Endocrine tumors of the digestive tract and pancreas: histogenesis, diagnosis and molecular basis

Rindi, Guido; Villanacci, Vincenzo; Ubiali, Alessandro; Scarpa, Aldo

doi:10.1586/14737159.1.3.323

Cited by 41 publications

(21 citation statements)

References 52 publications

(116 reference statements)

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“…In addition to hormones and biogenic amines, they are known to produce growth factors which by acting in an autocrine or paracrine manner regulate GEP-NET proliferation and differentiation [2,3,4,5,6]. …”

Section: Discussionmentioning

confidence: 99%

“…Of the utmost importance in the biology of GEP-NETs is, besides the production of biogenic amines and hormones, the production of growth factors, which can influence cell proliferation and differentiation of both tumors and host tissues acting as autocrine or paracrine stimuli. Depicted growth factors are VEGF, FGF, IGF-I, PDGF, TGF-α, TNF-α, and ILs [3,4,5,6]. Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine produced by many host immune cells as well as tumor cells.…”

Section: Introductionmentioning

confidence: 99%

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TNF-α Promoter Single Nucleotide Polymorphisms in Gastroenteropancreatic Neuroendocrine Tumors

Berković¹,

Čačev²,

Zjačić-Rotkvić³

et al. 2006

Neuroendocrinology

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Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) secrete biogenic amines, hormones and growth factors, tumor necrosis factor-α (TNF-α) being one of them. As the expression of TNF-α is mostly regulated at the transcriptional level, its promoter polymorphisms have been intensively studied as a potential determinant of TNF-α production and cancer susceptibility. We have analyzed for the first time the potential association between -238, -308, -857 and -1031 TNF-α promoter polymorphisms and GEP-NETs. The study included 65 individuals diagnosed with GEP-NET and 154 healthy age- and sex-matched controls. Although most of the patients had solitary GEP-NETs, 6 were diagnosed with GEP-NET as a part of multiple endocrine neoplasia type 1 and 1 as a part of neurofibromatosis type 1. The C allele at the -1031 position was more frequent in GEP-NET patients (p < 0.0005), suggesting its possible role in GEP-NET development. The significant difference between foregut and midgut GEP-NET patients was observed in the -308 high expression genotypes and -308A allele (high expression) which tend to occur more frequently in the foregut GEP-NETs (p = 0.0392 and p = 0.0350, respectively). When functional and nonfunctional pancreatic endocrine tumors were compared, there were no significant differences in the researched TNF-α SNPs. The results suggest the putative role of TNF-α -1031 polymorphism in the development of GEP-NET.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

TNF-α Promoter Single Nucleotide Polymorphisms in Gastroenteropancreatic Neuroendocrine Tumors

Berković¹,

Čačev²,

Zjačić-Rotkvić³

et al. 2006

Neuroendocrinology

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“…Aggressive metastases are usually seen in the liver and are rarely found in the chest. 8 Other subtypes of NET include gastrinomas, insulinomas, carcinoid, glucagonomas, and somatostatinomas, 5,9 and most are associated with specific clinical syndromes and laboratory abnormalities (eg, gastrinomas with ZollingerEllison syndrome, insulinomas with hypoglycemia). 10 …”

Section: Vipomasmentioning

confidence: 99%

2 History and Physical Examination

An¹,

Singh²

2008

Synopsis of Spine Surgery

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Hospital Physician July 2008 35P ancreatic cholera syndrome, also known as Verner-Morrison syndrome 1 and WDHA syndrome, is a constellation of symptoms caused by VIPomas, a rare subtype of neuroendocrine tumor (NET) that typically originates in the pancreas. In this syndrome, excessive production of vasoactive intestinal polypeptide (VIP) provokes secretory diarrhea with associated electrolyte imbalance. VIPomas account for less than 1% of all pancreatic tumors and are usually solitary lesions larger than 3 cm, with 75% occurring in the tail of the pancreas. More than 60% of VIPomas metastasize by the time of diagnosis. 2 Diagnosis is dependent on confirming the presence of hormone hypersecretion and localizing the tumor using available imaging modalities. This article presents the case of a woman with the classic presentation of VIPoma who required multiple hospitalizations due to life-threatening hypokalemia. The approach to diagnosis of VIPoma and management of components of pancreatic cholera syndrome are also discussed. CASE PRESENTATION History and Physical ExaminationA 42-year-old woman with no significant past medical history presented to her primary care physician with abdominal pain 15 days after an elective tubal ligation. Initially, the symptoms were thought to be related to the postoperative course and the patient was treated with opiates. However, symptoms persisted for 2 months and were associated with bouts of copious, watery, nonbloody diarrhea (occurring 3-4 times/day). She denied recent use of antibiotics or laxatives. Current medications were acetaminophen/oxycodone to control pain. She had no known drug allergies and denied a history of smoking or illicit drug use. Previous surgeries included the recent laparoscopic tubal ligation, cholecystectomy, breast augmentation, and tonsillectomy. Family history was noncontributory. The primary care physician ordered esophagogastroduodenoscopy and colonoscopy, both of which were unremarkable. Abdominal computed tomography (CT) performed 6 months prior as part of the preoperative evaluation for tubal ligation was also normal. The patient's symptoms worsened, with 8 to 10 bowel movements per day, generalized fatigue, and a 26-lb weight loss, leading to an emergency department (ED) visit.In the ED, the patient's vital signs included a temperature of 99.8°F, blood pressure of 109/60 mm Hg, a regular heart rate of 98 bpm, respiratory rate of 20 breaths/min, and oxygen saturation of 99% on room air. Physical examination revealed abdominal distension, increased bowel sounds with no palpable masses or organomegaly, and a normal rectal examination. Diagnostic StudiesLaboratory values on admission were notable for elevated alkaline phosphatase (348 U/L), aspartate aminotransferase (83 U/L), and alanine aminotransferase (49 U/L) levels. The potassium level was low at 2.4 mEq/L (normal, 3.5-5.0 mEq/L) and remained low despite daily oral potassium replacement. Stool cultures and samples for ovae, parasites, and Clostridium difficile toxin were negative.Repeat abdo...

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“…Enterochromaffin-like (ECL)-cell gastric NETs associated with chronic atrophic gastritis (type I gastric NETs) arise in association with ECL-cell hyperplasia and are often multiple [40]. LOH of 11q was present in only one of six such tumors examined.…”

Section: Loh and Mutation Analysismentioning

confidence: 99%

Molecular profiles of gastroenteropancreatic endocrine tumors

2007

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Neuroendocrine tumors of the gastroenteropancreatic system are defined by their endocrine phenotype and share many histopathological and clinical features. However, the fact that the hormone production of tumors depends on their site of origin, that the tumors differ in their biology, and that the association with familial syndromes is nonrandom suggests heterogeneity. It is therefore conceivable that the gastroenteropancreatic neuroendocrine tumors also differ in their molecular profile. This review summarizes and discusses the available data in this field.

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Endocrine tumors of the digestive tract and pancreas: histogenesis, diagnosis and molecular basis

Cited by 41 publications

References 52 publications

TNF-α Promoter Single Nucleotide Polymorphisms in Gastroenteropancreatic Neuroendocrine Tumors

TNF-α Promoter Single Nucleotide Polymorphisms in Gastroenteropancreatic Neuroendocrine Tumors

2 History and Physical Examination

Molecular profiles of gastroenteropancreatic endocrine tumors

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