Changing Incidence of Pancreatic Neoplasms

Fitzgerald, Timothy L.; Hickner, Zach; Schmitz, Matthew; Kort, Eric J.

doi:10.1097/mpa.0b013e318163a329

Cited by 157 publications

(57 citation statements)

References 13 publications

(10 reference statements)

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“…Approximately 4-7% of gastroenteropancreatic NETs originate in the pancreas, and these are referred to as pancreatic NETs (PNETs) [1]. Whilst there is evidence to suggest the possibility of an increasing incidence, PNETs currently arise in approximately 0.3 per 100,000 people in Western society [2,3]. The relatively indolent clinical course of PNETs, relative to that of the much more common pancreatic ductal adenocarcinoma (PDAC), explains why the overall prevalence of PNETs accounts for as many as 10% of pancreatic neoplasms despite the low incidence.…”

Section: Introductionmentioning

confidence: 99%

“…Given that the incidence of PNETs may be increasing [3], there is an emerging need for a clarification and further investigation of factors which might increase the risk of the development of PNETs within the population. Accordingly, we report a systematic review and meta-analysis to evaluate the association of diabetes mellitus, smoking, alcohol use, and first-degree family history of cancer with the risk of developing PNET.…”

Section: Introductionmentioning

confidence: 99%

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Diabetes, Smoking, Alcohol Use, and Family History of Cancer as Risk Factors for Pancreatic Neuroendocrine Tumors: A Systematic Review and Meta-Analysis

et al. 2015

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Background and Aims: Risk factors for pancreatic neuroendocrine tumors (PNETs) are not well understood. The aim of this systematic review was to assess if diabetes mellitus, smoking, alcohol use, and family history of cancer are risk factors for PNETs. Methods: MEDLINE and abstracts from the European and North American Neuroendocrine Tumor Societies (ENETS and NANETS) were searched for studies published until October 2013. Eligible studies were selected according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. Results: Five studies evaluating 4 individual populations were included (study accrual period 2000-2011) into the meta-analysis, involving 827 cases (range 160-309 per study) and 2,407 controls (range 233-924 per study). All studies had a case-control design and described regional series. The pooled adjusted odds ratio was 2.74 (95% CI: 1.63-4.62; p < 0.01; I² = 60.4%) for history of diabetes, 1.21 (95% CI: 0.92-1.58; p = 0.18; I² = 45.8%) for ever smoking, 1.37 (95% CI: 0.99-1.91; p = 0.06; I² = 0.0%) for heavy smoking, 1.09 (95% CI: 0.64-1.85; p = 0.75; I² = 85.2%) for ever alcohol use, 2.72 (95% CI: 1.25-5.91; p = 0.01; I² = 57.8%) for heavy alcohol use, and 2.16 (95% CI: 1.64-2.85; p < 0.01; I² = 0.0%) for first-degree family history of cancer. Conclusions: Diabetes mellitus and first-degree family history of cancer are associated with an increased risk of sporadic PNET. There was also a trend for diagnosis of sporadic PNET associated with heavy smoking. Alcohol use may be a risk factor for PNET, but there was considerable heterogeneity in the meta-analysis. These results suggest the need for a larger, homogeneous, international study for the clarification of risk factors for the occurrence of PNET.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Diabetes, Smoking, Alcohol Use, and Family History of Cancer as Risk Factors for Pancreatic Neuroendocrine Tumors: A Systematic Review and Meta-Analysis

et al. 2015

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“…Although PETs are generally considered rare neoplasms, their incidence has almost doubled in the last 20 years (Fitzgerald et al 2008). PETs represent w1% of all pancreatic cancers by incidence, but 10% by prevalence (Yao et al 2007), and are one of the most challenging forms of neuroendocrine tumours (NETs), with a worse prognosis compared with gastrointestinal carcinoids (Panzuto et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Src kinase activity coordinates cell adhesion and spreading with activation of mammalian target of rapamycin in pancreatic endocrine tumour cells

Florio¹,

Adesso²,

Pedrotti³

et al. 2011

Endocrine-Related Cancer

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Pancreatic endocrine tumours (PETs) are rare and heterogeneous neoplasms, often diagnosed at metastatic stage, for which no cure is currently available. Recently, activation of two pathways that support proliferation and invasiveness of cancer cells, the Src family kinase (SFK) and mammalian target of rapamycin (mTOR) pathways, was demonstrated in PETs. Since both pathways represent suitable targets for therapeutic intervention, we investigated their possible interaction in PETs. Western blot and immunofluorescence analyses indicated that SFK and mTOR activity correlate in PET cell lines. We also found that SFKs coordinate cell adhesion and spreading with activation of the mTOR pathway in PET cells. Live cell metabolic labelling and biochemical studies demonstrated that SFK activity enhance mTOR-dependent translation initiation. Furthermore, microarray analysis of the mRNAs associated with polyribosomes revealed that SFKs regulate mTOR-dependent translation of specific transcripts, with an enrichment in mRNAs encoding cell cycle proteins. Importantly, a synergic inhibition of proliferation was observed in PET cells concomitantly treated with SFK and mTOR inhibitors, without activation of the phosphatidylinositol 3-kinase/AKT pro-survival pathway. Tissue microarray analysis revealed activation of Src and mTOR in some PET samples, and identified phosphorylation of 4E-BP1 as an independent marker of poor prognosis in PETs. Thus, our work highlights a novel link between the SFK and mTOR pathways, which regulate the translation of mRNAs for cell cycle regulators, and suggest that crosstalk between these pathways promotes PET cell proliferation.

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“…Pancreatic neuroendocrine tumours (pNETs) are rare tumours accounting for 1% to 2% of all pancreatic neoplasms [1,2] with a peak incidence in the ages between 30 to 60 years [3,4] and a slight female preponderance. The identification of a pancreatic mass as a pNET remains challenging [5] but important as pNETs have a significantly better outcome as compared to other non-endocrine malignant tumours of the pancreas [6].…”

Section: Introductionmentioning

confidence: 99%

Diagnostic Performance of Endoscopic Ultrasound (EUS)/ Endoscopic Ultrasound – Fine Needle Aspiration (EUS-FNA) Cytology in Solid and Cystic Pancreatic Neuroendocrine Tumours

Mitra¹,

Nayar²,

Leeds³

et al. 2015

JGLD

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Background & Aims: Our study aimed to assess the sensitivity of EUS and EUS-FNA for pancreatic neuro-endocrine tumors (pNETs) and compare performance over two consecutive 4 year 2 month periods, to investigate the comparative performance between solid and cystic pNETs and determine the incremental yield of EUS±FNA in individuals with a mass not diagnosed as a pNET after cross-sectional imaging.Methods: A retrospective review of a prospectively maintained database was carried out to identify all pNET patients who underwent EUS-FNA between April 2003 and September 2011.Results: A final diagnosis of solid and cystic pNETs was made in 43 and 10 patients, respectively. Overall, the yield of combined EUS imaging and cytology was significantly higher than that of CT and/or MRI (p< 0.05) across all groups [solid (83.7% vs. 41.8%), cystic (70% vs. 10%) and combined solid-cystic (81.1% vs. 35.8%)]. The yield of combined EUS imaging and cytology was significantly better than EUS imaging alone (p<0.05) in the solid (83.7% vs. 58%) and combined pNET cohort (81.1% vs. 52.8%) of patients. After a non-diagnostic CT and or MRI, EUS/EUS-FNA confirmed pNET in 19 out of 25 patients (76.0%) with solid pNETs and 6 out of 9 patients (66.7%) with cystic pNETs.Conclusion: EUS and EUS-FNA had a significant clinical impact in the 25/34 of cases where pNET was not suspected after initial cross-sectional imaging.

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Changing Incidence of Pancreatic Neoplasms

Abstract: The incidence of most pancreatic neoplasms has changed a little; however, nonfunctional neuroendocrine neoplasms increased greater than 2-fold. The etiology of this change is unclear.

Cited by 157 publications

References 13 publications

Diabetes, Smoking, Alcohol Use, and Family History of Cancer as Risk Factors for Pancreatic Neuroendocrine Tumors: A Systematic Review and Meta-Analysis

Diabetes, Smoking, Alcohol Use, and Family History of Cancer as Risk Factors for Pancreatic Neuroendocrine Tumors: A Systematic Review and Meta-Analysis

Src kinase activity coordinates cell adhesion and spreading with activation of mammalian target of rapamycin in pancreatic endocrine tumour cells

Diagnostic Performance of Endoscopic Ultrasound (EUS)/ Endoscopic Ultrasound – Fine Needle Aspiration (EUS-FNA) Cytology in Solid and Cystic Pancreatic Neuroendocrine Tumours

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