4_2758.

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Spoletini, Gabriele, Domenico Tamburrino, Francesca Muffatti, Stefano Crippa, Valentina Andreasi, Stefano Partelli, and Massimo Falconi. "Guideline for the Management of Pancreatic Neuroendocrine Tumor." In Pancreatic Cancer, 161–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-47181-4_13.

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Xing, Fuyong, Hai Su, and Lin Yang. "An Integrated Framework for Automatic Ki-67 Scoring in Pancreatic Neuroendocrine Tumor." In Advanced Information Systems Engineering, 436–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40811-3_55.

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Тези доповідей конференцій з теми "Pancreatic neuroendocrine tumor"

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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Qi, Jenny Y., Paul C. Moore, Maike Thamsen, Rajarshi Ghosh, Micah J. Gliedt, Dustin J. Maly, Bradley J. Backes, Feroz R. Papa та Scott A. Oakes. "Abstract 2862: The balance of divergent IRE1α signaling regulates pancreatic neuroendocrine tumor growth". У 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.am2016-2862.

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Wan, Yidong, Lei Xu, Pengfei Yang, Zuozhen Cao, Chen Luo, Xiaoyong Shen, Yan Wu, Dan Ruan, and Tianye Niu. "Feasibility of predicting pancreatic neuroendocrine tumor grade using deep features from unsupervised learning." In Imaging Informatics for Healthcare, Research, and Applications, edited by Thomas M. Deserno and Po-Hao Chen. SPIE, 2020. http://dx.doi.org/10.1117/12.2548723.

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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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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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Park, Joo Kyung, Woo Hyun Paik, Ji Kon Ryu, Yong-Tae Kim, and Se-Hoon Lee. "Abstract A158: DAXX/ATRX and MEN1 genes are stong prognostic markers in pancreatic neuroendocrine tumor." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a158.

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Rizzo, Anthony J., Jacqueline A. Brosnan-Cashman, Mindy K. Graham, Alan K. Meeker, and Christopher M. Heaphy. "Abstract 3464: CRISPR-mediated inactivation of ATRX and DAXX in pancreatic neuroendocrine tumor cell lines." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3464.

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Gasmi, M., M. Giovannini, N. Lesavre, C. Boustière, B. Napoleon, S. Koch, G. Vanbervliet, J.-M. Gonzalez, and M. Barthet. "EUS-GUIDED RADIOFREQUENCY ABLATION MID-TERM RESULTS (MORE THAN TWO YEARS FOLLOW-UP) FOR PANCREATIC NEUROENDOCRINE TUMOR AND PANCREATIC CYSTIC NEOPLASMS." In ESGE Days. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1704037.

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Leu, Frank, Minesh Nandi, and Chung Wong. "Abstract 707: Anti-SSTR antibodies can reverse neuroendocrine tumor cellular dedifferentiation induced by neutralizing EMT regulator miR-200c in pancreatic neuroendocrine tumor BON cells while increase cell death." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-707.

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Salma, Shaik Amjad Ume, Jussara Hagen, Jacki Reilly, Ryan Sheehy, Nitija Tiwari, Jackson Nteeba, Scott K. Sherman, et al. "Abstract 1368: RABL6A, a novel critical regulator of Akt-mTOR signaling in pancreatic neuroendocrine tumor cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1368.

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