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1. Adissu HA, Turner PV: Insulinoma and squamous cell carcinoma with peripheral polyneuropathy in an aged Sprague-Dawley rat. J Am Assoc Lab Anim Sci; 2010 Nov;49(6):856-9
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  • [Title] Insulinoma and squamous cell carcinoma with peripheral polyneuropathy in an aged Sprague-Dawley rat.
  • Pancreatic islet cell adenoma, oral squamous cell carcinoma, peripheral polyneuropathy, and multiple age-associated degenerative lesions were diagnosed in an aged Sprague-Dawley rat presenting with polyuria, polydypsia, dehydration, anorexia, weight loss, and posterior weakness.
  • Microscopically, the islet cell adenoma was encapsulated by fibrous tissue and composed of packets of oval-to-polygonal monomorphic cells in a fibrovascular stroma.
  • The oral squamous cell carcinoma, grossly presenting as gingival ulceration, was composed of nests and cords of squamous epithelial cells that focally eroded and infiltrated the hard palate and resulted in degeneration of the maxillary nerve.
  • [MeSH-major] Carcinoma, Squamous Cell / veterinary. Gingival Neoplasms / veterinary. Insulinoma / veterinary. Pancreatic Neoplasms / veterinary. Peripheral Nervous System / pathology. Polyneuropathies / veterinary. Rats

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  • [Cites] Arch Toxicol. 1992;66(7):496-502 [1444814.001]
  • [Cites] J Neuropathol Exp Neurol. 1989 Jul;48(4):399-412 [2543797.001]
  • [Cites] J Am Anim Hosp Assoc. 1998 Nov-Dec;34(6):471-5 [9826281.001]
  • [Cites] Acta Neuropathol. 2004 Dec;108(6):503-14 [15365726.001]
  • [Cites] Toxicol Pathol. 2001 May-Jun;29(3):353-62 [11442021.001]
  • [Cites] Brain Res. 2002 Aug 23;947(1):84-9 [12144856.001]
  • [Cites] Diabetes Metab Res Rev. 2003 Sep-Oct;19(5):392-400 [12951647.001]
  • [Cites] J Natl Cancer Inst. 1967 Jul;39(1):17-32 [4291142.001]
  • [Cites] Diabetologia. 1968 Jan;4(1):44-7 [4907148.001]
  • [Cites] J Comp Pathol. 1982 Jan;92(1):139-47 [6279704.001]
  • [Cites] Acta Neuropathol. 1983;59(1):63-9 [6837269.001]
  • [Cites] Vet Pathol. 1983 May;20(3):291-7 [6308877.001]
  • [Cites] Vet Pathol. 1986 Jan;23(1):11-5 [3004001.001]
  • [Cites] J Vet Intern Med. 1987 Apr-Jun;1(2):86-90 [2851653.001]
  • [Cites] Lab Anim. 1998 Oct;32(4):457-66 [9807760.001]
  • (PMID = 21205453.001).
  • [ISSN] 1559-6109
  • [Journal-full-title] Journal of the American Association for Laboratory Animal Science : JAALAS
  • [ISO-abbreviation] J. Am. Assoc. Lab. Anim. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2994055
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2. National Toxicology Program: Toxicology and carcinogenesis studies of methylene blue trihydrate (Cas No. 7220-79-3) in F344/N rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2008 May;(540):1-224
Hazardous Substances Data Bank. METHYLENE BLUE .

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  • Spleen lesions associated with methylene blue trihydrate administration included hematopoietic cell proliferation, pigmentation, lymphoid depletion of the lymphoid follicles, and capsular fibrosis.
  • Liver lesions associated with methylene blue exposure included centrilobular necrosis in rats dying early, hematopoietic cell proliferation, and Kupffer cell pigmentation with erythrophagocytosis.
  • Lesions in the spleen associated with methylene blue trihydrate administration included hematopoietic cell proliferation, pigmentation, and congestion.
  • Liver lesions associated with methylene blue trihydrate administration included periportal degeneration, hematopoietic cell proliferation, and Kupffer cell pigmentation with erythrophagocytosis.
  • Spleen lesions in dosed rats included hematopoietic cell proliferation, congestion, lymphoid depletion of the lymphoid follicles, and capsular fibrosis.
  • In all dosed groups, the incidences of hematopoietic cell proliferation and pigmentation in the spleen were significantly greater than those in the vehicle controls.
  • In the liver, the incidences of hematopoietic cell proliferation were significantly increased in males and females in the 100 and 200 mg/kg groups, and the incidences of Kupffer cell pigmentation were significantly increased in groups administered 50 mg/kg or greater.
  • The incidences of pancreatic islet cell adenoma and adenoma or carcinoma (combined) were increased in all dosed groups of males, were significantly increased in 25 mg/kg males, and exceeded the historical range in controls (all routes).
  • The incidence of pancreatic islet cell hyperplasia was significantly increased in the 50 mg/kg males.
  • In the spleen, the incidence of hematopoietic cell proliferation in 50 mg/kg males was significantly increased; the incidences of capsular fibrosis were significantly increased in all dosed groups of males and in 5 and 50 mg/kg females.
  • The incidences of carcinoma and of adenoma or carcinoma (combined) of the small intestine occurred with a positive trend in males.
  • The incidences of hematopoietic cell proliferation of the spleen were significantly increased in 12.5 and 25 mg/kg males and in 25 mg/kg females.
  • [MeSH-minor] Administration, Oral. Anemia / chemically induced. Anemia / pathology. Animals. Body Weight / drug effects. CHO Cells. Chromosome Aberrations / chemically induced. Cricetinae. Cricetulus. DNA Damage. Female. Intestinal Neoplasms / chemically induced. Intestinal Neoplasms / pathology. Intestine, Small / drug effects. Intestine, Small / pathology. Islets of Langerhans / drug effects. Islets of Langerhans / pathology. Lymphoma / chemically induced. Lymphoma / pathology. Male. Methemoglobinemia / chemically induced. Methemoglobinemia / pathology. Mice. Mice, Inbred Strains. Pancreatic Neoplasms / chemically induced. Pancreatic Neoplasms / pathology. Rats. Rats, Inbred F344. Sister Chromatid Exchange / drug effects

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  • (PMID = 18685714.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Mutagens; T42P99266K / Methylene Blue
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3. Guardado-Mendoza R, Dick EJ Jr, Jimenez-Ceja LM, Davalli A, Chavez AO, Folli F, Hubbard GB: Spontaneous pathology of the baboon endocrine system. J Med Primatol; 2009 Dec;38(6):383-9
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  • [Title] Spontaneous pathology of the baboon endocrine system.
  • BACKGROUND: Study of endocrine pathology in animal models is critical to understanding endocrine pathology in humans.
  • METHODS: We evaluated 434 endocrine-related diagnoses from 4619 baboon necropsies, established the incidence of spontaneous endocrine pathology, and analyzed the clinical and biochemical data associated with the individual cases.
  • RESULTS: The most common diagnoses in descending order, were pancreatic islet cell amyloidosis (n = 259), ovarian cysts (n = 50), pituitary adenoma (n = 37), pancreatic islet cell adenoma (n = 20), granulosa cell tumor (n = 15), thyroid adenoma (n = 11), adrenal hyperplasia (n = 10), thyroid carcinoma (n = 8), and pheochromocytoma (n = 6).
  • The incidence of pancreatic islet cell amyloidosis progressively increased with age.
  • The incidence of pancreatic islet cell amyloidosis and adrenal pathology was similar to humans; the incidence of pituitary adenoma and thyroid pathology was lower than in humans.
  • CONCLUSIONS: Endocrine disease in baboons is common and shares clinical and biochemical characteristics with endocrine disease in humans.
  • [MeSH-major] Endocrine System Diseases / veterinary. Monkey Diseases / epidemiology. Papio

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  • [Cites] J Med Primatol. 2007 Apr;36(2):61-79 [17493137.001]
  • [Cites] Endocrinol Metab Clin North Am. 2005 Sep;34(3):677-705, x [16085166.001]
  • [Cites] Endocr Rev. 2008 May;29(3):303-16 [18314421.001]
  • [Cites] Gynecol Endocrinol. 2008 Aug;24(8):423-7 [18850378.001]
  • [Cites] Am J Clin Pathol. 2000 Feb;113(2):295-302 [10664633.001]
  • [Cites] Endocr Rev. 2000 Jun;21(3):245-91 [10857554.001]
  • [Cites] Aust N Z J Med. 2000 Dec;30(6):648-52 [11198571.001]
  • [Cites] Endocr Relat Cancer. 2001 Dec;8(4):287-305 [11733226.001]
  • [Cites] J Med Primatol. 2002 Apr;31(2):84-90 [12110051.001]
  • [Cites] Obes Res. 2003 Jan;11(1):75-80 [12529488.001]
  • [Cites] Comp Med. 2002 Dec;52(6):563-7 [12540172.001]
  • [Cites] J Med Primatol. 2003 Feb;32(1):48-56 [12733602.001]
  • [Cites] Endocr Rev. 2003 Aug;24(4):539-53 [12920154.001]
  • [Cites] Minerva Ginecol. 2004 Feb;56(1):41-51 [14973409.001]
  • [Cites] Mayo Clin Proc. 1983 Dec;58(12):802-4 [6645626.001]
  • [Cites] Vet Pathol. 1985 Mar;22(2):141-6 [3984159.001]
  • [Cites] Lab Anim Sci. 1986 Oct;36(5):529-33 [3534445.001]
  • [Cites] Acta Med Scand. 1986;220(3):225-32 [3776697.001]
  • [Cites] Clin Chem. 1992 Apr;38(4):486-92 [1568311.001]
  • [Cites] Lab Anim Sci. 1993 Jun;43(3):236-43 [8355484.001]
  • [Cites] Am J Surg Pathol. 2005 Feb;29(2):254-74 [15644784.001]
  • [Cites] N Engl J Med. 2005 Jun 9;352(23):2376-8 [15944422.001]
  • [Cites] Diabetes. 2008 Apr;57(4):899-908 [18174524.001]
  • (PMID = 19793179.001).
  • [ISSN] 1600-0684
  • [Journal-full-title] Journal of medical primatology
  • [ISO-abbreviation] J. Med. Primatol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / C06 RR016228; United States / NCRR NIH HHS / RR / P51 RR013986; United States / NCRR NIH HHS / RR / P51 RR013986-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Denmark
  • [Other-IDs] NLM/ NIHMS145553; NLM/ PMC2783813
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4. Auerbach SS, Bristol DW, Peckham JC, Travlos GS, Hébert CD, Chhabra RS: Toxicity and carcinogenicity studies of methylene blue trihydrate in F344N rats and B6C3F1 mice. Food Chem Toxicol; 2010 Jan;48(1):169-77
Hazardous Substances Data Bank. METHYLENE BLUE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The incidences of pancreatic islet cell adenoma and adenoma or carcinoma (combined) were increased in all dosed groups of male rats, but increases were statistically significant in 25mg/kg bw/day males only and the dose-response was non-linear.
  • There was a corresponding increase in the incidence of pancreatic islet cell hyperplasia but statistically significant only in the 50mg/kg bw/day male rats.
  • There were no significant increases in neoplastic transformation observed in the mice; however, positive trends were noted for adenoma or carcinoma (combined) of the small intestine and malignant lymphoma.
  • [MeSH-minor] Animals. Blood Cell Count. Body Weight / drug effects. Carcinogenicity Tests. Dose-Response Relationship, Drug. Female. Hematopoietic Stem Cells / drug effects. Hyperplasia / chemically induced. Hyperplasia / pathology. Kaplan-Meier Estimate. Lung / pathology. Male. Mammary Neoplasms, Experimental / chemically induced. Mammary Neoplasms, Experimental / pathology. Mice. Mice, Inbred Strains. Neoplasms / chemically induced. Neoplasms / pathology. Rats. Rats, Inbred F344. Sex Characteristics. Species Specificity. Survival Analysis

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  • [Copyright] Published by Elsevier Ltd.
  • (PMID = 19804809.001).
  • [ISSN] 1873-6351
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Grant] United States / FDA HHS / BB / 1 Z01 ESO45004-11 BB; United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; T42P99266K / Methylene Blue
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5. Fernando HS, Hawkyard SJ, Poon P, Musa M: Renal cell carcinoma with non-islet cell tumor hypoglycemia. Int J Urol; 2006 Jul;13(7):985-6
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  • [Title] Renal cell carcinoma with non-islet cell tumor hypoglycemia.
  • We report a case of an elderly gentleman with renal cell carcinoma presenting with the rare entity of non-islet cell tumor hypoglycemia (NICTH).
  • Non-islet cell tumor hypoglycemia syndrome is caused by the tumor producing insulin-like growth factor II, causing hypoglycemia.
  • [MeSH-major] Adenoma, Islet Cell / complications. Carcinoma, Renal Cell / complications. Hypoglycemia / etiology. Kidney Neoplasms / complications. Pancreatic Neoplasms / complications

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  • (PMID = 16882067.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 67763-96-6 / Insulin-Like Growth Factor I; 67763-97-7 / Insulin-Like Growth Factor II
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6. McElroy MK, Lowy AM, Weidner N: Case report: focal nesidioblastosis ("nesidioblastoma") in an adult. Hum Pathol; 2010 Mar;41(3):447-51
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  • [Title] Case report: focal nesidioblastosis ("nesidioblastoma") in an adult.
  • Adult nesidioblastosis is an uncommon cause of hyperinsulinemic hypoglycemia characterized by diffuse islet hyperplasia with beta-cell hypertrophy and atypia.
  • In contrast to infants, a focal form of adult nesidioblastosis (ie, "nesidioblastoma") has not been documented, although proposed.
  • [MeSH-major] Nesidioblastosis / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20004945.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose
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7. Izumiyama H, Gotyo N, Fukai N, Ozawa N, Doi M, Yoshimoto T, Arii S, Hirata Y: Glucose-responsive and octreotide-sensitive insulinoma. Intern Med; 2006;45(8):519-24
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  • Although MRI and CT scan of the abdomen failed to detect any mass lesions in the pancreas, Octreoscan revealed increased radioactive uptake around the pancreatic head region.
  • At surgery, two islet cell adenomas were identified in the pancreas and resected.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Glucose Tolerance Test. Insulinoma / drug therapy. Octreotide / therapeutic use. Pancreatic Neoplasms / drug therapy

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  • (PMID = 16702744.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Blood Glucose; 0 / Insulin; RWM8CCW8GP / Octreotide
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8. Gómez-Pérez FJ, Cuevas-Ramos D, Valdés PA, Aguilar-Salinas CA, Mehta R, Rull JA: Beta-cell adenomas without hyperinsulinemia with use of highly specific insulin radioimmunoassays: case report and review of literature. Endocr Pract; 2010 Jul-Aug;16(4):660-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Beta-cell adenomas without hyperinsulinemia with use of highly specific insulin radioimmunoassays: case report and review of literature.
  • OBJECTIVE: To report a case of a proinsulin-secreting islet cell adenoma in which the diagnosis was obscured by an ultraspecific insulin assay.
  • Magnetic resonance imaging and endoscopic ultrasonography confirmed the presence of a 2.5-cm tumor in the head of the pancreas.
  • A proinsulin-secreting islet cell tumor was diagnosed.
  • Surgical resection of the tumor was successfully accomplished, but diabetes mellitus developed 4 months postoperatively.
  • CONCLUSION: The diagnosis of a hypoglycemia-producing pancreatic adenoma can be missed when an ultraspecific insulin assay is used.
  • [MeSH-major] Insulinoma / blood. Insulinoma / diagnosis. Pancreatic Neoplasms / blood. Pancreatic Neoplasms / diagnosis. Proinsulin / blood

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  • (PMID = 20439243.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 9035-68-1 / Proinsulin
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9. Berrospi Espinoza F, Ruiz Figueroa E, Chavez Passiuri I, Celis Zapata J: [Laparoscopic treatment of insulinoma: surgical technique and perisurgical results]. Rev Gastroenterol Peru; 2005 Oct-Dec;25(4):366-70
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  • AIM: Our experience with the laparoscopic treatment of pancreatic insulinomas is reported.
  • RESULTS: All the patients were laparoscopically approached to attempt the tumor enucleation.
  • One patient developed a pancreatic fistula that closed spontaneously.
  • In all cases histological evaluation of the tumor showed benign islet cell tumor.
  • CONCLUSION: Laparoscopic enucleation of pancreatic insulinoma is a feasible and safe technique.
  • [MeSH-major] Insulinoma / surgery. Laparoscopy / methods. Pancreatic Neoplasms / surgery

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  • (PMID = 16333393.001).
  • [ISSN] 1022-5129
  • [Journal-full-title] Revista de gastroenterología del Perú : órgano oficial de la Sociedad de Gastroenterología del Perú
  • [ISO-abbreviation] Rev Gastroenterol Peru
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Peru
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10. Merritt JL 2nd, Davis DM, Pittelkow MR, Babovic-Vuksanovic D: Extensive acrochordons and pancreatic islet-cell tumors in tuberous sclerosis associated with TSC2 mutations. Am J Med Genet A; 2006 Aug 1;140(15):1669-72
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  • [Title] Extensive acrochordons and pancreatic islet-cell tumors in tuberous sclerosis associated with TSC2 mutations.
  • Acrochordons are frequently encountered benign skin lesions that may occasionally represent underlying pathology.
  • Pancreatic islet-cell tumors are rare neoplasms and few cases have been described in patients with tuberous sclerosis complex (TSC).
  • Further evaluation revealed pancreatic islet cell tumors.
  • Additionally, mutations in TSC2 gene may be a risk factor for developing pancreatic islet-cell tumors.
  • [MeSH-major] Adenoma, Islet Cell / genetics. Adenoma, Islet Cell / pathology. Mutation. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology. Skin Diseases / genetics. Tuberous Sclerosis / genetics. Tumor Suppressor Proteins / genetics


11. Krzysztof K, Wiktor B, Tadeusz Ł, Waldemar B, Magdalena K, Janusz D: Neuroendocrine tumours--analysis of own material--a nine--year retrospective study. Hepatogastroenterology; 2010 Mar-Apr;57(98):236-41

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The aim of this study was to present the author's observations of the histological tumor types, occurrence and its surgical treatment.
  • Ultrasonography, scintigraphy, computed tomography or magnetic resonance imaging of abdominal cavity, pelvis, thorax or neck--depend on the tumor localization--were done in every individual.
  • All cases were subjected to surgical procedure with an aim to resect the tumour completely.
  • RESULTS: In the present study were observed 6 cases of carcinoids localized in ileum, cecum and sigmoid colon, 1 case of gastrinoma in pancreatic head localization, 1 case of insulinoma localized in pancreatic tail, 1 case of vipoma localised in pancreatic head, 2 cases of nesidioblastoma and 1 case of microcystic adenoma with neuroendocrine differentiation in pancreatic tail localization and 1 case of nonspecific apudoma observed in ileum.
  • In adrenal glands we observed 10 benign and 1 malignant pheochromocytoma (one bilateral female case with Multiple Endocrine Neoplasia type 2A).

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  • (PMID = 20583420.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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12. Virgolini I, Traub-Weidinger T, Decristoforo C: Nuclear medicine in the detection and management of pancreatic islet-cell tumours. Best Pract Res Clin Endocrinol Metab; 2005 Jun;19(2):213-27
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  • [Title] Nuclear medicine in the detection and management of pancreatic islet-cell tumours.
  • Over the last decade somatostatin receptor scintigraphy using various derivatives of long-acting somatostatin analogues has gained its place in the management of pancreatic islet-cell tumours.
  • Scintigraphy is based on the high-affinity binding of such somatostatin analogues to receptors over-expressed by these tumour types.
  • Following the introduction of (111)In-DTPA-D-Phe(1)-octreotide, clinical studies with radiolabelled DOTA-Tyr(3)-octreotide and DOTA-Tyr(3)-octreotate derivatives have shown considerable improvement of imaging results with increased tumour uptake.
  • One of the newer developments, (68)Ga-labelled DOTA-Tyr(3)-octreotide, has shown promising results in patients with pancreatic islet-cell tumours, based on the high-affinity binding to the somatostatin receptor subtype 2 in combination with positron emission tomography (PET) technology.
  • Other peptides--such as ligands for the gastrin/CCK2 receptors or vasoactive intestinal peptide (VIP)--have also been studied for imaging pancreatic cell tumours.
  • When labelled with (90)Y or (177)Lu, some somatostatin analogues have been applied to patients in advanced stages of the disease.
  • [MeSH-major] Adenoma, Islet Cell / radionuclide imaging. Adenoma, Islet Cell / radiotherapy. Islets of Langerhans / radionuclide imaging. Pancreatic Neoplasms / radionuclide imaging. Pancreatic Neoplasms / radiotherapy

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  • (PMID = 15763696.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 51110-01-1 / Somatostatin
  • [Number-of-references] 56
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13. Herwick S, Miller FH, Keppke AL: MRI of islet cell tumors of the pancreas. AJR Am J Roentgenol; 2006 Nov;187(5):W472-80
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  • [Title] MRI of islet cell tumors of the pancreas.
  • OBJECTIVE: CT is the most widely used imaging technique for the diagnosis of islet cell tumors, but MRI may be better for detecting small lesions and metastases because of its optimal contrast resolution and ability to easily perform dynamic imaging.
  • CONCLUSION: Although classically considered well-defined, arterially enhancing lesions that are bright on T2-weighted sequences, pancreatic islet cell tumors have quite a broad spectrum of appearances.
  • MRI is well suited for detecting and characterizing pancreatic islet cell tumors as well as their local effects and metastases.
  • [MeSH-major] Adenoma, Islet Cell / diagnosis. Magnetic Resonance Imaging. Pancreatic Neoplasms / diagnosis

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  • (PMID = 17056877.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Zhang TP, Zhao YP, Zhu Y, Cai LX, Cui QC, Chen J: [Clinicopathologic features and surgical treatment of nonfunctioning islet cell tumors (78 case report)]. Zhonghua Yi Xue Za Zhi; 2005 Sep 28;85(37):2647-50
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  • [Title] [Clinicopathologic features and surgical treatment of nonfunctioning islet cell tumors (78 case report)].
  • OBJECTIVE: To investigate surgical treatment results and clinical pathological specifics in the treatment of non-functional islet cell tumor.
  • METHODS: To perform retrospective analysis of 78 cases of non-functional islet cell tumor treated at Peking Union Medical College Hospital from July 1968 through January 2005, and summarize clinical symptoms and signs, primary diagnosis before surgery, surgical treatment, pathologic specifics and immuno-histological analysis.
  • Insulin, glucagon, pancreatic polypeptide, somatostatin, vasoactive intestinal peptide and gastrin positive rates are 64.6% (42/65), 47.5% (22/53), 45.8% (22/48), 37.5% (21/56), 23.9% (11/46) and 22.6% (7/31).
  • CONCLUSIONS: Non-functional islet cell tumor lack specificity, Bus and CT are primary examination methods, immuno-histological analysis indicates various different hormones, but lacks the presence of related clinical symptoms.
  • Surgery is an effective form of treatment in the treatment of non-functional islet cell tumor, even with distal metastasis, immediate surgical removal and treatment, extend prognosis.
  • [MeSH-major] Adenoma, Islet Cell / surgery. Pancreatic Neoplasms / surgery

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  • (PMID = 16321328.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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15. Liu R, Hu MG, Luo Y: [Laparoscopic resection of pancreatic islet cell tumors]. Zhonghua Wai Ke Za Zhi; 2008 Dec 1;46(23):1768-70
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  • [Title] [Laparoscopic resection of pancreatic islet cell tumors].
  • OBJECTIVE: To summarize the surgical technique and clinical experience of total laparoscopic resection of the pancreatic islet cell tumors.
  • METHODS: From July 2002 to December 2007, 30 cases including 12 males and 18 females were diagnosed as pancreatic islet cell tumor.
  • Pancreatic leakage occurred in 3 cases, 2 of which were cured conservatively.
  • And the other one were cured by endoscopic retrograde cannulation of the pancreatic duct.
  • CONCLUSION: Total laparoscopic resection is a safe and effective method for pancreatic islet cell tumors.
  • [MeSH-major] Adenoma, Islet Cell / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery

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  • (PMID = 19094778.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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16. Varker KA, Campbell J, Shah MH: Phase II study of thalidomide in patients with metastatic carcinoid and islet cell tumors. Cancer Chemother Pharmacol; 2008 Apr;61(4):661-8
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  • [Title] Phase II study of thalidomide in patients with metastatic carcinoid and islet cell tumors.
  • PURPOSE: Carcinoid and islet cell tumors are known to be highly vascular.
  • There is no effective systemic therapy currently available for metastatic disease.
  • Tumor response was assessed at 12-week intervals using RECIST criteria.
  • Planned treatment duration was 24 weeks unless unacceptable toxicity or disease progression was observed.
  • Best response was stable disease (SD) in 11 of 16 response-evaluable patients (69%).
  • CONCLUSIONS: Thalidomide was fairly well tolerated in patients with metastatic carcinoid/islet cell tumors, but failed to reveal any objective responses.
  • [MeSH-major] Adenoma, Islet Cell / drug therapy. Angiogenesis Inhibitors / therapeutic use. Carcinoid Tumor / drug therapy. Carcinoid Tumor / secondary. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / secondary. Thalidomide / therapeutic use
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Pancreatic Hormones / blood. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17589846.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Biomarkers, Tumor; 0 / Pancreatic Hormones; 106477-83-2 / pancreastatin; 4Z8R6ORS6L / Thalidomide
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17. Desai AA, McGuigan JE, Draganov P: Zollinger-Ellison phenotype in the absence of hypergastrinemia and islet-cell tumor. Int J Gastrointest Cancer; 2005;35(2):157-61
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  • [Title] Zollinger-Ellison phenotype in the absence of hypergastrinemia and islet-cell tumor.
  • Patients with the Zollinger-Ellison syndrome are characterized by islet-cell tumors, striking gastric acid hypersecretion, and peptic ulcer disease.
  • It is a rare syndrome caused by non-beta cell islet-cell tumors (gastrinomas) located in or in proximity to the pancreas.
  • Exuberant secretion of gastrin from the gastrinomas produces severe gastric acid hypersecretion that often leads to impressive peptic ulcer disease and the constellation of symptoms listed above.
  • We describe a patient presenting with clinical manifestations characteristic of the ZES with strikingly elevated gastric acid secretion,multiple ulcers in the first and second portions of the duodenum and diarrhea, but in absence of islet-cell tumor and/or hypergastrinemia.
  • [MeSH-minor] Adenoma, Islet Cell. Gastrins / blood. Humans. Male. Middle Aged. Pancreatic Neoplasms. Phenotype

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  • [Cites] Am J Gastroenterol. 2003 Feb;98(2):301-7 [12591045.001]
  • [Cites] Ann Intern Med. 1984 Jul;101(1):7-13 [6145381.001]
  • [Cites] Gastroenterology. 1997 Oct;113(4):1129-35 [9322507.001]
  • [Cites] Int J Pancreatol. 1996 Apr;19(2):79-91 [8723550.001]
  • [Cites] Q J Med. 1983 Spring;52(206):256-67 [6137024.001]
  • [Cites] Gastroenterology. 1988 Jul;95(1):195-8 [3131179.001]
  • [Cites] Gastroenterology. 1973 Jul;65(1):140-65 [4354624.001]
  • [Cites] Gastroenterology. 1988 Sep;95(3):657-67 [3396814.001]
  • [Cites] Ann Surg. 1987 May;205(5):550-6 [3579402.001]
  • [Cites] Ann Surg. 1955 Oct;142(4):709-23; discussion, 724-8 [13259432.001]
  • [Cites] N Engl J Med. 1968 Jun 13;278(24):1308-13 [5648596.001]
  • [Cites] Gastroenterology. 1980 Dec;79(6):1324-31 [7439637.001]
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4682-6 [9354421.001]
  • [Cites] Ann Intern Med. 1985 Aug;103(2):215-7 [4014903.001]
  • [Cites] Curr Probl Surg. 1994 Feb;31(2):77-156 [7904550.001]
  • [Cites] Ann Intern Med. 1989 Nov 1;111(9):713-22 [2572194.001]
  • [Cites] Ann Intern Med. 1977 Dec;87(6):680-6 [931203.001]
  • [Cites] Dig Dis Sci. 1991 Oct;36(10):1371-6 [1914757.001]
  • (PMID = 15879632.001).
  • [ISSN] 1537-3649
  • [Journal-full-title] International journal of gastrointestinal cancer
  • [ISO-abbreviation] Int J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrins
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18. Liang H, Wang XN, Wang BG, Pan Y, Ding XW, Hao XS: [Management of nonfunctioning islet cell tumors of the pancreas]. Zhonghua Zhong Liu Za Zhi; 2007 Jun;29(6):457-60
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  • [Title] [Management of nonfunctioning islet cell tumors of the pancreas].
  • OBJECTIVE: To analyze the clinical and pathological features in order to investigate appropriate way of diagnosis and treatment for non-functional islet cell tumors of the pancreas (NFICT).
  • Twenty-eight patients were diagnosed as having non-functional islet cell carcinomas of the pancreas (NFICC) and 15 patients benign islet cell tumors.
  • Multicemtric tumor were found in one patient.
  • The resectability and curative resection rate in 28 patients with nonfunctioning islet cell carcinomas of the pancreas was 78.6% and 60.7%, respectively.
  • None of the 15 patients with benign nonfunctioning islet cell tumor of the pancreas died of this disease.
  • While the overall cumulative 5- and 10-year survival rate in 28 patients with non-functional islet cell carcinomas of the pancreas was only 58.1% and 29.0%, respectively.
  • CONCLUSION: Nonfunctioning islet cell tumor of the pancreas is frequently found in young female.
  • [MeSH-major] Adenoma, Islet Cell / therapy. Carcinoma, Islet Cell / therapy. Pancreatic Neoplasms / therapy

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  • (PMID = 17974283.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 50SG953SK6 / Mitomycin; 80168379AG / Doxorubicin; U3P01618RT / Fluorouracil; FAM protocol
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19. Nishie A, Obuchi M, Howe J, Dahmoush L, Stolpen A: Small islet cell tumour in the pancreas: diagnostic value of diffusion-weighted MRI. J Med Imaging Radiat Oncol; 2008 Aug;52(4):374-5
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  • [Title] Small islet cell tumour in the pancreas: diagnostic value of diffusion-weighted MRI.
  • We present a case of a small islet cell tumour that was clearly depicted on diffusion-weighted imaging using a free breathing approach and discuss the diagnostic value of this sequence.
  • [MeSH-major] Adenoma, Islet Cell / diagnosis. Diffusion Magnetic Resonance Imaging / methods. Pancreatic Neoplasms / diagnosis

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  • (PMID = 18811762.001).
  • [ISSN] 1754-9485
  • [Journal-full-title] Journal of medical imaging and radiation oncology
  • [ISO-abbreviation] J Med Imaging Radiat Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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20. Nakano K, Yamashita S, Soma I, Hayashi N, Higaki N, Murakami M, Hayashida H, Kan K, Ichihara T, Sakon M, Ayata M: [A case of nonfunctioning islet cell tumor with extensive calcification]. Nihon Shokakibyo Gakkai Zasshi; 2009 Oct;106(10):1494-9
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  • [Title] [A case of nonfunctioning islet cell tumor with extensive calcification].
  • Abdominal CT and magnetic resonance imaging (MRI) findings showed a calcified tumor 5 cm in diameter with a smooth surface.
  • The tumor mainly showed calcification at it center and a partially solid element around it margin which was enhanced in the early phase.
  • Pathological and immunohistochemical studies revealed a nonfunctioning islet cell tumor with calcification.
  • A nonfunctioning islet cell tumor with central calcification formation as it grew to a maximum diameter of 7 cm is rare.
  • When diagnosing pancreatic tumors it must be kept in mind that some nonfunctioning islet cell tumors of the pancreas can show nontypical features such as calcification formation.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Calcinosis. Pancreatic Neoplasms / pathology

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  • (PMID = 19834297.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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21. Ekeblad S: Islet cell tumours. Adv Exp Med Biol; 2010;654:771-89
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  • [Title] Islet cell tumours.
  • Pancreatic endocrine tumours can cause hormonal symptoms by over-secretion of hormones.
  • They are less aggressive than exocrine pancreatic cancer, but carry a variable prognosis.
  • The tumours are either sporadic or hereditary, as part of the multiple endocrine neoplasia type 1 syndrome.
  • Hereditary forms of pancreatic endocrine tumours are caused by mutations in the MEN1 gene.
  • Menin, the protein encoded by this gene, has been shown to interact with numerous transcription factors and proteins involved in cell-cycle control, shedding some light on the importance of the protein.
  • Several advances have been made in prognostication; a tumour-node-metastasis system has been evaluated and seems to have prognostic value, and several new molecular prognostic markers are under evaluation.
  • It is hoped that the tumour-node-metastasis system and other prognostic markers will be adopted in clinical routine and improve prognostication and treatment choices.
  • [MeSH-major] Adenoma, Islet Cell / therapy. Multiple Endocrine Neoplasia Type 1 / therapy

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  • (PMID = 20217524.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hormones
  • [Number-of-references] 81
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22. Yang W, Chen MH, Yan K, Wu W, Dai Y, Zhang H: Differential diagnosis of non-functional islet cell tumor and pancreatic carcinoma with sonography. Eur J Radiol; 2007 Jun;62(3):342-51
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  • [Title] Differential diagnosis of non-functional islet cell tumor and pancreatic carcinoma with sonography.
  • OBJECTIVE: To investigate the differential diagnosis of non-functional islet cell tumor (NFICT) and pancreatic ductal adenocarcinoma (pancreatic carcinoma) with clinical presentation and sonographic features.
  • MATERIALS AND METHODS: Twenty cases of NFICT were investigated in the study, and 41 cases of pancreatic carcinoma were included as the control group.
  • Among them, 5 NFICT and 32 pancreatic carcinomas underwent CEUS with SonoVue.
  • RESULTS: Statistic analysis showed four significant factors in differential diagnosis for NFICT and pancreatic carcinoma, including age (P<0.001), tumor size (P=0.006), tumor margin (P<0.001) and vascularity of tumor (P=0.004).
  • When the patient is younger than 60 years, and tumor is smaller than 5 cm with well-defined margin and hypervascular, it would be most likely a NFICT other than pancreatic carcinoma.
  • NFICT often shows early enhancement and more homogeneous infusion than pancreatic carcinoma on CEUS (P=0.005 and 0.008).
  • CONCLUSIONS: Sonography is able to provide useful differential information for NFICT, which is often misdiagnosed as pancreatic carcinoma.
  • [MeSH-major] Adenoma, Islet Cell / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Pancreas / ultrasonography. Pancreatic Neoplasms / diagnosis. Ultrasonography / methods

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  • (PMID = 17412543.001).
  • [ISSN] 0720-048X
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Phospholipids; 0 / contrast agent BR1; WS7LR3I1D6 / Sulfur Hexafluoride
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23. Noone TC, Hosey J, Firat Z, Semelka RC: Imaging and localization of islet-cell tumours of the pancreas on CT and MRI. Best Pract Res Clin Endocrinol Metab; 2005 Jun;19(2):195-211
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  • [Title] Imaging and localization of islet-cell tumours of the pancreas on CT and MRI.
  • Islet-cell tumours are neuroendocrine tumours that arise from the endocrine pancreas.
  • They range from benign to malignant.
  • Multiphase, post-contrast series are commended for the evaluation of islet-cell tumours with either modality.
  • [MeSH-major] Adenoma, Islet Cell / diagnosis. Magnetic Resonance Imaging / methods. Pancreatic Neoplasms / diagnosis. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Gastrinoma / diagnosis. Humans. Insulinoma / diagnosis. Islets of Langerhans / pathology. Multiple Endocrine Neoplasia Type 1 / diagnosis

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  • (PMID = 15763695.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 19
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24. Jiang KR, Miao Y, Xu ZK, Qian ZY, Dai CC, Xie L, Wu JL, Li Q, Xi CH, Guo F, Chen JM, Gao WT, Liu XL: [Diagnosis and surgical treatment for non-functional islet cell tumor: a retrospective analysis of 44 cases]. Zhonghua Wai Ke Za Zhi; 2009 Mar 1;47(5):326-8
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  • [Title] [Diagnosis and surgical treatment for non-functional islet cell tumor: a retrospective analysis of 44 cases].
  • OBJECTIVE: To evaluate the methods of diagnosis and surgical treatment for nonfunctional islet cell tumor (NICT).
  • METHODS: Forty-four patients with non-functional islet cell tumor treated at the First Affiliated Hospital of Nanjing Medical University during January 1968 to June 2008 were analyzed retrospectively.
  • Clinical manifestation: 15 cases (34.1%) of abdominal masses, 17 patients (38.6%) with epigastric or back pain, 5 cases of jaundice, 5 cases (11.4%) for upper abdominal fullness or vomiting, 10 cases (22.7%) of pancreatic tumor noticed by routine health checkups or imaging examinations.
  • RESULTS: pancreatic fistula in 7 patients (15.9%), intra-abdominal bleeding in 4 (9.1%), gastrojejunal anastomosis outlet obstruction in 1 (2.3%), biliary fistula in 2 (4.5%) and incisional infection in 3 (6.8%).
  • CONCLUSIONS: No specific clinical manifestation is recognized for non-functional islet cell tumor.
  • [MeSH-major] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / surgery. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery

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  • (PMID = 19595003.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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25. Koopmans KP, Neels OC, Kema IP, Elsinga PH, Sluiter WJ, Vanghillewe K, Brouwers AH, Jager PL, de Vries EG: Improved staging of patients with carcinoid and islet cell tumors with 18F-dihydroxy-phenyl-alanine and 11C-5-hydroxy-tryptophan positron emission tomography. J Clin Oncol; 2008 Mar 20;26(9):1489-95
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  • [Title] Improved staging of patients with carcinoid and islet cell tumors with 18F-dihydroxy-phenyl-alanine and 11C-5-hydroxy-tryptophan positron emission tomography.
  • PURPOSE: To evaluate and compare diagnostic sensitivity of positron emission tomography (PET) scanning in carcinoid and islet cell tumor patients with a serotonin and a catecholamine precursor as tracers.
  • PATIENTS AND METHODS: Carcinoid (n = 24) or pancreatic islet cell tumor (n = 23) patients with at least one lesion on conventional imaging including somatostatin receptor scintigraphy (SRS) and computed tomography (CT) scan underwent (11)C-5-hydroxytryptophan ((11)C-5-HTP) PET and 6-[F-18]fluoro-L-dihydroxy-phenylalanine ((18)F-DOPA) PET.
  • RESULTS: In carcinoid tumor patients, per-patient analysis showed sensitivities for (11)C-5-HTP PET, (18)F-DOPA PET, SRS, and CT of 100%, 96%, 86%, 96%, respectively, and in islet cell tumors of 100%, 89%, 78%, 87%, respectively.
  • In carcinoid patients, per-lesion analysis revealed sensitivities for (11)C-5-HTP PET, (11)C-5-HTP PET/CT, (18)F-DOPA PET, (18)F-DOPA PET/CT, SRS, SRS/CT, and CT alone of, respectively, 78%, 89%, 87%, 98%, 49%, 73%, and 63% and in islet cell tumors of 67%, 96%, 41%, 80%, 46%, 77%, and 68%, respectively.
  • In all carcinoid patients (18)F-DOPA PET and (11)C-5-HTP PET detected more lesions than SRS (P < .001). (11)C-5-HTP PET was superior to (18)F-DOPA PET in islet cell tumors (P < .0001).
  • CONCLUSION: (18)F-DOPA PET/CT is the optimal imaging modality for staging in carcinoid patients and (11)C-5-HTP PET/CT in islet cell tumor patients.
  • [MeSH-major] 5-Hydroxytryptophan. Adenoma, Islet Cell / radionuclide imaging. Carcinoid Tumor / radionuclide imaging. Dihydroxyphenylalanine. Pancreatic Neoplasms / radionuclide imaging. Positron-Emission Tomography. Tomography, X-Ray Computed

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  • [CommentIn] J Clin Oncol. 2008 Nov 10;26(32):5307-8; author reply 5308-9 [18854556.001]
  • (PMID = 18349401.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbon Radioisotopes; 0 / Radiopharmaceuticals; 0 / Receptors, Somatostatin; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 63-84-3 / Dihydroxyphenylalanine; C1LJO185Q9 / 5-Hydroxytryptophan
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26. Ikenaga N, Yamaguchi K, Konomi H, Fujii K, Sugitani A, Tanaka M: A minute nonfunctioning islet cell tumor demonstrating malignant features. J Hepatobiliary Pancreat Surg; 2005;12(1):84-7
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  • [Title] A minute nonfunctioning islet cell tumor demonstrating malignant features.
  • We report a patient with a minute nonfunctioning islet cell tumor, 8 mm in diameter, which demonstrated malignant features by histology.
  • Ultrasonography and computed tomography demonstrated a well-defined pancreatic tumor, 8 mm in diameter, in the body of the pancreas.
  • Serum levels of pancreatic hormones were within normal limits, and thus a tentative diagnosis was nonfunctioning islet cell tumor.
  • The size of the tumor remained unchanged for 1 1/2 years, but, at this time, the serum level of CA19-9 was elevated to 253 U/ml.
  • The resected specimen showed an endocrine tumor invading both the pancreatic parenchyma and the perineural spaces outside the tumor.
  • In general, minute nonfunctioning islet cell tumors have been considered to be completely benign, but the present tumor showed clear malignant features.
  • We might have to take surgical resection into consideration even if the size of such an endocrine tumor is minute.
  • [MeSH-major] Adenoma, Islet Cell / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery

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  • (PMID = 15754106.001).
  • [ISSN] 0944-1166
  • [Journal-full-title] Journal of hepato-biliary-pancreatic surgery
  • [ISO-abbreviation] J Hepatobiliary Pancreat Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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27. Du YC, Lewis BC, Hanahan D, Varmus H: Assessing tumor progression factors by somatic gene transfer into a mouse model: Bcl-xL promotes islet tumor cell invasion. PLoS Biol; 2007 Oct 16;5(10):e276
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessing tumor progression factors by somatic gene transfer into a mouse model: Bcl-xL promotes islet tumor cell invasion.
  • Tumors develop through multiple stages, implicating multiple effectors, but the tools to assess how candidate genes contribute to stepwise tumor progression have been limited.
  • We have developed a novel system in which progression of phenotypes in a mouse model of pancreatic islet cell tumorigenesis can be used to measure the effects of genes introduced by cell-type-specific infection with retroviral vectors.
  • Like RIP-Tag mice, RIP-Tag; RIP-tva bitransgenic mice develop isolated carcinomas by approximately 14 wk of age, after progression through well-defined stages that are similar to aspects of human tumor progression, including hyperplasia, angiogenesis, adenoma, and invasive carcinoma.
  • Similar infection with vectors carrying cDNA encoding either of two progression factors, a dominant-negative version of cadherin 1 (dnE-cad) or Bcl-xL, accelerated the formation of islet tumors with invasive properties and pancreatic lymph node metastasis.
  • To begin studying the mechanism by which Bcl-xL, an anti-apoptotic protein, promotes invasion and metastasis, RIP-Tag; RIP-tva pancreatic islet tumor cells were infected in vitro with RCASBP-Bcl-xL.
  • Although no changes were observed in rates of proliferation or apoptosis, Bcl-xL altered cell morphology, remodeled the actin cytoskeleton, and down-regulated cadherin 1; it also induced cell migration and invasion, as evaluated using two-chamber transwell assays.
  • In addition, myosin Va was identified as a novel Bcl-xL-interacting protein that might mediate the effects of Bcl-xL on tumor cell migration and invasion.


28. Cruz Cardona JA, Wamsley HL, Farina LL, Kiupel M: Metastatic pancreatic polypeptide-secreting islet cell tumor in a dog. Vet Clin Pathol; 2010 Sep;39(3):371-6
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  • [Title] Metastatic pancreatic polypeptide-secreting islet cell tumor in a dog.
  • Histologic evaluation determined the mass to be an islet cell tumor.
  • Approximately 98% of cells were positive by immunolabeling for pancreatic polypeptide (PP), and only rare cells were positive for insulin or somatostatin.
  • Pancreatic tumors that primarily produce PP are rare in dogs, and this is the first report of both the cytologic and histologic features of an islet cell tumor predominantly secreting PP.
  • Additional case studies are needed to further characterize the cytomorphologic features and clinical presentation of PP-secreting islet cell tumor, or polypeptidoma, in dogs.

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  • [Copyright] ©2010 American Society for Veterinary Clinical Pathology.
  • (PMID = 20698942.001).
  • [ISSN] 1939-165X
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 59763-91-6 / Pancreatic Polypeptide
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29. Caudill JL, Humphrey SK, Salomão DR: Islet cell tumor of the pancreas: increasing diagnosis after instituting ultrasonography-guided fine needle aspiration. Acta Cytol; 2008 Jan-Feb;52(1):45-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Islet cell tumor of the pancreas: increasing diagnosis after instituting ultrasonography-guided fine needle aspiration.
  • OBJECTIVE: To review the clinical and cytomorphologic features of pancreatic islet cell tumors (ICT).
  • STUDY DESIGN: Computer search identified patients with pancreatic ICT diagnosed by fine needle aspiration biopsy (FNAB) between January 1995 and December 2003.
  • Twenty-two patients underwent tumor resection.
  • CONCLUSION: Newer radiography and biopsy techniques to detect and examine smaller pancreatic masses have increased the number of pancreatic ICT diagnoses at our institution.
  • The distinctive cytomorphologic features of pancreatic ICT make it reliably diagnosable by FNAB.
  • [MeSH-major] Adenoma, Islet Cell / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy, Fine-Needle. Endosonography. Female. Humans. Islets of Langerhans / pathology. Islets of Langerhans / radiography. Islets of Langerhans / ultrasonography. Male. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 18323274.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Mascarenhas NB, Mulcahy MF, Lewandowski RJ, Salem R, Ryu RK: Hepatic abscess after yttrium-90 radioembolization for islet-cell tumor hepatic metastasis. Cardiovasc Intervent Radiol; 2010 Jun;33(3):650-3
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  • [Title] Hepatic abscess after yttrium-90 radioembolization for islet-cell tumor hepatic metastasis.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Embolization, Therapeutic / adverse effects. Liver Abscess / etiology. Liver Neoplasms / radiotherapy. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology

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  • (PMID = 19688373.001).
  • [ISSN] 1432-086X
  • [Journal-full-title] Cardiovascular and interventional radiology
  • [ISO-abbreviation] Cardiovasc Intervent Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Yttrium Radioisotopes
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31. Krysiak R, Okopień B, Herman ZS: [Insulinoma]. Pol Merkur Lekarski; 2007 Jan;22(127):70-4
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  • [Transliterated title] Wyspiak wydzielajacy insuline.
  • Insulinoma is considered the most common endocrine tumour of the pancreas with an annual prevalence of 4 cases per million people.
  • Contrary to the other endocrine tumours of this organ, over 90% of the insulinomas are benign in nature.
  • Effective management requires directed biochemical testing, careful choice of preoperative imaging tests, and complete pancreatic exploration by an experienced endocrine surgeon utilising intraoperative ultrasound.
  • The only curative treatment for insulinoma is complete resection of the tumour.
  • [MeSH-major] Adenoma, Islet Cell / complications. Adenoma, Islet Cell / diagnosis. Insulinoma / complications. Insulinoma / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Endocrine Surgical Procedures / methods. Gastrinoma / complications. Gastrinoma / diagnosis. Gastrinoma / metabolism. Gastrinoma / surgery. Humans. Hypoglycemia / complications. Insulin / metabolism. Pancreatectomy / methods. Prognosis. Rare Diseases

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  • (PMID = 17477096.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Insulin
  • [Number-of-references] 34
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32. Bourcier ME, Sherrod A, DiGuardo M, Vinik AI: Successful control of intractable hypoglycemia using rapamycin in an 86-year-old man with a pancreatic insulin-secreting islet cell tumor and metastases. J Clin Endocrinol Metab; 2009 Sep;94(9):3157-62
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  • [Title] Successful control of intractable hypoglycemia using rapamycin in an 86-year-old man with a pancreatic insulin-secreting islet cell tumor and metastases.
  • CONTEXT: Insulinomas are rare tumors of the pancreatic islet cells that produce insulin.
  • At present, streptozotocin is the only approved drug for the treatment of pancreatic islet cell tumors.
  • SETTING AND PATIENT: This report describes a case of an elderly gentleman with a metastatic pancreatic insulinoma and severe hypoglycemia.
  • He remained euglycemic for the past year with no evidence of tumor progression based on Octreoscan.
  • CONCLUSIONS: Rapamycin may provide a useful means of abrogating tumor growth and controlling hypoglycemia in malignant insulinomas by reducing the malignant beta-cell growth and proliferation as well as inhibiting insulin production.
  • [MeSH-major] Adenoma, Islet Cell / drug therapy. Hypoglycemia / drug therapy. Pancreatic Neoplasms / drug therapy. Sirolimus / therapeutic use

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  • (PMID = 19567519.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0J48LPH2TH / Hydrochlorothiazide; 5W494URQ81 / Streptozocin; W00SSD35VW / buthiazide; W36ZG6FT64 / Sirolimus
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33. Shimada K, Sakamoto Y, Esaki M, Kosuge T, Hiraoka N: Role of medial pancreatectomy in the management of intraductal papillary mucinous neoplasms and islet cell tumors of the pancreatic neck and body. Dig Surg; 2008;25(1):46-51
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  • [Title] Role of medial pancreatectomy in the management of intraductal papillary mucinous neoplasms and islet cell tumors of the pancreatic neck and body.
  • BACKGROUND/AIM: Medial pancreatectomy has been applied as a safe and effective alternative in benign diseases located in the pancreatic neck or body.
  • Four patients required an additional resection of the pancreatic remnant because of a positive surgical margin.
  • Three patients with islet cell tumor and 1 patient with solid pseudopapillary tumor had no malignant disease.
  • Postoperative complications occurred in 6 patients (43%): 5 had pancreatic fistulas and 1 had a gastric ulcer.
  • CONCLUSIONS: A medial pancreatectomy is a safe and effective alternative for the treatment of intraductal papillary mucinous neoplasm, islet cell tumor, or solid pseudopapillary tumor located in the neck or body of the pancreas.
  • [MeSH-major] Adenocarcinoma, Mucinous / surgery. Adenocarcinoma, Papillary / surgery. Adenoma, Islet Cell / surgery. Carcinoma, Intraductal, Noninfiltrating / surgery. Pancreatectomy. Pancreatic Neoplasms / surgery

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  • (PMID = 18292661.001).
  • [ISSN] 1421-9883
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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34. Yu R, Nissen NN, Dhall D, Heaney AP: Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature. Pancreas; 2008 May;36(4):428-31
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  • [Title] Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature.
  • We report a rare case of nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas.
  • A 60-year-old patient was incidentally found to harbor a pancreatic mass with markedly elevated glucagon levels but without glucagonoma syndrome.
  • She was initially diagnosed with glucagonoma, and the tumor was resected.
  • Pathological examination demonstrated that the tumor was a nonfunctioning islet cell tumor and revealed nesidioblastosis and hyperplasia of alpha cells and microglucagonoma in the apparently normal surgical margin.
  • No pancreatic tumors recurred 36 months after surgery.
  • This is the third case of alpha-cell nesidioblastosis reported in the English literature.
  • Somatostatin analog may be used to suppress glucagon secretion in alpha-cell hyperplasia.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / pathology. Glucagonoma / pathology. Islets of Langerhans / pathology. Nesidioblastosis / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18437091.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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35. Dromain C, Baudin E: [Endocrine pancreas]. J Radiol; 2005 Jun;86(6 Pt 2):797-804; quiz 805
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  • [Title] [Endocrine pancreas].
  • [Transliterated title] Pancréas endocrine.
  • Pancreatic endocrine tumors (PET) are characterised by their hormone synthesis capability and can be associated with an hereditary syndrome-related cancer.
  • The challenge for imaging is to localize the tumor.
  • [MeSH-major] Diagnostic Imaging. Islets of Langerhans / pathology. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / diagnosis. Endosonography. Humans. Magnetic Resonance Imaging. Positron-Emission Tomography. Somatostatin. Tomography, X-Ray Computed

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  • (PMID = 16142073.001).
  • [ISSN] 0221-0363
  • [Journal-full-title] Journal de radiologie
  • [ISO-abbreviation] J Radiol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 51110-01-1 / Somatostatin
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36. Anderson AA, Helmering J, Juan T, Li CM, McCormick J, Graham M, Baker DM, Damore MA, Véniant MM, Lloyd DJ: Pancreatic islet expression profiling in diabetes-prone C57BLKS/J mice reveals transcriptional differences contributed by DBA loci, including Plagl1 and Nnt. Pathogenetics; 2009;2(1):1
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  • [Title] Pancreatic islet expression profiling in diabetes-prone C57BLKS/J mice reveals transcriptional differences contributed by DBA loci, including Plagl1 and Nnt.
  • BACKGROUND: C57BLKS/J (BLKS) mice are susceptible to islet exhaustion in insulin-resistant states as compared with C57BL6/J (B6) mice, as observed by the presence of the leptin receptor (Lepr) allele, Leprdb/db.
  • Furthermore, DBA2/J (DBA) mice are also susceptible to beta-cell failure and share 25% of their genome with BLKS; thus the DBA genome may contribute to beta-cell dysfunction in BLKS mice.
  • RESULTS: Here we show that BLKS mice exhibit elevated insulin secretion, as evidenced by improved glucose tolerance and increased islet insulin secretion compared with B6 mice, and describe interstrain transcriptional differences in glucose response.
  • CONCLUSION: Two genes, Nicotinamide nucleotide transhydrogenase (Nnt) and Pleiomorphic adenoma gene like 1 (Plagl1), were 4 and 7.2-fold higher respectively in BLKS islets, and may be major contributors to increased insulin secretion by BLKS islets.
  • Several inflammatory glucose-responsive genes are expressed at a higher level in BLKS, suggesting an inflammatory component to BLKS islet dysfunction.
  • This study describes physiological differences between BLKS and B6 mice, and provides evidence for a causative role of the DBA genome in beta-cell dysfunction in BLKS mice.

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  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 12;105(6):2082-7 [18252823.001]
  • [Cites] Diabetologia. 2007 Dec;50(12):2476-85 [17922105.001]
  • [Cites] Ann Clin Biochem. 2007 Nov;44(Pt 6):570-2 [17961315.001]
  • [Cites] BMC Mol Biol. 2007;8:41 [17521427.001]
  • [Cites] PLoS Med. 2007 May;4(5):e158 [17472435.001]
  • [Cites] Endocrinology. 2007 Feb;148(2):575-84 [17110428.001]
  • [Cites] J Cell Physiol. 2007 Jan;210(1):16-25 [17063461.001]
  • [Cites] Biochem Soc Trans. 2006 Nov;34(Pt 5):806-10 [17052203.001]
  • [Cites] Diabetes. 2006 Jul;55(7):2153-6 [16804088.001]
  • [Cites] Nat Genet. 2006 Jun;38(6):688-93 [16682971.001]
  • [Cites] Diabetes. 2006 Jun;55(6):1625-33 [16731824.001]
  • [Cites] Diabetologia. 2006 Jun;49(6):1254-63 [16570159.001]
  • [Cites] Biochim Biophys Acta. 2006 Apr;1762(4):440-6 [16481151.001]
  • [Cites] Hum Mol Genet. 2000 Feb 12;9(3):453-60 [10655556.001]
  • [Cites] Cell. 2005 Aug 12;122(3):337-49 [16096055.001]
  • [Cites] Diabetologia. 2005 Apr;48(4):675-86 [15729571.001]
  • [Cites] Diabetes. 2005 Apr;54(4):1191-9 [15793261.001]
  • [Cites] Endocr J. 2004 Oct;51(5):499-504 [15516785.001]
  • [Cites] J Lipid Res. 1999 Jul;40(7):1328-35 [10393218.001]
  • [Cites] Immunogenetics. 1997;46(1):53-62 [9148789.001]
  • [Cites] Mamm Genome. 1995 Feb;6(2):131-3 [7766997.001]
  • [Cites] Am J Physiol. 1995 May;268(5 Pt 1):C1241-51 [7762618.001]
  • [Cites] Diabetologia. 1989 Sep;32(9):636-43 [2676665.001]
  • [Cites] Nature. 1990 Sep 13;347(6289):151-6 [1697648.001]
  • [Cites] Diabetologia. 1983 Nov;25(5):439-43 [6360782.001]
  • [Cites] Diabetes. 1981 Dec;30(12):1029-34 [7030828.001]
  • [Cites] Diabetes. 1978 Jan;27(1):1-7 [340309.001]
  • [Cites] J Clin Invest. 2004 Aug;114(3):339-48 [15286800.001]
  • [Cites] Endocrinology. 2004 Jul;145(7):3307-23 [15044376.001]
  • [Cites] Endocrinology. 2002 Jun;143(6):2085-92 [12021173.001]
  • [Cites] Nature. 2001 Dec 13;414(6865):788-91 [11742410.001]
  • [Cites] Diabetes. 2000 Nov;49(11):1946-54 [11078464.001]
  • [Cites] Diabetes. 2008 Apr;57(4):938-44 [18171713.001]
  • [Cites] PLoS One. 2008;3(5):e2165 [18478125.001]
  • [Cites] J Cell Physiol. 2008 Aug;216(2):558-67 [18452188.001]
  • [Cites] Cell Metab. 2006 Jan;3(1):35-45 [16399503.001]
  • (PMID = 19161594.001).
  • [ISSN] 1755-8417
  • [Journal-full-title] PathoGenetics
  • [ISO-abbreviation] Pathogenetics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2642818
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37. Hobson DJ, Turner PV: Spontaneous pancreatic islet cell tumor in a black and white colobus monkey (Colobus guereza kikuyuensis). J Med Primatol; 2008 Feb;37 Suppl 1:11-5
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  • [Title] Spontaneous pancreatic islet cell tumor in a black and white colobus monkey (Colobus guereza kikuyuensis).
  • Histologically, the mass had characteristics of a neuroendocrine or endocrine tumor.
  • Immunohistochemical stains for chromogranin, synaptophysin, insulin, and glucagon were positive, confirming the diagnosis of a mixed pancreatic islet cell tumor.
  • [MeSH-major] Adenoma, Islet Cell / veterinary. Colobus. Monkey Diseases / diagnosis. Pancreatic Neoplasms / veterinary

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  • (PMID = 18269522.001).
  • [ISSN] 0047-2565
  • [Journal-full-title] Journal of medical primatology
  • [ISO-abbreviation] J. Med. Primatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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38. House MG, Schulick RD: Endocrine tumors of the pancreas. Curr Opin Oncol; 2006 Jan;18(1):23-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endocrine tumors of the pancreas.
  • PURPOSE OF REVIEW: Neoplasms of the endocrine pancreas, commonly referenced as pancreatic islet cell tumors, are rare, often well differentiated endocrine neoplasms, whose biology remains poorly characterized.
  • This article reviews the current clinical management of pancreatic islet cell tumors and describes the molecular events that have been studied to guide future therapies of these peculiar neoplasms.
  • RECENT FINDINGS: While some islet cell tumors arise in association with the MEN-1 syndrome, the majority of these neoplasms are sporadic lesions whose underlying genetic and molecular events remain largely unknown.
  • Recent work has identified changes in gene expression occurring in metastatic and non-metastatic islet cell tumors, which appear to correlate with the occurrence of lymph node and liver metastases.
  • Epigenetic alterations of select tumor suppressor genes may influence patient survival, and the presence of gene promoter methylation may be used as a prognostic marker system.
  • In addition, multiple molecular alterations, including changes in expression of cellular proteins with migratory, cell cycle or angiogenic functions, have been demonstrated to influence islet cell tumor growth, invasion and metastatic spread.
  • SUMMARY: Understanding the molecular events underlying the biology of pancreatic islet cell tumors will aid the development of accurate prognostic markers and will guide improved therapeutic modalities in the future.
  • [MeSH-major] Adenoma, Islet Cell / therapy. Carcinoma, Islet Cell / therapy. Pancreatic Neoplasms / therapy

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  • [RetractionIn] Klastersky J. Curr Opin Oncol. 2006 Jul;18(4):414 [16721138.001]
  • (PMID = 16357560.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Retracted Publication; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / ELL protein, human; 0 / Transcriptional Elongation Factors
  • [Number-of-references] 51
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39. Anlauf M, Schlenger R, Perren A, Bauersfeld J, Koch CA, Dralle H, Raffel A, Knoefel WT, Weihe E, Ruszniewski P, Couvelard A, Komminoth P, Heitz PU, Klöppel G: Microadenomatosis of the endocrine pancreas in patients with and without the multiple endocrine neoplasia type 1 syndrome. Am J Surg Pathol; 2006 May;30(5):560-74
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  • [Title] Microadenomatosis of the endocrine pancreas in patients with and without the multiple endocrine neoplasia type 1 syndrome.
  • It has been suggested that microadenomatosis of the endocrine pancreas is a hallmark of the multiple endocrine neoplasia type 1 syndrome (MEN1).
  • This study attempts to elucidate the relationship between pancreatic microadenomatosis and the MEN1 and von Hippel-Lindau (VHL) syndromes.
  • Pancreatic tissue specimens from 37 patients (with either microadenomatosis or the MEN1 syndrome) were analyzed using immunohistochemistry, confocal laser scanning microscopy, and morphometric methods.
  • Pancreatic microadenomatosis was found in 35 of 37 patients, 28 of whom fulfilled the clinicopathologic criteria and 13 the genetic criteria for MEN1, whereas none of the patients had evidence of a VHL syndrome.
  • In microadenomatosis patients with and without the MEN1 syndrome, a subset of morphologically normal-appearing islets showed increased endocrine cell proliferation.
  • In conclusion, endocrine multihormonal microadenomatosis of the pancreas is a feature of MEN1.
  • In addition, a monohormonal type of pancreatic microadenomatosis was identified that consisted of either insulinomas or glucagon-producing tumors and was not associated with MEN1 or VHL.
  • [MeSH-major] Adenoma, Islet Cell / complications. Adenoma, Islet Cell / pathology. Multiple Endocrine Neoplasia Type 1 / complications. Multiple Endocrine Neoplasia Type 1 / pathology. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. DNA Mutational Analysis. Female. Humans. Immunohistochemistry. Male. Microscopy, Confocal. Middle Aged. Mutation. Polymerase Chain Reaction. von Hippel-Lindau Disease / complications. von Hippel-Lindau Disease / genetics. von Hippel-Lindau Disease / pathology


40. Couvelard A, Deschamps L, Rebours V, Sauvanet A, Gatter K, Pezzella F, Ruszniewski P, Bedossa P: Overexpression of the oxygen sensors PHD-1, PHD-2, PHD-3, and FIH Is associated with tumor aggressiveness in pancreatic endocrine tumors. Clin Cancer Res; 2008 Oct 15;14(20):6634-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of the oxygen sensors PHD-1, PHD-2, PHD-3, and FIH Is associated with tumor aggressiveness in pancreatic endocrine tumors.
  • PURPOSE: Tumor hypoxia is associated with poor prognosis and resistance to treatment.
  • Our aim was to assess the expression of proteins that act as cellular oxygen sensors, directly regulating the hypoxia inducible factor (HIF) pathway, i.e., prolyl hydroxylase domain proteins (PHD)-1, PHD-2, PHD-3, and FIH in pancreatic endocrine tumors (PET).
  • FIH stromal expression was found in 23% of PETs and correlated with higher FIH nuclear expression (P = 0.0004) and poorer disease-free survival (P = 0.0018).
  • CONCLUSION: HIF regulatory proteins are highly expressed in PET and their expression is correlated with tumor metastases, tumor recurrence, and prognosis.
  • These molecules that play an important role in the control of hypoxia-induced genes may have a function in the regulation of cellular proliferation and differentiation during endocrine tumorigenesis.
  • [MeSH-major] Cell Hypoxia. Dioxygenases / metabolism. Pancreatic Neoplasms / metabolism. Procollagen-Proline Dioxygenase / metabolism. Repressor Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Adenoma, Islet Cell / metabolism. Adenoma, Islet Cell / pathology. Adult. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / secondary. Cell Differentiation. Cell Proliferation. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Hypoxia-Inducible Factor-Proline Dioxygenases. Immunoenzyme Techniques. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lymphatic Metastasis. Male. Microcirculation. Mixed Function Oxygenases. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / metabolism. Neovascularization, Pathologic. Tissue Array Analysis

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  • (PMID = 18927305.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Repressor Proteins; EC 1.- / Mixed Function Oxygenases; EC 1.13.11.- / Dioxygenases; EC 1.14.11.- / HIF1AN protein, human; EC 1.14.11.2 / EGLN1 protein, human; EC 1.14.11.2 / Procollagen-Proline Dioxygenase; EC 1.14.11.29 / EGLN3 protein, human; EC 1.14.11.29 / Hypoxia-Inducible Factor-Proline Dioxygenases
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41. Zhou J, Dong M, Kong F, Li Y, Tian Y: Central pancreatectomy for benign tumors of the neck and body of the pancreas: report of eight cases. J Surg Oncol; 2009 Sep 1;100(3):273-6
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  • [Title] Central pancreatectomy for benign tumors of the neck and body of the pancreas: report of eight cases.
  • BACKGROUND: To discuss the advantage of central pancreatectomy in the patients with benign tumors of the neck and body of the pancreas.
  • The operation is carried out by exposition of the pancreatic neck and body involved by the lesion.
  • RESULTS: Central pancreatectomy was done in eight patients including five mucinous cystadenomas, one serious cystadenoma, one insulinoma and one nonfunctional islet cell tumor.
  • Pancreatic fistula occurred in three cases and was treated conservatively.
  • CONCLUSION: Central pancreatectomy is a safe technique for benign tumors of the pancreatic neck and body, especially when the enucleation is very difficult.
  • [MeSH-major] Pancreatectomy / methods. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adenoma, Islet Cell / surgery. Adult. Cystadenoma, Mucinous / surgery. Cystadenoma, Serous / surgery. Female. Humans. Insulinoma / surgery. Male. Middle Aged. Pancreatic Fistula / etiology. Pancreatic Fistula / therapy. Postoperative Complications. Retrospective Studies

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  • (PMID = 19267362.001).
  • [ISSN] 1096-9098
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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42. Ho AS, Picus J, Darcy MD, Tan B, Gould JE, Pilgram TK, Brown DB: Long-term outcome after chemoembolization and embolization of hepatic metastatic lesions from neuroendocrine tumors. AJR Am J Roentgenol; 2007 May;188(5):1201-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MATERIALS AND METHODS: Forty-six patients with carcinoid (n = 31) or islet cell (n = 15) tumors were treated.
  • Potential factors affecting survival, including presence of extrahepatic disease and resection of the primary lesion, were analyzed.
  • The mean overall survival times for the carcinoid (1,255 +/- 163 days) and islet cell tumor (1,311 +/- 403 days) subgroups were similar (p = 0.66).
  • The progression-free survival times for the carcinoid (602 +/- 144 days) and islet cell (501 +/- 107 days) tumor subgroups also were similar (p = 0.72).
  • The survival time of patients without known extrahepatic metastasis (n = 18; 1,571 +/- 291 days) trended toward significance compared with that of patients with known extrahepatic disease (n = 26; 770 +/- 112 days; p = 0.08).
  • Resection of the primary tumor in 19 of 46 patients did not affect survival (resection survival, 1,558 +/- 400 days; nonresection survival, 1,000 +/- 179 days; p = 0.44).
  • The presence of extrahepatic metastasis or an unresected primary tumor should not limit the use of hepatic artery chemoembolization or HAE.
  • [MeSH-minor] Adenoma, Islet Cell / therapy. Adult. Aged. Carcinoid Tumor / secondary. Carcinoid Tumor / therapy. Embolization, Therapeutic. Female. Hepatic Artery. Humans. Male. Middle Aged. Survival Analysis

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  • (PMID = 17449759.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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43. Hoff AO, Hauache OM: [Multiple endocrine neoplasia type 1 (MEN 1): clinical, biochemical and molecular diagnosis and treatment of the associated disturbances]. Arq Bras Endocrinol Metabol; 2005 Oct;49(5):735-46
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  • [Title] [Multiple endocrine neoplasia type 1 (MEN 1): clinical, biochemical and molecular diagnosis and treatment of the associated disturbances].
  • [Transliterated title] Neoplasia endócrina múltipla tipo 1: diagnóstico clínico, laboratorial e molecular e tratamento das doenças associadas.
  • Multiple endocrine neoplasia (MEN) syndromes include types 1 (MEN 1) and 2 (MEN 2), von Hippel-Lindau syndrome, neurofibromatosis type 1 and Carney complex.
  • These are complex genetic syndromes caused by activation or inactivation of different types of genes known to be involved in the regulation of cell proliferation.
  • MEN 1 is a hereditary syndrome, transmitted in an autosomic dominant fashion and caused by an inactivating mutation of the MEN 1 gene, characterized by the development of primary hyperparathyroidism, islet cell tumors and pituitary adenomas.
  • In addition, these patients can present with cutaneous manifestations such as angiofibromas and collagenomas, and can develop other neoplastic manifestations including carcinoids, thyroid tumors, adrenal adenomas, lipomas, pheochromocytomas and meningiomas.
  • The MEN 1 gene encodes a peptide which is a tumor suppressor gene called menin.
  • Several studies have demonstrated its importance in regulation of cell proliferation and have confirmed its role in the pathogenesis of the MEN 1 syndrome.
  • [MeSH-major] Multiple Endocrine Neoplasia Type 1. Mutation / genetics. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / genetics. Adenoma, Islet Cell / therapy. Genetic Testing. Humans. Hyperparathyroidism, Primary / diagnosis. Hyperparathyroidism, Primary / genetics. Hyperparathyroidism, Primary / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / therapy. Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / genetics. Pituitary Neoplasms / therapy

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  • (PMID = 16444356.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins
  • [Number-of-references] 84
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44. Pietras K, Hanahan D: A multitargeted, metronomic, and maximum-tolerated dose "chemo-switch" regimen is antiangiogenic, producing objective responses and survival benefit in a mouse model of cancer. J Clin Oncol; 2005 Feb 10;23(5):939-52
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  • PURPOSE: A transgenic mouse model has revealed parameters of the angiogenic switch during multistep tumorigenesis of pancreatic islets, and demonstrated efficacy of antiangiogenic therapies.
  • Pericytes have been revealed as functionally important for tumor neovasculature, using kinase inhibitors targeting their platelet-derived growth factor receptors (PDGFRs).
  • Additionally, vascular endothelial growth factor receptor (VEGFR) inhibitors and metronomic chemotherapy show modest benefit against early- but not late-stage disease.
  • MATERIALS AND METHODS: Seeking to improve efficacy against otherwise intractable end-stage pancreatic islet tumors, two receptor tyrosine kinase inhibitors, imatinib and SU11248, were used to disrupt PDGFR-mediated pericyte support of tumor endothelial cells in concert with maximum-tolerated dose (MTD) or metronomic chemotherapy and/or VEGFR inhibition.
  • RESULTS: Imatinib, despite equivocal efficacy as monotherapy, reduced pericyte coverage of tumor vessels and enhanced efficacy in combination with metronomic chemotherapy or VEGFR inhibition.
  • MTD using cyclophosphamide caused transitory regression, but then rapid regrowth, in contrast to metronomic cyclophosphamide plus imatinib, which produced stable disease.
  • The MTD regimen elicited apoptosis of tumor cells but not endothelial cells, whereas the other regimens increased endothelial cell apoptosis concordant with efficacy.
  • CONCLUSION: This study demonstrates a potentially tractable clinical strategy in a stringent preclinical model, wherein standard-of-care chemotherapy is followed by a novel maintenance regimen: PDFGR is targeted to disrupt pericyte support, while metronomic chemotherapy and/or VEGFR inhibitors target consequently sensitized endothelial cells, collectively destabilizing pre-existing tumor vasculature and inhibiting ongoing angiogenesis.
  • [MeSH-minor] Adenoma, Islet Cell / drug therapy. Animals. Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Alkylating / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Benzamides. Clinical Protocols. Cyclophosphamide / therapeutic use. Disease Models, Animal. Endothelial Cells / drug effects. Imatinib Mesylate. Indoles / administration & dosage. Indoles / therapeutic use. Mice. Mice, Transgenic. Pancreatic Neoplasms / blood supply. Pancreatic Neoplasms / drug therapy. Piperazines / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. Pyrroles / administration & dosage. Pyrroles / therapeutic use. Remission Induction

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  • (PMID = 15557593.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Benzamides; 0 / Indoles; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Pyrroles; 0 / sunitinib; 8A1O1M485B / Imatinib Mesylate; 8N3DW7272P / Cyclophosphamide; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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45. Haddad LB, Scatton O, Randone B, Andraus W, Massault PP, Dousset B, Soubrane O: Pancreatic fistula after pancreaticoduodenectomy: the conservative treatment of choice. HPB (Oxford); 2009 May;11(3):203-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic fistula after pancreaticoduodenectomy: the conservative treatment of choice.
  • BACKGROUND: A pancreatic fistula (PF) is the most common complication after pancreaticoduodenectomy (PD), and its reported incidence varies from 2% to 28%.
  • The main indications for PD were pancreatic duct carcinoma in 52 patients (44.5%), ampullary carcinoma or adenoma in 18 (15.4%) and islet cell tumour in 11 (9.4%).
  • The medium delay between the pancreatic resection and reoperation was 10 days (range, 3-32 days).
  • There is no advantage in performing completion pancreatectomy (CP) instead of extensive drainage as a result of the same mortality and morbidity rates and the risk of endocrine insufficiency.

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  • [Cites] Arch Surg. 2004 Jan;139(1):16-9 [14718268.001]
  • [Cites] Br J Surg. 2000 Jul;87(7):883-9 [10931023.001]
  • [Cites] World J Surg. 2003 Jun;27(6):709-14 [12732998.001]
  • [Cites] Arch Surg. 2006 Jun;141(6):574-9; discussion 579-80 [16785358.001]
  • [Cites] Ann Surg. 2005 Dec;242(6):767-71, discussion 771-3 [16327486.001]
  • [Cites] Br J Surg. 2005 Sep;92(9):1117-23 [15931656.001]
  • [Cites] Arch Surg. 2005 Sep;140(9):849-54; discussion 854-6 [16172293.001]
  • [Cites] Surgery. 2005 Jul;138(1):8-13 [16003309.001]
  • [Cites] World J Surg. 2005 Feb;29(2):212-6 [15654661.001]
  • [Cites] J Gastrointest Surg. 2004 Dec;8(8):951-9 [15585382.001]
  • [Cites] J Gastrointest Surg. 2004 Nov;8(7):766-72; discussion 772-4 [15531229.001]
  • [Cites] World J Surg. 1999 Feb;23(2):164-71; discussion 171-2 [9880426.001]
  • [Cites] Ann Surg. 1997 Sep;226(3):248-57; discussion 257-60 [9339931.001]
  • [Cites] J Am Coll Surg. 1997 Jul;185(1):18-24 [9208956.001]
  • [Cites] Br J Surg. 1996 Feb;83(2):176-9 [8689156.001]
  • [Cites] Ann Surg. 1995 Oct;222(4):580-8; discussion 588-92 [7574936.001]
  • [Cites] Br J Surg. 1995 Sep;82(9):1270-3 [7552016.001]
  • [Cites] Ann Surg. 1995 Jun;221(6):721-31; discussion 731-3 [7794076.001]
  • [Cites] Cancer. 1995 Apr 15;75(8):2069-76 [7697596.001]
  • [Cites] Arch Surg. 1995 Mar;130(3):295-9; discussion 299-300 [7887797.001]
  • [Cites] Br J Surg. 1994 Feb;81(2):265-9 [8156354.001]
  • [Cites] Am J Surg. 1994 Oct;168(4):295-8 [7524375.001]
  • [Cites] Ann Surg. 1993 Sep;218(3):229-37; discussion 237-8 [8103982.001]
  • [Cites] Ann Surg. 1993 May;217(5):430-5; discussion 435-8 [8098202.001]
  • [Cites] Arch Surg. 1992 Aug;127(8):945-9; discussion 949-50 [1353671.001]
  • [Cites] World J Surg. 1992 May-Jun;16(3):521-4 [1350387.001]
  • [Cites] Am J Surg. 1992 Jan;163(1):125-30; discussion 130-1 [1733360.001]
  • [Cites] Ann Surg. 1988 Jan;207(1):39-47 [3276272.001]
  • [Cites] Ann Surg. 1990 Apr;211(4):447-58 [2322039.001]
  • [Cites] Surg Gynecol Obstet. 1978 Jun;146(6):959-62 [653575.001]
  • [Cites] J Am Coll Surg. 2004 Aug;199(2):198-203 [15275873.001]
  • [Cites] Arch Surg. 2004 Jul;139(7):718-25; discussion 725-7 [15249403.001]
  • [Cites] Arch Surg. 2003 Dec;138(12):1310-4; discussion 1315 [14662530.001]
  • [Cites] J Am Coll Surg. 2003 Apr;196(4):556-64; discussion 564-5; author reply 565 [12691930.001]
  • [Cites] Ann Surg. 2003 Jan;237(1):57-65 [12496531.001]
  • [Cites] Br J Surg. 2002 Oct;89(10):1245-51 [12296891.001]
  • [Cites] Dig Surg. 2001;18(6):453-7; discussion 458 [11799295.001]
  • [Cites] J Gastrointest Surg. 2000 Nov-Dec;4(6):567-79 [11307091.001]
  • [Cites] Arch Surg. 2001 Apr;136(4):391-8 [11296108.001]
  • [Cites] Am J Surg. 2000 Aug;180(2):117-20 [11044525.001]
  • [Cites] Ann Surg. 2000 Sep;232(3):419-29 [10973392.001]
  • [Cites] J Gastrointest Surg. 2003 Jul-Aug;7(5):672-82 [12850681.001]
  • (PMID = 19590648.001).
  • [ISSN] 1365-182X
  • [Journal-full-title] HPB : the official journal of the International Hepato Pancreato Biliary Association
  • [ISO-abbreviation] HPB (Oxford)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2697888
  • [Keywords] NOTNLM ; pancreatic fistula / pancreatic resection / pancreaticoduodenectomy / postoperative complications
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46. Cavard C, Terris B, Grimber G, Christa L, Audard V, Radenen-Bussiere B, Simon MT, Renard CA, Buendia MA, Perret C: Overexpression of regenerating islet-derived 1 alpha and 3 alpha genes in human primary liver tumors with beta-catenin mutations. Oncogene; 2006 Jan 26;25(4):599-608
MedlinePlus Health Information. consumer health - Liver Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of regenerating islet-derived 1 alpha and 3 alpha genes in human primary liver tumors with beta-catenin mutations.
  • We used PCR-based subtractive hybridization to compare gene expression between malignant and benign components of a human HCC occurring in pre-existing adenoma activated for beta-catenin.
  • They encode the Regenerating islet-derived 3 alpha (REG3A/HIP/PAP/REG-III) and 1 alpha (REG1A) proteins, both involved in liver and pancreatic regeneration and proliferation.
  • [MeSH-major] Antigens, Neoplasm / genetics. Biomarkers, Tumor / genetics. Carcinoma, Hepatocellular / genetics. Gene Expression Regulation, Neoplastic. Lectins, C-Type / genetics. Lithostathine / genetics. Liver Neoplasms / genetics. Mutation. beta Catenin / genetics
  • [MeSH-minor] Adenoma / genetics. Adult. Cell Line, Tumor. Colonic Neoplasms / genetics. Hepatoblastoma / genetics. Humans. Male. Signal Transduction

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  • (PMID = 16314847.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Lithostathine; 0 / REG1A protein, human; 0 / beta Catenin; 0 / pancreatitis-associated protein
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47. Hofer MD, Chang MC, Hirko KA, Rubin MA, Nosé V: Immunohistochemical and clinicopathological correlation of the metastasis-associated gene 1 (MTA1) expression in benign and malignant pancreatic endocrine tumors. Mod Pathol; 2009 Jul;22(7):933-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical and clinicopathological correlation of the metastasis-associated gene 1 (MTA1) expression in benign and malignant pancreatic endocrine tumors.
  • Pancreatic endocrine tumors are rare tumors with unpredictable clinical behavior.
  • No histological features or immunohistochemical markers reliably predict malignant progression and the molecular basis of progression of pancreatic endocrine tumors remains unknown.
  • The metastasis-associated gene 1 is thought to play a role in transcription repression and estrogen receptor interaction and is overexpressed in several human cancers, including endocrine neoplasms.
  • The purpose of this study was to analyze the expression of metastasis-associated gene 1 in pancreatic endocrine tumors for its possible role in malignant progression.
  • Twenty-seven pancreatic endocrine tumors were identified from our archive.
  • The clinical follow-up data were examined and tumors were classified according to the 2004 World Health Organization criteria as benign behavior (WHO 1.1), uncertain behavior (WHO 1.2), well-differentiated endocrine carcinoma (WHO 2), and poorly differentiated endocrine carcinoma (WHO 3).
  • Metastasis-associated gene 1 expression was significantly higher in malignant tumors (n=17) with a mean staining intensity of 3.8 compared with 2.9 in benign tumors (n=10, P=0.046).
  • The expression levels were significantly associated with WHO class (P=0.028), as well as size of tumor (P=0.029), and mitotic rate (P=0.035).
  • We show that metastasis-associated gene 1 expression is significantly associated with malignant behavior in pancreatic endocrine tumors.
  • This may suggest a potential role for metastasis-associated gene 1 in the malignant progression and metastasis and its use as biomarker for malignant pancreatic endocrine tumors.
  • [MeSH-major] Adenoma, Islet Cell / enzymology. Carcinoma, Islet Cell / enzymology. Histone Deacetylases / metabolism. Islets of Langerhans / enzymology. Pancreatic Neoplasms / enzymology. Repressor Proteins / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Female. Fluorescent Antibody Technique, Indirect. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Invasiveness. Retrospective Studies

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  • (PMID = 19377441.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Repressor Proteins; EC 3.5.1.- / Mta1 protein, human; EC 3.5.1.98 / Histone Deacetylases
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48. Ramachandra C, Manjunath S, Joseph B, Appaji L, Kumari BS, Rao CR, Prabhakaran PS: Mixed exocrine-endocrine pancreatic carcinoma in childhood. Indian J Gastroenterol; 2005 May-Jun;24(3):116
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  • [Title] Mixed exocrine-endocrine pancreatic carcinoma in childhood.
  • A 7-year-old boy with mixed exocrine-endocrine pancreatic cancer is presented.
  • This may be the second reported case of such a tumor in childhood.
  • [MeSH-major] Adenoma, Islet Cell / epidemiology. Carcinoma, Acinar Cell / epidemiology. Pancreatic Neoplasms / epidemiology

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  • (PMID = 16041106.001).
  • [ISSN] 0254-8860
  • [Journal-full-title] Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology
  • [ISO-abbreviation] Indian J Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] India
  • [Number-of-references] 5
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49. Swain JM, Adams RB, Farnell MB, Que FG, Sarr MG: Gastric and pancreatoduodenal resection for malignant lesions after previous gastric bypass--diagnosis and methods of reconstruction. Surg Obes Relat Dis; 2010 Nov-Dec;6(6):670-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: Of the available patients, 7 were identified with 2 remnant gastric cancers (2 signet ring cell adenocarcinomas), 4 pancreatic neoplasms (2 adenocarcinomas and 2 neuroendocrine cancers), and 1 ampullary cancer.
  • The pancreatic and duodenal neoplasms required pancreatoduodenectomy, with 4 of 5 patients also undergoing remnant gastrectomy.
  • The patients after pancreatoduodenectomy required biliary and pancreatic reconstruction with the pancreaticobiliary limb, Roux limb, or proximal common channel, depending on the limb length.
  • [MeSH-major] Digestive System Surgical Procedures / methods. Duodenal Neoplasms / surgery. Gastrectomy / methods. Gastric Bypass. Pancreatic Neoplasms / surgery. Pancreaticoduodenectomy / methods. Stomach Neoplasms / surgery
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / epidemiology. Adenoma, Islet Cell / surgery. Aged. Carcinoma, Neuroendocrine / diagnosis. Carcinoma, Neuroendocrine / epidemiology. Carcinoma, Neuroendocrine / surgery. Common Bile Duct Neoplasms / diagnosis. Common Bile Duct Neoplasms / epidemiology. Common Bile Duct Neoplasms / surgery. Female. Humans. Male. Middle Aged. Retrospective Studies

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  • [Copyright] Copyright © 2010 American Society for Metabolic and Bariatric Surgery. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20627707.001).
  • [ISSN] 1878-7533
  • [Journal-full-title] Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery
  • [ISO-abbreviation] Surg Obes Relat Dis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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50. Klimstra DS: Nonductal neoplasms of the pancreas. Mod Pathol; 2007 Feb;20 Suppl 1:S94-112
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  • Although the majority of pancreatic neoplasms are infiltrating ductal adenocarcinomas or other neoplasms with ductal differentiation, neoplasms with acinar, endocrine, mixed, or uncertain differentiation constitute a diverse and distinctive group.
  • The most common and best-characterized nonductal neoplasms are pancreatic endocrine neoplasm, acinar cell carcinoma, pancreatoblastoma, and solid pseudopapillary neoplasm.
  • [MeSH-major] Adenocarcinoma, Papillary / pathology. Adenoma, Islet Cell / pathology. Carcinoma, Acinar Cell / pathology. Carcinoma, Islet Cell / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor. Humans

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  • (PMID = 17486055.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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51. Gnacńska M, Lewczuk A, Sworczak K: [Insulinoma misdiagnosed and treated as epilepsy]. Pol Merkur Lekarski; 2008 Mar;24(141):251-3
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  • [Transliterated title] Wyspiak trzustki mylnie rozpoznany i leczony jako padaczka--opis przypadku.
  • Although insulinoma constitutes almost 90% of neuroendocrine tumors localized in the pancreas, it is a rare disease.
  • Quite commonly prior to the diagnosis there is a history of several years and misdiagnosis as neurological or cardiological disease is not infrequent.
  • The image of pancreas was normal in the acquired abdominal ultrasound and in CT a tumor was found in the tail of pancreas.
  • [MeSH-major] Epilepsy / diagnosis. Insulinoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 18634294.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
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52. Peranteau WH, Bathaii SM, Pawel B, Hardy O, Alavi A, Stanley CA, Adzick NS: Multiple ectopic lesions of focal islet adenomatosis identified by positron emission tomography scan in an infant with congenital hyperinsulinism. J Pediatr Surg; 2007 Jan;42(1):188-92
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  • [Title] Multiple ectopic lesions of focal islet adenomatosis identified by positron emission tomography scan in an infant with congenital hyperinsulinism.
  • Congenital hyperinsulinism (HI) exists in 2 histologic forms, focal and diffuse, and rarely has been attributed to lesions in ectopic pancreatic tissue.
  • We present a case of HI resulting from focal pancreatic and ectopic pancreatic lesions.
  • Surgical exploration found pancreatic rests in the jejunum responsible for the hot spots seen on PET.
  • Pathology confirmed the presence of focal HI lesions in the pancreatic head and small intestinal specimens.
  • This case supports the ability of ectopic pancreatic tissue to contribute to the pathology of HI.
  • [MeSH-major] Adenoma, Islet Cell / diagnosis. Congenital Hyperinsulinism / diagnosis. Jejunal Neoplasms / diagnosis. Pancreatic Neoplasms / diagnosis


53. Hamir AN, Kunkle RA, Miller JM, Cutlip RC, Richt JA, Kehrli ME Jr, Williams ES: Age-related lesions in laboratory-confined raccoons (Procyon lotor) inoculated with the agent of chronic wasting disease of mule deer. J Vet Diagn Invest; 2007 Nov;19(6):680-6
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  • [Title] Age-related lesions in laboratory-confined raccoons (Procyon lotor) inoculated with the agent of chronic wasting disease of mule deer.
  • This communication documents age-associated pathologic changes and final observations on experimental transmission of chronic wasting disease (CWD) by the intracerebral route to raccoons (Procyon lotor).
  • Six years after inoculation, none of the 3 remaining CWD-inoculated raccoons had shown clinical signs of neurologic disorder, and the experiment was terminated.
  • Age-related lesions observed in these raccoons included islet-cell pancreatic amyloidosis (5/6), cystic endometrial hyperplasia (3/4), cerebrovascular mineralization (5/6), neuroaxonal degeneration (3/6), transitional-cell adenoma of the urinary bladder (1/6), and myocardial inclusions (4/6).
  • [MeSH-major] Aging. Deer. Raccoons. Wasting Disease, Chronic / pathology. Wasting Disease, Chronic / transmission

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  • (PMID = 17998557.001).
  • [ISSN] 1040-6387
  • [Journal-full-title] Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
  • [ISO-abbreviation] J. Vet. Diagn. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Prions
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54. Almeida MQ, Stratakis CA: Solid tumors associated with multiple endocrine neoplasias. Cancer Genet Cytogenet; 2010 Nov;203(1):30-6
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  • [Title] Solid tumors associated with multiple endocrine neoplasias.
  • We present an update on molecular and clinical genetics of solid tumors associated with the various multiple endocrine neoplasias (MEN) syndromes.
  • MEN type 1 (MEN1) describes the association of pituitary, parathyroid, and pancreatic islet cell tumors with a variety of many other lesions.
  • Other pheochromocytoma-associated syndromes include von Hippel-Lindau disease; neurofibromatosis 1; the recently defined paraganglioma syndromes type 1, 3, and 4; Carney-Stratakis syndrome; and the Carney triad.
  • In the Carney triad, patients can manifest gastrointestinal stromal tumors, lung chondroma, paraganglioma, adrenal adenoma and pheochromocytoma, esophageal leiomyoma, and other conditions.
  • The Carney complex is yet another form of MEN that is characterized by skin tumors and pigmented lesions, myxomas, schwannomas, and various endocrine neoplasias.
  • [MeSH-major] Multiple Endocrine Neoplasia / complications. Neoplasms / genetics
  • [MeSH-minor] Adrenal Gland Neoplasms / genetics. Germ-Line Mutation. Humans. Multiple Endocrine Neoplasia Type 1 / complications. Multiple Endocrine Neoplasia Type 2a / complications. Pheochromocytoma / genetics. Thyroid Neoplasms / etiology

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • [Cites] Science. 2000 Feb 4;287(5454):848-51 [10657297.001]
  • [Cites] J Urol. 1999 Sep;162(3 Pt 1):659-64 [10458336.001]
  • [Cites] Nat Genet. 2000 Sep;26(1):89-92 [10973256.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Oct;85(10):3860-5 [11061550.001]
  • [Cites] Nat Genet. 2000 Nov;26(3):268-70 [11062460.001]
  • [Cites] Hum Mol Genet. 2000 Dec 12;9(20):3037-46 [11115848.001]
  • [Cites] Am J Hum Genet. 2001 Jul;69(1):49-54 [11404820.001]
  • [Cites] Cytokine Growth Factor Rev. 2001 Dec;12(4):361-73 [11544105.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Sep;86(9):4041-6 [11549623.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Dec;86(12):5658-71 [11739416.001]
  • [Cites] N Engl J Med. 2002 May 9;346(19):1459-66 [12000816.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Aug;89(8):3737-8 [15292298.001]
  • [Cites] Medicine (Baltimore). 1968 Sep;47(5):371-409 [4386574.001]
  • [Cites] Clin Endocrinol Metab. 1980 Jul;9(2):299-315 [6994943.001]
  • [Cites] Br J Dermatol. 1980 Oct;103(4):421-9 [7437308.001]
  • [Cites] N Engl J Med. 1981 Dec 31;305(27):1617-27 [6796886.001]
  • [Cites] J Am Acad Dermatol. 1984 Jan;10(1):72-82 [6693605.001]
  • [Cites] Medicine (Baltimore). 1985 Jul;64(4):270-83 [4010501.001]
  • [Cites] Endocr Rev. 1987 Nov;8(4):391-405 [2891500.001]
  • [Cites] N Engl J Med. 1990 Mar 15;322(11):723-7 [1968616.001]
  • [Cites] Cell. 1990 Jul 13;62(1):187-92 [1694727.001]
  • [Cites] Science. 1993 May 28;260(5112):1317-20 [8493574.001]
  • [Cites] Nature. 1993 Jun 3;363(6428):458-60 [8099202.001]
  • [Cites] Semin Dermatol. 1995 Jun;14(2):90-8 [7640202.001]
  • [Cites] Clin Endocrinol (Oxf). 1995 Jul;43(1):123-7 [7641404.001]
  • [Cites] Oncogene. 1995 Nov 16;11(10):2039-45 [7478523.001]
  • [Cites] Oncogene. 1996 Feb 1;12(3):481-7 [8637703.001]
  • [Cites] J Clin Endocrinol Metab. 1953 Jan;13(1):20-47 [13022748.001]
  • [Cites] Am J Med. 1953 Mar;14(3):318-27 [13030489.001]
  • [Cites] Curr Mol Med. 2004 Dec;4(8):833-42 [15579030.001]
  • [Cites] Cell Mol Life Sci. 2004 Dec;61(23):2954-64 [15583857.001]
  • [Cites] Am J Surg Pathol. 2005 Feb;29(2):254-74 [15644784.001]
  • [Cites] Am J Gastroenterol. 2006 Feb;101(2):266-73 [16454829.001]
  • [Cites] Endocr Relat Cancer. 2006 Jun;13(2):415-25 [16728571.001]
  • [Cites] N Engl J Med. 2006 Jun 22;354(25):2729-31 [16790714.001]
  • [Cites] Nat Genet. 2006 Jul;38(7):794-800 [16767104.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 17;103(42):15558-63 [17030811.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Nov;91(11):4505-9 [16912137.001]
  • [Cites] Curr Opin Oncol. 2007 Jan;19(1):24-9 [17133108.001]
  • [Cites] Curr Opin Genet Dev. 2007 Feb;17(1):71-7 [17208433.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4537-40 [17510376.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Jul;92(7):2784-92 [17426081.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Aug;92(8):2938-43 [17535989.001]
  • [Cites] J Med Genet. 2007 Sep;44(9):586-7 [17557926.001]
  • [Cites] N Engl J Med. 2007 Sep 6;357(10):1054-6 [17804857.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2008 Feb;4(2):111-5 [18212813.001]
  • [Cites] N Engl J Med. 2008 Feb 14;358(7):750-2 [18272904.001]
  • [Cites] Expert Rev Anticancer Ther. 2008 Apr;8(4):625-32 [18402529.001]
  • [Cites] Nat Rev Cancer. 2008 Aug;8(8):592-603 [18650835.001]
  • [Cites] J Am Acad Dermatol. 2008 Nov;59(5):801-10 [18804312.001]
  • [Cites] Cancer Res. 2009 Apr 15;69(8):3650-6 [19351833.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Jun;94(6):2085-91 [19293268.001]
  • [Cites] Pigment Cell Melanoma Res. 2009 Oct;22(5):580-7 [19650827.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Oct;94(10):3656-62 [19723753.001]
  • [Cites] Clin Cancer Res. 2009 Oct 15;15(20):6378-85 [19825962.001]
  • [Cites] Surg Clin North Am. 2009 Oct;89(5):1193-204 [19836492.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2009 Dec;23(6):713-22 [19942148.001]
  • [Cites] Clin Cancer Res. 2009 Dec 1;15(23):7119-23 [19934298.001]
  • [Cites] Genet Med. 2009 Dec;11(12):825-35 [19904212.001]
  • [Cites] Genet Med. 2010 Jan;12(1):1-11 [20027112.001]
  • [Cites] Medicine (Baltimore). 1997 Jan;76(1):21-9 [9064485.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 Nov;47(5):507-12 [9425388.001]
  • [Cites] J Pediatr Endocrinol Metab. 2000 Apr;13(4):373-9 [10776991.001]
  • (PMID = 20951316.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS241024; NLM/ PMC2957471
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55. Chun MG, Mao JH, Chiu CW, Balmain A, Hanahan D: Polymorphic genetic control of tumor invasion in a mouse model of pancreatic neuroendocrine carcinogenesis. Proc Natl Acad Sci U S A; 2010 Oct 5;107(40):17268-73
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  • [Title] Polymorphic genetic control of tumor invasion in a mouse model of pancreatic neuroendocrine carcinogenesis.
  • Cancer is a disease subject to both genetic and environmental influences.
  • In this study, we used the RIP1-Tag2 (RT2) mouse model of islet cell carcinogenesis to identify a genetic locus that influences tumor progression to an invasive growth state.
  • RT2 mice inbred into the C57BL/6 (B6) background develop both noninvasive pancreatic neuroendocrine tumors (PNET) and invasive carcinomas with varying degrees of aggressiveness.
  • A gene residing in this locus, the anaplastic lymphoma kinase (Alk), was expressed at significantly lower levels in PNETs from invasion-resistant C3H mice compared with invasion-susceptible B6 mice, and pharmacological inhibition of Alk led to reduced tumor invasiveness in RT2 B6 mice.
  • Collectively, our results demonstrate that tumor invasion is subject to polymorphic genetic control and identify Alk as a genetic modifier of invasive tumor growth.

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  • [Cites] Biochem J. 2000 Dec 15;352 Pt 3:601-10 [11104663.001]
  • [Cites] PLoS Genet. 2010 Sep;6(9):e1001120 [20862307.001]
  • [Cites] Cancer Cell. 2002 May;1(4):339-53 [12086849.001]
  • [Cites] Nat Genet. 2003 Mar;33 Suppl:238-44 [12610533.001]
  • [Cites] Nat Rev Genet. 2003 Sep;4(9):721-34 [12951573.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2406-10 [15059892.001]
  • [Cites] Nature. 1985 May 9-15;315(6015):115-22 [2986015.001]
  • [Cites] Carcinogenesis. 1993 Nov;14(11):2353-8 [8242866.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] Nat Genet. 1995 Aug;10(4):424-9 [7670492.001]
  • [Cites] Nat Genet. 1995 Nov;11(3):241-7 [7581446.001]
  • [Cites] Am J Pathol. 1996 Dec;149(6):1899-917 [8952526.001]
  • [Cites] Nature. 1998 Mar 12;392(6672):190-3 [9515965.001]
  • [Cites] Int J Cancer. 1998 Aug 12;77(4):640-4 [9679770.001]
  • [Cites] Science. 1999 Apr 30;284(5415):808-12 [10221914.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18147-52 [15608061.001]
  • [Cites] Nat Genet. 2005 Mar;37(3):243-53 [15711544.001]
  • [Cites] Oncogene. 2005 Jun 9;24(25):4037-51 [15806157.001]
  • [Cites] Nat Genet. 2005 Oct;37(10):1055-62 [16142231.001]
  • [Cites] Blood. 2006 Jan 15;107(2):689-97 [16189272.001]
  • [Cites] Genes Dev. 2006 Mar 1;20(5):543-56 [16481467.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 2;104(1):270-5 [17185414.001]
  • [Cites] J Clin Oncol. 2007 Feb 10;25(5):587-95 [17290067.001]
  • [Cites] Nature. 2007 Feb 15;445(7129):761-5 [17230190.001]
  • [Cites] Nature. 2007 Jun 28;447(7148):1087-93 [17529967.001]
  • [Cites] Nat Rev Cancer. 2008 Jan;8(1):11-23 [18097461.001]
  • [Cites] Med Res Rev. 2008 May;28(3):372-412 [17694547.001]
  • [Cites] Nat Genet. 2008 May;40(5):623-30 [18372905.001]
  • [Cites] Cancer Res. 2008 May 15;68(10):3591-600 [18483240.001]
  • [Cites] Cell. 2008 Jul 25;134(2):215-30 [18662538.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2008 Sep;13(3):337-42 [18661105.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):930-5 [18724359.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):975-8 [18923525.001]
  • [Cites] Nature. 2009 Mar 26;458(7237):505-8 [19136944.001]
  • [Cites] Oncogene. 2009 Sep 17;28(37):3296-306 [19633684.001]
  • [Cites] Breast Cancer Res. 2009;11(5):R75 [19825179.001]
  • [Cites] Genes Dev. 2010 Feb 1;24(3):241-55 [20080943.001]
  • [Cites] Mol Cancer. 2010;9:51 [20205715.001]
  • [Cites] Int J Cancer. 2010 Jun 1;126(11):2603-13 [19847808.001]
  • [Cites] Proc Natl Acad Sci U S A. 2010 Jun 15;107(24):10791-8 [20457905.001]
  • [Cites] Nat Genet. 2001 Dec;29(4):459-64 [11694878.001]
  • (PMID = 20855625.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5R01CA45234-24; United States / NCI NIH HHS / CA / U01-CA84244; United States / NICHD NIH HHS / HD / U01 HD043430; United States / NCI NIH HHS / CA / R01 CA045234; United States / NICHD NIH HHS / HD / U01-HD43430; United States / NCI NIH HHS / CA / U01 CA084244
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NVP-TAE684; 0 / Pyrimidines; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Other-IDs] NLM/ PMC2951397
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56. Lewis RB, Lattin GE Jr, Paal E: Pancreatic endocrine tumors: radiologic-clinicopathologic correlation. Radiographics; 2010 Oct;30(6):1445-64
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  • [Title] Pancreatic endocrine tumors: radiologic-clinicopathologic correlation.
  • Pancreatic endocrine tumors (PETs) are primarily well-differentiated tumors composed of cells that resemble normal islet cells but that arise from pancreatic ductal cells.
  • Most are sporadic, but some are associated with familial syndromes such as multiple endocrine neoplasia type 1, von Hippel-Lindau syndrome, and neurofibromatosis type 1.
  • At imaging, PETs typically appear as well-defined hypervascular masses, a finding indicative of their rich capillary network.
  • Knowledge of the characteristic clinical, pathologic, and radiologic features of PETs is important in the evaluation and management of patients with a suspected clinical syndrome or a pancreatic mass.
  • [MeSH-major] Diagnostic Imaging. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / epidemiology. Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / epidemiology. Carcinoma, Islet Cell / pathology. Diagnosis, Differential. Humans. Multiple Endocrine Neoplasia Type 1 / pathology. Neurofibromatosis 1 / pathology. Prevalence. von Hippel-Lindau Disease / pathology

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  • [Copyright] © RSNA, 2010.
  • (PMID = 21071369.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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57. Long KB, Srivastava A, Hirsch MS, Hornick JL: PAX8 Expression in well-differentiated pancreatic endocrine tumors: correlation with clinicopathologic features and comparison with gastrointestinal and pulmonary carcinoid tumors. Am J Surg Pathol; 2010 May;34(5):723-9
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  • [Title] PAX8 Expression in well-differentiated pancreatic endocrine tumors: correlation with clinicopathologic features and comparison with gastrointestinal and pulmonary carcinoid tumors.
  • PAX (paired box) genes encode a family of transcription factors that regulate organogenesis and cell-lineage specification in multiple organ systems.
  • In the pancreas, PAX proteins play a critical role in islet cell differentiation.
  • We recently observed that islet cells show strong, diffuse staining for PAX8 by immunohistochemistry.
  • However, PAX8 expression has not previously been examined in pancreatic endocrine tumors (PETs).
  • Expression of PAX8 was significantly associated with WHO category 1.1 ("benign" behavior) compared with category 1.2 (uncertain behavior) or 2 (well-differentiated endocrine carcinoma) (positive in 100%, 64%, and 52% of tumors, respectively; P<0.05).
  • In summary, PAX8 is expressed in normal pancreatic islet cells and in a high proportion of primary and metastatic PETs.
  • PAX8 immunostaining may be helpful in determining the primary site for a WDNET metastatic to the liver, as ileal (PAX8 negative) and pancreatic (PAX8 positive) tumors most often present as a metastasis from an occult primary.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoid Tumor / pathology. Carcinoma, Islet Cell / secondary. Gastrointestinal Neoplasms / pathology. Lung Neoplasms / pathology. Paired Box Transcription Factors / metabolism. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Female. Humans. Immunohistochemistry. Islets of Langerhans / metabolism. Islets of Langerhans / pathology. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lymph Nodes / pathology. Male. Middle Aged

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  • [CommentIn] Am J Surg Pathol. 2011 Dec;35(12):1906-8 [22067332.001]
  • (PMID = 20414099.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / PAX8 protein, human; 0 / Paired Box Transcription Factors
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58. Hamzah J, Nelson D, Moldenhauer G, Arnold B, Hämmerling GJ, Ganss R: Vascular targeting of anti-CD40 antibodies and IL-2 into autochthonous tumors enhances immunotherapy in mice. J Clin Invest; 2008 May;118(5):1691-9
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  • In this study, we used a tumor-homing peptide to engineer anti-CD40 agonist antibodies and recombinant IL-2 such that they were selectively delivered into spontaneously arising tumors in a transgenic mouse model of islet cell carcinogenesis.
  • Intravenous injection of these agents, either separately or together, led to accumulation in the vicinity of tumor neovessels without toxic side effects.
  • Combined, local anti-CD40 and IL-2 therapy reduced tumor vascularity and significantly delayed tumor growth in mice.
  • Remarkably, tumor-bearing mice remained disease-free long-term when targeted anti-CD40 and IL-2 were combined with transfers of preactivated antitumor immune cells.
  • In this therapeutic setting, triggering of CD40 on endothelial cells induced an inflammatory response of the vessel wall and facilitated effector cell accumulation in the tumor parenchyma while IL-2 promoted antigen-specific immune cell persistence.
  • We believe this is a novel and highly effective anticancer approach, whereby tumor stroma is "conditioned" for enhanced immune cell entry and survival, facilitating immune-mediated tumor destruction and leading to a sustained antitumor response.
  • [MeSH-major] Adenoma, Islet Cell. Antibodies. Antigens, CD40 / immunology. Immunotherapy, Adoptive. Interleukin-2 / immunology. Pancreatic Neoplasms

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  • [Cites] Biol Blood Marrow Transplant. 2004 Aug;10(8):534-9 [15282531.001]
  • [Cites] Trends Immunol. 2007 Nov;28(11):467-73 [17981086.001]
  • [Cites] Nature. 1985 May 9-15;315(6015):115-22 [2986015.001]
  • [Cites] Mol Cell Biol. 1985 Dec;5(12):3610-6 [3915782.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7487-91 [2217180.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2985-9 [1532662.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 6;91(25):12135-9 [7527552.001]
  • [Cites] J Exp Med. 1995 Jul 1;182(1):33-40 [7540655.001]
  • [Cites] Cell Immunol. 1999 Dec 15;198(2):87-95 [10648122.001]
  • [Cites] J Vet Med Sci. 2000 Oct;62(10):1101-4 [11073083.001]
  • [Cites] J Immunol Methods. 2001 Feb 1;248(1-2):139-47 [11223075.001]
  • [Cites] J Exp Med. 2001 Dec 3;194(11):1549-59 [11733570.001]
  • [Cites] J Exp Med. 2002 Feb 18;195(4):423-35 [11854356.001]
  • [Cites] Int J Cancer. 2002 Feb 20;97(6):719-25 [11857345.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1659-65 [11861281.001]
  • [Cites] Cancer Res. 2002 Mar 1;62(5):1462-70 [11888921.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Apr 16;99(8):5561-6 [11929985.001]
  • [Cites] J Immunol. 2003 Mar 1;170(5):2727-33 [12594303.001]
  • [Cites] J Immunol. 2003 Nov 15;171(10):5051-63 [14607902.001]
  • [Cites] Cancer Cell. 2003 Nov;4(5):383-91 [14667505.001]
  • [Cites] Cancer Cell. 2003 Nov;4(5):393-403 [14667506.001]
  • [Cites] Expert Opin Biol Ther. 2004 Apr;4(4):455-68 [15102596.001]
  • [Cites] J Immunol. 2004 May 15;172(10):5861-9 [15128765.001]
  • [Cites] Immunity. 1995 Jun;2(6):573-85 [7796292.001]
  • [Cites] J Leukoc Biol. 1995 Aug;58(2):209-16 [7543921.001]
  • [Cites] J Exp Med. 1995 Dec 1;182(6):1857-64 [7500031.001]
  • [Cites] J Exp Med. 1996 Aug 1;184(2):747-52 [8760829.001]
  • [Cites] Immunity. 1996 Oct;5(4):319-30 [8885865.001]
  • [Cites] Nature. 1998 Feb 5;391(6667):591-4 [9468137.001]
  • [Cites] J Immunol. 1997 Dec 1;159(11):5640-7 [9548507.001]
  • [Cites] Nature. 1998 Jun 4;393(6684):478-80 [9624004.001]
  • [Cites] Nature. 1998 Jun 4;393(6684):480-3 [9624005.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3957-62 [10097145.001]
  • [Cites] Nat Med. 1999 May;5(5):548-53 [10229232.001]
  • [Cites] Nat Med. 1999 Jul;5(7):774-9 [10395322.001]
  • [Cites] Nat Med. 1999 Jul;5(7):780-7 [10395323.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1094-101 [15459006.001]
  • [Cites] Nat Rev Cancer. 2005 Jun;5(6):436-46 [15928674.001]
  • [Cites] Nat Biotechnol. 2005 Sep;23(9):1137-46 [16151407.001]
  • [Cites] Am J Pathol. 2006 Mar;168(3):786-95 [16507894.001]
  • [Cites] J Leukoc Biol. 2006 Oct;80(4):685-90 [16864602.001]
  • [Cites] J Exp Med. 2006 Oct 30;203(11):2441-50 [17043144.001]
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):876-83 [17327609.001]
  • [Cites] Nat Med. 2007 Mar;13(3):354-60 [17334371.001]
  • [Cites] Cancer Cell. 2007 Jun;11(6):539-54 [17560335.001]
  • [Cites] J Immunol. 2007 Nov 15;179(10):6686-95 [17982058.001]
  • [Cites] Eur J Immunol. 2004 Oct;34(10):2635-41 [15368278.001]
  • (PMID = 18398504.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD40; 0 / GTPase-Activating Proteins; 0 / Interleukin-2; 0 / Peptides; 0 / Ralbp1 protein, mouse; 0 / Recombinant Fusion Proteins
  • [Other-IDs] NLM/ PMC2289791
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59. Jager PL, Chirakal R, Marriott CJ, Brouwers AH, Koopmans KP, Gulenchyn KY: 6-L-18F-fluorodihydroxyphenylalanine PET in neuroendocrine tumors: basic aspects and emerging clinical applications. J Nucl Med; 2008 Apr;49(4):573-86
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

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  • Subsequently, this review provides an overview of current clinical applications in neuroendocrine tumors, including carcinoid tumors, pancreatic islet cell tumors, pheochromocytoma, paraganglioma, medullary thyroid cancer, hyperinsulinism, and various other clinical entities.
  • [MeSH-minor] Adenoma, Islet Cell / radionuclide imaging. Humans. Hyperinsulinism / radionuclide imaging. Pancreatic Neoplasms / radionuclide imaging. Pheochromocytoma / radionuclide imaging. Thyroid Neoplasms / radionuclide imaging

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  • (PMID = 18344441.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 2C598205QX / fluorodopa F 18; 63-84-3 / Dihydroxyphenylalanine
  • [Number-of-references] 78
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60. Xian X, Håkansson J, Ståhlberg A, Lindblom P, Betsholtz C, Gerhardt H, Semb H: Pericytes limit tumor cell metastasis. J Clin Invest; 2006 Mar;116(3):642-51
The Lens. Cited by Patents in .

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  • [Title] Pericytes limit tumor cell metastasis.
  • Previously we observed that neural cell adhesion molecule (NCAM) deficiency in beta tumor cells facilitates metastasis into distant organs and local lymph nodes.
  • Here, we show that NCAM-deficient beta cell tumors grew leaky blood vessels with perturbed pericyte-endothelial cell-cell interactions and deficient perivascular deposition of ECM components.
  • Conversely, tumor cell expression of NCAM in a fibrosarcoma model (T241) improved pericyte recruitment and increased perivascular deposition of ECM molecules.
  • Together, these findings suggest that NCAM may limit tumor cell metastasis by stabilizing the microvessel wall.
  • To directly address whether pericyte dysfunction increases the metastatic potential of solid tumors, we studied beta cell tumorigenesis in primary pericyte-deficient Pdgfb(ret/ret) mice.
  • This resulted in beta tumor cell metastases in distant organs and local lymph nodes, demonstrating a role for pericytes in limiting tumor cell metastasis.
  • These data support a new model for how tumor cells trigger metastasis by perturbing pericyte-endothelial cell-cell interactions.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Neoplasm Metastasis / pathology. Neoplasm Metastasis / prevention & control. Pancreatic Neoplasms / pathology. Pericytes / physiology
  • [MeSH-minor] Animals. Cell Communication / genetics. Endothelium, Vascular / metabolism. Endothelium, Vascular / pathology. Fibrosarcoma / blood supply. Fibrosarcoma / genetics. Fibrosarcoma / metabolism. Fibrosarcoma / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Neovascularization, Pathologic / metabolism. Neural Cell Adhesion Molecules / deficiency. Neural Cell Adhesion Molecules / genetics. Neural Cell Adhesion Molecules / physiology

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  • [Cites] Am J Pathol. 1991 Jun;138(6):1335-47 [1711288.001]
  • [Cites] Cell Struct Funct. 1986 Sep;11(3):245-52 [3768962.001]
  • [Cites] Eur J Cancer. 1996 Dec;32A(14):2451-60 [9059333.001]
  • [Cites] Anticancer Res. 1997 Mar-Apr;17(2B):1227-30 [9137477.001]
  • [Cites] Science. 1997 Jul 11;277(5323):242-5 [9211853.001]
  • [Cites] Am J Surg. 1997 Sep;174(3):251-7 [9324132.001]
  • [Cites] Nat Med. 1999 Mar;5(3):286-91 [10086383.001]
  • [Cites] Curr Top Pathol. 1999;93:27-33 [10339896.001]
  • [Cites] Development. 1999 Jun;126(14):3047-55 [10375497.001]
  • [Cites] Cancer Res. 2004 Dec 1;64(23):8630-8 [15574770.001]
  • [Cites] Science. 2005 Jan 7;307(5706):58-62 [15637262.001]
  • [Cites] Curr Opin Genet Dev. 2005 Feb;15(1):102-11 [15661540.001]
  • [Cites] Expert Rev Mol Diagn. 2005 Mar;5(2):221-30 [15833051.001]
  • [Cites] Tumour Biol. 2005 Mar-Apr;26(2):103-12 [15897690.001]
  • [Cites] Circ Res. 2005 Sep 16;97(6):512-23 [16166562.001]
  • [Cites] Oncology. 2005;69(2):159-66 [16127287.001]
  • [Cites] Brain Res Bull. 2000 Mar 15;51(5):363-9 [10715555.001]
  • [Cites] Am J Pathol. 2000 Apr;156(4):1363-80 [10751361.001]
  • [Cites] Dev Dyn. 2001 Jan;220(1):60-73 [11146508.001]
  • [Cites] EMBO J. 2001 Feb 15;20(4):672-82 [11179212.001]
  • [Cites] Pancreas. 2001 Mar;22(2):122-5 [11249065.001]
  • [Cites] J Cell Biol. 2001 Apr 30;153(3):543-53 [11331305.001]
  • [Cites] Cells Tissues Organs. 2001;169(1):1-11 [11340256.001]
  • [Cites] Nature. 2001 May 17;411(6835):375-9 [11357145.001]
  • [Cites] Bioessays. 2001 Jun;23(6):494-507 [11385629.001]
  • [Cites] Cancer Res. 2001 Oct 15;61(20):7627-34 [11606404.001]
  • [Cites] Circulation. 2002 Jan 1;105(1):112-7 [11772885.001]
  • [Cites] Glycobiology. 2002 Jan;12(1):47-63 [11825886.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):801-13 [11891179.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):985-1000 [11891196.001]
  • [Cites] Physiol Rev. 2002 Jul;82(3):673-700 [12087132.001]
  • [Cites] EMBO J. 2002 Aug 15;21(16):4307-16 [12169633.001]
  • [Cites] Nat Rev Cancer. 2002 Jun;2(6):442-54 [12189386.001]
  • [Cites] Nat Genet. 2003 Jan;33(1):49-54 [12469122.001]
  • [Cites] J Clin Invest. 2003 May;111(9):1287-95 [12727920.001]
  • [Cites] Nat Med. 2003 Jun;9(6):685-93 [12778167.001]
  • [Cites] Br J Dermatol. 2003 May;148(5):971-80 [12786828.001]
  • [Cites] Genes Dev. 2003 Aug 1;17(15):1835-40 [12897053.001]
  • [Cites] J Clin Invest. 2003 Oct;112(8):1142-51 [14561699.001]
  • [Cites] J Cell Biol. 2003 Oct 27;163(2):209-13 [14581448.001]
  • [Cites] Clin Chem. 2004 Mar;50(3):509-15 [14726469.001]
  • [Cites] PLoS Biol. 2003 Nov;1(2):E52 [14624252.001]
  • [Cites] Cancer Res. 2004 Apr 15;64(8):2725-33 [15087386.001]
  • [Cites] Circ Res. 2004 Apr 30;94(8):1067-74 [15031262.001]
  • [Cites] Nature. 1985 May 9-15;315(6015):115-22 [2986015.001]
  • [Cites] Nature. 1994 Feb 3;367(6462):455-9 [8107803.001]
  • (PMID = 16470244.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecules
  • [Other-IDs] NLM/ PMC1361347
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61. Borka K, Kaliszky P, Szabó E, Lotz G, Kupcsulik P, Schaff Z, Kiss A: Claudin expression in pancreatic endocrine tumors as compared with ductal adenocarcinomas. Virchows Arch; 2007 May;450(5):549-57
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  • [Title] Claudin expression in pancreatic endocrine tumors as compared with ductal adenocarcinomas.
  • We aimed to analyze protein and messenger RNA (mRNA) expressions of different CLDNs in human pancreatic endocrine tumors (PET) and ductal adenocarcinomas.
  • Normal acini and ducts showed strong CLDNs 1, -3, -4, and -7 and scattered CLDN 2 protein expressions, while Langerhans islands revealed only CLDN 3 and -7 expressions.
  • CLDN 2 expression was found in the half of ductal adenocarcinomas, while the vast majority of endocrine tumors were negative.
  • CLDN 1, -4, and -7 immunohistochemistry was positive in all adenocarcinomas, whereas endocrine tumors were completely negative for CLDNs 1 and -4.
  • CLDN 3 and -7 proteins were detected in all endocrine tumors, while CLDN 3 in ductal adenocarcinomas was negative.
  • The mRNA expression of CLDNs showed differences between endocrine tumors and ductal adenocarcinomas, similar as found for protein expression.
  • High expressions of CLDN 3 in endocrine tumors and CLDN 4 in ductal carcinomas might attract them as targets for adjuvant therapy.
  • [MeSH-major] Adenoma, Islet Cell / metabolism. Carcinoma, Islet Cell / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Membrane Proteins / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor. Female. Gene Expression. Humans. Immunoenzyme Techniques. Male. Middle Aged. RNA, Messenger / metabolism. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] Virchows Arch. 2006 Jan;448(1):52-8 [16220299.001]
  • [Cites] Oncogene. 2003 Apr 3;22(13):2021-33 [12673207.001]
  • [Cites] Am J Pathol. 2002 May;160(5):1745-54 [12000726.001]
  • [Cites] Breast Cancer Res. 2005;7(2):R296-305 [15743508.001]
  • [Cites] Pathologe. 2003 Jul;24(4):265-71 [14513272.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Aug;19(4):649-56 [16183533.001]
  • [Cites] J Cell Biol. 1999 Oct 4;147(1):195-204 [10508866.001]
  • [Cites] Neuroendocrinology. 2004;80 Suppl 1:12-5 [15477709.001]
  • [Cites] Hum Pathol. 2005 Feb;36(2):162-9 [15754293.001]
  • [Cites] Diagn Mol Pathol. 2004 Dec;13(4):234-40 [15538114.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6265-71 [14559813.001]
  • [Cites] Clin Cancer Res. 2004 Jul 1;10 (13):4427-36 [15240533.001]
  • [Cites] Pancreas. 2004 Mar;28(2):181-90 [15028951.001]
  • [Cites] Genes Cells. 1998 Sep;3(9):569-73 [9813107.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):5583-7 [11733531.001]
  • [Cites] J Mol Histol. 2004 Nov;35(8-9):811-22 [15609094.001]
  • [Cites] J Cell Biol. 1998 Jun 29;141(7):1539-50 [9647647.001]
  • [Cites] J Clin Invest. 2005 Jul;115(7):1765-76 [15965503.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2567-75 [12855632.001]
  • [Cites] Pancreas. 2006 May;32(4):396-402 [16670622.001]
  • [Cites] Anticancer Res. 2006 Mar-Apr;26(2A):1167-70 [16619519.001]
  • [Cites] Oncol Rep. 2005 Feb;13(2):193-9 [15643498.001]
  • [Cites] Cancer Res. 2001 Nov 1;61(21):7878-81 [11691807.001]
  • [Cites] J Clin Endocrinol Metab. 1975 Nov;41(5):841-4 [1102552.001]
  • [Cites] Hum Pathol. 2006 May;37(5):555-61 [16647953.001]
  • [Cites] Am J Clin Pathol. 2004 Feb;121(2):226-30 [14983936.001]
  • [Cites] Virchows Arch. 2005 Dec;447(6):961-8 [16133365.001]
  • [Cites] Curr Opin Oncol. 2006 Jan;18(1):23-9 [16357560.001]
  • [Cites] BMC Cancer. 2006 Jul 12;6:186 [16836752.001]
  • [Cites] Cancer Immunol Immunother. 2005 May;54(5):431-45 [15750830.001]
  • [Cites] Mod Pathol. 2006 Mar;19(3):460-9 [16439986.001]
  • [Cites] Med Electron Microsc. 2003 Sep;36(3):147-56 [14505058.001]
  • [Cites] Virchows Arch. 2006 Apr;448(4):428-34 [16328347.001]
  • [Cites] J Cell Sci. 2004 May 15;117(Pt 12):2435-47 [15159449.001]
  • [Cites] Gastroenterology. 2001 Feb;120(2):411-22 [11159882.001]
  • [Cites] Nucleic Acids Res. 2002 May 1;30(9):e36 [11972351.001]
  • [Cites] Histopathology. 2005 May;46(5):551-60 [15842637.001]
  • [Cites] Pathol Int. 2005 Feb;55(2):63-9 [15693851.001]
  • [Cites] Cancer. 2002 Aug 15;95(4 Suppl):923-7 [12209672.001]
  • [Cites] Am J Pathol. 2004 Mar;164(3):903-14 [14982844.001]
  • [Cites] Oncologist. 2006 Jun;11(6):612-23 [16794240.001]
  • [Cites] Gynecol Oncol. 2006 Nov;103(2):591-8 [16797678.001]
  • [Cites] J Clin Pathol. 2005 Nov;58(11):1121-5 [16254096.001]
  • [Cites] Hepatogastroenterology. 1998 May-Jun;45(21):855-66 [9684147.001]
  • [Cites] Curr Opin Oncol. 2005 Jan;17(1):24-7 [15608508.001]
  • [Cites] Pathol Oncol Res. 2005;11(1):26-31 [15800679.001]
  • (PMID = 17429687.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins; 0 / RNA, Messenger
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62. Shah OJ, Robbani I, Nazir P, Khan AB: Central pancreatectomy: a new technique for resection of selected pancreatic tumors. Hepatobiliary Pancreat Dis Int; 2009 Feb;8(1):93-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Central pancreatectomy: a new technique for resection of selected pancreatic tumors.
  • BACKGROUND: Pancreatic tumors located in the neck region usually require pancreaticoduodenectomy or splenopancreatectomy.
  • For small benign tumors enucleation is not usually feasible due to their size and localization; then pancreatectomy is often needed.
  • Central pancreatectomy consists of a limited resection of the midportion of the pancreas and can be offered in benign and low-grade malignant tumors of the neck of the pancreas.
  • The study aimed to evaluate whether central pancreatectomy has a place in pancreatic surgery.
  • RESULTS: Four patients, two with serous cystadenoma, and one with an islet cell tumor, and one with a hydatid cyst, were identified for the procedure.
  • The mean tumor size was 3 cm, the mean operative time was 217.5 minutes, and the mean blood loss was 382.5 ml.
  • No endocrine or exocrine deficiency was observed in any patient during a mean follow-up of 22.7 months.
  • CONCLUSIONS: Central pancreatectomy is a procedure that offers excellent results in benign and low-grade malignant tumors.
  • It preserves functional elements (endocrine and exocrine) of the pancreas and also eliminates the infective and hematological effects of splenectomy.
  • Thus, central pancreatectomy should be included in the armamentarium of pancreatic surgery, and in order to obtain good results, proper indications and adequate experience are recommended.
  • [MeSH-major] Cystadenoma / surgery. Echinococcosis / surgery. Pancreas / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adenoma, Islet Cell / pathology. Adenoma, Islet Cell / surgery. Adult. Biopsy. Female. Follow-Up Studies. Humans. Male. Postoperative Complications

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  • (PMID = 19208523.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] China
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63. Levy MJ, Smyrk TC, Reddy RP, Clain JE, Harewood GC, Kendrick ML, Pearson RK, Petersen BT, Rajan E, Topazian MD, Wang KK, Wiersema MJ, Yusuf TE, Chari ST: Endoscopic ultrasound-guided trucut biopsy of the cyst wall for diagnosing cystic pancreatic tumors. Clin Gastroenterol Hepatol; 2005 Oct;3(10):974-9
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  • [Title] Endoscopic ultrasound-guided trucut biopsy of the cyst wall for diagnosing cystic pancreatic tumors.
  • The aim of this study was to determine whether the tissue obtained by endoscopic ultrasound-guided trucut biopsy (EUS TCB) is sufficient for histologic diagnosis of cystic pancreatic tumors (CPTs).
  • Final diagnoses included serous cystadenoma (SCA, n=5), islet cell tumor (n=2), mixed seromucinous lesion (n=1), polycystic disease of the pancreas (n=1), and pseudocyst (n=1).
  • In the fourth patient with an SCA, the TCB result ruled out metastatic disease from locally recurrent lung cancer, allowing a narrowed radiation field.
  • EUS TCB confirmed the need for surgery in 2 patients with an islet cell tumor.
  • [MeSH-major] Biopsy / methods. Endoscopy, Gastrointestinal / methods. Pancreatic Cyst / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adenoma, Islet Cell / pathology. Adult. Aged. Aged, 80 and over. Cystadenoma, Serous / pathology. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Pancreatic Pseudocyst / pathology

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  • [CommentIn] Clin Gastroenterol Hepatol. 2005 Oct;3(10):964-6 [16234040.001]
  • (PMID = 16234042.001).
  • [ISSN] 1542-3565
  • [Journal-full-title] Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
  • [ISO-abbreviation] Clin. Gastroenterol. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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64. Recaldini C, Carrafiello G, Bertolotti E, Angeretti MG, Fugazzola C: Contrast-enhanced ultrasonograpic findings in pancreatic tumors. Int J Med Sci; 2008;5(4):203-8
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  • [Title] Contrast-enhanced ultrasonograpic findings in pancreatic tumors.
  • OBJECTIVE: The purpose of this article is to present the potentials and limits of contrast-enhanced ultrasonography (CEUS) in the characterization of pancreatic tumors, usually hypoechoic or cystic at B-mode ultrasound.
  • CONCLUSION: As regards hypoechoic lesions at B-mode ultrasound, CEUS often can distinguish among adenocarcinoma, islet cell tumor and serous microcystic adenoma.
  • [MeSH-major] Contrast Media / chemistry. Pancreas / ultrasonography. Pancreatic Neoplasms / diagnosis. Ultrasonography / methods

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  • [Cites] AJR Am J Roentgenol. 2001 Aug;177(2):367-71 [11461864.001]
  • [Cites] World J Gastroenterol. 2006 Jul 14;12(26):4181-4 [16830370.001]
  • [Cites] Radiol Med. 2001 Jul-Aug;102(1-2):23-31 [11677434.001]
  • [Cites] Eur Radiol. 2001;11(10):1939-51 [11702126.001]
  • [Cites] Eur Radiol. 2002 Jan;12(1):151-65 [11868093.001]
  • [Cites] AJR Am J Roentgenol. 2002 Sep;179(3):725-30 [12185053.001]
  • [Cites] J Ultrasound Med. 2002 Sep;21(9):983-91 [12216764.001]
  • [Cites] Scand J Gastroenterol. 2002 Nov;37(11):1313-20 [12465731.001]
  • [Cites] Abdom Imaging. 2004 Mar-Apr;29(2):246-58 [15290954.001]
  • [Cites] Gastrointest Radiol. 1991 Winter;16(1):53-61 [1991611.001]
  • [Cites] Am J Gastroenterol. 2005 Jan;100(1):144-52 [15654794.001]
  • [Cites] Pancreatology. 2005;5(4-5):398-402 [15985763.001]
  • [Cites] AJR Am J Roentgenol. 2005 Nov;185(5):1193-200 [16247133.001]
  • [Cites] Radiographics. 2005 Nov-Dec;25(6):1471-84 [16284129.001]
  • [Cites] Radiology. 2006 Mar;238(3):912-9 [16439566.001]
  • [Cites] Eur Radiol. 2001;11(9):1626-30 [11511881.001]
  • (PMID = 18645620.001).
  • [ISSN] 1449-1907
  • [Journal-full-title] International journal of medical sciences
  • [ISO-abbreviation] Int J Med Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Contrast Media
  • [Other-IDs] NLM/ PMC2467517
  • [Keywords] NOTNLM ; contrast-enhanced ultrasonography / pancreatic tumors
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65. Gumbs AA, Grès P, Madureira F, Gayet B: Laparoscopic vs open resection of pancreatic endocrine neoplasms: single institution's experience over 14 years. Langenbecks Arch Surg; 2008 May;393(3):391-5
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  • [Title] Laparoscopic vs open resection of pancreatic endocrine neoplasms: single institution's experience over 14 years.
  • BACKGROUND: Laparoscopic resection of benign pancreatic endocrine neoplasms (PENs) has become the standard of care for tumors in the pancreatic tail.
  • Over a 14-year period, we have resected both benign and malignant tumors of the entire pancreas laparoscopically and compared our survival and complication rates with open controls.
  • CONCLUSIONS: Laparoscopic resection of benign and malignant PENs has similar overall complication and 5-year survival rates as the open technique; however, the laparoscopic approach is associated with shorter operative times.
  • [MeSH-major] Adenoma, Islet Cell / surgery. Insulinoma / surgery. Laparoscopy / methods. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Postoperative Complications / etiology. Postoperative Complications / surgery. Reoperation. Retrospective Studies

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  • [Cites] Langenbecks Arch Surg. 2005 Apr;390(2):134-40 [15609056.001]
  • [Cites] Surg Laparosc Endosc Percutan Tech. 2000 Jun;10 (3):168-73 [10872980.001]
  • [Cites] Acta Chir Belg. 1999 Oct;99(5):249-52 [10582077.001]
  • [Cites] Surg Clin North Am. 2000 Aug;80(4):1151-70 [10987029.001]
  • [Cites] J Laparoendosc Adv Surg Tech A. 2004 Jun;14(3):173-7 [15245671.001]
  • [Cites] Surgery. 1996 Dec;120(6):1051-4 [8957494.001]
  • [Cites] Surg Endosc. 2004 Mar;18(3):402-6 [14735345.001]
  • [Cites] Arch Surg. 1988 May;123(5):550-3 [3358679.001]
  • [Cites] Endocr Pract. 2002 Sep-Oct;8(5):329-34 [15251834.001]
  • [Cites] Surg Endosc. 2007 Jan;21(1):103-8 [17008952.001]
  • [Cites] World J Surg. 1999 Aug;23(8):825-34 [10415209.001]
  • [Cites] World J Surg. 2004 Dec;28(12 ):1239-47 [15517485.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2005;12(6):451-5 [16365817.001]
  • [Cites] J Surg Oncol. 2002 Sep;81(1):45-53; discussion 54 [12210027.001]
  • [Cites] Am J Surg. 1996 Jul;172(1):15-20 [8686795.001]
  • [Cites] World J Surg. 2006 Oct;30(10 ):1916-9; discussion 1920-1 [16855802.001]
  • [Cites] J Gastrointest Surg. 1997 Jan-Feb;1(1):20-5; discussion 25-6 [9834326.001]
  • [Cites] Surgery. 1998 Dec;124(6):1050-5 [9854582.001]
  • [Cites] Surg Endosc. 2007 Apr;21(4):579-86 [17180287.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2002;9(6):710-22 [12658405.001]
  • [Cites] Surg Endosc. 2004 Mar;18(3):407-11 [14752628.001]
  • [Cites] Ann Surg. 2004 Aug;240(2):205-13 [15273542.001]
  • [Cites] J Gastrointest Surg. 2005 Mar;9(3):381-8 [15749601.001]
  • [Cites] Surgery. 2000 Sep;128(3):386-91 [10965308.001]
  • [Cites] Ann Surg. 2002 Aug;236(2):149-58 [12170019.001]
  • [Cites] Hepatogastroenterology. 2005 Mar-Apr;52(62):620-4 [15816491.001]
  • [Cites] World J Surg. 2002 Aug;26(8):1057-65 [12016486.001]
  • [Cites] Surg Oncol Clin N Am. 1998 Oct;7(4):881-91 [9735139.001]
  • (PMID = 18196267.001).
  • [ISSN] 1435-2451
  • [Journal-full-title] Langenbeck's archives of surgery
  • [ISO-abbreviation] Langenbecks Arch Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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66. Strosberg J, Hoffe S, Gardner N, Choi J, Kvols L: Effective treatment of locally advanced endocrine tumors of the pancreas with chemoradiotherapy. Neuroendocrinology; 2007;85(4):216-20
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  • [Title] Effective treatment of locally advanced endocrine tumors of the pancreas with chemoradiotherapy.
  • BACKGROUND/AIMS: The use of chemoradiation in the management of locally advanced pancreatic endocrine tumors has not been reported in the medical literature.
  • Given the sensitivity of pancreatic endocrine tumors to cytotoxic agents including streptozocin, doxorubicin and 5-FU, we have hypothesized that the combination of concurrent and sequential chemotherapy and radiation will yield higher response rates than acheivable with chemotherapy alone.
  • METHODS: Six patients with locally advanced pancreatic endocrine tumors were treated with a protocol consisting of radiation concurrent with infusional 5-FU (or capecitabine) along with induction and consolidation chemotherapy (streptozocin and doxorubicin).
  • With a median follow-up of 29 months, all six patients in the study have had continued reduction in tumor size from the time of the first posttreatment scan to the most recent scan.
  • None of the patients have experienced local or metastatic disease progression.
  • CONCLUSION: The combination of concurrent and sequential chemoradiotherapy appears to be a highly effective treatment for locally advanced pancreatic endocrine tumors.
  • [MeSH-major] Adenoma, Islet Cell / drug therapy. Adenoma, Islet Cell / radiotherapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / radiotherapy

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  • [Copyright] Copyright 2007 S. Karger AG, Basel.
  • (PMID = 17541257.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 5W494URQ81 / Streptozocin; 6804DJ8Z9U / Capecitabine; 80168379AG / Doxorubicin; U3P01618RT / Fluorouracil
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67. Roggin KK, Rudloff U, Blumgart LH, Brennan MF: Central pancreatectomy revisited. J Gastrointest Surg; 2006 Jun;10(6):804-12
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  • This limited resection has the advantage of conserving normal, uninvolved pancreatic parenchyma, thus reducing the possibility of postoperative exocrine and endocrine dysfunction.
  • While the incidence of postoperative endocrine insufficiency may be as low as 4%, procedural morbidity, specifically pancreatic fistula, appears to exceed the published rates for standard resections (i.e., distal/subtotal pancreatectomy or pancreaticoduodenectomy).
  • We have reviewed our prospective pancreatic cancer database to determine the utilization of central pancreatectomy in a major cancer center with expertise in pancreatic surgery.
  • Six (60%) had postoperative complications including three cases (30%) of pancreatic fistula.
  • At a median follow-up of 13.6 months (mean, 25.2 months), only one patient had mild endocrine insufficiency and no patients had clinically significant exocrine dysfunction.
  • The associated morbidity of central pancreatectomy may outweigh any potential benefit in long-term pancreatic secretory function.
  • [MeSH-major] Pancreatectomy / methods. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adenoma, Islet Cell / surgery. Cystadenoma, Serous / surgery. Humans. Pancreatic Fistula / etiology. Retrospective Studies

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  • [Cites] Ann Surg. 1999 May;229(5):693-8; discussion 698-700 [10235528.001]
  • [Cites] Ann Surg. 1989 Mar;209(3):273-8 [2923514.001]
  • [Cites] Langenbecks Arch Surg. 2005 Jun;390(3):266-71 [15864637.001]
  • [Cites] Surgery. 1984 Oct;96(4):608-16 [6435270.001]
  • [Cites] Arch Surg. 2001 Apr;136(4):391-8 [11296108.001]
  • [Cites] Ann Surg. 2003 Jan;237(1):57-65 [12496531.001]
  • [Cites] Hepatogastroenterology. 1995 Sep-Oct;42(5):730-3 [8751242.001]
  • [Cites] World J Surg. 2003 May;27(5):595-8 [12715230.001]
  • [Cites] N Engl J Med. 1990 Mar 29;322(13):898-903 [2179721.001]
  • [Cites] Am J Surg. 2002 Jan;183(1):42-52 [11869701.001]
  • [Cites] Ann Surg. 2002 Nov;236(5):612-8 [12409667.001]
  • [Cites] Am J Surg. 2005 Feb;189(2):223-8 [15720996.001]
  • [Cites] J Am Coll Surg. 2004 Jun;198(6):871-6 [15194067.001]
  • [Cites] Surgery. 2002 Nov;132(5):836-43 [12464868.001]
  • [Cites] Surgery. 1993 May;113(5):532-5 [8488471.001]
  • [Cites] Ann Surg. 2002 Jun;235(6):803-13 [12035036.001]
  • [Cites] Ann Surg. 1995 Oct;222(4):580-8; discussion 588-92 [7574936.001]
  • [Cites] Ann Surg. 1976 Oct;184(4):403-13 [1015887.001]
  • [Cites] J Surg Oncol. 2001 Jun;77(2):132-5 [11398167.001]
  • [Cites] S Afr J Surg. 1989 Jun;27(2):67-8 [2749413.001]
  • [Cites] N Engl J Med. 2004 Sep 16;351(12):1218-26 [15371579.001]
  • [Cites] Surg Today. 1993;23(8):733-6 [8400678.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 1999;6(3):303-11 [10526067.001]
  • [Cites] Surgery. 1992 May;111(5):489-94 [1317976.001]
  • [Cites] Arch Surg. 2002 Feb;137(2):164-8 [11822953.001]
  • [Cites] Am J Surg. 1995 Jan;169(1):65-9; discussion 69-70 [7818000.001]
  • [Cites] Ann Surg. 2000 Dec;232(6):786-95 [11088073.001]
  • [Cites] J Am Coll Surg. 2001 Sep;193(3):281-7 [11548798.001]
  • [Cites] J Am Coll Surg. 1994 Nov;179(5):545-52 [7952456.001]
  • [Cites] Ann Surg. 2001 Sep;234(3):313-21; discussion 321-2 [11524584.001]
  • [Cites] Chirurgie. 1998 Sep;123(4):363-7 [9828510.001]
  • [Cites] Arch Surg. 1998 Mar;133(3):327-31 [9517749.001]
  • [Cites] Hepatogastroenterology. 1999 Jul-Aug;46(28):2585-8 [10522046.001]
  • [Cites] Dis Colon Rectum. 1993 Jun;36(6):602-6 [7684667.001]
  • [Cites] Br J Surg. 2000 Apr;87(4):434-8 [10759738.001]
  • [Cites] Am J Surg. 1967 Jan;113(1):77-84 [6016711.001]
  • [Cites] J Gastrointest Surg. 2004 Jul-Aug;8(5):532-8 [15239986.001]
  • [Cites] Ann Surg. 1996 May;223(5):506-11; discussion 511-2 [8651741.001]
  • [Cites] J Am Coll Surg. 2000 Jun;190(6):715-6 [10873008.001]
  • [Cites] Arch Surg. 1991 Mar;126(3):359-64 [1998479.001]
  • [Cites] J Am Coll Surg. 2000 Jun;190(6):711-6 [10873007.001]
  • [Cites] Br J Surg. 2003 Feb;90(2):190-6 [12555295.001]
  • [Cites] Br J Surg. 1988 Jul;75(7):719 [3416130.001]
  • [Cites] J Gastrointest Surg. 1998 Nov-Dec;2(6):509-16; discussion 516-7 [10457309.001]
  • [Cites] Arch Surg. 2000 Jun;135(6):644-8; discussion 648-50 [10843359.001]
  • [Cites] J Gastrointest Surg. 2004 May-Jun;8(4):493-501 [15120376.001]
  • (PMID = 16769536.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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68. Yao VJ, Ozawa MG, Varner AS, Kasman IM, Chanthery YH, Pasqualini R, Arap W, McDonald DM: Antiangiogenic therapy decreases integrin expression in normalized tumor blood vessels. Cancer Res; 2006 Mar 01;66(5):2639-49
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  • [Title] Antiangiogenic therapy decreases integrin expression in normalized tumor blood vessels.
  • Tumor blood vessels normalized by antiangiogenic therapy may provide improved delivery of chemotherapeutic agents during a window of time but it is unknown how protein expression in tumor vascular endothelial cells changes.
  • We evaluated the distribution of RGD-4C phage, which binds alpha(v)beta(3), alpha(v)beta(5), and alpha(5)beta(1) integrins on tumor blood vessels before and after antiangiogenic therapy.
  • Cellular distribution of RGD-4C phage in surviving tumor vessels matched the alpha(5)beta(1) integrin expression.
  • The reduction in integrin expression on tumor vessels after antiangiogenic therapy raises the possibility that integrin-targeted delivery of diagnostics or therapeutics may be compromised.
  • Efficacious delivery of drugs may benefit from identification by in vivo phage display of targeting peptides that bind to tumor blood vessels normalized by antiangiogenic agents.
  • [MeSH-major] Adenoma, Islet Cell / blood supply. Bacteriophage M13 / metabolism. Endothelial Cells / virology. Imidazoles / pharmacology. Indazoles / pharmacology. Integrin alpha5beta1 / biosynthesis. Integrin alphaVbeta3 / biosynthesis. Pancreatic Neoplasms / blood supply

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  • (PMID = 16510583.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-24136; United States / NHLBI NIH HHS / HL / P01 HL024136; United States / NCI NIH HHS / CA / P50-CA90270; United States / NCI NIH HHS / CA / CA88106; United States / NCI NIH HHS / CA / CA90810; United States / NHLBI NIH HHS / HL / HL-59157
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Imidazoles; 0 / Indazoles; 0 / Integrin alpha5beta1; 0 / Integrin alphaVbeta3; 0 / Oligopeptides; 78VO7F77PN / arginyl-glycyl-aspartic acid; C9LVQ0YUXG / axitinib
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69. de Sá SV, Corrêa-Giannella ML, Machado MC, de Souza JJ, Pereira MA, Patzina RA, Siqueira SA, Machado MC, Giannella-Neto D: Somatostatin receptor subtype 5 (SSTR5) mRNA expression is related to histopathological features of cell proliferation in insulinomas. Endocr Relat Cancer; 2006 Mar;13(1):69-78
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  • [Title] Somatostatin receptor subtype 5 (SSTR5) mRNA expression is related to histopathological features of cell proliferation in insulinomas.
  • Insulinomas are rare endocrine neoplasias that constitute the most frequent islet cell tumours.
  • Somatostatin (SST) analogs are tentatively used to inhibit insulin secretion and control tumour growth in patients with local invasion or inoperative metastasis, but variable responses have been reported.
  • Histopathological and immunohistochemical analysis for some features associated with tumour aggressiveness and semi-quantitative RT-PCR for SSTR1-5 and real-time qPCR for SSTR5 were performed.
  • SSTR5 mRNA was positively correlated with histopathological features related to tumour aggressiveness (large tumour diameter, well-differentiated endocrine tumour with uncertain behaviour and higher number of cells with nuclear atypia).
  • The observed positive correlation between SSTR5 expression and tumour size suggests that the use of SST analogues more specific to SSTR5 in the treatment of insulinomas deserves attention.
  • [MeSH-major] Cell Proliferation. Insulinoma / pathology. Pancreatic Neoplasms / pathology. RNA, Messenger / metabolism. Receptors, Somatostatin / genetics
  • [MeSH-minor] Adenoma, Islet Cell. Adolescent. Adult. Aged. Female. Humans. Liver Neoplasms / genetics. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Male. Middle Aged. Pituitary Hormones / metabolism. Pituitary Neoplasms / genetics. Pituitary Neoplasms / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16601280.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Pituitary Hormones; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 5
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70. Buscaglia JM, Giday SA, Kantsevoy SV, Jagannath SB, Magno P, Wolfgang CL, Daniels JA, Canto MI, Okolo Iii PI: Patient- and cyst-related factors for improved prediction of malignancy within cystic lesions of the pancreas. Pancreatology; 2009;9(5):631-8
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  • BACKGROUND AND AIMS: Early diagnosis of cancer in pancreatic cysts is important for timely referral to surgery.
  • The aim of this study was to develop a predictive model for pancreatic cyst malignancy to improve patient selection for surgical resection.
  • METHODS: We performed retrospective analyses of endoscopic ultrasound (EUS) and pathology databases identifying pancreatic cysts with available final pathological diagnoses.
  • RESULTS: 270 patients with pancreatic cysts were identified and analyzed (41% men, mean age 61.8 years).
  • Final pathological diagnoses were branch-duct IPMN (n = 118, 50% malignant), serous cystadenoma (n = 71), pseudocyst (n = 37), mucinous cyst adenoma/adenocarcinoma (n = 36), islet cell tumor (n = 4), simple cyst (n = 3), and ductal adenocarcinoma with cystic degeneration (n = 1).
  • CONCLUSIONS: Risk factors other than cyst size are important for determination of malignancy in pancreatic cysts.
  • [MeSH-major] Pancreas / ultrasonography. Pancreatic Cyst / ultrasonography

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19657218.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Carcinoembryonic Antigen
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71. Maione F, Molla F, Meda C, Latini R, Zentilin L, Giacca M, Seano G, Serini G, Bussolino F, Giraudo E: Semaphorin 3A is an endogenous angiogenesis inhibitor that blocks tumor growth and normalizes tumor vasculature in transgenic mouse models. J Clin Invest; 2009 Nov;119(11):3356-72
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  • [Title] Semaphorin 3A is an endogenous angiogenesis inhibitor that blocks tumor growth and normalizes tumor vasculature in transgenic mouse models.
  • Tumor growth and progression rely upon angiogenesis, which is regulated by pro- and antiangiogenic factors, including members of the semaphorin family.
  • By analyzing 3 different mouse models of multistep carcinogenesis, we show here that during angiogenesis, semaphorin 3A (Sema3A) is expressed in ECs, where it serves as an endogenous inhibitor of angiogenesis that is present in premalignant lesions and lost during tumor progression.
  • Pharmacologic inhibition of endogenous Sema3A during the angiogenic switch, the point when pretumoral lesions initiate an angiogenic phase that persists throughout tumor growth, enhanced angiogenesis and accelerated tumor progression.
  • By contrast, when, during the later stages of carcinogenesis following endogenous Sema3A downmodulation, Sema3A was ectopically reintroduced into islet cell tumors by somatic gene transfer, successive waves of apoptosis ensued, first in ECs and then in tumor cells, resulting in reduced vascular density and branching and inhibition of tumor growth and substantially extended survival.
  • Further, long-term reexpression of Sema3A markedly improved pericyte coverage of tumor blood vessels, something that is thought to be a key property of tumor vessel normalization, and restored tissue normoxia.
  • We conclude, therefore, that Sema3A is an endogenous and effective antiangiogenic agent that stably normalizes the tumor vasculature.
  • [MeSH-minor] Adenoma, Islet Cell / blood supply. Adenoma, Islet Cell / physiopathology. Animals. Antigens, CD29 / metabolism. Cell Hypoxia. Cell Movement. Disease Models, Animal. Female. Gene Expression Regulation, Neoplastic. Humans. Mice. Mice, Inbred C57BL. Mice, Transgenic. Uterine Cervical Neoplasms / blood supply. Uterine Cervical Neoplasms / physiopathology

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  • [Cites] Exp Cell Res. 2006 Mar 10;312(5):584-93 [16445911.001]
  • [Cites] Diabetes. 2006 Apr;55(4):875-84 [16567506.001]
  • [Cites] Trends Biochem Sci. 2006 Apr;31(4):231-9 [16530415.001]
  • [Cites] Blood. 2006 May 15;107(10):3892-901 [16424390.001]
  • [Cites] Endothelium. 2006 Mar-Apr;13(2):81-91 [16728327.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1661-7 [16684957.001]
  • [Cites] Nat Med. 2006 Dec;12(12):1380-9 [17099709.001]
  • [Cites] J Clin Invest. 2000 Feb;105(3):261-70 [10675351.001]
  • [Cites] Mech Dev. 2000 Oct;97(1-2):35-45 [11025205.001]
  • [Cites] Nat Cell Biol. 2000 Oct;2(10):737-44 [11025665.001]
  • [Cites] Mech Dev. 2001 Nov;109(1):115-9 [11677062.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):193-202 [12086877.001]
  • [Cites] Nat Med. 2002 Sep;8(9):918-21 [12205444.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11854-9 [12192090.001]
  • [Cites] J Clin Invest. 2002 Oct;110(7):933-41 [12370271.001]
  • [Cites] Int J Cancer. 2003 Apr 20;104(4):496-503 [12584749.001]
  • [Cites] J Clin Invest. 2003 May;111(9):1287-95 [12727920.001]
  • [Cites] Nature. 2003 Jul 24;424(6947):391-7 [12879061.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):42985-91 [12933805.001]
  • [Cites] Cancer Cell. 2003 Nov;4(5):383-91 [14667505.001]
  • [Cites] Cancer Cell. 2003 Nov;4(5):393-403 [14667506.001]
  • [Cites] Nat Med. 2004 Feb;10(2):145-7 [14745444.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):1008-15 [14871832.001]
  • [Cites] Genes Dev. 2004 Feb 15;18(4):435-47 [14977921.001]
  • [Cites] Mol Cell Neurosci. 2004 Apr;25(4):722-31 [15080899.001]
  • [Cites] Biochem Soc Trans. 2004 Jun;32(Pt3):421-5 [15157151.001]
  • [Cites] J Clin Invest. 2004 Sep;114(5):623-33 [15343380.001]
  • [Cites] Nature. 1985 May 9-15;315(6015):115-22 [2986015.001]
  • [Cites] Nature. 1989 May 4;339(6219):58-61 [2469964.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Oct 1;90(19):9051-5 [7692444.001]
  • [Cites] J Biol Chem. 1995 Oct 27;270(43):25570-7 [7592728.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 2;93(7):2930-5 [8610145.001]
  • [Cites] Cell. 1996 Aug 9;86(3):353-64 [8756718.001]
  • [Cites] Am J Pathol. 1996 Dec;149(6):1899-917 [8952526.001]
  • [Cites] Clin Ther. 2006 Nov;28(11):1779-802 [17212999.001]
  • [Cites] Cancer Cell. 2007 Jan;11(1):53-67 [17222790.001]
  • [Cites] Cancer Res. 2007 Feb 15;67(4):1451-60 [17308083.001]
  • [Cites] J Biol Chem. 2007 Sep 7;282(36):26294-305 [17569671.001]
  • [Cites] Cell. 2007 Nov 2;131(3):463-75 [17981115.001]
  • [Cites] Front Biosci. 2008;13:2653-9 [17981740.001]
  • [Cites] Cancer Metastasis Rev. 2007 Dec;26(3-4):421-31 [17768598.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2674-80 [18180379.001]
  • [Cites] Nat Med. 2008 Mar;14(3):255-7 [18278052.001]
  • [Cites] Circ Res. 2008 Mar 14;102(5):562-70 [18202311.001]
  • [Cites] Trends Biochem Sci. 2008 Apr;33(4):161-70 [18374575.001]
  • [Cites] J Exp Med. 2008 May 12;205(5):1155-71 [18458115.001]
  • [Cites] Nature. 2008 May 15;453(7193):410-4 [18418378.001]
  • [Cites] Nat Rev Cancer. 2008 Aug;8(8):632-45 [18580951.001]
  • [Cites] PLoS One. 2008;3(9):e3287 [18818766.001]
  • [Cites] Nat Rev Cancer. 2008 Dec;8(12):942-56 [19029957.001]
  • [Cites] Cancer Cell. 2009 Mar 3;15(3):220-31 [19249680.001]
  • [Cites] Cancer Res. 1997 Apr 1;57(7):1294-300 [9102216.001]
  • [Cites] Science. 1999 Apr 30;284(5415):808-12 [10221914.001]
  • [Cites] J Neurochem. 1999 Sep;73(3):961-71 [10461885.001]
  • [Cites] J Clin Invest. 2004 Nov;114(9):1260-71 [15520858.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):553-63 [15607960.001]
  • [Cites] Science. 2005 Jan 7;307(5706):58-62 [15637262.001]
  • [Cites] Am J Pathol. 2005 Jul;167(1):193-211 [15972964.001]
  • [Cites] Nature. 2005 Jul 14;436(7048):193-200 [16015319.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6167-77 [16024618.001]
  • [Cites] Nat Cell Biol. 2005 Sep;7(9):870-9 [16113679.001]
  • [Cites] Cancer Res. 2005 Sep 15;65(18):8317-23 [16166308.001]
  • [Cites] Circ Res. 2005 Sep 16;97(6):512-23 [16166562.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):299-309 [16226705.001]
  • [Cites] Cancer Lett. 2006 Jan 8;231(1):1-11 [16356825.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):198-211 [16397233.001]
  • [Cites] Nat Clin Pract Oncol. 2006 Jan;3(1):24-40 [16407877.001]
  • [Cites] Annu Rev Med. 2006;57:1-18 [16409133.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2006 Mar;290(3):H1220-5 [16258027.001]
  • [Cites] J Natl Cancer Inst. 2006 Feb 15;98(4):255-61 [16478744.001]
  • [Cites] Exp Cell Res. 2006 Mar 10;312(5):651-8 [16325811.001]
  • (PMID = 19809158.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Grant] Italy / Telethon / / GGP04127; Italy / Telethon / / GGP09175; United States / NIDDK NIH HHS / DK / DK59936; United States / NIAAA NIH HHS / AA / P60 AA11999
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD29; 0 / Semaphorin-3A
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72. Jabbour SA, Davidovici BB, Wolf R: Rare syndromes. Clin Dermatol; 2006 Jul-Aug;24(4):299-316
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  • Dermatologists may also encounter patients presenting with skin lesions that reflect an underlying endocrine disorder not commonly seen in daily practice.
  • Some of these endocrine disorders include glucagonoma, neurofibromatosis type 1, McCune-Albright syndrome, multiple endocrine neoplasia, the Carney complex, carcinoid tumors, and mastocytosis.
  • McCune-Albright syndrome is characterized by café-au-lait spots, polyostotic fibrous dysplasia, sexual precocity, and hyperfunction of multiple endocrine glands.
  • Multiple endocrine neoplasia type 2A is characterized by medullary thyroid cancer, pheochromocytoma, and primary parathyroid hyperplasia.
  • In some patients with multiple endocrine neoplasia type 2A, cutaneous lichen amyloidosis may also be present.
  • Multiple endocrine neoplasia type 2B is characterized by medullary thyroid cancer and pheochromocytoma but not hyperparathyroidism.
  • Multiple endocrine neoplasia type 1 is an autosomal dominant predisposition to tumors of the parathyroid glands (four-gland hyperplasia), anterior pituitary, and pancreatic islet cells; hence, the mnemonic device of the "3 Ps"; multiple cutaneous lesions (angiofibromas and collagenomas) are frequent in patients with multiple endocrine neoplasia type 1.
  • Carney complex may be viewed as a form of multiple endocrine neoplasia because affected patients often have tumors of two or more endocrine glands, including primary pigmented nodular adrenocortical disease (some with Cushing's syndrome), pituitary adenoma, testicular neoplasms, thyroid adenoma or carcinoma, and ovarian cysts.
  • Additional unusual manifestations include psammomatous melanotic schwannoma, breast ductal adenoma, and a rare bone tumor, osteochondromyxoma.
  • Mast cell diseases include all disorders of mast cell proliferation.
  • [MeSH-major] Endocrine System Diseases / genetics. Endocrine System Diseases / pathology. Mastocytosis, Cutaneous / pathology. Multiple Endocrine Neoplasia / genetics. Multiple Endocrine Neoplasia / pathology

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  • (PMID = 16828412.001).
  • [ISSN] 0738-081X
  • [Journal-full-title] Clinics in dermatology
  • [ISO-abbreviation] Clin. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 155
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73. Davies K, Conlon KC: Neuroendocrine tumors of the pancreas. Curr Gastroenterol Rep; 2009 Apr;11(2):119-27
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  • Pancreatic endocrine tumors are rare neoplasms accounting for less than 5% of pancreatic malignancies.
  • Signs and symptoms are usually related to hormone hypersecretion in the case of functioning tumors and to tumor size or metastases with nonfunctioning tumors.
  • Surgical resection remains the treatment of choice even in the face of metastatic disease.
  • Further development of novel diagnostic and treatment modalities offers potential to greatly improve quality of life and prolong disease-free survival for patients with pancreatic endocrine tumors.
  • [MeSH-major] Adenoma, Islet Cell. Carcinoma, Islet Cell. Pancreatic Neoplasms

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  • [Cites] J Clin Oncol. 2002 Jun 1;20(11):2633-42 [12039924.001]
  • [Cites] Cancer. 1991 Sep 15;68(6):1329-34 [1678681.001]
  • [Cites] World J Surg. 2008 May;32(5):904-17 [18264824.001]
  • [Cites] World J Surg. 2002 Aug;26(8):985-90 [12016479.001]
  • [Cites] Ann Surg. 2007 Feb;245(2):273-81 [17245182.001]
  • [Cites] Ann Oncol. 1999;10 Suppl 4:182-4 [10436817.001]
  • [Cites] J Gastroenterol. 2007 Jun;42(6):497-500 [17671766.001]
  • [Cites] J Gastrointest Surg. 2006 Jan;10(1):138-45 [16368504.001]
  • [Cites] Gastroenterology. 1968 Dec;55(6):677-86 [4302500.001]
  • [Cites] Ann Surg. 2006 Sep;244(3):410-9 [16926567.001]
  • [Cites] Arch Surg. 1984 May;119(5):508-14 [6143548.001]
  • [Cites] Endocr Relat Cancer. 2008 Jun;15(2):409-27 [18508996.001]
  • [Cites] Eur J Surg Oncol. 2008 Mar;34(3):324-32 [17967523.001]
  • [Cites] Am J Med. 1999 Mar;106(3):307-10 [10190379.001]
  • [Cites] Ann Surg Oncol. 2008 Dec;15(12):3532-7 [18825460.001]
  • [Cites] AJR Am J Roentgenol. 2003 Oct;181(4):987-92 [14500214.001]
  • [Cites] Dig Dis Sci. 1991 Jul;36(7):933-42 [2070707.001]
  • [Cites] N Engl J Med. 1992 Jun 25;326(26):1721-6 [1317506.001]
  • [Cites] World J Surg. 1993 Jul-Aug;17 (4):427-32 [8362525.001]
  • [Cites] Transplantation. 1998 Nov 27;66(10):1307-12 [9846513.001]
  • [Cites] Medicine (Baltimore). 1996 Mar;75(2):53-63 [8606627.001]
  • [Cites] Curr Probl Surg. 1990 Jun;27(6):301-86 [1973365.001]
  • [Cites] N Engl J Med. 1977 Apr 28;296(17):963-7 [321960.001]
  • [Cites] Mayo Clin Proc. 1991 Jul;66(7):711-9 [1677058.001]
  • [Cites] Ann Surg. 2008 Jan;247(1):165-72 [18156937.001]
  • [Cites] Arch Surg. 2002 Feb;137(2):164-8 [11822953.001]
  • [Cites] Ann Surg. 1955 Oct;142(4):709-23; discussion, 724-8 [13259432.001]
  • [Cites] N Engl J Med. 1986 May 1;314(18):1145-51 [3007986.001]
  • [Cites] Ann Surg Oncol. 2001 Apr;8(3):249-53 [11314942.001]
  • [Cites] Am J Med. 1958 Sep;25(3):374-80 [13571250.001]
  • [Cites] Surg Clin North Am. 1987 Apr;67(2):379-93 [3031836.001]
  • [Cites] Curr Opin Oncol. 1999 Jan;11(1):32-7 [9914875.001]
  • [Cites] Pathol Res Pract. 1988 Apr;183(2):155-68 [2898775.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Aug;82(8):2622-8 [9253344.001]
  • [Cites] J Gastrointest Surg. 1998 Sep-Oct;2(5):473-82 [18335273.001]
  • [Cites] Arch Surg. 2006 Aug;141(8):765-9; discussion 769-70 [16924083.001]
  • [Cites] J Med Res. 1902 Nov;8(2):385-95 [19971505.001]
  • [Cites] J Clin Oncol. 2007 Dec 10;25(35):5609-15 [18065733.001]
  • [Cites] Radiology. 1993 Mar;186(3):799-802 [8381551.001]
  • [Cites] Am J Surg. 1990 Feb;159(2):258-64 [2154144.001]
  • (PMID = 19281699.001).
  • [ISSN] 1534-312X
  • [Journal-full-title] Current gastroenterology reports
  • [ISO-abbreviation] Curr Gastroenterol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrins; 0 / Insulin; 51110-01-1 / Somatostatin; 9007-92-5 / Glucagon
  • [Number-of-references] 44
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74. Kwekkeboom DJ, Teunissen JJ, Bakker WH, Kooij PP, de Herder WW, Feelders RA, van Eijck CH, Esser JP, Kam BL, Krenning EP: Radiolabeled somatostatin analog [177Lu-DOTA0,Tyr3]octreotate in patients with endocrine gastroenteropancreatic tumors. J Clin Oncol; 2005 Apr 20;23(12):2754-62
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  • [Title] Radiolabeled somatostatin analog [177Lu-DOTA0,Tyr3]octreotate in patients with endocrine gastroenteropancreatic tumors.
  • PURPOSE: There are few treatment options for patients with metastasized or inoperable endocrine gastroenteropancreatic (GEP) tumors.
  • We observed complete remission in three patients (2%), partial remission in 32 patients (26%), minor response (tumor diameter decrease of 25% to 50%) in 24 patients (19%), stable disease (SD) in 44 patients (35%), and progressive disease (PD) in 22 patients (18%).
  • Higher remission rates were positively correlated with high uptake on pretherapy somatostatin receptor imaging and a limited number of liver metastases, whereas PD was significantly more frequent in patients with a low performance score and extensive disease.
  • Median time to progression in 103 patients who either had SD or tumor regression was more than 36 months.
  • CONCLUSION: Treatment with 177Lu-octreotate results in tumor remission in a high percentage of patients with GEP tumors.
  • Results are better in patients with a limited tumor load.
  • [MeSH-major] Adenoma, Islet Cell / drug therapy. Carcinoid Tumor / drug therapy. Endocrine Gland Neoplasms / drug therapy. Organometallic Compounds / adverse effects. Organometallic Compounds / therapeutic use. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Male. Middle Aged. Octreotide / analogs & derivatives. Receptors, Somatostatin. Treatment Outcome

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  • (PMID = 15837990.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / (177lutetium-DOTA(O)Tyr3)octreotate; 0 / Organometallic Compounds; 0 / Receptors, Somatostatin; RWM8CCW8GP / Octreotide
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75. Chen G, A J, Wang M, Farley S, Lee LY, Lee LC, Sawicki MP: Menin promotes the Wnt signaling pathway in pancreatic endocrine cells. Mol Cancer Res; 2008 Dec;6(12):1894-907
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  • [Title] Menin promotes the Wnt signaling pathway in pancreatic endocrine cells.
  • Menin is a tumor suppressor protein mutated in patients with multiple endocrine neoplasia type 1.
  • We show that menin is essential for canonical Wnt/beta-catenin signaling in cultured rodent islet tumor cells.
  • Likewise, multiple endocrine neoplasia type 1 disease associated missense mutations of menin abrogate the ability to increase TCF reporter gene activity.
  • Based on these studies, we hypothesized that Wnt signaling could inhibit islet cell proliferation because loss of menin function is thought to increase endocrine tumor cell proliferation.
  • TGP61 rodent islet tumor cells treated with a glycogen synthase kinase 3beta inhibitor that increases Wnt pathway signaling had decreased cell proliferation compared with vehicle-treated cells.
  • Collectively, these data suggest that menin has an essential role in Wnt/beta-catenin signaling through a mechanism that eventually affects histone trimethylation of the downstream target gene Axin2, and activation of Wnt/beta-catenin signaling inhibits islet tumor cell proliferation.
  • [MeSH-major] Adenoma, Islet Cell / metabolism. Multiple Endocrine Neoplasia Type 1 / metabolism. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins / metabolism. Wnt Proteins / metabolism

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  • (PMID = 19074834.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 095148
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AXIN2 protein, human; 0 / Axin Protein; 0 / Axin2 protein, mouse; 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CTNNB1 protein, human; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Histones; 0 / MEN1 protein, human; 0 / Men1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / TCF3 protein, human; 0 / TCF4 protein, human; 0 / Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin
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76. Choi EK, Park SH, Kim DY, Kim KW, Byun JH, Lee MG, Ha HK: Unusual manifestations of primary pancreatic neoplasia: Radiologic-pathologic correlation. J Comput Assist Tomogr; 2006 Jul-Aug;30(4):610-7
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  • [Title] Unusual manifestations of primary pancreatic neoplasia: Radiologic-pathologic correlation.
  • Primary pancreatic lesions may present with unusual features ranging from cystic change in ductal adenocarcinoma and islet cell tumors to ductal communication in solid pseudopapillary and mucinous tumors.
  • Consideration of unusual variations of primary pancreatic neoplasm in the differential diagnosis of solid and cystic pancreatic lesions is necessary for their proper diagnostic work-up and management.
  • We present the rare imaging manifestations and corresponding pathologic correlation of a representative group of primary pancreatic tumors, including pancreatic adenocarcinoma, islet cell tumor, solid pseudopapillary tumor, and serous/mucinous cystic tumors.
  • [MeSH-major] Pancreatic Neoplasms / radiography. Tomography, X-Ray Computed / methods
  • [MeSH-minor] Adenocarcinoma, Mucinous / pathology. Adenocarcinoma, Mucinous / radiography. Adenoma, Islet Cell / pathology. Adenoma, Islet Cell / radiography. Contrast Media. Cystadenoma / pathology. Cystadenoma / radiography. Diagnosis, Differential. Humans

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  • (PMID = 16845292.001).
  • [ISSN] 0363-8715
  • [Journal-full-title] Journal of computer assisted tomography
  • [ISO-abbreviation] J Comput Assist Tomogr
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 14
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77. Christein JD, Smoot RL, Farnell MB: Central pancreatectomy: a technique for the resection of pancreatic neck lesions. Arch Surg; 2006 Mar;141(3):293-9
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  • [Title] Central pancreatectomy: a technique for the resection of pancreatic neck lesions.
  • Although historically used for traumatic pancreatic transection and chronic pancreatitis, it currently is reserved for selective management of pancreatic neck lesions that are benign or have low malignant potential.
  • Our objectives were to describe the technique and determine the safety and effectiveness of central pancreatectomy in the excision of benign or low-malignant potential lesions of the pancreatic neck.
  • INTERVENTION: Patients with pancreatic neck or proximal body masses underwent central pancreatectomy at the Mayo Clinic, Rochester, Minn.
  • On follow-up, long-term endocrine and exocrine function were determined based on laboratory values and patient history.
  • RESULTS: Abnormalities included 3 islet cell tumors, 2 serous cystadenomas, a mucinous cystadenoma, a lymphoepithelial cyst, and a recurrent liposarcoma.
  • Mean tumor size was 2.8 cm and mean operative time was 4.8 hours with a mean blood loss of 381 mL.
  • The most common complication was pancreatic leak (5 patients [63%]).
  • One patient transiently required oral pancreatic enzyme supplementation.
  • CONCLUSIONS: Central pancreatectomy may preserve endocrine and exocrine function.
  • The most common complication is pancreatic leak.
  • Caution is necessary when using central pancreatectomy in the treatment of pancreatic neck lesions.
  • The precise role of central pancreatectomy in the management of benign or low-malignant potential lesions of the neck of the pancreas remains in evolution.
  • [MeSH-major] Pancreatectomy / methods. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adenoma, Islet Cell / radiography. Adenoma, Islet Cell / surgery. Cystadenoma, Serous / radiography. Cystadenoma, Serous / surgery. Female. Humans. Liposarcoma / surgery. Male. Mesenteric Veins / surgery. Middle Aged. Neoplasm Recurrence, Local / surgery. Reoperation. Retrospective Studies. Tomography, X-Ray Computed

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  • (PMID = 16549696.001).
  • [ISSN] 0004-0010
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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78. Alzahrani AS, Al-Khaldi N, Shi Y, Al-Rijjal RA, Zou M, Baitei EY, Amin T: Diagnosis by serendipity: Cushing syndrome attributable to cortisol-producing adrenal adenoma as the initial manifestation of multiple endocrine neoplasia type 1 due to a rare splicing site MEN1 gene mutation. Endocr Pract; 2008 Jul-Aug;14(5):595-602
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  • [Title] Diagnosis by serendipity: Cushing syndrome attributable to cortisol-producing adrenal adenoma as the initial manifestation of multiple endocrine neoplasia type 1 due to a rare splicing site MEN1 gene mutation.
  • OBJECTIVE: To report a case that highlights the potential for Cushing syndrome to be the first manifestation of multiple endocrine neoplasia type 1 (MEN 1) syndrome and to describe the rare underlying genetic mutation and the heterogeneous manifestations of the syndrome within the same family.
  • RESULTS: A 16-year-old girl who was not known to have any medical illness and had no known family history of MEN 1 syndrome presented with Cushing syndrome attributable to a cortisol-producing adrenal adenoma.
  • She did not have clinical, biochemical, or radiologic evidence of islet cell pancreatic tumors.
  • Most cases are due to corticotropin-producing pituitary adenomas.
  • [MeSH-major] Adrenocortical Adenoma / pathology. Cushing Syndrome / diagnosis. Hydrocortisone / secretion. Multiple Endocrine Neoplasia Type 1 / pathology


79. Muscarella LA, Barbano R, Augello B, Formica V, Micale L, Zelante L, D'Agruma L, Merla G: An 11-bp duplication in the promoter region of the VHL gene in a patient with cerebellar hemangioblastoma and renal oncocytoma. J Hum Genet; 2007;52(6):485-91
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  • Central nervous system hemangioblastomas are benign vascular tumours that may present sporadically or as manifestation of the von Hippel-Lindau (VHL) disease.
  • VHL Syndrome is a rare autosomal dominant disorder characterized, besides hemangioblastomas, by susceptibility to multifocal and bilateral renal cell carcinoma and cysts, retinal angiomas, pheochromocytoma, epididymis cystoadenoma, pancreatic cysts and/or islet cell tumours.
  • Germline mutations of VHL tumour suppressor gene cause the VHL disease, while somatic mutations have been associated with sporadic hemangioblastomas and clear-cell renal carcinomas.
  • [MeSH-major] Adenoma, Oxyphilic / genetics. Cerebellar Neoplasms / genetics. Hemangioblastoma / genetics. Kidney Neoplasms / genetics. Promoter Regions, Genetic. Von Hippel-Lindau Tumor Suppressor Protein / genetics. von Hippel-Lindau Disease / genetics


80. Lindberg D, Akerström G, Westin G: Mutational analyses of WNT7A and HDAC11 as candidate tumour suppressor genes in sporadic malignant pancreatic endocrine tumours. Clin Endocrinol (Oxf); 2007 Jan;66(1):110-4
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  • [Title] Mutational analyses of WNT7A and HDAC11 as candidate tumour suppressor genes in sporadic malignant pancreatic endocrine tumours.
  • OBJECTIVE: We and others have reported loss of heterozygosity (LOH) on chromosome 3p25 in sporadic malignant pancreatic endocrine tumours (PETs).
  • A common region of deletion on chromosome 3p25 contains numerous genes, including VHL and PPARgamma, that have been excluded previously as candidate tumour suppressor genes by DNA sequencing analysis.
  • CONCLUSION: The absence of tumour-specific somatic events in WNT7A and HDAC11 suggests that these genes are unlikely to have a classical tumour suppressor gene role in sporadic malignant PETs.
  • The putative 3p25 tumour suppressor remains to be identified.
  • [MeSH-major] Adenoma, Islet Cell / genetics. Genes, Tumor Suppressor. Histone Deacetylases / genetics. Loss of Heterozygosity. Pancreatic Neoplasms / genetics. Wnt Proteins / genetics

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  • (PMID = 17201809.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / WNT7A protein, human; 0 / Wnt Proteins; EC 3.5.1.98 / HDAC11 protein, human; EC 3.5.1.98 / Histone Deacetylases
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81. Abe H, Murakami T, Kubota M, Kim T, Hori M, Kudo M, Hashimoto K, Nakamori S, Dono K, Tomoda K, Monden M, Nakamura H: Quantitative tissue blood flow evaluation of pancreatic tumor: comparison between xenon CT technique and perfusion CT technique based on deconvolution analysis. Radiat Med; 2005 Aug;23(5):364-70
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  • [Title] Quantitative tissue blood flow evaluation of pancreatic tumor: comparison between xenon CT technique and perfusion CT technique based on deconvolution analysis.
  • PURPOSE: There has been one report that tissue blood flow (TBF) quantification with xenon CT was effective in predicting the therapeutic response to an anticancer drug in pancreatic cancer.
  • The purpose of this study was to evaluate the correlation between the TBF of pancreatic tumors calculated with xenon CT and those with perfusion CT, in order to evaluate whether perfusion CT could replace xenon CT.
  • MATERIALS AND METHODS: Nine patients with pathologically proved pancreatic tumors who underwent both xenon CT and perfusion CT were included.
  • RESULTS: Quantitative TBF of pancreatic tumors measured by perfusion CT ranged from 22.1 to 196.2 ml/min/100 g (mean+/-SD, 52.6+/-54.8 ml/min/100 g).
  • CONCLUSION: The TBF of pancreatic tumors measured by xenon CT and perfusion CT techniques showed a close linear correlation.
  • We can expect that perfusion CT based on the deconvolution algorithm may replace xenon CT to predict the effect of pancreatic tumor treatment with anticancer drugs.
  • [MeSH-major] Adenocarcinoma / blood supply. Adenoma, Islet Cell / blood supply. Contrast Media / administration & dosage. Pancreatic Neoplasms / blood supply. Tomography, Spiral Computed / methods. Tomography, X-Ray Computed / methods. Xenon / administration & dosage

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  • (PMID = 16342909.001).
  • [ISSN] 0288-2043
  • [Journal-full-title] Radiation medicine
  • [ISO-abbreviation] Radiat Med
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Contrast Media; 3H3U766W84 / Xenon
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82. Couvelard A, O'Toole D, Turley H, Leek R, Sauvanet A, Degott C, Ruszniewski P, Belghiti J, Harris AL, Gatter K, Pezzella F: Microvascular density and hypoxia-inducible factor pathway in pancreatic endocrine tumours: negative correlation of microvascular density and VEGF expression with tumour progression. Br J Cancer; 2005 Jan 17;92(1):94-101
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  • [Title] Microvascular density and hypoxia-inducible factor pathway in pancreatic endocrine tumours: negative correlation of microvascular density and VEGF expression with tumour progression.
  • Tumour-associated angiogenesis is partly regulated by the hypoxia-inducible factor (HIF) pathway.
  • Endocrine tumours are highly vascularised and the molecular mechanisms of their angiogenesis are not fully delineated.
  • The aim of this study is to evaluate angiogenesis and expression of HIF-related molecules in a series of patients with pancreatic endocrine tumours (PETs).
  • The expression of vascular endothelial growth factor (VEGF), HIF-1alpha, HIF-2alpha and carbonic anhydrase 9 (CA9) was examined by immunohistochemistry in 45 patients with PETs and compared to microvascular density (MVD), endothelial proliferation, tumour stage and survival.
  • Microvascular density was significantly higher in benign PETs than in PETs of uncertain prognosis, well-differentiated and poorly differentiated carcinomas (mean values: 535, 436, 252 and 45 vessels mm(-2), respectively, P < 0.0001).
  • The regulation of HIF signalling appears to be specific in pancreatic endocrine tumours.
  • [MeSH-major] Adenoma, Islet Cell / blood supply. Adenoma, Islet Cell / metabolism. Neovascularization, Pathologic. Pancreatic Neoplasms / blood supply. Pancreatic Neoplasms / metabolism. Vascular Endothelial Growth Factors / metabolism
  • [MeSH-minor] Adult. Basic Helix-Loop-Helix Transcription Factors. Carbonic Anhydrases / metabolism. Disease Progression. Female. Humans. Hypoxia-Inducible Factor 1, alpha Subunit. Male. Microcirculation. Transcription Factors / metabolism

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  • [Cites] Eur J Cancer. 1998 Apr;34(5):609-18 [9713263.001]
  • [Cites] Neuroendocrinology. 1986;43(2):159-65 [3523276.001]
  • [Cites] Gut. 1998 Sep;43(3):422-7 [9863490.001]
  • [Cites] Clin Cancer Res. 1997 Aug;3(8):1309-16 [9815813.001]
  • [Cites] J Pathol. 1998 Nov;186(3):313-8 [10211122.001]
  • [Cites] Oncogene. 1999 Sep 20;18(38):5356-62 [10498889.001]
  • [Cites] J Clin Invest. 1997 Jul 15;100(2):404-10 [9218518.001]
  • [Cites] Cancer Res. 1999 Nov 15;59(22):5830-5 [10582706.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Mar;85(3):1159-62 [10720055.001]
  • [Cites] Cancer Res. 2000 Mar 1;60(5):1388-93 [10728704.001]
  • [Cites] Br J Cancer. 2000 Apr;82(8):1441-5 [10780524.001]
  • [Cites] J Endocrinol. 2000 May;165(2):475-81 [10810311.001]
  • [Cites] Cancer. 2000 May 15;88(10):2239-45 [10820344.001]
  • [Cites] Cancer. 2000 Jun 1;88(11):2606-18 [10861440.001]
  • [Cites] Am J Pathol. 2000 Aug;157(2):411-21 [10934146.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4693-6 [10987269.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):7075-83 [11156414.001]
  • [Cites] Curr Opin Cell Biol. 2001 Apr;13(2):167-71 [11248550.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6394-9 [11522632.001]
  • [Cites] Nature. 2001 Aug 30;412(6850):877-84 [11528470.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Oct;32(2):177-81 [11550286.001]
  • [Cites] Br J Cancer. 2001 Sep 14;85(6):881-90 [11556841.001]
  • [Cites] Novartis Found Symp. 2001;240:212-25; discussion 225-31 [11727931.001]
  • [Cites] Int J Cancer. 2002 Feb 20;97(6):719-25 [11857345.001]
  • [Cites] Nat Rev Cancer. 2002 Jan;2(1):38-47 [11902584.001]
  • [Cites] Br J Cancer. 2002 Apr 22;86(8):1276-82 [11953885.001]
  • [Cites] Semin Cell Dev Biol. 2002 Feb;13(1):29-37 [11969369.001]
  • [Cites] J Clin Oncol. 2002 Jun 1;20(11):2633-42 [12039924.001]
  • [Cites] Pancreas. 2002 Aug;25(2):122-9 [12142733.001]
  • [Cites] Clin Cancer Res. 2002 Aug;8(8):2595-604 [12171890.001]
  • [Cites] J Surg Oncol. 2002 Sep;81(1):45-53; discussion 54 [12210027.001]
  • [Cites] Nat Rev Cancer. 2002 Sep;2(9):673-82 [12209156.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Nov;87(11):4961-5 [12414859.001]
  • [Cites] Microsc Res Tech. 2003 Feb 1;60(2):181-5 [12539172.001]
  • [Cites] Hum Pathol. 2003 Jan;34(1):18-27 [12605362.001]
  • [Cites] Histopathology. 2003 May;42(5):482-91 [12713626.001]
  • [Cites] Virology. 1992 Apr;187(2):620-6 [1312272.001]
  • [Cites] J Natl Cancer Inst. 1992 Dec 16;84(24):1875-87 [1281237.001]
  • [Cites] Am J Pathol. 1995 Jul;147(1):9-19 [7541613.001]
  • [Cites] Br J Cancer. 1995 Aug;72(2):319-23 [7543771.001]
  • [Cites] Hum Pathol. 1995 Nov;26(11):1196-200 [7590692.001]
  • [Cites] Mol Endocrinol. 1995 Dec;9(12):1760-70 [8614412.001]
  • [Cites] Genomics. 1996 May 1;33(3):480-7 [8661007.001]
  • [Cites] Histopathology. 1997 Mar;30(3):294-301 [9088964.001]
  • [Cites] Am J Pathol. 1997 Nov;151(5):1417-23 [9358768.001]
  • [Cites] Am J Clin Pathol. 1998 Mar;109(3):286-93 [9495200.001]
  • [Cites] Histopathology. 1998 Feb;32(2):133-8 [9543669.001]
  • [Cites] Mod Pathol. 1998 Apr;11(4):329-33 [9578082.001]
  • [Cites] J Pathol. 1998 Feb;184(2):119-22 [9602700.001]
  • [Cites] Nat Med. 2003 Jun;9(6):653-60 [12778163.001]
  • [Cites] Nat Med. 2003 Jun;9(6):677-84 [12778166.001]
  • [Cites] Nat Rev Cancer. 2003 Jun;3(6):401-10 [12778130.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):133-46 [12957288.001]
  • [Cites] Gastroenterology. 2003 Oct;125(4):1094-104 [14517793.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12596-601 [9770531.001]
  • (PMID = 15558070.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factors; 0 / endothelial PAS domain-containing protein 1; EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2361752
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83. Elsayes KM, Narra VR, Abou El Abbass HA, Aly TS, Radwan SM, Chen ZM: Pancreatic tumors: diagnostic patterns by 3D gradient-echo post contrast magnetic resonance imaging with pathologic correlation. Curr Probl Diagn Radiol; 2006 Jul-Aug;35(4):125-39
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  • [Title] Pancreatic tumors: diagnostic patterns by 3D gradient-echo post contrast magnetic resonance imaging with pathologic correlation.
  • Magnetic resonance (MR) imaging has considerable potential in characterizing pancreatic masses.
  • Certain features can be used by the radiologist to establish a definitive diagnosis for most pancreatic tumors including ductal adenocarcinoma, islet cell tumors, solid and papillary epithelial neoplasms, micro- and macrocystic adenoma, and metastases.
  • In this article, special emphasis will be placed on the impact of 3D GRE sequence in the diagnosis of pancreatic neoplasms with pathologic correlation.
  • [MeSH-major] Contrast Media. Imaging, Three-Dimensional. Magnetic Resonance Imaging. Pancreatic Neoplasms / diagnosis

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  • (PMID = 16814000.001).
  • [ISSN] 0363-0188
  • [Journal-full-title] Current problems in diagnostic radiology
  • [ISO-abbreviation] Curr Probl Diagn Radiol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
  • [Number-of-references] 37
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84. Maser C, Toset A, Roman S: Gastrointestinal manifestations of endocrine disease. World J Gastroenterol; 2006 May 28;12(20):3174-9
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  • [Title] Gastrointestinal manifestations of endocrine disease.
  • The hormonal interactions among the systems throughout the body are not fully understood; many vague clinical symptoms may in fact be manifestations of underlying endocrine diseases.
  • The aim of the following review is to discuss gastrointestinal manifestations of surgically correctable endocrine diseases, focusing on abnormalities of thyroid function, cancer and finally autoimmune diseases.
  • We also review manifestations of pancreatic endocrine tumors, and multiple endocrine neoplasia.
  • [MeSH-major] Endocrine System Diseases / complications. Gastrointestinal Diseases / etiology. Gastrointestinal Tract / physiopathology
  • [MeSH-minor] Adenoma, Islet Cell / complications. Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / physiopathology. Adenoma, Islet Cell / surgery. Humans. Neuroendocrine Tumors / complications. Neuroendocrine Tumors / diagnosis. Neuroendocrine Tumors / physiopathology. Neuroendocrine Tumors / surgery. Thyroid Diseases / complications. Thyroid Diseases / diagnosis. Thyroid Diseases / physiopathology. Thyroid Diseases / surgery

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  • [Cites] J Clin Endocrinol Metab. 2000 Jan;85(1):286-92 [10634400.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Sep;55(3):357-62 [11589679.001]
  • [Cites] Dig Dis Sci. 2001 Dec;46(12):2631-5 [11768252.001]
  • [Cites] Ann Surg. 2002 May;235(5):648-54; discussion 654-5 [11981210.001]
  • [Cites] Histopathology. 1997 Sep;31(3):231-6 [9354893.001]
  • [Cites] Hepatogastroenterology. 1997 Sep-Oct;44(17):1500-8 [9356880.001]
  • [Cites] Scand J Gastroenterol. 1998 Jan;33(1):88-92 [9489914.001]
  • [Cites] World J Surg. 1998 Jul;22(7):738-42; discussion 743 [9606291.001]
  • [Cites] World J Surg. 1998 Dec;22(12):1231-6 [9841749.001]
  • [Cites] Surgery. 1998 Dec;124(6):1050-5 [9854582.001]
  • [Cites] Am J Gastroenterol. 1998 Dec;93(12):2391-6 [9860398.001]
  • [Cites] Mod Pathol. 1999 Apr;12(4):400-11 [10229505.001]
  • [Cites] Am J Pathol. 1999 Jul;155(1):7-9 [10393829.001]
  • [Cites] Arch Surg. 1999 Aug;134(8):818-22; discussion 822-3 [10443803.001]
  • [Cites] Arch Intern Med. 1999 Aug 9-23;159(15):1726-30 [10448775.001]
  • [Cites] N Engl J Med. 1999 Aug 26;341(9):635-44 [10460814.001]
  • [Cites] Exp Biol Med (Maywood). 2004 Nov;229(10):1007-16 [15522836.001]
  • [Cites] World J Surg. 2004 Sep;28(9):886-9 [15593462.001]
  • [Cites] Neth J Med. 2004 Sep;62(8):293-6 [15588071.001]
  • [Cites] World J Surg. 2004 Dec;28(12):1231-8 [15517477.001]
  • [Cites] World J Surg. 2004 Dec;28(12):1239-47 [15517485.001]
  • [Cites] Nihon Geka Gakkai Zasshi. 2005 Aug;106(8):472-8 [16119110.001]
  • [Cites] World J Surg. 2002 Oct;26(10):1291-6 [12205549.001]
  • [Cites] Ann N Y Acad Sci. 2002 Sep;970:159-69 [12381551.001]
  • [Cites] Clin Endocrinol (Oxf). 2002 Dec;57(6):821-5 [12460333.001]
  • [Cites] Diabetes Care. 2003 Jan;26(1):82-8 [12502662.001]
  • [Cites] Pathology. 2003 Feb;35(1):42-6 [12701683.001]
  • [Cites] Eur Radiol. 2004 May;14(5):923-5 [12955450.001]
  • [Cites] World J Gastroenterol. 2004 Jun 15;10(12):1806-9 [15188511.001]
  • [Cites] Hepatobiliary Pancreat Dis Int. 2004 Aug;3(3):469-72 [15313691.001]
  • [Cites] Dysphagia. 2004 Spring;19(2):120-4 [15382800.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Oct;89(10):4944-8 [15472189.001]
  • [Cites] N Engl J Med. 1968 May 9;278(19):1056-8 [5644968.001]
  • [Cites] Ann Intern Med. 1973 May;78(5):669-75 [4711771.001]
  • [Cites] J Clin Gastroenterol. 1984 Oct;6(5):437-40 [6501830.001]
  • [Cites] Nihon Geka Gakkai Zasshi. 1986 Jun;87(6):671-9 [3526120.001]
  • [Cites] Ann Surg. 1987 Mar;205(3):230-9 [3548610.001]
  • [Cites] Br J Surg. 1987 May;74(5):377-80 [3036290.001]
  • [Cites] Gastroenterology. 1989 Oct;97(4):911-9 [2777044.001]
  • [Cites] Gastroenterology. 1991 Jan;100(1):99-106 [1983854.001]
  • [Cites] Tissue Antigens. 1990 Sep;36(3):136-7 [2278049.001]
  • [Cites] Am J Med. 1992 Feb;92(2):183-8 [1543203.001]
  • [Cites] J Clin Gastroenterol. 1992 Jan;14(1):56-8 [1556409.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Sep;75(3):745-9 [1517363.001]
  • [Cites] Cancer. 1993 Feb 1;71(3):745-50 [8431855.001]
  • [Cites] Ann Surg. 1993 Feb;217(2):101-8 [8382467.001]
  • [Cites] Histopathology. 1994 Dec;25(6):549-61 [7698732.001]
  • [Cites] Ann Intern Med. 1995 Aug 15;123(4):269-73 [7611592.001]
  • [Cites] J Clin Pathol. 1996 Jul;49(7):611-3 [8813970.001]
  • [Cites] Am J Surg Pathol. 1996 Oct;20(10):1161-81 [8827022.001]
  • [Cites] J Endocrinol. 1996 Dec;151(3):431-7 [8994388.001]
  • [Cites] Int J Colorectal Dis. 1997;12(4):240-2 [9272455.001]
  • (PMID = 16718836.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 58
  • [Other-IDs] NLM/ PMC4087959
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85. Oue N, Mitani Y, Aung PP, Sakakura C, Takeshima Y, Kaneko M, Noguchi T, Nakayama H, Yasui W: Expression and localization of Reg IV in human neoplastic and non-neoplastic tissues: Reg IV expression is associated with intestinal and neuroendocrine differentiation in gastric adenocarcinoma. J Pathol; 2005 Oct;207(2):185-98
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  • Regenerating islet-derived family, member 4 (Reg IV) is a candidate marker for cancer and inflammatory bowel disease.
  • Insulin-producing beta cells of the endocrine pancreas were positive for Reg IV.
  • No association was found between Reg IV expression and clinical characteristics such as tumour stage and patient prognosis.
  • Of 36 colorectal adenocarcinomas, 13 (36.1%) were positive for Reg IV, which was associated with tumour stage (p = 0.0379, Fisher's exact test).
  • These data suggest that Reg IV is expressed by gastrointestinal and pancreatic tumours, including adenocarcinomas and carcinoid tumours, and that Reg IV is associated with intestinal and neuroendocrine differentiation of the stomach and gastric carcinoma.
  • [MeSH-minor] Adenoma / chemistry. Biomarkers, Tumor / analysis. Blotting, Western / methods. Breast Neoplasms / chemistry. Carcinoid Tumor / chemistry. Cell Differentiation / physiology. Cell Line, Tumor. Colon / metabolism. Colorectal Neoplasms / chemistry. Female. Humans. Immunohistochemistry / methods. Intestine, Small / metabolism. Lung Neoplasms / chemistry. Pancreas / metabolism. Pancreatic Neoplasms / chemistry. Phenotype. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Stomach / metabolism

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  • [Copyright] Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16086444.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Neoplasm Proteins; 0 / REG4 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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86. Musunuru S, Chen H, Rajpal S, Stephani N, McDermott JC, Holen K, Rikkers LF, Weber SM: Metastatic neuroendocrine hepatic tumors: resection improves survival. Arch Surg; 2006 Oct;141(10):1000-4; discussion 1005
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  • RESULTS: From January 1996 through May 2004, 48 patients with liver-only neuroendocrine metastases were identified (median follow-up, 20 months), including 36 carcinoid and 12 islet cell tumors.
  • No difference was noted in the percentage of liver involved with tumor between the 3 groups.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Adenoma, Islet Cell / therapy. Carcinoid Tumor / pathology. Carcinoid Tumor / therapy. Liver Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Catheter Ablation. Disease-Free Survival. Embolization, Therapeutic. Female. Hepatectomy. Hepatic Artery. Humans. Male. Octreotide / therapeutic use. Retrospective Studies. Treatment Outcome

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  • (PMID = 17043278.001).
  • [ISSN] 0004-0010
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; RWM8CCW8GP / Octreotide
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87. Nakahara T, Norberg SM, Shalinsky DR, Hu-Lowe DD, McDonald DM: Effect of inhibition of vascular endothelial growth factor signaling on distribution of extravasated antibodies in tumors. Cancer Res; 2006 Feb 01;66(3):1434-45
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  • Antibodies and other macromolecular therapeutics can gain access to tumor cells via leaky tumor vessels.
  • We addressed this issue by examining the distribution of extravasated antibodies in islet cell tumors of RIP-Tag2 transgenic mice and implanted Lewis lung carcinomas using fluorescence and confocal microscopic imaging.
  • Anti-E-cadherin antibody, which targets epitopes on tumor cells of RIP-Tag2 adenomas, was the only antibody to achieve detectable levels within tumor cell clusters at 6 hours after i.v. injection.
  • Treatment for 7 days with AG-013736, a potent inhibitor of VEGF signaling, reduced the tumor vascularity by 86%.
  • The overall area density of extravasated IgG/antibodies decreased after treatment but the change was less than the reduction in vascularity and actually increased when expressed per surviving tumor vessel.
  • Accumulation of anti-E-cadherin antibody in tumor cell clusters was similarly affected.
  • The patchy pattern of antibodies in stroma after treatment qualitatively resembled untreated tumors and surprisingly coincided with sleeves of basement membrane left behind after pruning of tumor vessels.
  • Together, the findings suggest that antibody transport increases from surviving tumor vessels after normalization by inhibition of VEGF signaling.
  • Antibodies preferentially distribute to tumor stroma but also accumulate on tumor cells if binding sites are accessible.
  • [MeSH-major] Adenoma, Islet Cell / blood supply. Adenoma, Islet Cell / immunology. Antibodies, Neoplasm / metabolism. Carcinoma, Lewis Lung / blood supply. Carcinoma, Lewis Lung / immunology. Immunoglobulin G / metabolism. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 16452199.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL 59157; United States / NHLBI NIH HHS / HL / P01 HL024136; United States / NCI NIH HHS / CA / P50 CA 90270; United States / NHLBI NIH HHS / HL / HL 24136; United States / NCI NIH HHS / CA / CA 82923
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Cadherins; 0 / Imidazoles; 0 / Immunoglobulin G; 0 / Indazoles; 0 / Vascular Endothelial Growth Factor A; 9001-31-4 / Fibrin; C9LVQ0YUXG / axitinib
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88. Sobczak I, Galabova-Kovacs G, Sadzak I, Kren A, Christofori G, Baccarini M: B-Raf is required for ERK activation and tumor progression in a mouse model of pancreatic beta-cell carcinogenesis. Oncogene; 2008 Aug 14;27(35):4779-87
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  • [Title] B-Raf is required for ERK activation and tumor progression in a mouse model of pancreatic beta-cell carcinogenesis.
  • The extracellular signal-regulated kinase (ERK) pathway is required for the proliferation of cancer cell lines harboring activating BRAF or, to a lesser extent, activating RAS mutations.
  • It is still unclear, however, whether the pathway is required in vivo for tumor development, particularly in tumors in which B-Raf is not mutationally activated.
  • To address the question of whether B-Raf contributed to tumor angiogenesis in vivo we conditionally ablated B-Raf in a model of pancreatic islet carcinoma driven by the functional inactivation of tumor suppressors (RIP1Tag2), which critically depends on angiogenesis for growth.
  • We find that B-Raf is dispensable for the proliferation of tumor cells in culture, but necessary for ERK activation and for the expression of angiogenic factors by tumor cells in vivo and in vitro.
  • The progression from adenoma to carcinoma is also significantly impaired.
  • Thus, endogenous B-Raf contributes to the development of RIP1Tag2 tumors by supporting the stromal response and tumor progression.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Extracellular Signal-Regulated MAP Kinases / metabolism. Islets of Langerhans / pathology. Pancreatic Neoplasms / pathology. Proto-Oncogene Proteins B-raf / physiology
  • [MeSH-minor] Animals. Base Sequence. DNA Primers. Disease Models, Animal. Disease Progression. Enzyme Activation. Immunohistochemistry. Mice. Mice, Knockout. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor beta / metabolism. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism


89. Sakurai A, Katai M, Yamashita K, Mori J, Fukushima Y, Hashizume K: Long-term follow-up of patients with multiple endocrine neoplasia type 1. Endocr J; 2007 Apr;54(2):295-302
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  • [Title] Long-term follow-up of patients with multiple endocrine neoplasia type 1.
  • Whether early surgical treatment of non-functioning pancreas islet cell tumor (NFPT) provides a favorable quality of life and life expectancy in patients with multiple endocrine neoplasia type 1 (MEN1) remains controversial.
  • [MeSH-major] Adenoma, Islet Cell / etiology. Adenoma, Islet Cell / surgery. Multiple Endocrine Neoplasia Type 1 / complications. Pancreatic Neoplasms / etiology. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adult. Asian Continental Ancestry Group. Diabetes Mellitus / etiology. Disease Progression. Female. Follow-Up Studies. Glucose Intolerance / etiology. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasms, Second Primary / radiography. Pancreas / physiopathology. Pancreatectomy / adverse effects. Pancreatectomy / methods. Tomography, X-Ray Computed


90. Chen M, Rahman L, Voeller D, Kastanos E, Yang SX, Feigenbaum L, Allegra C, Kaye FJ, Steeg P, Zajac-Kaye M: Transgenic expression of human thymidylate synthase accelerates the development of hyperplasia and tumors in the endocrine pancreas. Oncogene; 2007 Jul 19;26(33):4817-24
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  • [Title] Transgenic expression of human thymidylate synthase accelerates the development of hyperplasia and tumors in the endocrine pancreas.
  • In addition, TS gene expression has been linked with cell-cycle regulation and cell proliferation through the ability of retinoblastoma protein to repress the transcriptional activation of E2F target genes such as TS.
  • To investigate the role of deregulated TS activity in tumor development, we generated transgenic mice that express high levels of catalytically active human TS (hTS) exclusively in the pancreas and low levels of hTS in multiple other tissues.
  • Analyses of pancreatic tissue in TS transgenic mice revealed abnormalities within the endocrine pancreas, ranging from pancreatic islet hyperplasia to the detection of islet cell tumors.
  • Overexpression of hTS in murine islets provides a new model to study genetic alterations associated with the progression from normal cells to hyperplasia to islet cell tumors, and suggests that this mouse model may be useful for regulating TS activity in vivo for development of cancer prevention and new therapies.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Islets of Langerhans / pathology. Pancreatic Neoplasms / pathology. Thymidylate Synthase / metabolism

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  • (PMID = 17297449.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.1.1.45 / Thymidylate Synthase
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91. Kapran Y, Bauersfeld J, Anlauf M, Sipos B, Klöppel G: Multihormonality and entrapment of islets in pancreatic endocrine tumors. Virchows Arch; 2006 Apr;448(4):394-8
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  • [Title] Multihormonality and entrapment of islets in pancreatic endocrine tumors.
  • We analyzed pancreatic endocrine tumors (PETs) from 200 patients for the incidence of multihormonality and entrapped islets and correlated the results with clinicopathological features.
  • Classified according to the WHO classification, there were 32 well-differentiated benign PETs, 85 well-differentiated PETs with uncertain behavior, and 83 well-differentiated malignant PETs.
  • All tumors were immunostained for pancreatic hormones (insulin, glucagon, somatostatin, and pancreatic polypeptide) and for additional hormones such as gastrin, vasoactive intestinal polypeptide, calcitonin, seratonin, and adrenocorticotropic hormone.
  • Multihormonality was found in 34% of all PETs and it was a frequent finding in the tumors of the uncertain behavior (38.8%) group.
  • Islet entrapment was found in 57 tumors (28.5%) and was significantly more frequent in PETs with uncertain and malignant behavior than benign ones (p=0.01).
  • In 57 cases, we also investigated whether ductule entrapment accompanied islet entrapment.
  • Ductule entrapment did not show significant correlation with malignancy and was a more frequent finding in nonfunctioning tumors.
  • We conclude that the incidence of multihormonality in PETs is not as high as suggested previously and islet entrapping may reflect aggressive tumor growth and may be a complementary criterion for predicting the biological behavior of PETs.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / pathology. Islets of Langerhans / pathology. Pancreatic Hormones / metabolism. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cell Count. Child. Child, Preschool. Female. Humans. Male. Middle Aged

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  • [Cites] Semin Diagn Pathol. 2000 May;17(2):104-8 [10839610.001]
  • [Cites] Pathol Res Pract. 1992 Feb;188(1-2):191-8 [1317556.001]
  • [Cites] Cancer. 1985 Sep 15;56(6):1420-9 [2992737.001]
  • [Cites] Semin Diagn Pathol. 1984 Nov;1(4):285-96 [6100974.001]
  • [Cites] Cancer. 1982 Mar 1;49(5):908-15 [6277456.001]
  • [Cites] Virchows Arch. 1996 Dec;429(6):323-33 [8982376.001]
  • [Cites] Am J Surg Pathol. 2004 Jun;28(6):813-20 [15166675.001]
  • [Cites] Virchows Arch. 2003 Mar;442(3):258-65 [12647216.001]
  • [Cites] Am J Surg Pathol. 2003 Apr;27(4):461-8 [12657930.001]
  • [Cites] Hum Pathol. 1996 Nov;27(11):1124-34 [8912819.001]
  • [Cites] Hum Pathol. 1982 Mar;13(3):263-71 [7076209.001]
  • [Cites] Am J Surg Pathol. 1996 Nov;20(11):1378-84 [8898842.001]
  • [Cites] Virchows Arch. 2004 Sep;445(3):231-5 [15517367.001]
  • [Cites] Surg Today. 1992;22(4):305-12 [1392340.001]
  • [Cites] Histopathology. 1978 Nov;2(6):389-99 [215502.001]
  • [Cites] Am J Surg Pathol. 1982 Jul;6(5):387-99 [6127037.001]
  • [Cites] Histopathology. 2002 Aug;41(2):122-6 [12147089.001]
  • [Cites] Am J Pathol. 1975 May;79(2):271-84 [167586.001]
  • [Cites] Virchows Arch. 2003 May;442(5):444-52 [12692724.001]
  • (PMID = 16418841.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Pancreatic Hormones
  •  go-up   go-down


92. Evert M, Schildhaus HU, Schneider-Stock R, Dombrowski F: Cystic cholangiomas after transplantation of pancreatic islets into the livers of diabetic rats. Virchows Arch; 2006 Jun;448(6):776-87
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  • [Title] Cystic cholangiomas after transplantation of pancreatic islets into the livers of diabetic rats.
  • Islet transplantation is increasingly used as a therapy for human type 1 diabetes mellitus.
  • In our study, we investigated the effect of the transplantation of a low number (n = 350) of pancreatic islets into the right liver part on the neighboring portal bile ducts.
  • A few days after low-number islet transplantation, cholangiocytes adjacent to the grafts showed an increase in proliferative activity.
  • During the next 12-24 months, many peri-insular ductules progressed via tumor-like cystic lesions to large cystic cholangiomas, accompanied by a translocation of the insulin receptor into the cytoplasm and an increase in expression of insulin-related signaling proteins (Insulin-receptor-substrate-1, Raf-1, Mek-1).
  • After 24 months, 53% of rats with low-number transplantation exhibited at least one cholangioma >10 mm, significantly outnumbering tumor development in the transplant-free left liver part and in any control group.
  • A graft cell origin of the tumors was excluded by Y chromosome in situ hybridization in cross-gender transplantations.
  • Conclusively, low-number intrahepatic islet transplantation, most likely acting by permanent local hyperinsulinism, leads to prolonged cholangiocellular proliferation in streptozotocin- and in autoimmune-diabetic rats, resulting in the development of benign cystic cholangiomas.
  • [MeSH-major] Adenoma, Bile Duct / etiology. Bile Duct Neoplasms / etiology. Bile Ducts, Intrahepatic / pathology. Diabetes Mellitus, Experimental / complications. Diabetes Mellitus, Type 1 / complications. Islets of Langerhans Transplantation / adverse effects
  • [MeSH-minor] Animals. Blood Glucose / analysis. Body Weight. Cell Proliferation. Female. Fluorescent Antibody Technique, Indirect. Immunoenzyme Techniques. Liver / pathology. Liver / surgery. Male. Rats. Rats, Inbred BB. Rats, Inbred Lew

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  • [Cites] J Neurocytol. 1997 Apr;26(4):191-206 [9192286.001]
  • [Cites] Pathol Res Pract. 2003;199(6):373-9 [12924437.001]
  • [Cites] Prog Liver Dis. 1996;14:161-97 [9055578.001]
  • [Cites] Am J Pathol. 1989 May;134(5):1069-86 [2470253.001]
  • [Cites] Diabetes. 2001 Apr;50(4):710-9 [11289033.001]
  • [Cites] Transplantation. 1977 Aug;24(2):152-4 [143091.001]
  • [Cites] Transplantation. 1977 Feb;23(2):182-5 [402048.001]
  • [Cites] Lab Invest. 1994 Nov;71(5):688-99 [7967522.001]
  • [Cites] Hepatology. 1996 Jan;23(1):62-70 [8550050.001]
  • [Cites] Diabetes. 2004 May;53(5):1311-7 [15111501.001]
  • [Cites] J Clin Invest. 2004 Oct;114(7):877-83 [15467822.001]
  • [Cites] J Gastroenterol. 2003;38(3):278-82 [12673452.001]
  • [Cites] Carcinogenesis. 1991 Feb;12(2):225-31 [1704820.001]
  • [Cites] Am J Pathol. 1996 Apr;148(4):1249-56 [8644865.001]
  • [Cites] Am J Pathol. 1997 Mar;150(3):1071-87 [9060843.001]
  • [Cites] Mech Dev. 2003 Jan;120(1):117-30 [12490302.001]
  • [Cites] AJR Am J Roentgenol. 2001 Feb;176(2):471-4 [11159098.001]
  • [Cites] Diabetes. 1977 Mar;26(3):201-14 [402300.001]
  • [Cites] Transplantation. 1994 Aug 15;58(3):349-54 [8053060.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1833-43 [16452245.001]
  • [Cites] Ann Surg. 1995 Oct;222(4):562-75; discussion 575-9 [7574935.001]
  • [Cites] Z Krebsforsch Klin Onkol Cancer Res Clin Oncol. 1976 Dec 9;87(3):239-55 [189519.001]
  • [Cites] J Hepatol. 1998 Apr;28(4):709-16 [9566841.001]
  • [Cites] Hepatology. 2004 Jun;39(6):1499-507 [15185290.001]
  • [Cites] Transplant Proc. 2004 May;36(4):1111-6 [15194387.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 1998 Oct;34(9):704-10 [9794222.001]
  • [Cites] Diabetes. 1996 Aug;45(8):1108-14 [8690159.001]
  • [Cites] Hepatology. 1999 May;29(5):1453-62 [10216129.001]
  • [Cites] Stain Technol. 1960 Nov;35:313-23 [13741297.001]
  • [Cites] Am J Pathol. 1997 Jun;150(6):2167-80 [9176407.001]
  • [Cites] Cell Biol Toxicol. 2004 Mar;20(2):83-96 [15242184.001]
  • [Cites] N Engl J Med. 2000 Jul 27;343(4):230-8 [10911004.001]
  • [Cites] Cancer Res. 2005 Aug 1;65(15):7013-22 [16061688.001]
  • [Cites] Lab Invest. 2005 Jan;85(1):99-108 [15543204.001]
  • [Cites] Am J Pathol. 1998 Apr;152(4):1025-38 [9546363.001]
  • [Cites] Biochem Biophys Res Commun. 1988 Oct 14;156(1):131-6 [3178826.001]
  • [Cites] Lab Invest. 2000 Sep;80(9):1399-411 [11005208.001]
  • [Cites] Cytogenet Cell Genet. 1995;69(3-4):246-52 [7698023.001]
  • [Cites] Nat Rev Immunol. 2004 Apr;4(4):259-68 [15057784.001]
  • [Cites] Toxicol Pathol. 1991;19(4 Pt 2):561-70 [1668599.001]
  • [Cites] Diabetes Metab Rev. 1987 Jul;3(3):725-50 [3301238.001]
  • [Cites] Am J Pathol. 1999 Mar;154(3):683-91 [10079246.001]
  • [Cites] Diabetes. 2002 Jul;51(7):2148-57 [12086945.001]
  • [Cites] Jikken Dobutsu. 1983 Apr;32(2):77-84 [6225653.001]
  • [Cites] J Clin Invest. 1986 Nov;78(5):1339-48 [3095376.001]
  • [Cites] Gastroenterology. 2004 Oct;127(4):1198-209 [15480997.001]
  • [Cites] Cancer Res. 1991 May 15;51(10):2611-20 [1708696.001]
  • [Cites] FASEB J. 1999 Jul;13(10):1195-205 [10385610.001]
  • [Cites] Z Krebsforsch Klin Onkol Cancer Res Clin Oncol. 1971;76(3):193-215 [4330373.001]
  • [Cites] J Clin Invest. 1992 Oct;90(4):1284-9 [1401065.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2003 Jul;285(1):G31-6 [12606307.001]
  • [Cites] Cancer Res. 2004 Nov 1;64(21):8093-100 [15520221.001]
  • [Cites] Cancer. 1981 Jun 15;47(12):2936-40 [7260880.001]
  • [Cites] Hepatology. 1996 Jan;23(1):71-9 [8550051.001]
  • [Cites] Autoimmunity. 1993;15(2):107-12 [8218836.001]
  • [Cites] Transplantation. 1979 Jan;27(1):71-3 [155910.001]
  • (PMID = 16601979.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Blood Glucose
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93. Ishikawa T, Itoh A, Kawashima H, Ohno E, Matsubara H, Itoh Y, Nakamura Y, Nakamura M, Miyahara R, Hayashi K, Ishigami M, Katano Y, Ohmiya N, Goto H, Hirooka Y: Usefulness of EUS combined with contrast-enhancement in the differential diagnosis of malignant versus benign and preoperative localization of pancreatic endocrine tumors. Gastrointest Endosc; 2010 May;71(6):951-9
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  • [Title] Usefulness of EUS combined with contrast-enhancement in the differential diagnosis of malignant versus benign and preoperative localization of pancreatic endocrine tumors.
  • BACKGROUND: Pancreatic endocrine tumors (PETs) develop in relatively few patients, but they are often difficult to diagnose because of their small size and various clinical symptoms.
  • OBJECTIVE: The aim of this study was to investigate the usefulness of EUS combined with contrast enhancement (CE-EUS) in the preoperative localization of PETs and the differentiation between malignant and benign PETs.
  • [MeSH-major] Pancreas / ultrasonography. Pancreatic Neoplasms / ultrasonography
  • [MeSH-minor] Adenoma, Islet Cell / pathology. Adenoma, Islet Cell / ultrasonography. Adult. Aged. Carcinoma, Islet Cell / pathology. Carcinoma, Islet Cell / ultrasonography. Contrast Media. Diagnosis, Differential. Endosonography. Female. Humans. Male. Middle Aged. Neuroendocrine Tumors / pathology. Neuroendocrine Tumors / ultrasonography. Retrospective Studies. Young Adult

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  • [Copyright] 2010 American Society for Gastrointestinal Endoscopy. Published by Mosby, Inc. All rights reserved.
  • (PMID = 20438884.001).
  • [ISSN] 1097-6779
  • [Journal-full-title] Gastrointestinal endoscopy
  • [ISO-abbreviation] Gastrointest. Endosc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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94. La Rosa S, Klersy C, Uccella S, Dainese L, Albarello L, Sonzogni A, Doglioni C, Capella C, Solcia E: Improved histologic and clinicopathologic criteria for prognostic evaluation of pancreatic endocrine tumors. Hum Pathol; 2009 Jan;40(1):30-40
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  • [Title] Improved histologic and clinicopathologic criteria for prognostic evaluation of pancreatic endocrine tumors.
  • Currently used histopathologic criteria for the diagnosis of pancreatic endocrine tumors are still under discussion as far as to their capacity to identify prognostically different tumor subsets, which are potentially helpful for patient management.
  • One hundred fifty-five pancreatic endocrine tumors encompassing all the main histologic types and stages, operated with intention to cure and then followed up for a median 126 months, were carefully investigated histologically to identify prognostically informative parameters at univariable, bivariable, and multivariable analysis.
  • Ki67 index, mitotic rate, neuroinvasion with or without vascular, peritumoral or stromal infiltrative patterns, as well as tumor size, and association with endocrine syndromes other than insulinoma proved effective in predicting recurrence and disease-specific death among well-differentiated tumors.
  • The TNM system proved to be highly predictive of patient outcome and easy to combine with histologic and clinicopathologic parameters to classify pancreatic endocrine tumors into groups of increasing malignant potential.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / metabolism. Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / metabolism. Carcinoma, Islet Cell / pathology. Carcinoma, Pancreatic Ductal / diagnosis. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / pathology. Humans. Insulinoma / diagnosis. Insulinoma / metabolism. Insulinoma / pathology. Ki-67 Antigen / analysis. Mitotic Index. Necrosis / pathology. Neoplasm Invasiveness. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Rate. Tumor Burden

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  • (PMID = 18715612.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
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95. Yamaguchi T, Takahashi H, Kagawa R, Takeda R, Sakata S, Yamamoto M, Iwasa Y: Nonfunctioning pancreatic endocrine tumor presenting with hemorrhage from isolated gastric varices. Am Surg; 2005 Dec;71(12):1027-30
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  • [Title] Nonfunctioning pancreatic endocrine tumor presenting with hemorrhage from isolated gastric varices.
  • Hemorrhage from gastric varices due to left-sided portal hypertension is an unusual presentation for pancreatic endocrine tumor.
  • A case of pancreatic endocrine tumor presenting with gastric variceal hemorrhage secondary to left-sided portal hypertension associated with splenic vein occlusion is presented.
  • Surveys to identify the cause of gastric varices by an abdominal CT, MRCP, and abdominal angiography revealed splenic vein occlusion secondarily attributed to the pancreatic tail tumor and splenomegaly.
  • The pancreatic tumor was suspected to be a resectable endocrine tumor.
  • By the histological examination, the diagnosis of nonfunctioning pancreatic endocrine tumor with malignant potential was determined.
  • In this case, the unusual presentation for pancreatic endocrine tumors such as a gastric variceal hemorrhage had an advantage that led to early presentation prior to the development of metastases with possible curative surgery.
  • [MeSH-major] Adenoma, Islet Cell / diagnosis. Esophageal and Gastric Varices / diagnosis. Gastrointestinal Hemorrhage / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 16447473.001).
  • [ISSN] 0003-1348
  • [Journal-full-title] The American surgeon
  • [ISO-abbreviation] Am Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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96. Rothenstein J, Cleary SP, Pond GR, Dale D, Gallinger S, Moore MJ, Brierley J, Siu LL: Neuroendocrine tumors of the gastrointestinal tract: a decade of experience at the Princess Margaret Hospital. Am J Clin Oncol; 2008 Feb;31(1):64-70
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  • Pathological distribution demonstrated that 72% were NET/carcinoids, 21% were islet cell tumors, and 6% were small cell carcinomas.
  • At presentation, 53% of patients had distant metastases and 46% had loco-regional disease.
  • [MeSH-major] Adenoma, Islet Cell / therapy. Carcinoid Tumor / therapy. Carcinoma, Small Cell / therapy. Gastrointestinal Neoplasms / therapy. Neuroendocrine Tumors / therapy

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  • (PMID = 18376230.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
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97. Frankel WL: Update on pancreatic endocrine tumors. Arch Pathol Lab Med; 2006 Jul;130(7):963-6
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  • [Title] Update on pancreatic endocrine tumors.
  • Endocrine tumors of the pancreas represent 1% to 2% of all pancreatic neoplasms.
  • The morphologic spectrum of these tumors can be variable, and the differential diagnosis includes chronic pancreatitis with neuroendocrine hyperplasia, ductal adenocarcinoma, solid pseudopapillary tumor, acinar cell carcinoma, and pancreatoblastoma.
  • It is important to be aware that unusual morphologic variants of pancreatic endocrine tumors are common, and immunohistochemical stains can help avoid misdiagnosis.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Carcinoma, Acinar Cell / diagnosis. Carcinoma, Pancreatic Ductal / diagnosis. Carcinoma, Papillary / diagnosis. Diagnosis, Differential. Humans. Islets of Langerhans / pathology. Neoplasms, Germ Cell and Embryonal / diagnosis. Pancreatitis, Chronic / diagnosis. Prognosis

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
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  • (PMID = 16831051.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 26
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98. Christante D, Pommier S, Givi B, Pommier R: Hepatic artery chemoinfusion with chemoembolization for neuroendocrine cancer with progressive hepatic metastases despite octreotide therapy. Surgery; 2008 Dec;144(6):885-93; discussion 893-4
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  • METHODS: Patients with neuroendocrine cancer and diffuse hepatic metastases were treated with hepatic artery chemoinfusion and chemoembolization when they demonstrated disease progression despite octreotide therapy.
  • The overall response rate was 80% for patients with carcinoid or islet cell neoplasms.
  • Median disease-specific survival was 39 months from the first treatment; 1- and 5-year survival rates were 78% and 27%, respectively.
  • CONCLUSION: Survival after initiating this regimen was over 3 years for the majority of patients exhibiting progression of extensive, unresectable hepatic disease despite octreotide therapy.
  • [MeSH-minor] Adenoma, Islet Cell / drug therapy. Adult. Aged. Carcinoid Tumor / drug therapy. Carcinoid Tumor / secondary. Chemoembolization, Therapeutic. Digestive System Neoplasms / pathology. Disease Progression. Female. Hepatic Artery. Humans. Infusions, Intra-Arterial. Male. Middle Aged. Retrospective Studies. Survival Analysis. Young Adult

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  • [CommentIn] Surgery. 2008 Dec;144(6):895-8 [19040994.001]
  • (PMID = 19040993.001).
  • [ISSN] 1532-7361
  • [Journal-full-title] Surgery
  • [ISO-abbreviation] Surgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; RWM8CCW8GP / Octreotide; U3P01618RT / Fluorouracil
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99. Deng H, Shi J, Wilkerson M, Meschter S, Dupree W, Lin F: Usefulness of S100P in diagnosis of adenocarcinoma of pancreas on fine-needle aspiration biopsy specimens. Am J Clin Pathol; 2008 Jan;129(1):81-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Even though the cytologic criteria for pancreatic ductal adenocarcinoma (PDA) on fine-needle aspiration biopsy (FNAB) specimens have been well defined, a diagnostic challenge is still present.
  • We immunohistochemically evaluated the diagnostic value of S100P on cell-block and/or smear preparations in 58 cases of FNAB specimens of the pancreas.
  • The 58 cases were divided into 4 groups: 1, 32 cases of PDA; 2, 6 cases with an atypical or "suspicious" diagnosis; 3, 14 cases of benign or reactive ductal epithelium; and 4, 6 cases of endocrine tumor.
  • S100P is a sensitive and specific marker for the detection of PDA on FNAB specimens on cell-block and smear preparations.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Pancreatic Ductal / diagnosis. Carrier Proteins / metabolism. Nuclear Proteins / metabolism. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / metabolism. Biopsy, Fine-Needle. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / metabolism. Diagnosis, Differential. Epithelial Cells / metabolism. Epithelial Cells / pathology. Humans. Immunoenzyme Techniques. Islets of Langerhans / metabolism. Islets of Langerhans / pathology. Pancreatic Ducts / metabolism. Pancreatic Ducts / pathology

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  • (PMID = 18089492.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / Nuclear Proteins; 0 / S100PBP protein, human
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100. Namasivayam S, Salman K, Mittal PK, Martin D, Small WC: Hypervascular hepatic focal lesions: spectrum of imaging features. Curr Probl Diagn Radiol; 2007 May-Jun;36(3):107-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Common hypervascular liver lesions include hemangioma, focal nodular hyperplasia, hepatocellular adenoma, hepatocellular carcinoma, fibrolamellar carcinoma, and metastases from primary tumors such as islet cell tumor, carcinoid, renal cell carcinoma, melanoma, and thyroid carcinoma.
  • [MeSH-minor] Adenoma / diagnosis. Hemangioendothelioma / diagnosis. Hemangioma. Humans. Liver / blood supply. Liver Cirrhosis / diagnosis. Melanoma / diagnosis. Melanoma / pathology. Melanoma / secondary. Necrosis. Neoplasm Invasiveness. Portal Vein / pathology

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  • (PMID = 17484954.001).
  • [ISSN] 0363-0188
  • [Journal-full-title] Current problems in diagnostic radiology
  • [ISO-abbreviation] Curr Probl Diagn Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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