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1. Ueda J, Nakamura Y, Aimoto T, Hiroi M, Cho K, Yamahatsu K, Kawamoto M, Uchida E: Laparoscopic distal pancreatectomy preserving spleen and splenic vessels for pancreatic insulinoma. J Nippon Med Sch; 2010 Jun;77(3):175-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Laparoscopic distal pancreatectomy preserving spleen and splenic vessels for pancreatic insulinoma.
  • We describe a 43-year-old woman who underwent laparoscopic distal pancreatectomy preserving the spleen and splenic vessels for the treatment of insulinoma in the pancreatic body.
  • The patient experienced cold sweats on fasting, received diagnosis of insulinoma, and was referred to our hospital for laparoscopic surgery.
  • Blood biochemistry studies showed low fasting blood glucose of 42 mg/dL, serial immunoreactive insulin of 15.2 microU/mL, and a Fajans index (immunoreactive insulin/blood glucose) of 0.36 (normal <0.30).
  • Contrast-enhanced early-phase computed tomography of the abdomen showed a circular, intensely stained, 1.6-cm-diameter tumor in the pancreatic body close to the main pancreatic duct.
  • A solitary insulinoma of the pancreatic body was diagnosed on the basis of the result of hematologic studies, and diagnostic imaging results.
  • Because of the location of the tumor, we elected to perform distal pancreatectomy preserving the spleen and splenic vessels, rather than enucleation.
  • Insulin and blood glucose levels were monitored during surgery.
  • Before removal of the tumor, insulin levels remained consistently high, never decreasing to less than 10 microU/mL.
  • After surgery, insulin levels decreased rapidly, to less than 5 microU/mL within 30 minutes and subsequently remained at the new low level, leading us to conclude that the entire tumor had been removed.
  • [MeSH-major] Insulinoma / diagnosis. Insulinoma / surgery. Laparoscopy / methods. Pancreatectomy / methods. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery. Spleen / surgery
  • [MeSH-minor] Adult. Blood Glucose / metabolism. Female. Humans. Insulin / blood. Splenic Artery / surgery. Splenic Vein / surgery. Tomography, X-Ray Computed / methods. Treatment Outcome

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  • (PMID = 20610903.001).
  • [ISSN] 1345-4676
  • [Journal-full-title] Journal of Nippon Medical School = Nippon Ika Daigaku zasshi
  • [ISO-abbreviation] J Nippon Med Sch
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin
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2. Xue HD, Jin ZY, Liu W, Wang Y, Zhao WM: [Perfusion characteristics of normal pancreas and insulinoma on multi-slice spiral CT]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao; 2006 Feb;28(1):68-70
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  • [Title] [Perfusion characteristics of normal pancreas and insulinoma on multi-slice spiral CT].
  • OBJECTIVE: To investigate the perfusion characteristics of normal pancreas and insulinoma on multi-slice spiral CT (MSCT).
  • METHODS: Totally 21 subjects with suspected insulinoma were enrolled.
  • Perfusion characteristics, including blood flow (BF), patlak blood volume (pBV), time to peak (TTP), permeability, and peak enhancement (PE) of insulinomas and normal pancreas parenchyma were analyzed based on the MSCT data sets subsequently.
  • RESULTS: Benign insulinoma was pathologically confirmed in 12 out of the 21 subjects, while the remaining 9 subjects were normal.
  • In both normal and tumor-suffered subjects (n = 19), perfusion parameters of normal pancreatic parachyma were measured as follows: BF (p) = 104.
  • In subjects with insulinoma (n = 11), perfusion parameters of tumor tissue were measured as follows: F (i) = 206.5 +/- 42.2, BV (i) = 315.9 +/- 79.0, TFP (i) = 123.2 +/- 18.8, Permeability (i) = 102.5 +/- 54.
  • Results of F, BV, and peak enhancement in these two kinds of tissue showed significant differences (P < 0.01), while there were no significant difference (P > 0.05) in TTP and permeability between normal pancreatic parenchyma and insulinoma.
  • CONCLUSIONS: Benign insulinoma has perfusion characteristics of increased blood flow and blood volume, but its TTP is consistent with normal pancreas and has normal permeability.
  • MSCT allows further understanding of the blood flow of the normal pancreas and its benign tumor insulinoma.
  • [MeSH-major] Insulinoma / radiography. Pancreas / radiography. Pancreatic Neoplasms / radiography. Tomography, Spiral Computed / methods

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  • (PMID = 16548193.001).
  • [ISSN] 1000-503X
  • [Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae
  • [ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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3. Priego P, Sanjuanbenito A, Martínez Molina E, Lobo E, García Teruel D, Morales V, Rodríguez G, Fresneda V: [Diagnosis and treatment of pancreatic insulinoma]. Rev Esp Enferm Dig; 2007 Apr;99(4):218-22
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  • [Title] [Diagnosis and treatment of pancreatic insulinoma].
  • [Transliterated title] Manejo diagnóstico y terapéutico del insulinoma pancreático.
  • INTRODUCTION: insulinoma is the most frequent pancreatic endocrine tumor.
  • The aim of this study was to evaluate the experience in the management and treatment of this kind of tumor at Hospital Ramón y Cajal.
  • MATERIAL AND METHODS: between January 1999 and July 2006, 12 patients were operated on in our hospital (9 females and 3 males) who had been diagnosed with insulinoma, with a mean age of 56 years (16-72 years).
  • Intraoperative ultrasonography confirmed the presence of an insulinoma in 100% of cases.
  • Two patients developed a pancreatic fistula, and one a pancreatic pseudocyst that healed spontaneously without surgery.
  • However, the initial procedure of choice would be pancreas palpation and intraoperative ultrasonography.
  • Surgery cured 100% of cases, and the procedure selected depends on size, location, distance from the main pancreatic duct, and relation to multiple endocrine neoplasm 1 (MEN-1).
  • [MeSH-major] Insulinoma / diagnosis. Insulinoma / surgery. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery

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  • (PMID = 17590104.001).
  • [ISSN] 1130-0108
  • [Journal-full-title] Revista española de enfermedades digestivas : organo oficial de la Sociedad Española de Patología Digestiva
  • [ISO-abbreviation] Rev Esp Enferm Dig
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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4. Berrospi Espinoza F, Celis Zapata J, Ruiz Figueroa E, Chavez Passiuri I, Reaño G: [Localization of pancreatic insulinoma with ultrasonography laparoscopy]. Rev Gastroenterol Peru; 2007 Jan-Mar;27(1):91-4
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  • [Title] [Localization of pancreatic insulinoma with ultrasonography laparoscopy].
  • [Transliterated title] Localización de insulinoma pancreático con ultrasonografía laparoscópica.
  • The case of a 51-year-old woman with a clinical history of hipoglicemia caused by a presumed pancreatic insulinoma is reported.
  • Laboratory tests pointed out for a insulinoma, but imaginologic studies could not locate the tumor.
  • By means of the ultrasonography device the tumor was located at the uncinate process of the pancreas and, eventually treated by laparoscopic enucleation.
  • [MeSH-major] Insulinoma / diagnosis. Laparoscopy / methods. Pancreatic Neoplasms / diagnosis. Ultrasonography, Interventional

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  • (PMID = 17431441.001).
  • [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] Case Reports; English Abstract; Journal Article
  • [Publication-country] Peru
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5. Mai W, Cáceres AV: Dual-phase computed tomographic angiography in three dogs with pancreatic insulinoma. Vet Radiol Ultrasound; 2008 Mar-Apr;49(2):141-8
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  • [Title] Dual-phase computed tomographic angiography in three dogs with pancreatic insulinoma.
  • This article describes the findings in three dogs with histopathologically confirmed pancreatic insulinoma using dual-phase computed tomographic angiography (CTA).
  • In all three dogs, dual-phase CTA findings identified lesions not seen on ultrasonography, including the actual identification of the primary pancreatic neoplasm in two dogs.
  • In two dogs, the insulinomas were found to have a strong enhancement during the arterial phase of the study but not at the other phases, which stresses the importance of dual-phase computed tomography for the diagnosis of this type of pancreatic neoplasia, in agreement with current knowledge in humans.
  • [MeSH-major] Dog Diseases / diagnosis. Insulinoma / veterinary. Pancreatic Neoplasms / veterinary. Tomography, X-Ray Computed

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  • (PMID = 18418994.001).
  • [ISSN] 1058-8183
  • [Journal-full-title] Veterinary radiology & ultrasound : the official journal of the American College of Veterinary Radiology and the International Veterinary Radiology Association
  • [ISO-abbreviation] Vet Radiol Ultrasound
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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6. Aoki T, Hui H, Umehara Y, Licalzi S, Demetriou AA, Rozga J, Perfetti R: Intrasplenic Transplantation of Encapsulated Genetically Engineered Mouse Insulinoma Cells Reverses Streptozotocin-Induced Diabetes in Rats. Cell Transplant; 2005 Jul;14(6):411-421

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  • [Title] Intrasplenic Transplantation of Encapsulated Genetically Engineered Mouse Insulinoma Cells Reverses Streptozotocin-Induced Diabetes in Rats.
  • Pancreatic islet transplantation is limited by shortage of donor organs.
  • Although β-cell lines could be used, their secretion of insulin is characteristically glucose independent and immunoisolation is required.
  • Here we show that intrasplenic transplantation of encapsulated glucose-responsive mouse insulinoma cells reversed streptozotocin (STZ)-induced diabetes in rats.
  • MIN-6 cells derived from a transgenic mouse expressing SV 40 large T antigen in pancreatic β-cells were transfected with minigene encoding for human glucagon-like-peptide-1 under the control of rat insulin promoter.
  • The cells were encapsulated in alginate/poly-L-lysine and used for cell transplantation in STZ-diabetic rats.
  • In group I rats (n = 6) 20 million encapsulated cells were injected into the spleen.
  • Plasma insulin level was measured every other week (RIA).
  • In rats transplanted with cells the n-FBG was 100-150 mg/dl until the end of the study.
  • After splenectomy, all cell recipients became diabetic (glucose 400 ± 20 mg/dl).
  • Transplanted rats showed increase in body weight and insulin production (3.3 ± 1.0 ng/ml versus 0.92 ± 0.3 ng/ml; p < 0.01) and had normal IPGTT.
  • Spleens contained capsules with insulin-positive cells.
  • Overall, data from this work indicate that intrasplenic transplantation of xenogeneic encapsulated insulin-producing cells without immunosuppression reversed diabetes in rats.
  • Excellent survival and function of the transplanted cells was due to the fact that the cells were separated from the bloodstream by the immunoisolatory membrane only and insulin was delivered directly to the liver (i.e., in a physiological manner).

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  • (PMID = 28876105.001).
  • [ISSN] 1555-3892
  • [Journal-full-title] Cell transplantation
  • [ISO-abbreviation] Cell Transplant
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Diabetes / Encapsulation / Insulin / Insulinoma cells / Pancreatic islets / Streptozotocin / Transplantation technique
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7. Anaye A, Mathieu A, Closset J, Bali MA, Metens T, Matos C: Successful preoperative localization of a small pancreatic insulinoma by diffusion-weighted MRI. JOP; 2009;10(5):528-31
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  • [Title] Successful preoperative localization of a small pancreatic insulinoma by diffusion-weighted MRI.
  • CONTEXT: Insulinoma is the most common functioning endocrine tumor of the pancreas responsible for fasting hypoglycemia resulting from autonomous insulin hypersecretion.
  • Most insulinomas are small and difficult to localize with conventional imaging.
  • We successfully localized a small insulinoma in our patient using diffusion-weighted magnetic resonance imaging before surgery.
  • CASE REPORT: We report the case of a female patient with a clinical suspicion of insulinoma.
  • A preoperative MR with diffusion-weighted imaging was performed and localized a small nodule in the pancreatic tail.
  • Histologic examination identified a neuroendocrine tumor compatible with an insulinoma.
  • CONCLUSION: Diffusion-weighted imaging can be useful in detecting and localizing small insulinomas, especially for those with no hypervascular pattern.
  • [MeSH-major] Diffusion Magnetic Resonance Imaging. Insulinoma / radiography. Pancreatic Neoplasms / radiography

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  • (PMID = 19734630.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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8. Gupta S, McGrath B, Cavener DR: PERK regulates the proliferation and development of insulin-secreting beta-cell tumors in the endocrine pancreas of mice. PLoS One; 2009 Nov 24;4(11):e8008
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  • [Title] PERK regulates the proliferation and development of insulin-secreting beta-cell tumors in the endocrine pancreas of mice.
  • BACKGROUND: PERK eIF2alpha kinase is required for the proliferation of the insulin-secreting beta- cells as well as insulin synthesis and secretion.
  • In addition, PERK signaling has been found to be an important factor in determining growth and angiogenesis of specific types of tumors, and was attributed to PERK-dependent regulation of the hypoxic stress response.
  • In this report we examine the role of PERK in regulating proliferation and angiogenesis of transformed beta-cells in the development of insulinomas.
  • METHODOLOGY: The SV40 Large T-antigen (Tag) was genetically introduced into the insulin secreting beta-cells of Perk KO mice under the control of an inducible promoter.
  • Tumor growth and the related parameters of cell proliferation were measured.
  • In late stage insulinomas the degree of vascularity was determined.
  • PRINCIPAL FINDINGS: The formation and growth of insulinomas in Perk-deficient mice was dramatically ablated with much fewer tumors, which averaged 38-fold smaller than seen in wild-type control mice.
  • Beta-cell proliferation was ablated in Perk-deficient mice associated with reduced tumor growth.
  • In the small number of large encapsulated insulinomas that developed in Perk-deficient mice, we found a dramatic reduction in tumor vascularity compared to similar sized insulinomas in wild-type mice.
  • Although insulinoma growth in Perk-deficient mice was largely impaired, beta-cell mass was increased sufficiently by T-antigen induction to rescue the hypoinsulinemia and diabetes in these mice.
  • CONCLUSIONS: We conclude that PERK has two roles in the development of beta-cell insulinomas, first to support rapid cell proliferation during the initial transition to islet hyperplasia and later to promote angiogenesis during the progression to late-stage encapsulated tumors.

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  • (PMID = 19956728.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK062049; United States / NIGMS NIH HHS / GM / R01 GM056957; United States / NIDDK NIH HHS / DK / R01-DK062049; United States / NIGMS NIH HHS / GM / R01-GM56957
  • [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 / Antigens, Viral, Tumor; 0 / Blood Glucose; EC 2.7.10.- / PERK kinase; EC 2.7.11.1 / eIF-2 Kinase
  • [Other-IDs] NLM/ PMC2776514
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9. Dai MH, Zhao YP, Liao Q, Liu ZW, Hu Y, Guo JC: [Surgical treatment of pancreatic insulinoma by laparoscopy]. Zhonghua Wai Ke Za Zhi; 2006 Feb 1;44(3):165-8
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  • [Title] [Surgical treatment of pancreatic insulinoma by laparoscopy].
  • OBJECTIVE: To evaluate the safety and outcome of laparoscopic insulinoma resection.
  • METHODS: Twenty-five patients with insulinoma were admitted and divided into two groups: laparoscopic group (10 patients) and laparotomy group (15 patients).
  • All tumors of two groups were located at the body or tail of pancreas preoperatively by abdominal CT and digital subtraction angiography (DSA).
  • There were no differences in preoperative location and size of tumors between two groups.
  • However, one case of pancreatic leakage developed in laparoscopic group, comparably, 3 cases of pancreatic leakage, 2 cases of celiac sepsis and 5 cases of fluid accumulation in thoracic cavity developed in laparotomy group.
  • CONCLUSIONS: Laparoscopic resection of pancreatic insulinoma is safe and feasible for tumors located at the body or tail of the pancreas.
  • Its application for tumors located at the pancreatic head needs further evaluation.
  • [MeSH-major] Insulinoma / surgery. Laparoscopy. Pancreatectomy / methods. Pancreatic Neoplasms / surgery

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  • (PMID = 16635344.001).
  • [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] Comparative Study; English Abstract; Journal Article
  • [Publication-country] China
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10. Owecki M, Czepczyriński R, Biczysko M, Stawny B, Drews M, Sowiński J: [Usefullness of scintigraphy with somatostatin analogues in the imaging of insulinoma of the pancreas]. Pol Merkur Lekarski; 2006 Jan;20(115):77-80
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  • [Title] [Usefullness of scintigraphy with somatostatin analogues in the imaging of insulinoma of the pancreas].
  • [Transliterated title] Przydatność scyntygrafii z uzyciem analogów somatostatyny w obrazowaniu wyspiaka trzustki typu insulinoma.
  • We present a case of a 74-years-old female with insulinoma of the pancreas.
  • The fast was terminated after 5 hours and 40 minutes because of neuroglycopenic symptoms with the serum glucose and insulin levels of 40 mg/dl and 34,01 microU/ml respectively.
  • The tumor was invisible in ultrasound, abdominal CT scan and MRL The only means that enabled preoperative visualization was 111-Indium labeled octreotide scintigraphy (OctreoScan).
  • Laparotomy was performed, and a tumor was disclosed in intraoperative ultrasonography within the head of the pancreas.
  • The tumor of 37 mm diameter was excised.
  • Histopatological examination revealed benign insulinoma.
  • The patient with proper glucose levels and insulin concentration of 3,04 microU/ml was discharged in good health.
  • This case confirms high usefulness of preoperative OctreoScan and intraoperative ultrasonography in the approach to a patient with insulinoma.
  • [MeSH-major] Indium Radioisotopes. Insulinoma / radionuclide imaging. Pancreatic Neoplasms / radionuclide imaging. Radionuclide Imaging. Somatostatin / analogs & derivatives

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  • (PMID = 16617742.001).
  • [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
  • [Chemical-registry-number] 0 / Indium Radioisotopes; 51110-01-1 / Somatostatin; G083B71P98 / pentetreotide
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11. Ungureanu CD, David L, Braşoveanu V, Herlea V, Coculescu M, Popescu I: [Double localization of pancreatic insulinoma. Diagnostic and therapeutic difficulties]. Chirurgia (Bucur); 2005 Sep-Oct;100(5):489-94
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  • [Title] [Double localization of pancreatic insulinoma. Diagnostic and therapeutic difficulties].
  • [Transliterated title] Insulinom pancreatic cu dublă localizare. Dificultăţi de diagnostic si atitudine terapeutică.
  • Insulinomas are the most common cause of hypoglycemia resulting from endogenous hyperinsulinism.
  • Because most of insulinomas are less than 2 cm in size and rarely they not may be visible by CT scan or transabdominal ultrasonography.
  • We report a case of double insulinoma located in the head of the pancreas in which the diagnosis and surgical treatment presented difficulties which determined a particular clinical evolution.
  • [MeSH-major] Insulinoma / diagnosis. Insulinoma / surgery. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery

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  • (PMID = 16372677.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] rum
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Romania
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12. Kuroki T, Tajima Y, Tsutsumi R, Mishima T, Kitasato A, Adachi T, Kanematsu T: Intraoperative pancreatography and gastric-wall-covering method for the prevention of pancreatic leakage after enucleation of insulinoma in the pancreas. J Hepatobiliary Pancreat Surg; 2006;13(4):314-6
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  • [Title] Intraoperative pancreatography and gastric-wall-covering method for the prevention of pancreatic leakage after enucleation of insulinoma in the pancreas.
  • Pancreatic leakage is one of the most common complications following pancreatic surgery.
  • Although several surgical techniques and several devices for the management of pancreatic ducts have been advocated to prevent pancreatic leakage, its incidence is still not acceptable.
  • We report our new surgical technique, a gastric-wall-covering method, for the prevention of pancreatic leakage in the enucleation of insulinoma in the pancreas, along with intraoperative pancreatography for navigation surgery of the pancreatic duct.
  • Our novel techniques help to prevent pancreatic leakage following pancreatic surgery, including partial resection of the pancreas.
  • [MeSH-major] Digestive System Surgical Procedures / methods. Insulinoma / surgery. Pancreatic Neoplasms / surgery. Postoperative Complications / prevention & control. Stomach / surgery
  • [MeSH-minor] Female. Humans. Intraoperative Period. Middle Aged. Pancreatic Ducts / ultrasonography. Suture Techniques

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  • (PMID = 16858542.001).
  • [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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13. Pugliese R, Boniardi M, Sansonna F, Maggioni D, Scandroglio I, Costanzi A, Rapetti R, Oppizzi G, Loli P: [Video-laparoscopic excision of pancreatic insulinoma. Experience with 3 cases]. Chir Ital; 2008 Jan-Feb;60(1):9-13
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  • [Title] [Video-laparoscopic excision of pancreatic insulinoma. Experience with 3 cases].
  • [Transliterated title] Trattamento chirurgico videolaparoscopico dell'insulinoma pancreatico. Esperienza di tre casi.
  • Laparoscopic treatment of lesions of the distal pancreas has gained favour worldwide in the last decade.
  • The objective of this study was to analyze 3 cases of insulinoma successfully treated with the laparoscopic approach.
  • From 2000 to 2007 in our institution 3 patients with insulinoma of the left pancreas were treated with a laparoscopic approach.
  • The insulinoma was diagnosed by helical CT scan, Two cases were treated by left pancreatectomy and one by enucleation.
  • Morbidity consisted in one mild pancreatic fistula after left pancreatectomy that was healed by conservative treatment after 24 days.
  • During the follow-up insulinoma symptoms have disappeared in all patients.
  • This study confirms the feasibility of laparoscopic resection for insulinoma.
  • [MeSH-major] Insulinoma / surgery. Laparoscopy / methods. Pancreatectomy / methods. Pancreatic Neoplasms / surgery. Video-Assisted Surgery / methods

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  • (PMID = 18389742.001).
  • [ISSN] 0009-4773
  • [Journal-full-title] Chirurgia italiana
  • [ISO-abbreviation] Chir Ital
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Blood Glucose
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14. Morita S, Machida H, Kuwatsuru R, Saito N, Suzuki K, Iihara M, Obara T, Mitsuhashi N: Preoperative localization of pancreatic insulinoma by super selective arterial stimulation with venous sampling. Abdom Imaging; 2007 Jan-Feb;32(1):126-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preoperative localization of pancreatic insulinoma by super selective arterial stimulation with venous sampling.
  • Although most insulinomas are small, they have been successfully detected by computed tomography and magnetic resonance imaging recently.
  • However, preoperative localization of the insulinomas by arterial stimulation with venous sampling is crucial when they show atypical findings on these imaging modalities.
  • We report a case of a large benign insulinoma located at the pancreatic tail; this tumor was diagnosed correctly by super selective arterial stimulation with venous sampling.
  • [MeSH-major] Calcium. Insulin / blood. Insulinoma / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Aged. Angiography / methods. Contrast Media. Humans. Injections, Intra-Arterial. Magnetic Resonance Imaging. Male. Pancreas / blood supply. Preoperative Care. Splenic Artery / radiography. Tomography, X-Ray Computed

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  • (PMID = 16932851.001).
  • [ISSN] 0942-8925
  • [Journal-full-title] Abdominal imaging
  • [ISO-abbreviation] Abdom Imaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Insulin; SY7Q814VUP / Calcium
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15. Tomita T, Masuzaki H, Noguchi M, Iwakura H, Fujikura J, Tanaka T, Ebihara K, Kawamura J, Komoto I, Kawaguchi Y, Fujimoto K, Doi R, Shimada Y, Hosoda K, Imamura M, Nakao K: GPR40 gene expression in human pancreas and insulinoma. Biochem Biophys Res Commun; 2005 Dec 30;338(4):1788-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GPR40 gene expression in human pancreas and insulinoma.
  • To assess gene expression of a membrane-bound G-protein-coupled fatty acid receptor, GPR40, in the human pancreas and islet cell tumors obtained at surgery were analyzed.
  • The mRNA level of the GPR40 gene in isolated pancreatic islets was approximately 20-fold higher than that in the pancreas, and the level was comparable to or rather higher than that of the sulfonylurea receptor 1 gene, which is known to be expressed abundantly in human pancreatic beta cells.
  • A large amount of GPR40 mRNA was detected in tissue extracts from two cases of insulinoma, whereas the expression was undetectable in glucagonoma or gastrinoma.
  • The present study demonstrates that GPR40 mRNA is expressed predominantly in pancreatic islets in humans and that GPR40 mRNA is expressed solely in human insulinoma among islet cell tumors.
  • These results indicate that GPR40 is probably expressed in pancreatic beta cells in the human pancreas.
  • [MeSH-major] Insulinoma / metabolism. Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Receptors, G-Protein-Coupled / biosynthesis

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  • (PMID = 16289108.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FFAR1 protein, human; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled
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16. Akca A, Mann K, Starke A, Lammers BJ, Goretzki PE: [Insulinoma associated with pregnancy]. Dtsch Med Wochenschr; 2010 Jul;135(30):1484-6
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  • [Title] [Insulinoma associated with pregnancy].
  • [Transliterated title] Postpartales Insulinom.
  • INVESTIGATION AND DIAGNOSIS: The following examination showed a low basal blood glucose level as well as pathological levels of insulin and C-peptide.
  • These findings together with the Whipple trias (hypoglycaemia, neurological symptoms and rapid improvement after infusion of glucose) were highly suspicious of an insulinoma.
  • Whereas CT, MRI and DOTATOC-PET were negative, endoscopic ultrasound showed a mass of 13 mm in the tail of the pancreas.
  • TREATMENT AND COURSE: The tumour was resected from the tail of the pancreas by laparoscopic enucleation.
  • Histological examination revealed an endocrine tumour (insulinoma) of the pancreas.
  • CONCLUSION: Despite its rarity, an insulinoma represents an important differential diagnosis of hypoglycaemia during and right after pregnancy.
  • [MeSH-major] Insulinoma / diagnosis. Insulinoma / surgery. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery. Pregnancy Complications, Neoplastic / diagnosis. Pregnancy Complications, Neoplastic / surgery

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  • [Copyright] Georg Thieme Verlag KG Stuttgart, New York.
  • (PMID = 20648406.001).
  • [ISSN] 1439-4413
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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17. 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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  • [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.
  • METHODS: We describe the case of a 46-year-old woman, who presented with fasting hypoglycemia and appropriately low insulin values.
  • During the entire fasting test, highly specific insulin remained at <3 mIU/L, with a median value (and interquartile range) of 0.9 (0.8 to 2.3) mIU/L, when the glucose concentration was <50 mg/dL.
  • 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
  • [MeSH-minor] Diagnosis, Differential. Endosonography. Female. Humans. Hypoglycemia / blood. Insulin / blood. Magnetic Resonance Imaging. Middle Aged. Radioimmunoassay

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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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18. Kutsuna N, Yamazaki S, Itoh Y, Wakabayashi K, Iwama A, Watanabe Y, Haraguchi Y, Ueda T, Takayama T: Arterial stimulation and venous sampling (ASVS) is useful for recurrent lesions of insulinoma: a case report. Surg Laparosc Endosc Percutan Tech; 2009 Aug;19(4):e138-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arterial stimulation and venous sampling (ASVS) is useful for recurrent lesions of insulinoma: a case report.
  • We encountered a recurrent case of benign solitary insulinoma in the pancreatic tail, which may have been caused by an inadequate surgical margin in the use of an ultrasonic dissector.
  • A 45-year-old man was referred with hypoglycemia and diagnosed solitary insulinoma in the pancreas.
  • Laparoscopic pancreatic enucleation was performed using an ultrasonic dissector.
  • The tumor was extracted and the surgical margins were microscopically negative.
  • He underwent resection of all visible lesions with omentum and wide excision of the soft tissue surrounding the pancreas after preoperative arterial stimulation and venous sampling test.
  • [MeSH-major] Calcium Gluconate / administration & dosage. Gastrointestinal Agents / administration & dosage. Insulin / blood. Insulinoma / blood. Pancreatic Neoplasms / blood

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  • (PMID = 19692865.001).
  • [ISSN] 1534-4908
  • [Journal-full-title] Surgical laparoscopy, endoscopy & percutaneous techniques
  • [ISO-abbreviation] Surg Laparosc Endosc Percutan Tech
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrointestinal Agents; 0 / Insulin; SQE6VB453K / Calcium Gluconate
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19. Limmer S, Huppert PE, Juette V, Lenhart A, Welte M, Wietholtz H: Radiofrequency ablation of solitary pancreatic insulinoma in a patient with episodes of severe hypoglycemia. Eur J Gastroenterol Hepatol; 2009 Sep;21(9):1097-101
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiofrequency ablation of solitary pancreatic insulinoma in a patient with episodes of severe hypoglycemia.
  • Insulinomas are rare neuroendocrine tumors of the pancreas.
  • In this case, we describe the successful use of computed tomography (CT)-guided radiofrequency ablation (RFA) of an insulinoma in an 80-year-old female patient.
  • An insulinoma measuring 1.5 cm in diameter was localized by endoscopic ultrasound and CT scan in the tail of the pancreas.
  • Owing to a high surgical risk caused by the patient's comorbidities and poor physical condition, the resection of the tumor was not considered.
  • Using CT-guided percutaneous RFA, the insulinoma was successfully ablated.
  • A control-CT, 5 weeks after RFA, revealed no residual tumor.
  • In conclusion, we found RFA suitable for the treatment of pancreatic insulinomas.
  • [MeSH-major] Catheter Ablation. Hypoglycemia / etiology. Insulinoma / surgery. Pancreatic Neoplasms / surgery

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  • (PMID = 19685572.001).
  • [ISSN] 1473-5687
  • [Journal-full-title] European journal of gastroenterology & hepatology
  • [ISO-abbreviation] Eur J Gastroenterol Hepatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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20. Iseri T, Yamada K, Chijiwa K, Nishimura R, Matsunaga S, Fujiwara R, Sasaki N: Dynamic computed tomography of the pancreas in normal dogs and in a dog with pancreatic insulinoma. Vet Radiol Ultrasound; 2007 Jul-Aug;48(4):328-31
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  • [Title] Dynamic computed tomography of the pancreas in normal dogs and in a dog with pancreatic insulinoma.
  • To establish optimal imaging conditions for enhanced computed tomography (CT) for canine pancreatic tumors, 10 healthy beagles were subjected to dynamic CT.
  • This technique was then applied to a dog with suspected insulinoma.
  • The changes in mean peak enhancement and the delay time of the aorta and pancreas were determined.
  • In normal beagles, maximal arterial and pancreatic CT enhancement was observed at 15 +/- 2 s (795 +/- 52 Housfield unit [HU]) and 28 +/- 9 s (118 +/- 16HU) after contrast medium injection, respectively.
  • Multiphase enhanced CT was performed in a pug with suspected insulinoma using the CT protocol defined for the normal beagles with some parameters modified; the images were acquired at the arterial (14 s after contrast medium injection), pancreatic (after 28 s), and equilibrium (after 90 s) phases; scanning was followed by exploratory laparotomy.
  • CT images were characterized by an enhanced mass in the left pancreatic lobe at the arterial phase, during which the difference between the CT values of the mass and normal pancreas was the highest.
  • Histopathologic diagnosis of the pancreatic mass was insulinoma.
  • Thus, it appears that enhanced CT imaging can be used to delineate the pancreas from a pancreatic mass, and it may be helpful in deciding the need for surgery.
  • [MeSH-major] Dog Diseases / diagnosis. Dogs / anatomy & histology. Insulinoma / veterinary. Pancreas / anatomy & histology. Pancreatic Neoplasms / veterinary. Tomography, X-Ray Computed / veterinary

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  • (PMID = 17691631.001).
  • [ISSN] 1058-8183
  • [Journal-full-title] Veterinary radiology & ultrasound : the official journal of the American College of Veterinary Radiology and the International Veterinary Radiology Association
  • [ISO-abbreviation] Vet Radiol Ultrasound
  • [Language] eng
  • [Publication-type] Case Reports; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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21. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Laparoscopic treatment of insulinoma: surgical technique and perisurgical results].
  • [Transliterated title] Tratamiento laparoscópico del Insulinoma pancreático. Técnica quirúrgica y resultados peri operatorios.
  • AIM: Our experience with the laparoscopic treatment of pancreatic insulinomas is reported.
  • PATIENTS AND METHODS: Four patients with clinical and radiological diagnosis of insulinoma were treated between January 2000 and September 2005.
  • RESULTS: All the patients were laparoscopically approached to attempt the tumor enucleation.
  • In three cases complete enucleation was possible; the remaining case was converted to perform the resection of the middle portion of the pancreas.
  • 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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22. Andronesi D, Andronesi A, Tonea A, Andrei S, Herlea V, Lupescu I, Ionescu-Târgovişte C, Coculescu M, Fica S, Ionescu M, Gheorghe C, Popescu I: [Insulinoma of the pancreas: analysis of a clinical series of 30 cases]. Chirurgia (Bucur); 2009 Nov-Dec;104(6):675-85
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Insulinoma of the pancreas: analysis of a clinical series of 30 cases].
  • [Transliterated title] Insulinomul pancreatic--analiza unei serii clinice de 30 de cazuri.
  • Insulinoma is the most frequent neuroendocrine pancreatic tumor and is the main cause for hypoglicemia due to endogenous hyperinsulinism.
  • We performed an analysis of a clinical series in order to study the clinical and biological spectrum of presentation, the preoperatory imagistic diagnosis and results of the surgical approach.
  • Between 1986-2009, 30 patients with symptoms suggesting an insulinoma were hospitalized in our department.
  • Preoperatory localization of insulinomas was possible in 16 patients.
  • Intraoperatory ultrasound was performed in 16 patients and its sensitivity in detection of insulinomas was 93%; the combination between intraoperative ultrasound and manual exploration of pancreas by the surgeon reached a 100% sensitivity.
  • Before the intraoperatory ultrasound was used the tumor excision was predominantly done by extensive pancreatic resection, while after this was available in our centre more conservative (enucleo-resection) procedures were chosen.
  • The dimensions of the tumor were less than 2 cm in most of the patients; 2 had nesidioblastosis and 2 had multiple insulinomas; all 28 patients proved to have benign insulinomas at histological specimens.
  • The most common complication following extensive pancreatic resections was acute pancreatitis, while after enucleation pancreatic fistula occurred more frequently.
  • CONCLUSIONS: Due to small dimensions, the preoperative diagnosis of insulinomas is usually difficult, ecoendoscopy being the most sensitive method.
  • Intraoperative ultrasound is essential for insulinoma localization and for chosing the optimal type of excision.
  • In benign insulinomas the prognosis is excellent, surgical resection being curative in all cases.
  • [MeSH-major] Insulinoma / surgery. Insulinoma / ultrasonography. Pancreatectomy / methods. Pancreatic Neoplasms / surgery. Pancreatic Neoplasms / ultrasonography. Ultrasonography, Interventional
  • [MeSH-minor] Adult. Aged. Female. Humans. Laparoscopy / adverse effects. Magnetic Resonance Imaging. Male. Middle Aged. Pancreatic Fistula / etiology. Pancreatitis / etiology. Retrospective Studies. Robotics. Sensitivity and Specificity. Treatment Outcome

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  • (PMID = 20187465.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] rum
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Romania
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23. Rott G, Biggemann M, Pfohl M: Embolization of an insulinoma of the pancreas with trisacryl gelatin microspheres as definitive treatment. Cardiovasc Intervent Radiol; 2008 May-Jun;31(3):659-62
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  • [Title] Embolization of an insulinoma of the pancreas with trisacryl gelatin microspheres as definitive treatment.
  • Insulinomas are rare, mostly benign neuroendocrine tumors, originating in 99% of cases from the pancreas, that synthesize and secrete insulin, causing symptomatic hypoglycemia.
  • We present the case of an 84-year-old woman with a symptomatic insulinoma who refused surgery and was treated with arterial embolization using trisacryl gelatin microspheres as definitive treatment.
  • [MeSH-major] Acrylic Resins / administration & dosage. Embolization, Therapeutic / methods. Gelatin / administration & dosage. Insulinoma / therapy. Pancreatic Neoplasms / therapy

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  • (PMID = 17922161.001).
  • [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 / Acrylic Resins; 0 / trisacryl gelatin microspheres; 9000-70-8 / Gelatin
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24. 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
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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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  • (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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25. Winer JH, Choi HS, Gibbs-Strauss SL, Ashitate Y, Colson YL, Frangioni JV: Intraoperative localization of insulinoma and normal pancreas using invisible near-infrared fluorescent light. Ann Surg Oncol; 2010 Apr;17(4):1094-100
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  • [Title] Intraoperative localization of insulinoma and normal pancreas using invisible near-infrared fluorescent light.
  • BACKGROUND: Neuroendocrine tumors of the pancreas, such as insulinoma, are difficult to localize, and complete resection is essential for cure.
  • Our hypothesis is that a near-infrared (NIR) fluorophore exhibiting uptake in insulinoma could provide high-sensitivity detection intraoperatively.
  • MB was injected as a rapid intravenous bolus at doses ranging from 0.25 to 2 mg/kg into wildtype rats and pigs, and into insulinoma-bearing transgenic mice.
  • The signal-to-background ratios (SBR) of tissues and tumors were quantified using FLARE software.
  • At doses > or =1 mg/kg, certain normal tissues, such as pancreas, accumulate MB and remain NIR fluorescent for up to 1 h with an SBR > or = 1.6.
  • Interestingly, insulinoma exhibits even higher MB signal than normal pancreas, resulting in insulinoma-to-pancreas ratios of 3.7 and insulinoma-to-muscle ratios of 16.2.
  • MB permitted high-sensitivity, real-time localization of primary, multicentric, and metastatic insulinoma and permitted differentiation among tumor, normal pancreas, and other abdominal structures.
  • CONCLUSION: A single intravenous injection of a clinically available, commonly used NIR fluorophore provides prolonged intraoperative localization of normal pancreas and insulinoma using invisible NIR fluorescent light.

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  • (PMID = 20033320.001).
  • [ISSN] 1534-4681
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA115296-03; United States / NCI NIH HHS / CA / R01 CA115296; United States / NCI NIH HHS / CA / R01 CA115296-03; United States / NCI NIH HHS / CA / R01-CA-115296
  • [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 / Fluorescent Dyes; T42P99266K / Methylene Blue
  • [Other-IDs] NLM/ NIHMS158806; NLM/ PMC2841719
  • [Keywords] NOTNLM ; Intraoperative Imaging / Methylene Blue / Near-Infrared Fluorescence / Neuroendocrine Tumors / Pancreas
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26. Pakhetra R, Priya G, Jyotsna VP, Seith A, Ammini AC: Insulinoma: reversal of brain magnetic resonance imaging changes following resection. Neurol India; 2008 Apr-Jun;56(2):192-4
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  • [Title] Insulinoma: reversal of brain magnetic resonance imaging changes following resection.
  • Insulinoma presents with myriad manifestations and severe neurological deficit may develop due to delay in diagnosis.
  • There was complete reversal of neurological deficit and brain magnetic resonance imaging changes of hypoglycemia on follow-up after resection of pancreatic insulinoma.
  • This is the first report which shows reversal of hypoglycemic changes in MRI after resection of insulinoma.
  • Insulinoma, pre and post surgery provides a model for study of the effect of hypoglycemia and its improvement after euglycemia.
  • [MeSH-major] Brain / pathology. Insulinoma / pathology. Magnetic Resonance Imaging / methods
  • [MeSH-minor] Adult. Female. Humans. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery

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  • (PMID = 18688148.001).
  • [ISSN] 0028-3886
  • [Journal-full-title] Neurology India
  • [ISO-abbreviation] Neurol India
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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27. Miron A, Calu V, Giulea C, Fica S, Barbu C, Stefan C: Laparoscopically treated pancreatic insulinoma. Case report. J Med Life; 2010 Apr-Jun;3(2):186-90
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  • [Title] Laparoscopically treated pancreatic insulinoma. Case report.
  • Usually, insulinomas are small sized, insulin secreting, benign tumors of the pancreas, and require surgical treatment.
  • We report the case of a female patient, of 61 years old, with pancreatic insulinoma localized in the junction between the head and the istm of the pancreas, of 1,4 cm in size, which induced hypoglycemia due to endogenous insulin hypersecretion.
  • The tumor was removed by laparoscopic enucleation in March 2009.
  • [MeSH-major] Insulinoma / surgery. Pancreatic Neoplasms / surgery

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  • [Cites] Surg Endosc. 1999 Apr;13(4):406-8 [10094758.001]
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  • (PMID = 20968207.001).
  • [ISSN] 1844-122X
  • [Journal-full-title] Journal of medicine and life
  • [ISO-abbreviation] J Med Life
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Blood Glucose
  • [Other-IDs] NLM/ PMC3019046
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28. Bonfig W, Kann P, Rothmund M, Schwarz HP: Recurrent hypoglycemic seizures and obesity: delayed diagnosis of an insulinoma in a 15 year-old boy--final diagnostic localization with endosonography. J Pediatr Endocrinol Metab; 2007 Sep;20(9):1035-8
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  • [Title] Recurrent hypoglycemic seizures and obesity: delayed diagnosis of an insulinoma in a 15 year-old boy--final diagnostic localization with endosonography.
  • Insulinoma in children and adolescents is extremely rare.
  • We present a case of insulinoma with onset of symptoms at the age of 12.5 years.
  • Diagnosis was made very soon after the first symptoms, but diagnostic localization was delayed, since conventional MRI did not reveal the insulinoma.
  • A solitary insulinoma in the pancreatic tail was enucleated laparoscopically.
  • [MeSH-major] Hypoglycemia / physiopathology. Insulinoma / ultrasonography. Obesity / physiopathology. Pancreatic Neoplasms / ultrasonography. Seizures / physiopathology


29. Horino T, Takao T, Hashimoto K: A case with insulinoma diagnosed and localized preoperatively using contrast-enhanced ultrasonography (CEUS) and arterial stimulation and venous sampling (ASVS). Endocr J; 2006 Feb;53(1):141-6
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  • [Title] A case with insulinoma diagnosed and localized preoperatively using contrast-enhanced ultrasonography (CEUS) and arterial stimulation and venous sampling (ASVS).
  • We report a case with insulinoma diagnosed and localized preoperatively using a combination of contrast-enhanced ultrasonography (CEUS) and arterial stimulation and venous sampling (ASVS).
  • Fajans' ratio, Grunt's ratio, and Turner's ratio, which are reported to be indexes for endogenous hyperinsulinemia in insulinoma, were all negative.
  • CEUS showed a small low echoic lesion in the pancreatic body with blood flow and ASVS showed that the insulin levels in the hepatic vein were extremely increased by calcium injection to the splenic artery, indicating an insulinoma in the pancreatic body preoperatively.
  • An open intra-abdominal operation was performed and an insulinoma was confirmed in the pancreatic body.
  • Enucleation of tumor was undertaken and symptomatic hypoglycemia improved.
  • [MeSH-major] Angiography / methods. Insulinoma / blood supply. Insulinoma / ultrasonography. Pancreatic Neoplasms / blood supply. Pancreatic Neoplasms / ultrasonography. Ultrasonography / methods

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  • (PMID = 16543684.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] SY7Q814VUP / Calcium
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30. 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.
  • Approximately 5 to 10% of these tumors are cancerous, and control of insulin secretion and hypoglycemia may be difficult in these patients.
  • Malignant insulinomas generally respond poorly to traditional chemotherapeutic agent regimens.
  • 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 required diazoxide, a thiazide diuretic, phenytoin, and a constant infusion of glucose to control the hypoglycemia and elevated insulin levels.
  • RESULTS: On the mTOR (mammalian target of rapamycin) agent rapamycin, he was weaned off all drugs except for the thiazide diuretic and maintained euglycemia with a reduction of circulating insulin levels.
  • 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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31. Sotoudehmanesh R, Hedayat A, Shirazian N, Shahraeeni S, Ainechi S, Zeinali F, Kolahdoozan S: Endoscopic ultrasonography (EUS) in the localization of insulinoma. Endocrine; 2007 Jun;31(3):238-41
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  • [Title] Endoscopic ultrasonography (EUS) in the localization of insulinoma.
  • OBJECTIVE: Endoscopic ultrasonography has been accepted as a sensitive modality for preoperative tumor localization in pancreas.
  • We have aimed to determine the performance characteristics of endoscopic ultrasonography in pancreatic insulinoma localization and evaluation of relationship between the tumor size and serum-c peptide level, lowest glucose level and insulin level.
  • METHODS: Patients suspicious to insulinoma according to clinical and laboratory findings were included.
  • Endoscopic ultrasonography was performed and if a tumor was identified, the patient was referred for surgery.
  • In one patient, a tumor was identified both by transabdominal ultrasonography and abdominal CT scan.
  • The overall sensitivity and accuracy of endoscopic ultrasonography for detection of insulinoma was 89.5% and 83.7% respectively.
  • The sensitivity of endoscopic ultrasonography for detection of lesions in pancreatic head, body and tail was 92.6%, 78.9%, and 40.0%, respectively.
  • There was no relationship between c-peptide, lowest blood glucose, insulin blood levels and tumor size in surgery.
  • CONCLUSION: EUS is an accurate method for detection of insulinoma.
  • The accuracy depends on the location of the tumor and is greatest for tumors in the pancreatic head.
  • [MeSH-major] Endosonography / methods. Insulinoma / diagnostic imaging. Pancreatic Neoplasms / diagnostic imaging
  • [MeSH-minor] Adolescent. Adult. Aged. Blood Glucose / metabolism. C-Peptide / blood. Female. Humans. Insulin / blood. Male. Middle Aged. Neoplasm Staging. Pancreatectomy. Sensitivity and Specificity. Ultrasonography, Interventional / methods

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  • (PMID = 17906369.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / C-Peptide; 0 / Insulin
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32. Bachmann J, Kleeff J, Bergmann F, Shrikhande SV, Hartschuh W, Büchler MW, Friess H: Pancreatic metastasis of Merkel cell carcinoma and concomitant insulinoma: case report and literature review. World J Surg Oncol; 2005 Sep 1;3:58

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic metastasis of Merkel cell carcinoma and concomitant insulinoma: case report and literature review.
  • BACKGROUND: Merkel cell carcinomas are rare neoplasm of neuroendocrine origin, usually observed in elderly people in areas with abundant sunlight, and predominantly located on the head and neck, extremities, and trunk.
  • In many patients, a local recurrence after resection of the primary tumour and even distant metastases can be found.
  • CASE PRESENTATION: We report an unusual occurrence of pancreatic metastases from a previously diagnosed Merkel cell carcinoma with the discovery of a concomitant insulinoma.
  • An 82-year old lady suffered from recurrent attacks of hypoglycemia and presented with an abdominal mass, 2 years prior she had an excision done on her eyebrow that was reported as Merkel cell carcinoma.
  • Final histopathology of the mass was a poorly differentiated endocrine carcinoma in the pancreatic tail, in the peripancreatic tissue and in the surrounding soft tissue consistent with metastatic Merkel cell carcinoma in addition to an insulinoma of the pancreatic body.
  • CONCLUSION: This is the first documented case of a metastatic Merkel cell carcinoma and a concomitant insulinoma, suggesting either a mere coincidence or an unknown neuroendocrine tumor syndrome.

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  • (PMID = 16137328.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1208966
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33. Cazabat L, Chanson P: [Hypoglycemia and insulinoma]. Ann Endocrinol (Paris); 2009 Sep;70 Suppl 1:S2-11
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  • [Title] [Hypoglycemia and insulinoma].
  • [Transliterated title] Hypoglycémie et insulinome.
  • Insulinomas are rare causes of hypoglycemia.
  • A mixed-meal test may also help to diagnose the very rare cases of postprandial hypoglycemia related to non insulinoma pancreatogenic hypoglycemic syndrome (NIPHS) or to some rare insulinomas.
  • Only when diagnosis of hypoglycemic hyperinsulinism is made, the tumor localization process may be initiated.
  • This may be difficult due to the small size of insulinomas (generally < 1 cm).
  • First results with a very new technique, the GLP-1 receptor imaging, are promising for localizing very small tumors.
  • This localization aims to allow a sparing surgery; enucleation of benign tumors, if possible, allows a pancreatic tissue preservation in patients with quite normal survival.
  • [MeSH-major] Hypoglycemia / etiology. Insulinoma / complications. Pancreatic Neoplasms / complications

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  • (PMID = 19878764.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 82
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34. Tao P, Xu D, Lin S, Ouyang GL, Chang Y, Chen Q, Yuan Y, Zhuo X, Luo Q, Li J, Li B, Ruan L, Li Q, Li Z: Abnormal expression, highly efficient detection and novel truncations of midkine in human tumors, cancers and cell lines. Cancer Lett; 2007 Aug 8;253(1):60-7
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  • [Title] Abnormal expression, highly efficient detection and novel truncations of midkine in human tumors, cancers and cell lines.
  • We detected aberrant Midkine (MK) expressions in human insulinoma and pancreatic cancer tissues by immunohistochemistry, revealing its potential role in tumorigenesis/carcinogenesis.
  • With a nested-touchdown PCR program we were able to detect the tMK in all human tumor/cancer tissues and cancer/tumor cell lines.
  • Detection of MK in the peripheral cells and precancerous lesions implies its potential for early cancer/tumor diagnosis.
  • Furthermore, we have discovered two novel truncations of the MK, tMKB and tMKC, respectively, in the disease specimens.
  • [MeSH-major] Cytokines / genetics. Insulinoma / genetics. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Adult. Amino Acid Sequence. Cell Line, Tumor. Humans. Molecular Sequence Data. Mutation. Pancreas / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17379400.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Cytokines; 137497-38-2 / midkine
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35. Fabbri HC, Mello MP, Soardi FC, Esquiaveto-Aun AM, Oliveira DM, Denardi FC, Moura-Neto A, Garmes HM, Baptista MT, Matos PS, Lemos-Marini SH, D'Souza-Li LF, Guerra-Júnior G: Long-term follow-up of an 8-year-old boy with insulinoma as the first manifestation of a familial form of multiple endocrine neoplasia type 1. Arq Bras Endocrinol Metabol; 2010 Nov;54(8):754-60
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  • [Title] Long-term follow-up of an 8-year-old boy with insulinoma as the first manifestation of a familial form of multiple endocrine neoplasia type 1.
  • Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant hereditary cancer syndrome characterized mostly by parathyroid, enteropancreatic, and anterior pituitary tumors.
  • His diagnosis was pancreatic insulinoma.
  • At a first evaluation, the father presented only gastric ulceration but subsequently developed hyperparathyroidism and lung carcinoid tumor.
  • Molecular study showed a G to A substitution in intron 4, at nine nucleotides upstream of the splicing acceptor site, causing a splicing mutation.
  • [MeSH-major] Insulinoma / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Pancreatic Neoplasms / genetics. Proto-Oncogene Proteins / genetics


36. Apodaca-Torrez FR, Triviño T, Lobo EJ, Goldenberg A, Benvenuto MR, Ardeng JC: [Pancreatic insulinomas]. Cir Esp; 2006 Jul;80(1):3-8
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  • [Title] [Pancreatic insulinomas].
  • [Transliterated title] Insulinoma de páncreas.
  • Insulinoma is the most frequent neuroendocrine pancreatic tumor.
  • The most frequently performed surgical procedures were pancreatic resection in 10 patients and laparotomic enucleation in the remaining 10.
  • The most frequent surgical complication was pancreatic fistula.
  • [MeSH-major] Insulinoma. Pancreatic Neoplasms

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  • (PMID = 16796946.001).
  • [ISSN] 0009-739X
  • [Journal-full-title] Cirugía española
  • [ISO-abbreviation] Cir Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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37. Strong VE, Shifrin A, Inabnet WB: Rapid intraoperative insulin assay: a novel method to differentiate insulinoma from nesidioblastosis in the pediatric patient. Ann Surg Innov Res; 2007;1:6
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  • [Title] Rapid intraoperative insulin assay: a novel method to differentiate insulinoma from nesidioblastosis in the pediatric patient.
  • Causes can include nesidioblastosis, pancreatic islet cell tumors such as insulinoma, and associations with multiple endocrine neoplasia syndromes.
  • Although new, improved imaging techniques have allowed for more precise preoperative localization of insulinomas, the differentiation of nesidioblastosis and insulinoma, particularly in children, can be challenging.
  • To improve intraoperative localization and confirmation of successful resection of insulinoma, a novel hormonal assay, the rapid intraoperative insulin assay, is reported for the first time in a pediatric patient.
  • This intraoperative radioimmunoassay for insulin yields results within several minutes and confirms complete resection of insulinoma.
  • CASE DESCRIPTION: We present a case of pancreatic insulinoma in a child with symptoms of severe hypoglycemia, causing seizures.
  • The insulinoma was enucleated laparoscopically, and rapid intra-operative insulin assay used to determine the success of the procedure.
  • DISCUSSION AND EVALUATION: This rapid intra-operative test provides a valuable adjunct for determining complete excision in complicated cases of recurrent or questionable insulinoma.
  • Although not a common problem, for pediatric patients in whom the diagnosis is not clear, this test may provide a novel approach to confirming disease.

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  • (PMID = 17958895.001).
  • [ISSN] 1750-1164
  • [Journal-full-title] Annals of surgical innovation and research
  • [ISO-abbreviation] Ann Surg Innov Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2116998
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38. Toniato A, Meduri F, Foletto M, Avogaro A, Pelizzo M: Laparoscopic treatment of benign insulinomas localized in the body and tail of the pancreas: a single-center experience. World J Surg; 2006 Oct;30(10):1916-9; discussion 1920-1
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  • [Title] Laparoscopic treatment of benign insulinomas localized in the body and tail of the pancreas: a single-center experience.
  • BACKGROUND: The increasingly widespread use of minimally invasive surgery has allowed surgeons to exploit this approach for complex procedures, such as pancreatic resections, though its actual role outside simple operations remains debated.
  • METHODS: This is a study of 12 consecutive patients, 5 men and 7 women, with pancreatic insulinoma who were treated at our institution from 2000 to September 2005.
  • RESULTS: Successful laparoscopic resection was performed in 11 out of 12 patients: 4 had tumor enucleation, and 7 had distal pancreatectomy; among these latter 5 had spleen-preserving distal pancreatectomy.
  • The median tumor size was 18 mm, and all the insulinomas were benign.
  • CONCLUSIONS: The laparoscopic approach proved to be feasible and safe, although the average operative time was longer and demanded good surgical skills as well as precise localization of the tumor and definition of its nature.
  • Tumors located in the body or tail of the pancreas that are benign in nature can better benefit of laparoscopic approach.
  • [MeSH-major] Insulinoma / surgery. Laparoscopy. Pancreas. Pancreatectomy / methods. Pancreatic Neoplasms / surgery

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  • (PMID = 16855802.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Pagliarini DJ, Wiley SE, Kimple ME, Dixon JR, Kelly P, Worby CA, Casey PJ, Dixon JE: Involvement of a mitochondrial phosphatase in the regulation of ATP production and insulin secretion in pancreatic beta cells. Mol Cell; 2005 Jul 22;19(2):197-207
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Involvement of a mitochondrial phosphatase in the regulation of ATP production and insulin secretion in pancreatic beta cells.
  • Reversible phosphorylation is the cell's most prevalent form of posttranslational modification, yet its role in the regulation of mitochondrial functions is poorly understood.
  • Knockdown of PTPMT1 expression in the pancreatic insulinoma cell line INS-1 832/13 alters the mitochondrial phosphoprotein profile and markedly enhances both ATP production and insulin secretion.
  • These data define PTPMT1 as a potential drug target for the treatment of type II diabetes and strengthen the notion that mitochondria are an underappreciated site of signaling by reversible phosphorylation.

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  • [CommentIn] Mol Cell. 2005 Aug 5;19(3):291-2 [16061174.001]
  • (PMID = 16039589.001).
  • [ISSN] 1097-2765
  • [Journal-full-title] Molecular cell
  • [ISO-abbreviation] Mol. Cell
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / F32 DK067799; United States / PHS HHS / / 18024; United States / NIGMS NIH HHS / GM / 2 T32 GM07752-25
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 8L70Q75FXE / Adenosine Triphosphate; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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40. Ketari-Jamoussi S, Debbiche-Chedly A, Ben Dhaou B, Boussema F, Cherif O, Cherif AR, Ben Ayed M, Bouzaine A, Rokbani L: [Giant insulinoma]. Ann Endocrinol (Paris); 2009 Mar;70(1):71-5
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  • [Title] [Giant insulinoma].
  • [Transliterated title] Un insulinome géant : à propos d'un cas.
  • Islet-cell tumors are the most common neuroendocrine tumors that arise from the endocrine pancreas.
  • The insulinoma is difficult to localize since it is very small in size, often not exceeding 2cm.
  • We report an exceptional case of giant insulinoma initially revealed by a pseudo-polycythemia in an 80-year-old man.
  • Routine biological investigations showed elevated hematocrit and haemoglobin, suggesting Vaquez disease.
  • Imaging studies showed a voluminous tumor located between the pancreas and the spleen.
  • The presence of an insulinoma was confirmed on the basis of an elevated level of proinsulin at the time of an asymptomatic episode of hypoglycemia.
  • Histopathological examination revealed a malignant, well-differentiated neuroendocrine malignant tumor.
  • [MeSH-major] Insulinoma / pathology. Insulinoma / surgery. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery

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  • (PMID = 18937931.001).
  • [ISSN] 0003-4266
  • [Journal-full-title] Annales d'endocrinologie
  • [ISO-abbreviation] Ann. Endocrinol. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 9035-68-1 / Proinsulin
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41. Jonnakuty C, Gragnoli C: Karyotype of the human insulinoma CM cell line--beta cell model in vitro? J Cell Physiol; 2007 Dec;213(3):661-2
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  • [Title] Karyotype of the human insulinoma CM cell line--beta cell model in vitro?
  • The CM cell line is derived from a human pancreatic insulinoma and is used as a beta cell model for the study of the pathogenesis of diabetes, as it appears to maintain the characteristics of beta cells.
  • However, a karyotype study of the CM cell line was not previously performed.
  • We aimed at karyotyping the CM cell line to confirm its human origin, diploid karyotype, and chromosomal structure.
  • We karyotyped the CM cells at earlier passages with the standard Giemsa technique.
  • The karyotyping procedure confirmed the human origin of the CM cell line.
  • However, the karyotype showed 64 chromosomes with structural abnormalities, including chromosome 11, in which the insulin gene is located.
  • Our Medline search of other existing insulinoma cell lines of rodent, mouse and hamster origin did not show any karyotype performed.
  • As the CM cell karyotype reveals significant structural and numerical chromosomal abnormalities, we question the use of such a cell line as an in vitro beta cell model.
  • We suggest that insulinoma cell lines established in vitro to study beta cell function should have a karyotype performed to exclude chromosomal aberrations.
  • [MeSH-major] Chromosome Aberrations. Insulinoma / genetics. Islets of Langerhans / cytology. Models, Biological. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Cell Line, Tumor. Chromosomes, Human, Pair 11. Diploidy. Humans. In Vitro Techniques. Insulin / genetics. Karyotyping / methods

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  • [Copyright] 2007 Wiley-Liss, Inc.
  • [CommentIn] J Cell Physiol. 2008 Aug;216(2):568 [18300264.001]
  • (PMID = 17492774.001).
  • [ISSN] 1097-4652
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Editorial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin
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42. Arao T, Okada Y, Hirose A, Tanaka Y: A rare case of adult-onset nesidioblastosis treated successfully with diazoxide. Endocr J; 2006 Feb;53(1):95-100

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Abdominal CT revealed no pancreatic tumor, and angiography of splenic artery showed no definite tumor stain within the pancreas.
  • Based on the results of selective arterial calcium stimulation and hepatic venous sampling (ASVS), the provisional diagnosis was a small insulinoma in the pancreatic body.
  • However, histopathological and immunohistochemical examinations of the resected tissue showed hypertrophy of islets of Langerhans islands and beta cells around pancreatic ducts.
  • [MeSH-minor] Angiography. Blood Glucose / analysis. Diagnosis, Differential. Humans. Hyperinsulinism / blood. Hypoglycemia / blood. Insulin-Secreting Cells / pathology. Insulinoma / diagnosis. Insulinoma / pathology. Liver / blood supply. Male. Middle Aged. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology

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  • (PMID = 16543678.001).
  • [ISSN] 0918-8959
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Vasodilator Agents; O5CB12L4FN / Diazoxide
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43. Cheon H, Cho JM, Kim S, Baek SH, Lee MK, Kim KW, Yu SW, Solinas G, Kim SS, Lee MS: Role of JNK activation in pancreatic beta-cell death by streptozotocin. Mol Cell Endocrinol; 2010 Jun 10;321(2):131-7
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  • [Title] Role of JNK activation in pancreatic beta-cell death by streptozotocin.
  • c-Jun N-terminal kinase (JNK) is activated by cellular stress and plays critical roles in diverse types of cell death.
  • However, role of JNK in beta-cell injury is obscure.
  • We investigated the role for JNK in streptozotocin (STZ)-induced beta-cell death.
  • STZ induced JNK activation in insulinoma or islet cells.
  • JNK inhibitors attenuated insulinoma or islet cell death by STZ.
  • PARP-1 siRNA attenuated insulinoma cell death and JNK activation after STZ treatment, which was reversed by MKP (MAP kinase phosphatase)-1 siRNA.
  • These results suggest that JNK is activated by STZ downstream of PARP-1 through inactivation of phosphatases such as MKP, which plays important roles in STZ-induced beta-cell death.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Cell Death / drug effects. Enzyme Activation / drug effects. Insulin-Secreting Cells / drug effects. JNK Mitogen-Activated Protein Kinases / metabolism. Streptozocin / pharmacology

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  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20176078.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Enzyme Inhibitors; 0 / Poly(ADP-ribose) Polymerase Inhibitors; 0 / Reactive Oxygen Species; 5W494URQ81 / Streptozocin; EC 2.4.2.30 / Parp1 protein, mouse; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
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44. Lee SR, Choi MC, Ahn KJ: A case of multiple endocrine neoplasia type 1 with primary liver gastrinoma. J Korean Med Sci; 2010 Jun;25(6):953-6
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  • Gastrinoma is the most frequent functional pancreaticoduodenal endocrine tumor in patients with multiple endocrine neoplasia type 1 (MEN 1).
  • We reported the case of a 39 yr old female patient with a history of repeated peptic ulcers and a hypoglycemia episode.
  • Abdominal CT indicated a well-defined liver mass and a pancreatic head mass.
  • Somatostatin-receptor scintigraphy with [(111)In] DTPA octreotide demonstrated a strong uptake of the radiotracer in the left lateral segment at the site of the hepatic mass.
  • After operation, immunohistochemical staining was consistent with pancreatic insulinoma and primary hepatic gastrinoma.
  • As the liver is a common site of metastases from gastrinoma, primary liver gastrinoma has not yet been reported with MEN 1.
  • [MeSH-minor] Adult. Female. Humans. Hypoglycemia / etiology. Insulinoma / complications. Insulinoma / diagnosis. Insulinoma / pathology. Mastectomy, Segmental. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / pathology. Peptic Ulcer / etiology. Tomography, X-Ray Computed

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  • (PMID = 20514321.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2877224
  • [Keywords] NOTNLM ; Gastrinoma / Insulinoma / Multiple Endocrine Neoplasia Type 1
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45. Reubi JC, Perren A, Rehmann R, Waser B, Christ E, Callery M, Goldfine AB, Patti ME: Glucagon-like peptide-1 (GLP-1) receptors are not overexpressed in pancreatic islets from patients with severe hyperinsulinaemic hypoglycaemia following gastric bypass. Diabetologia; 2010 Dec;53(12):2641-5
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  • [Title] Glucagon-like peptide-1 (GLP-1) receptors are not overexpressed in pancreatic islets from patients with severe hyperinsulinaemic hypoglycaemia following gastric bypass.
  • AIMS/HYPOTHESIS: Glucagon-like peptide-1 (GLP-1) receptors are highly overexpressed in benign insulinomas, permitting in vivo tumour visualisation with GLP-1 receptor scanning.
  • The present study sought to evaluate the GLP-1 receptor status in vitro in other pancreatic disorders leading to hyperinsulinaemic hypoglycaemia, specifically after gastric bypass surgery.
  • METHODS: Fresh frozen pancreatic tissue samples (n=7) from six gastric bypass surgery patients suffering from hyperinsulinaemic hypoglycaemia were evaluated for GLP-1 receptor content using in vitro receptor autoradiography, and compared with normal pancreas and with pancreatic insulinoma tissues.
  • RESULTS: GLP-1 receptor analysis of the pancreatic tissues, which histopathologically were compatible with nesidioblastosis and originated from post-bypass hypoglycaemic patients, revealed a mean density value of GLP-1 receptors in the islets of 1,483 ± 183 dpm/mg tissue.
  • The density of islet GLP-1 receptor in post-gastric bypass patients did not differ from that of normal pancreas (1,563 ± 104 dpm/mg tissue, n = 10).
  • Receptor density in pancreatic acini was low in post-bypass and control conditions.
  • In contrast, benign insulinomas showed a high density of GLP-1 receptors, with a mean value of 8,302 ± 1,073 dpm/mg tissue (n = 6).
  • CONCLUSIONS/INTERPRETATION: In contrast to insulinoma, hyperinsulinaemic hypoglycaemia after gastric bypass surgery is not accompanied by overexpression of GLP-1 receptor in individual islets.
  • These GLP-1 receptor data support the notion that the islet pathobiology of post-gastric bypass hypoglycaemia is distinctly different from that of benign insulinomas.
  • [MeSH-minor] Adult. Aged. Autoradiography. Female. Glucagon-Like Peptide-1 Receptor. Humans. Insulinoma / metabolism. Insulinoma / pathology. Male. Middle Aged. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Severity of Illness Index. Up-Regulation

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  • (PMID = 20835917.001).
  • [ISSN] 1432-0428
  • [Journal-full-title] Diabetologia
  • [ISO-abbreviation] Diabetologia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / GLP1R protein, human; 0 / Glucagon-Like Peptide-1 Receptor; 0 / Receptors, Glucagon
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46. Diaz AG, Lucas S, Ferraina P, Ferraro A, Puchulu F, Paes De Lima A, Maselli Mdel C, Gomez RM, Bruno OD: [Clinical experience in 37 cases of insulinoma]. Medicina (B Aires); 2006;66(6):499-504
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical experience in 37 cases of insulinoma].
  • [Transliterated title] Experiencia clinica sobre 37 casos de insulinoma.
  • Insulinoma is the most frequent pancreatic islet cell tumor.
  • Diagnosis is established through demonstration of inappropriately elevated insulin serum concentrations in the presence of hypoglycemia.
  • The aim of this study is to show our experience in the management of insulinoma.
  • Mean fasting serum glucose was 32.4 +/- 8.7 mg/dl, insulin 38.2 +/- 39.7 microU/ml (RIA, n=11) or 23.8 +/- 18.1 microU/ml (chemoluminescence, n=26) and C-peptide 1.15 +/- 1.60 nmol/l (n=14).
  • In 22 patients, a solitary tumor was excised (61.1%).
  • Six cases presented multiple insulinomas.
  • Five patients had malignant insulinomas.
  • In 3 patients another tumour (glucagonoma) was found (1 of them with MEN 1).
  • [MeSH-major] Insulinoma. Pancreatic Neoplasms
  • [MeSH-minor] Adolescent. Adult. Aged. Biopsy. Blood Glucose / analysis. Fasting. Female. Humans. Hypoglycemia / etiology. Insulin / blood. Male. Middle Aged. Pancreatectomy. Retrospective Studies

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  • (PMID = 17240619.001).
  • [ISSN] 0025-7680
  • [Journal-full-title] Medicina
  • [ISO-abbreviation] Medicina (B Aires)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Argentina
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin
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47. Kang CM, Park SH, Kim KS, Choi JS, Lee WJ, Kim BR: Surgical experiences of functioning neuroendocrine neoplasm of the pancreas. Yonsei Med J; 2006 Dec 31;47(6):833-9
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  • [Title] Surgical experiences of functioning neuroendocrine neoplasm of the pancreas.
  • We present our surgical experiences with functioning neuroendocrine neoplasms of the pancreas to define its natural history, and to suggest its proper management.
  • From June 1990 to June 2005, patients with diagnosis of functioning neuroendocrine (islet cell) neoplasms of the pancreas were retrospectively reviewed.
  • Twelve patients (86%) had insulinoma, two (14%) had gastrinoma.
  • One (7%) with pancreatic insulinoma was multiple endocrine neoplasia type 1.
  • Intraoperative ultrasound scan (sensitivity, 83%) was the most powerful modality for tumor localization.
  • Fifteen neoplasms with median tumor size 1 cm (range 0-3 cm) were resected.
  • Four insulinomas (26.7%) were located in the head of the pancreas and 5 (36%), in the tail.
  • Another 5 (36%) insulinomas and 1 (7%) gastrinoma were located around the neck area near the SMV or PV.
  • 100% of patients with functioning neuroendocrine neoplasms of the pancreas have survived.
  • The overall disease free 10-year survival was found to be about 81%.
  • Exact localization of tumor by intraoperative ultrasound and surgical removal are promising for good prognosis.
  • [MeSH-major] Insulinoma / surgery. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Gastrinoma / surgery. Gastrinoma / ultrasonography. Humans. Male. Middle Aged. Neoplasm Metastasis. Postoperative Complications. Prognosis. Retrospective Studies

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  • (PMID = 17191313.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2687824
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48. Bose AK, Mocanu MM, Carr RD, Brand CL, Yellon DM: Glucagon-like peptide 1 can directly protect the heart against ischemia/reperfusion injury. Diabetes; 2005 Jan;54(1):146-51
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  • Glucagon-like peptide 1 (GLP-1), a gut incretin hormone that stimulates insulin secretion, also activates antiapoptotic signaling pathways such as phosphoinositide 3-kinase and mitogen-activated protein kinase in pancreatic and insulinoma cells.
  • This finding may represent a new therapeutic potential for this class of drug currently undergoing clinical trials in the treatment of type 2 diabetes.
  • [MeSH-minor] Animals. Blood Pressure / drug effects. Butadienes / pharmacology. Chromones / pharmacology. Disease Models, Animal. Enzyme Inhibitors / pharmacology. Glucagon-Like Peptide 1. Heart Rate / drug effects. In Vitro Techniques. Insulin / secretion. MAP Kinase Signaling System / drug effects. MAP Kinase Signaling System / physiology. Male. Morpholines / pharmacology. Myocardial Infarction / pathology. Myocardial Infarction / prevention & control. Nitriles / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Rats. Rats, Sprague-Dawley. Time Factors

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  • (PMID = 15616022.001).
  • [ISSN] 0012-1797
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Butadienes; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Insulin; 0 / Morpholines; 0 / Nitriles; 0 / Peptide Fragments; 0 / Protein Precursors; 0 / U 0126; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 89750-14-1 / Glucagon-Like Peptide 1; 9007-92-5 / Glucagon; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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49. Soucek L, Lawlor ER, Soto D, Shchors K, Swigart LB, Evan GI: Mast cells are required for angiogenesis and macroscopic expansion of Myc-induced pancreatic islet tumors. Nat Med; 2007 Oct;13(10):1211-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mast cells are required for angiogenesis and macroscopic expansion of Myc-induced pancreatic islet tumors.
  • Myc is a pleiotropic transcription factor that is overexpressed in many human cancers and instructs many extracellular aspects of the tumor tissue phenotype, including remodeling of tumor stroma and angiogenesis.
  • Here we show in a beta-cell tumor model that activation of Myc in vivo triggers rapid recruitment of mast cells to the tumor site-a recruitment that is absolutely required for macroscopic tumor expansion.
  • In addition, treatment of established beta-cell tumors with a mast cell inhibitor rapidly triggers hypoxia and cell death of tumor and endothelial cells.
  • Inhibitors of mast cell function may therefore prove therapeutically useful in restraining expansion and survival of pancreatic and other cancers.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Mast Cells / metabolism. Neovascularization, Pathologic / etiology. Pancreatic Neoplasms / blood supply. Proto-Oncogene Proteins c-myc / physiology
  • [MeSH-minor] Animals. Bone Marrow Cells / cytology. Cells, Cultured. Chemokine CCL2 / metabolism. Chemokine CCL5 / metabolism. Femur / cytology. Gene Expression Regulation, Neoplastic. Immunohistochemistry. Mice. Mice, Inbred C57BL. Mice, Transgenic. Oligonucleotide Array Sequence Analysis


50. Crespel A, Barbaud A, Andrieu JM, Oziole E, Coubes P, Gélisse P: [Insulinoma presenting as pseudo-drug-resistant focal epilepsy]. Rev Neurol (Paris); 2009 May;165(5):493-5
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  • [Title] [Insulinoma presenting as pseudo-drug-resistant focal epilepsy].
  • [Transliterated title] Un insulinome se présentant comme une épilepsie focale pharmacorésistante.
  • INTRODUCTION: We describe a case of insulinoma presenting as a refractory frontal lobe epilepsy in a 44-year-old man with a history of severe head trauma.
  • Insulinoma was diagnosed based on the presence of episodes of hypoglycemia, abnormal insulin/blood glucose ratio and a tumor in the pancreas (echo-ultrasound).
  • CONCLUSION: Insulinoma should be considered in patients with no reason for having drug-resistant epilepsy, especially when seizures occur early in the morning or when episodes of neuropsychiatric symptoms with sweating are present.
  • [MeSH-major] Epilepsies, Partial / etiology. Insulinoma / diagnosis
  • [MeSH-minor] Adult. Blood Glucose / metabolism. Humans. Hypoglycemia / etiology. Insulin / blood. Male. Pancreatectomy. Seizures / epidemiology. Treatment Outcome. Weight Gain

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  • (PMID = 18926551.001).
  • [ISSN] 0035-3787
  • [Journal-full-title] Revue neurologique
  • [ISO-abbreviation] Rev. Neurol. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin
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51. Dadan J, Wojskowicz P, Wojskowicz A: Neuroendocrine tumors of the pancreas. Wiad Lek; 2008;61(1-3):43-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuroendocrine tumors of the pancreas.
  • The neuroendocrine tumors (NET) of the pancreas are very rare lesions with frequency of about 3 to 10 per 1 000 000 inhabitants.
  • The neuroendocrine tumors composes a heterogeneous group of tumors.
  • The gastro-entero-pancreatic tumors (GEP) constitute 70% of all NET and 2% of all digestive system tumors.
  • There have been several attempts to classify those lesions and since 2000 exists WHO classification which divides NET according to malignancy and histologic structure.
  • The most often NET of the pancreas are insulinoma, gastrinoma, glucagonoma, somatostatinoma, VIPoma.
  • There is a recommendation to assay hormonal activity, measure concentration of specific peptides, biogenic amines and hormones produced by NET cells to establish diagnosis.
  • Those tests are useful in monitoring treatment and in prognostication course of the disease.
  • Imaging methods especially useful in localization GEP-NET are: ultrasound (US), endoscopic ultrasound (EUS), somatostatin receptor scintigraphy (SRS), computer tomography (CT), magnetic resonance (MR) and angiography.
  • Surgical treatment depends on progression of disease as well as on localization of tumor and consists in both radical methods and palliative operations.
  • Although NET of pancreas are very rare. they are still important diagnostic and therapeutic problem and requires interdisciplinary co-operation.
  • The neuroendocrine tumors should be treated in centers with highest rank of references.
  • [MeSH-major] Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Gastrinoma / diagnosis. Gastrinoma / metabolism. Gastrinoma / therapy. Glucagonoma / diagnosis. Glucagonoma / metabolism. Glucagonoma / therapy. Humans. Insulinoma / diagnosis. Insulinoma / metabolism. Insulinoma / therapy. Somatostatinoma / diagnosis. Somatostatinoma / metabolism. Somatostatinoma / therapy. Vipoma / diagnosis. Vipoma / metabolism. Vipoma / therapy

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  • (PMID = 18717042.001).
  • [ISSN] 0043-5147
  • [Journal-full-title] Wiadomości lekarskie (Warsaw, Poland : 1960)
  • [ISO-abbreviation] Wiad. Lek.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 30
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52. Marek B, Kajdaniuk D, Kos-Kudła B, Foltyn W, Borgiel-Marek H, Matyja V, Pakuła D: [Insulinoma--diagnosis and treatment]. Endokrynol Pol; 2007 Jan-Feb;58(1):58-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Insulinoma--diagnosis and treatment].
  • [Transliterated title] Insulinoma--diagnostyka i leczenie.
  • Insulinomas are the most common functioning endocrine tumors of pancreas.
  • Approximately 10% are multiple, less than 10% can be malignant and 5-10% associated with the MEN-1 syndrome.
  • Insulinomas are the most common cause of hypoglycemia resulting from endogenous hyperinsulinism.
  • The aim of this lecture is to present the up-to-date information concerning the prevalence, diagnosis and treatment of insulinoma.
  • [MeSH-major] Insulinoma. Multiple Endocrine Neoplasia Type 1. Pancreatic Neoplasms

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  • (PMID = 17354206.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 39
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53. Park S, Kim SW, Lee BL, Jung EJ, Kim WH: Expression of E-cadherin and beta-catenin in the adenoma-carcinoma sequence of ampulla of Vater cancer. Hepatogastroenterology; 2006 Jan-Feb;53(67):28-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of E-cadherin and beta-catenin in the adenoma-carcinoma sequence of ampulla of Vater cancer.
  • BACKGROUND/AIMS: Ampullary carcinoma is uncommon but provides a good model for adenoma-carcinoma sequence.
  • During the adenoma-carcinoma transition, the tumor cells should acquire the ability to invade.
  • The E-cadherin-catenin complex connects the adjacent epithelial cells at the zona adherens, and this adhesion interferes with the tumor cell invasion.
  • METHODOLOGY: 111 cases of ampullary carcinoma were investigated with E-cadherin and beta-catenin expression with immunohistochemistry and the result was compared with their clinicopathologic and survival results.
  • RESULTS: Expressional loss of E-cadherin was detected in 3 (6.1%) adenomas and 73 (65.8%) carcinomas, and the expressional loss was significantly associated with tumor cell differentiation (p<0.05) and survival (p<0.05) in carcinoma.
  • In beta-catenin immunostaining, 4 (8.2%) adenomas and 45 (40.5%) carcinomas showed abnormal staining patterns either as nuclear staining or as a loss of membrane staining.
  • The cases with membranous loss of beta-catenin expression were correlated with poor survival rate.
  • CONCLUSIONS: Alteration of E-cadherin and beta-catenin is a late event during the adenoma-carcinoma sequence in ampullary neoplasms, and the loss of membranous expression of both E-cadherin and beta-catenin is closely correlated with less differentiated histology and poor prognosis.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Ampulla of Vater. Cadherins / biosynthesis. Carcinoma / metabolism. Carcinoma / pathology. Common Bile Duct Neoplasms / metabolism. Common Bile Duct Neoplasms / pathology. beta Catenin / biosynthesis

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  • (PMID = 16506371.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Cadherins; 0 / beta Catenin
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54. Soreide K, Buter TC, Janssen EA, Gudlaugsson E, Skaland I, Körner H, Baak JP: Cell-cycle and apoptosis regulators (p16INK4A, p21CIP1, beta-catenin, survivin, and hTERT) and morphometry-defined MPECs predict metachronous cancer development in colorectal adenoma patients. Cell Oncol; 2007;29(4):301-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell-cycle and apoptosis regulators (p16INK4A, p21CIP1, beta-catenin, survivin, and hTERT) and morphometry-defined MPECs predict metachronous cancer development in colorectal adenoma patients.
  • BACKGROUND AND AIMS: Although adenomas may be precursors to colorectal cancers (CRC), knowledge concerning the development of metachronous CRC is scarce.
  • We assessed whether differential expression of cell-cycle and apoptosis-regulating proteins and a monotonous population of elongated cells (MPECs) in colorectal adenomas could predict metachronous CRC.
  • METHODS: Application of immunohistochemistry on tissue microarrays in consecutive, population-based colorectal adenomas.
  • RESULTS: Of 171 patients with colorectal adenoma 86% (n=147) were eligible for study; 10 (7%) developed metachronous CRC.
  • Elevated expression of cell-cycle regulators p16(INK4A), p21(CIP1), and cytoplasmic/nuclear beta-catenin correlated with increased CRC risk (all P<0.0001), as did elevated expression of the anti-apoptosis protein survivin (P<0.0001) and human telomerase reverse transcriptase (hTERT; P<0.001).
  • Survivin, hTERT, and nuclear beta-catenin were the most predictive molecular markers (hazard ratios [HRs]: 6.3, 9.4, and 5.8, respectively).
  • Within adenomas containing MPECs, several molecular markers further defined high-risk patients.
  • CONCLUSIONS: Among several markers predictive for metachronous CRC development in colorectal adenomas, MPECs, survivin and hTERT may, when validated, provide information superior to conventional histology, with relevance for the clinical management of patients with colorectal adenoma.
  • [MeSH-major] Adenoma / pathology. Apoptosis Regulatory Proteins / metabolism. Cell Cycle Proteins / metabolism. Colorectal Neoplasms / pathology. Neoplasms, Second Primary / pathology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Demography. Female. Humans. Immunohistochemistry. Inhibitor of Apoptosis Proteins. Kaplan-Meier Estimate. Male. Microtubule-Associated Proteins / metabolism. Middle Aged. Multivariate Analysis. Neoplasm Proteins / metabolism. Proportional Hazards Models. Telomerase / metabolism. beta Catenin / metabolism

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  • (PMID = 17641414.001).
  • [ISSN] 1570-5870
  • [Journal-full-title] Cellular oncology : the official journal of the International Society for Cellular Oncology
  • [ISO-abbreviation] Cell. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / beta Catenin; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC4617994
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55. Twardowschy CA, Leite SA, Outi TY, Dykyj MT: [Insulinoma presenting as seizure: case report]. Arq Neuropsiquiatr; 2005 Sep;63(3A):685-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Insulinoma presenting as seizure: case report].
  • [Transliterated title] Insulinoma apresentando-se como crise convulsiva: relato de caso.
  • Insulinoma is a rare disease presenting with episodic neuroglycopenic and/or adrenergic symptoms.
  • We describe the case of a 36 year-old female that had been in treatment for complex partial seizures during 4 years without improvement.
  • A 72-hour fast test showed hypoglycemic symptoms with raised insulin and C-peptide.
  • The insulinoma localization was possible during exploratory laparatomy; image methods did not reveal the tumor.
  • Histological findings confirmed an insulinoma.
  • We conclude that blood glucose level should be requested during the investigation of convulsive and behavioral disorders since an insulinoma can present like them.
  • [MeSH-major] Hypoglycemia / etiology. Insulinoma / complications. Pancreatic Neoplasms / complications. Seizures / etiology

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  • (PMID = 16172725.001).
  • [ISSN] 0004-282X
  • [Journal-full-title] Arquivos de neuro-psiquiatria
  • [ISO-abbreviation] Arq Neuropsiquiatr
  • [Language] por
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Brazil
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56. Butte JM, Montero PH, Solar A, Torres J, Olmos PR, Goñi I, Quintana JC, Martínez J, Llanos O: Cervical metastases of glucagonoma in a patient with multiple endocrine neoplasia type 1: report of a case. Surg Today; 2008;38(12):1137-43
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cervical metastases of glucagonoma in a patient with multiple endocrine neoplasia type 1: report of a case.
  • Multiple endocrine neoplasia type 1 (MEN 1) is a syndrome characterized by tumors of the parathyroid glands, pancreatic islet cells, duodenum, and pituitary gland.
  • Computed tomography (CT) showed two hypervascular lesions in the tail of the pancreas and cervical ultrasound showed multiple hypoechogenic ovoid images in the neck.
  • A cervical CT scan confirmed two 15-mm lymph nodes in the left cervical region and 111In-DOTATOC imaging showed focal abnormal somatostatin expression in the pancreatic tail and the cervical nodes.
  • The patient had asymptomatic hypoglycemic episodes, with blood sugar levels as low as 30 mg/dl, which raised our suspicion of MEN 1 associated with pancreatic insulinoma.
  • Histopathological examination revealed 12 pancreatic tumors as well as metastases in four cervical lymph nodes.
  • A follow-up CT scan, 18 months after surgery, showed new tumors in the head of the pancreas and in the duodenal wall.
  • A pancreatoduodenectomy was performed and histopathological examination revealed nine nonfunctioning endocrine tumors in the pancreas, one tumor in the duodenal wall, and metastases in two peripancreatic lymph nodes.
  • [MeSH-major] Glucagonoma / pathology. Multiple Endocrine Neoplasia Type 1 / pathology. Pancreatic Neoplasms / pathology


57. Shibata H, Takano H, Ito M, Shioya H, Hirota M, Matsumoto H, Kakudo Y, Ishioka C, Akiyama T, Kanegae Y, Saito I, Noda T: Alpha-catenin is essential in intestinal adenoma formation. Proc Natl Acad Sci U S A; 2007 Nov 13;104(46):18199-204
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-catenin is essential in intestinal adenoma formation.
  • Although the molecular mechanism of tumor initiation is complex, several modifier genes have been identified using mouse models, including the ApcMin mouse.
  • Among the familial adenomatous polyposis mouse lines carrying a truncation mutation at codon 580 in Apc (Apc580D), one line (line19-Apc(580D/+)) showed a remarkably reduced incidence of intestinal adenomas (<5% compared with other lines).
  • In all adenomas generated in line19-Apc(580D/+), somatic recombination between the Apc and Ctnna1 loci retained the wild-type Ctnna1 allele.
  • These data strongly indicate that simultaneous inactivation of alpha-catenin and Apc during tumor initiation suppresses adenoma formation in line19-Apc(580D/+), suggesting that alpha-catenin plays an essential role in the initiation of intestinal adenomas.
  • Although accumulating evidence obtained from human colon tumors with invasive or metastatic potential has established a tumor-suppressive role for alpha-catenin in late-stage tumorigenesis, the role of alpha-catenin in the initiation of intestinal tumorigenesis is not well documented, especially compared with that of beta-catenin.
  • A mouse model used in this study focused on the early stage of tumor initiation and clearly indicated an essential role for alpha-catenin.
  • Thus, alpha-catenin has dual roles in intestinal tumorigenesis, a supporting role in tumor initiation, and a suppressive role in tumor progression.
  • [MeSH-major] Adenoma / pathology. Intestinal Neoplasms / pathology. alpha Catenin / physiology

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  • (PMID = 17989230.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / alpha Catenin
  • [Other-IDs] NLM/ PMC2084320
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58. Bioulac-Sage P, Blanc JF, Rebouissou S, Balabaud C, Zucman-Rossi J: Genotype phenotype classification of hepatocellular adenoma. World J Gastroenterol; 2007 May 21;13(19):2649-54
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  • [Title] Genotype phenotype classification of hepatocellular adenoma.
  • Studies that compare tumor genotype with phenotype have provided the basis of a new histological/molecular classification of hepatocellular adenomas.
  • Based on two molecular criteria (presence of a TCF1/HNF1 alpha or beta-catenin mutation), and an additional histological criterion (presence or absence of an inflammatory infiltrate), subgroups of hepatocellular adenoma can be defined and distinguished from focal nodular hyperplasia.
  • Analysis of 96 hepatocellular adenomas performed by a French collaborative network showed that they can be divided into four broad subgroups: the first one is defined by the presence of mutations in TCF1 gene inactivating the hepatocyte nuclear factor 1 (HNF1 alpha); the second by the presence of beta-catenin activating mutations; the category without mutations of HNF1 alpha or beta-catenin is further divided into 2 subgroups depending on the presence or absence of inflammation.
  • It is hoped that immunohistological tools will improve significantly diagnosis of liver biopsy in our ability to distinguish hepatocellular adenoma from focal nodular hyperplasia (FNH), and to delineate clinically meaningful entities within each group to define the best clinical management.
  • [MeSH-major] Adenoma, Liver Cell / classification. Genotype. Liver Neoplasms / classification. Phenotype
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Focal Nodular Hyperplasia / diagnosis. Hepatocyte Nuclear Factor 1-alpha / genetics. Humans. Liver / pathology. Mutation / genetics. beta Catenin / genetics

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  • (PMID = 17569132.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / beta Catenin
  • [Number-of-references] 23
  • [Other-IDs] NLM/ PMC4147112
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59. Miyai S, Yoshimura S, Iwasaki Y, Takekoshi S, Lloyd RV, Osamura RY: Induction of GH, PRL, and TSH beta mRNA by transfection of Pit-1 in a human pituitary adenoma-derived cell line. Cell Tissue Res; 2005 Nov;322(2):269-77
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  • [Title] Induction of GH, PRL, and TSH beta mRNA by transfection of Pit-1 in a human pituitary adenoma-derived cell line.
  • The functional development of pituitary cells depends on the expression of a combination of transcription factors and co-factors.
  • Pituitary-specific transcription factor-1 (Pit-1) is required for the expression of growth hormone (GH), prolactin (PRL), and the thyroid-stimulating hormone beta subunit (TSH beta) and acts synergistically with the estrogen receptor (ER) and GATA-binding protein 2 (GATA-2) to induce PRL and TSH beta expression, respectively.
  • In addition to being expressed in follicle-stimulating hormone, luteinizing hormone (LH), and TSH cells, alpha SU is reported to co-localize with GH in pituitary cells.
  • These findings have led to the suggestion that the expression of Pit-1 in cells of the alpha SU-based gonadotropin cell lineage might also lead to the expression of GH.
  • In this study, we transfected HP 75 cells (derived from a human non-functioning pituitary adenoma that expressed alpha SU and LH beta) with Pit-1 by using an adenovirus FLAG-Pit-1 construct.
  • Most of the transfected cells expressed GH mRNA, with fewer cells expressing PRL and TSH beta mRNA.
  • The HP 75 cells expressed the genes for ER and GATA-2, thus allowing their expression of GH, PRL, and TSH beta mRNA in response to Pit-1.
  • These results support the hypothesis that GH can be induced in cells that possess an active alpha SU gene and shed light on the basic molecular mechanism that drives the development of GH, PRL, and TSH beta expression in the alpha SU-based gonadotroph lineage.
  • [MeSH-major] Adenoma / metabolism. Human Growth Hormone / metabolism. Pituitary Neoplasms / metabolism. Prolactin / metabolism. RNA, Messenger / metabolism. Thyrotropin, beta Subunit / metabolism. Transcription Factor Pit-1 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Lineage. GATA2 Transcription Factor / genetics. GATA2 Transcription Factor / metabolism. Glycoprotein Hormones, alpha Subunit / genetics. Glycoprotein Hormones, alpha Subunit / metabolism. Humans. Pituitary Gland / cytology. Pituitary Gland / growth & development. Pituitary Gland / metabolism. Receptors, Estrogen / genetics. Receptors, Estrogen / metabolism. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism

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  • (PMID = 16133148.001).
  • [ISSN] 0302-766X
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / GATA2 Transcription Factor; 0 / Glycoprotein Hormones, alpha Subunit; 0 / RNA, Messenger; 0 / Receptors, Estrogen; 0 / Recombinant Fusion Proteins; 0 / Thyrotropin, beta Subunit; 0 / Transcription Factor Pit-1; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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60. Kauhanen S, Seppänen M, Minn H, Gullichsen R, Salonen A, Alanen K, Parkkola R, Solin O, Bergman J, Sane T, Salmi J, Välimäki M, Nuutila P: Fluorine-18-L-dihydroxyphenylalanine (18F-DOPA) positron emission tomography as a tool to localize an insulinoma or beta-cell hyperplasia in adult patients. J Clin Endocrinol Metab; 2007 Apr;92(4):1237-44
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  • [Title] Fluorine-18-L-dihydroxyphenylalanine (18F-DOPA) positron emission tomography as a tool to localize an insulinoma or beta-cell hyperplasia in adult patients.
  • CONTEXT AND OBJECTIVE: Fluorine-18-L-dihydroxyphenylalanine (18F-DOPA) positron emission tomography (PET) is a promising method in localizing neuroendocrine tumors.
  • The current study was set up to determine the potential of 18F-DOPA PET in identifying the insulin-secreting tumors or beta-cell hyperplasia of the pancreas in adults.
  • PATIENTS AND METHODS: We prospectively studied 10 patients with confirmed hyperinsulinemic hypoglycemia and presumed insulin-secreting tumor using 18F-DOPA PET.
  • Semiquantitative PET findings in the pancreas using standardized uptake values were compared to standardized uptake values of seven consecutive patients with nonpancreatic neuroendocrine tumors.
  • RESULTS: By visual inspection of 18F-DOPA PET images, it was possible in nine of 10 patients to localize the pancreatic lesion, subsequently confirmed by histological analysis.
  • 18F-DOPA uptake was enhanced in six of seven solid insulinomas and in the malignant insulinoma and its hepatic metastasis.
  • Two patients with beta-cell hyperplasia showed increased focal uptake of 18F-DOPA in the affected areas.
  • As compared to CT or MRI, 18F-DOPA PET was more sensitive in localizing diseased pancreatic tissue.
  • CONCLUSION: 18F-DOPA PET was useful in most patients with insulinoma and negative CT, MRI, and ultrasound results.
  • In agreement with previous findings in infants, preoperative 18F-DOPA imaging seems to be a method of choice for the detection of beta-cell hyperplasia in adults.
  • It should be considered for the detection of insulinoma or beta-cell hyperplasia in patients with confirmed hyperinsulinemic hypoglycemias when other diagnostic work-up is negative.
  • [MeSH-major] Dihydroxyphenylalanine / analogs & derivatives. Insulin-Secreting Cells / radionuclide imaging. Insulinoma / radionuclide imaging. Pancreatic Neoplasms / radionuclide imaging

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  • (PMID = 17227804.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 42877-15-6 / 5-fluorodopa; 63-84-3 / Dihydroxyphenylalanine
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61. Foley PJ, Scheri RP, Smolock CJ, Pippin J, Green DW, Drebin JA: Targeted suppression of beta-catenin blocks intestinal adenoma formation in APC Min mice. J Gastrointest Surg; 2008 Aug;12(8):1452-8

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  • [Title] Targeted suppression of beta-catenin blocks intestinal adenoma formation in APC Min mice.
  • INTRODUCTION: Mutations involving the adenomatous polyposis coli (APC) tumor suppressor gene leading to activation of beta-catenin have been identified in the majority of sporadic colonic adenocarcinomas and in essentially all colonic tumors from patients with Familial Adenomatous Polyposis.
  • The C57BL/6J-APC(min) (Min) mouse, which carries a germ line mutation in the murine homolog of the APC gene is a useful model for intestinal adenoma formation linked to loss of APC activity.
  • One of the critical downstream molecules regulated by APC is beta-catenin; molecular targeting of beta-catenin is, thus, an attractive chemopreventative strategy in colon cancer.
  • Antisense oligodeoxynucleotides (AODNs) capable of downregulating murine beta-catenin have been identified.
  • ANALYSIS OF beta-CATENIN PROTEIN EXPRESSION IN LIVER TISSUE AND INTESTINAL ADENOMAS: Adenomas harvested from mice treated for 7 days with beta-catenin AODNs demonstrated clear downregulation of beta-catenin expression, which was accompanied by a significant reduction in proliferation.
  • Min mice treated systemically with beta-catenin AODNs over a 6-week period had a statistically significant reduction in the number of intestinal adenomas.
  • These studies provide direct evidence that targeted suppression of beta-catenin inhibits the formation of intestinal adenomas in APC-mutant mice.
  • Furthermore, these studies suggest that molecular targeting of beta-catenin holds significant promise as a chemopreventative strategy in colon cancer.
  • [MeSH-major] Adenomatous Polyposis Coli / therapy. Colonic Neoplasms / therapy. Gene Expression Regulation, Neoplastic. Gene Targeting / methods. RNA, Neoplasm / genetics. beta Catenin / genetics
  • [MeSH-minor] Animals. Blotting, Northern. Blotting, Western. Cell Proliferation. Disease Progression. Female. Immunohistochemistry. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Neoplasms, Experimental. Treatment Outcome

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  • (PMID = 18521697.001).
  • [ISSN] 1873-4626
  • [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
  • [Grant] United States / NCI NIH HHS / CA / R01 CA100189
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CTNNB1 protein, mouse; 0 / RNA, Neoplasm; 0 / beta Catenin
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62. Bioulac-Sage P, Laumonier H, Couchy G, Le Bail B, Sa Cunha A, Rullier A, Laurent C, Blanc JF, Cubel G, Trillaud H, Zucman-Rossi J, Balabaud C, Saric J: Hepatocellular adenoma management and phenotypic classification: the Bordeaux experience. Hepatology; 2009 Aug;50(2):481-9
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  • [Title] Hepatocellular adenoma management and phenotypic classification: the Bordeaux experience.
  • We took advantage of the reported genotype/phenotype classification to analyze our surgical series of hepatocellular adenoma (HCA).
  • We identified 46 HNF1alpha-inactivated HCAs (44 women), 63 inflammatory HCAs (IHCA, 53 women) of which nine were also beta-catenin-activated, and seven beta-catenin-activated HCAs (all women); six additional cases had no known phenotypic marker and six others could not be phenotypically analyzed.
  • No differences were observed in solitary or multiple tumors in terms of hemorrhagic manifestations between groups.
  • Steatosis (tumor), microadenomas (resected specimen), and additional benign nodules were more frequently observed in HNF1alpha-inactivated HCAs (P < 0.01) than in IHCAs.
  • Body mass index > 25, peliosis (tumor), and steatosis in background liver were more frequent in IHCA (P < 0.01).
  • Six patients of 128 developed hepatocellular carcinoma (HCC) (all were beta-catenin-activated, whether inflammatory or not).
  • CONCLUSION: There were noticeable clinical differences between HNF1alpha-inactivated HCA and IHCA; there was no increased risk of bleeding or HCC related to the number of HCAs; beta-catenin-activated HCAs are at higher risk of HCC.
  • As a consequence, we believe that management of HCA needs to be adapted to the phenotype of these tumors.
  • [MeSH-major] Adenoma, Liver Cell / classification. Liver Neoplasms / classification
  • [MeSH-minor] Adult. Aged. C-Reactive Protein / metabolism. Fatty Acid-Binding Proteins / metabolism. Female. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Male. Middle Aged. Phenotype. Serum Amyloid A Protein / metabolism. Young Adult. beta Catenin / metabolism

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  • (PMID = 19585623.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acid-Binding Proteins; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Serum Amyloid A Protein; 0 / beta Catenin; 9007-41-4 / C-Reactive Protein
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63. Bioulac-Sage P, Laumonier H, Laurent C, Zucman-Rossi J, Balabaud C: Hepatocellular adenoma: what is new in 2008. Hepatol Int; 2008 Sep;2(3):316-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hepatocellular adenoma: what is new in 2008.
  • Patients (85%) with hepatocellular adenoma (HCA) are women taking oral contraceptives.
  • An HNF1alpha germline mutation is observed in less than 5% of HCA cases and can be associated with MODY 3 diabetes. (2) An activating beta-catenin mutation was found in 10% of HCA.
  • These beta-catenin activated HCAs are observed in men and women, and specific risk factors, such as male hormone administration or glycogenosis, are associated with their development.
  • Immunohistochemistry studies show that these HCAs overexpress beta-catenin (nuclear and cytoplasmic) and glutamine synthetase.
  • This group of tumours has a higher risk of malignant transformation into hepatocellular carcinoma. (3) Inflammatory HCAs are observed in 40% of the cases, and they are most frequent in women but are also found in men.
  • In this group, GGT is frequently elevated, with a biological inflammatory syndrome present.
  • An additional 10% of inflammatory HCAs express beta-catenin, and are also at risk of malignant transformation. (4) Currently, less than 10% of HCAs are unclassified.

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  • (PMID = 19669260.001).
  • [ISSN] 1936-0533
  • [Journal-full-title] Hepatology international
  • [ISO-abbreviation] Hepatol Int
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2716879
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64. Koga Y, Yao T, Hirahashi M, Kumashiro Y, Ohji Y, Yamada T, Tanaka M, Tsuneyoshi M: Flat adenoma-carcinoma sequence with high-malignancy potential as demonstrated by CD10 and beta-catenin expression: a different pathway from the polypoid adenoma-carcinoma sequence. Histopathology; 2008 Apr;52(5):569-77
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  • [Title] Flat adenoma-carcinoma sequence with high-malignancy potential as demonstrated by CD10 and beta-catenin expression: a different pathway from the polypoid adenoma-carcinoma sequence.
  • The aim was to examine phenotypic expression in colorectal neoplasia and to elucidate changes in such expression through the adenoma-carcinoma sequence.
  • Nuclear beta-catenin was more frequently expressed in NPG-LGN than in PG-LGN.
  • CONCLUSIONS: From the viewpoint of the expression of CD10 and beta-catenin, it would appear that NPG-LGN differs significantly from PG-LGN, thereby indicating that NPG-LGN is a precursor of CD10+ carcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma / pathology. Colonic Polyps / pathology. Colorectal Neoplasms / pathology. Neprilysin / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Cell Nucleus / metabolism. Cell Nucleus / pathology. Disease Progression. Early Diagnosis. Female. Humans. Immunohistochemistry. Intestinal Mucosa / metabolism. Intestinal Mucosa / pathology. Male. Neoplasm Invasiveness

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  • (PMID = 18370954.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / beta Catenin; EC 3.4.24.11 / Neprilysin
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65. Cavallaro G, Cucina A, Coluccia P, Petramala L, Cotesta D, Polistena A, Zinnamosca L, Letizia C, Rosato L, Cavallaro A, De Toma G: Role of growth factors on human parathyroid adenoma cell proliferation. World J Surg; 2010 Jan;34(1):48-54

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of growth factors on human parathyroid adenoma cell proliferation.
  • INTRODUCTION: Primary hyperparathyroidism (pHPT) is caused by a single monoclonal adenoma in more than 80% of patients.
  • Among the latter, insulin-like growth factor 1 (IGF-1), basic fibroblastic growth factor (bFGF), vascular endothelial growth factor (VEGF), and transforming growth factor beta 1 (TGF-beta1) and their effects have been extensively evaluated in different kinds of endocrine disease.
  • METHODS: Parathyroid cell cultures were prepared from six human adenomatous parathyroid glands that were surgically removed.
  • After 7 days of culture, the cells were refed with DMEM supplemented with 2% FCS alone (control group), or containing hrTGFbeta1, or hrIGF-I, or hrbFGF, or hrVEGF.
  • Then, after 48-hour incubation, cell count was performed by a particle count and size analyzer, and prevalence of cell cycle was analyzed by using a flow cytometer.
  • RESULTS: Cell count (x10000) in the control group was 3.73 +/- 0.32.
  • Low-dose TGF-beta1 stimulation resulted in 5.25 +/- 0.38 cells, and high-dose TGF-beta1 stimulation resulted in 2.35 +/- 0.37 cells.
  • IGF-1 stimulation resulted in 5.4 +/- 0.65 cells, bFGF stimulation in 5.68 +/- 0.86 cells, and VEGF stimulation resulted in 6.03 +/- 1.03 cells.
  • Cytometry showed different results in the percentage of cells in S-phase, in particular 22.65 +/- 4.98% of IGF-1-stimulated cells were found in S-phase compared with 7.55 +/- 3.2% of control group cells (p < 0.0001).
  • CONCLUSIONS: Growth factors seem to play an important role in parathyroid adenoma cell proliferation; IGF-1, bFGF, VEGF, and low-dose TGF-beta1 promote cell proliferation, whereas high-dose TGF-beta1 inhibits these phenomena.
  • [MeSH-major] Adenoma / pathology. Cell Proliferation / drug effects. Fibroblast Growth Factor 2 / pharmacology. Insulin-Like Growth Factor I / pharmacology. Parathyroid Neoplasms / pathology. Transforming Growth Factor beta1 / pharmacology. Vascular Endothelial Growth Factor A / pharmacology
  • [MeSH-minor] Analysis of Variance. Cells, Cultured. Female. Flow Cytometry. Humans. Male. Middle Aged

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  • (PMID = 20020293.001).
  • [ISSN] 1432-2323
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta1; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2; 67763-96-6 / Insulin-Like Growth Factor I
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66. Shcherbinina MB, Kosinskaia SV, Fateeva TV, Gaĭdar IuA: [Insulinoma]. Klin Med (Mosk); 2008;86(2):70-6
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  • [Title] [Insulinoma].
  • The authors review statistical, pathogenic, and clinical aspects of insulinima, a rare pancreatic tumor growing from beta-cells of islets of Langerhans.
  • Its functioning is associated with periodical impulsive ejection of insulin, its precursors, and relative peptides in large quantities, which results in hypoglycemic state.
  • When consciousness remains, the leading clinical syndrome is vegetative dysfunction.
  • The article describes diagnostic methods in insulinoma; their informative value is evaluated.
  • The authors describe their own observation of insulinoma, which illustrates difficulties in its revealing.
  • At the same time, the authors affirm that sufficient information make it possible for doctors to establish timely diagnosis of this disease.
  • [MeSH-major] Insulinoma. Pancreatic Neoplasms

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  • (PMID = 18368799.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Number-of-references] 18
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67. Davis JR, McNeilly JR, Norris AJ, Pope C, Wilding M, McDowell G, Holland JP, McNeilly AS: Fetal gonadotrope cell origin of FSH-secreting pituitary adenoma - insight into human pituitary tumour pathogenesis. Clin Endocrinol (Oxf); 2006 Nov;65(5):648-54
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  • [Title] Fetal gonadotrope cell origin of FSH-secreting pituitary adenoma - insight into human pituitary tumour pathogenesis.
  • OBJECTIVE: The pathogenesis of human pituitary adenomas remains unclear, but we report a case of FSH-secreting pituitary adenoma whose monohormonal phenotype suggests it was of fetal origin.
  • MEASUREMENTS: Endocrine studies were performed before and after curative surgery, with assessment of tumour hormone secretion in vitro, and immunostaining of tumour tissue for a series of gonadotrope proteins.
  • RESULTS: Immunocytochemistry showed that tumour cells were monohormonal for FSH.
  • Normal components of gonadotrope signalling pathways were expressed, including oestrogen receptor-alpha, activin receptors, secretogranin-II and chromogranin-A. beta-glycan, the putative inhibin coreceptor, was absent.
  • Tumour culture in vitro confirmed secretion of FSH with minimal LH, that was unsuppressed by oestradiol or inhibin-A.
  • Human fetal pituitary tissue contained FSH-only cells at 18 weeks gestation, whereas normal adult pituitary tissue contained only bihormonal gonadotropes.
  • CONCLUSIONS: We propose that this pituitary adenoma represents an indolent tumour of monohormonal fetal gonadotrope cells that originated early in gestation.
  • Pituitary tumours may therefore arise from abnormal persistence of fetal cell types, with extremely slow growth over many years until reaching a size threshold to generate an endocrine syndrome.
  • Understanding fetal pituitary architecture and function may be more informative for new insights into pituitary tumour pathogenesis than classical theories of cancer biology that invoke unrestrained cell proliferation.
  • [MeSH-major] Adenoma / embryology. Gonadotrophs / secretion. Pituitary Neoplasms / embryology
  • [MeSH-minor] Adult. Estradiol / blood. Female. Follicle Stimulating Hormone / analysis. Follicle Stimulating Hormone / blood. Follicle Stimulating Hormone / secretion. Humans. Immunohistochemistry / methods. Immunoradiometric Assay / methods. Luteinizing Hormone / blood. Pituitary Gland, Anterior / embryology. Pituitary Gland, Anterior / secretion. Polycystic Ovary Syndrome / blood. Polycystic Ovary Syndrome / embryology. Polycystic Ovary Syndrome / etiology. Tissue Culture Techniques

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  • (PMID = 17054468.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 4TI98Z838E / Estradiol; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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68. Kang WY, Chen WT, Wu MT, Chai CY: The expression of CD66a and possible roles in colorectal adenoma and adenocarcinoma. Int J Colorectal Dis; 2007 Aug;22(8):869-74
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  • [Title] The expression of CD66a and possible roles in colorectal adenoma and adenocarcinoma.
  • BACKGROUND: The aim of our study was to analyze the expression and possible role of CD66a in colorectal adenoma and adenocarcinoma and the relationship between its expression and pre-operation serum carcinoembryonic antigen (CEA) level and tumor stage in patients with colorectal adenocarcinomas.
  • METHODS: Paraffin-embedded sections from 184 patients including 42 colorectal adenomas with low-grade dysplasia, 43 adenomas with high-grade dysplasia, and 99 adenocarcinomas were collected for this study.
  • Immunohistochemical analysis was performed, and the expression and the location of CD66a were evaluated and were correlated with beta-catenin nuclear expression.
  • RESULTS: The expression of CD66a was found not only in the apical membrane of neoplastic glands but also in secretion within the lumen of the neoplastic glands including adenomas and adenocarcinomas.
  • Expressions of secreted CD66a were of higher level in adenocarcinoma than in adenoma with high-grade dysplasia and adenoma with low-grade dysplasia (p < 0.0001).
  • High expression of secreted CD66a was also associated with tumor stage, invasion, and pre-operation serum CEA level of patients with colorectal adenocarcinoma.
  • CONCLUSIONS: This study implied that CD66a can function both as an epithelial cell adhesion protein or alternatively as secreted CD66a.
  • In addition, a high expression of CD66a was significantly correlated with tumor invasion, stage, and pre-operation serum CEA level.
  • [MeSH-major] Adenocarcinoma / immunology. Adenoma / immunology. Antigens, CD / analysis. Cell Adhesion Molecules / analysis. Colorectal Neoplasms / immunology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoembryonic Antigen / blood. Cell Nucleus / chemistry. Female. Humans. Lymph Nodes / pathology. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Staging. beta Catenin / analysis

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  • (PMID = 17143599.001).
  • [ISSN] 0179-1958
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD66 antigens; 0 / CTNNB1 protein, human; 0 / Carcinoembryonic Antigen; 0 / Cell Adhesion Molecules; 0 / beta Catenin
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69. Gurlo T, Ryazantsev S, Huang CJ, Yeh MW, Reber HA, Hines OJ, O'Brien TD, Glabe CG, Butler PC: Evidence for proteotoxicity in beta cells in type 2 diabetes: toxic islet amyloid polypeptide oligomers form intracellularly in the secretory pathway. Am J Pathol; 2010 Feb;176(2):861-9
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  • [Title] Evidence for proteotoxicity in beta cells in type 2 diabetes: toxic islet amyloid polypeptide oligomers form intracellularly in the secretory pathway.
  • The islet in type 2 diabetes mellitus (T2DM) is characterized by a deficit in beta cells and islet amyloid derived from islet amyloid polypeptide (IAPP), a protein co-expressed with insulin by beta cells.
  • Using an antibody specific for toxic oligomers and cryo-immunogold labeling in human IAPP transgenic mice, human insulinoma and pancreas from humans with and without T2DM, we sought to establish the abundance and sites of formation of IAPP toxic oligomers.

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  • (PMID = 20042670.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK059579; United States / NIDDK NIH HHS / DK / DK059579
  • [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 / Amyloid; 0 / Islet Amyloid Polypeptide
  • [Other-IDs] NLM/ PMC2808091
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70. Mathur A, Gorden P, Libutti SK: Insulinoma. Surg Clin North Am; 2009 Oct;89(5):1105-21
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  • [Title] Insulinoma.
  • Insulinoma is a rare neuroendocrine tumor with an incidence of 4 per 1 million persons per year, which may occur as a unifocal sporadic event in patients without an inherited syndrome or as a part of multiple endocrine neoplasia type 1.
  • Once the diagnosis is established, the insulinoma is preoperatively localized within the pancreas with the goal of surgical excision for cure.
  • This review discusses the historical background, diagnosis, and management of sporadic insulinoma.
  • [MeSH-major] Insulinoma / surgery. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Combined Modality Therapy. Diagnosis, Differential. Diagnostic Imaging. Humans. Liver Transplantation. Neoplasm Metastasis

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  • (PMID = 19836487.001).
  • [ISSN] 1558-3171
  • [Journal-full-title] The Surgical clinics of North America
  • [ISO-abbreviation] Surg. Clin. North Am.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 DK999999
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 69
  • [Other-IDs] NLM/ NIHMS410902; NLM/ PMC3470467
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71. Valente TO, Bertevello PL, Waitzberg DL, Gama-Rodrigues J: [Laparoscopic surgical treatment of insulinomas with the use of intraoperative ultrasonography]. Arq Gastroenterol; 2007 Jan-Mar;44(1):22-8
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  • [Title] [Laparoscopic surgical treatment of insulinomas with the use of intraoperative ultrasonography].
  • [Transliterated title] Tratamento cirúrgico videolaparoscópico de insulinomas utilizando ultra-sonografia intra-operatória.
  • BACKGROUND: Insulinoma are insulin productive tumors originated from the pancreatic beta cells with an incidence of 4/1 million persons.
  • It is more prevalent between the 5th and 6th decade, in women (2:1) and from the endocrine pancreatic tumor is the more frequent (50% to 60%).
  • Insulinoma behave as a benign tumor when the diameter is inferior to 2 cm.
  • METHODS: Five patients were studied (3 man and 2 women) with age from 20 to 53 years old, clinically diagnosed with insulinoma.
  • After image work out it was proposed nuclear resection of the insulinoma by laparoscopic technique associated to intraoperative ultrasonography.
  • RESULTS: The patients had a complete remission of tumor related hypoglycemia and one patient developed a pancreatic fistula and other a pancreatic pseudocist with good postoperative resolution.
  • CONCLUSIONS: The videolaparoscopic approach for the surgical treatment of insulinoma is feasible.
  • [MeSH-major] Insulinoma / surgery. Laparoscopy / methods. Pancreatic Neoplasms / surgery. Ultrasonography, Interventional

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  • (PMID = 17639178.001).
  • [ISSN] 0004-2803
  • [Journal-full-title] Arquivos de gastroenterologia
  • [ISO-abbreviation] Arq Gastroenterol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Brazil
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72. Yang GZ, Li J, Ding HY: [Nipple adenoma: report of 18 cases with review of literatures]. Zhonghua Bing Li Xue Za Zhi; 2009 Sep;38(9):614-6
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  • [Title] [Nipple adenoma: report of 18 cases with review of literatures].
  • OBJECTIVE: To investigate the clinicopathological and immunohistochemical features, diagnosis and differential diagnosis of nipple adenoma of the breast.
  • METHODS: Morphological observation and immunohistochemistry were applied to 18 cases of nipple adenoma with a review of the related literatures.
  • The glandular epithelium showed various type of proliferation, forming thick layers or complex structures such as papillae, micropapillae, tufts, fronds, arcades or bridges accompanying with solid or cribriform cell nests.
  • The tumor cells were crowding, lack of an uniform morphology and polarity with intact myoepithelial cells around the ducts.
  • CONCLUSIONS: Nipple adenoma is an infrequent type of benign breast neoplasm, presenting as sclerosing papilloma, papillomatosis or florid sclerosing adenosis.
  • A correct diagnosis is based on the peculiar location and morphology of the tumor, and immunohistochemistry is helpful in some cases.
  • [MeSH-major] Adenoma / pathology. Breast Neoplasms / pathology. Nipples / pathology

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  • (PMID = 20079190.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CK-34 beta E12; 0 / Keratin-5; 68238-35-7 / Keratins
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73. Araújo VC, Demasi AP, Furuse C, Altemani A, Alves VA, Freitas LL, Araújo NS: Collagen type I may influence the expression of E-cadherin and beta-catenin in carcinoma ex-pleomorphic adenoma. Appl Immunohistochem Mol Morphol; 2009 Jul;17(4):312-8
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  • [Title] Collagen type I may influence the expression of E-cadherin and beta-catenin in carcinoma ex-pleomorphic adenoma.
  • Carcinoma ex-pleomorphic adenoma (CXPA) is an aggressive salivary gland malignancy, usually derived from a long-standing or a recurrent benign tumor, the pleomorphic adenoma (PA).
  • In the context of dynamic reciprocity, changes in the composition and structure of extracellular matrix proteins and cell surface receptors have been frequently associated with dysfunctional adhesion and invasive behavior of tumor cells.
  • In this study, different progression stages of CXPA were investigated regarding the expression of the major extracellular matrix proteins, collagen type I, and of E-cadherin and beta-catenin, the components of adherens junctions.
  • By immunohistochemical analysis, we have demonstrated that direct contact of tumor cells with fibrillar type I collagen, particularly near the invasive front and in invasive areas prevailing small nests of CXPA cells, could be associated with reduced expression of the E-cadherin and beta-catenin adhesion molecules and with invasive behavior of epithelial, but not of CXPA with myoepithelial component.

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  • (PMID = 19276972.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / Collagen Type I; 0 / Neoplasm Proteins; 0 / beta Catenin
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74. Krysiak R, Okopień B, Herman ZS: [Insulinoma]. Pol Merkur Lekarski; 2007 Jan;22(127):70-4
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  • [Title] [Insulinoma].
  • 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.
  • The clinical presentation of this neoplasm depends on excessive production of insulin and pro-insulin and is characterised by the symptoms of neuroglycopenia and catecholamine response.
  • 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.
  • The aim of this paper is to critically discuss contemporary diagnosis and treatment of this neoplasm on the basis of progress made in recent years.
  • [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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75. Schulenburg A, Cech P, Herbacek I, Marian B, Wrba F, Valent P, Ulrich-Pur H: CD44-positive colorectal adenoma cells express the potential stem cell markers musashi antigen (msi1) and ephrin B2 receptor (EphB2). J Pathol; 2007 Oct;213(2):152-60
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  • [Title] CD44-positive colorectal adenoma cells express the potential stem cell markers musashi antigen (msi1) and ephrin B2 receptor (EphB2).
  • The majority of colorectal adenomas contain a mutation in the APC gene activating the wnt pathway.
  • As wnt signalling preserves stem cell functions, it would be expected that stem cells would be enriched in adenomas.
  • We have shown expression of the wnt target gene CD44, which may characterize the expanded stem cell compartment, in colorectal tumours.
  • To investigate this possibility, we performed an immunohistological survey of CD44 expression in relation to the proliferation marker Ki67 and apoptosis in colorectal tumour tissue, and have isolated a CD44-positive subpopulation of the human colorectal adenoma cell line LT97 for cell biological analysis.
  • While CD44-positive cells attached and grew to reconstitute the original culture, the CD44-negative cells rapidly underwent apoptosis and were unable to resume growth.
  • In comparison to unsorted growing LT97 cells, the CD44-positive cells had shifted beta-catenin into the nucleus and expressed beta-catenin target genes, such as ephrin B receptor (ephB2) and musashi antigen (msi1).
  • By contrast, CD44-negative cultures contained no cells with nuclear beta-catenin.
  • In summary, the CD44-positive cells accumulating in colorectal tumours have increased survival capacity both in vivo and in vitro.
  • They also express markers typical of colorectal progenitor cells, msi1 and ephB2, in the premalignant progenitor population.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / metabolism. Colorectal Neoplasms / metabolism. Nerve Tissue Proteins / metabolism. RNA-Binding Proteins / metabolism. Receptor, EphB2 / metabolism
  • [MeSH-minor] Antigens, CD44 / metabolism. Apoptosis. Cell Proliferation. Cell Survival. Flow Cytometry. Humans. Neoplasm Proteins / metabolism. Neoplastic Stem Cells / metabolism. Polymerase Chain Reaction / methods. Tumor Cells, Cultured. beta Catenin / metabolism

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  • (PMID = 17708598.001).
  • [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 / Antigens, CD44; 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / MSI1 protein, human; 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / RNA-Binding Proteins; 0 / beta Catenin; EC 2.7.10.1 / Receptor, EphB2
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76. do Prado RF, Consolaro A, Taveira LA: Expression of betacatenin in carcinoma in pleomorphic adenoma, pleomorphic adenoma and normal salivary gland: an immunohistochemical study. Med Oral Patol Oral Cir Bucal; 2006 May;11(3):E247-51
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  • [Title] Expression of betacatenin in carcinoma in pleomorphic adenoma, pleomorphic adenoma and normal salivary gland: an immunohistochemical study.
  • OBJECTIVES: Pleomorphic adenomas are the most frequent type of epithelial salivary gland neoplasms, and their malignant counterpart, the carcinoma in pleomorphic adenomas, is much less common.
  • Beta-catenin is a cell adhesion molecule associated with the invasion and metastasis of carcinomas of the head and neck, esophagus.
  • The objective of this study was to detect the expression of beta-catenin in pleomorphic adenomas, carcinomas in pleomorphic adenomas and normal salivary glands to discuss its role in the development of these two lesions.
  • STUDY DESIGN: The expression of beta-catenin (BD Transduction Laboratories) was analyzed by immunohistochemistry in formalin-fixed, paraffin embedded specimens by the avidin-biotin-peroxidase complex method in 16 pleomorphic adenomas (12 from minor salivary glands), 3 carcinomas in pleomorphic adenomas (all from palate) and 10 normal salivary glands as control group (5 from major and 5 from minor salivary glands).
  • RESULTS: All cases of glands, adenomas and carcinomas in pleomorphic adenomas have membranous and cytoplasmic immunostaining.
  • Nuclear beta-catenin immunostaining was not observed.
  • The antibody presented a fine granular arrangement in the cytoplasm and cellular membrane of duct and acinic cells.
  • Higher beta-catenin index rates were seen mainly in salivary gland ducts and in ductal structures in the adenomas and carcinomas in pleomorphic adenomas.
  • There was protein loss in pleomorphic adenomas and cytoplasmic accumulation in carcinoma in pleomorphic adenomas.
  • CONCLUSIONS: The present study showed participation of the loss of beta-catenin adhesion molecule in the development of pleomorphic adenoma, and that the cytoplasmic accumulation of the molecule takes part in the malignant transformation of the pleomorphic adenoma into carcinoma in pleomorphic adenoma.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Carcinoma / metabolism. Neoplasms, Multiple Primary / metabolism. Salivary Gland Neoplasms / metabolism. Salivary Glands / metabolism. beta Catenin / biosynthesis

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  • (PMID = 16648762.001).
  • [ISSN] 1698-6946
  • [Journal-full-title] Medicina oral, patología oral y cirugía bucal
  • [ISO-abbreviation] Med Oral Patol Oral Cir Bucal
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / beta Catenin
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77. Wouters RS, van den Ouweland JM, Pouwels JG, Wolffenbuttel BH: [Missed hyperinsulinaemia in a patient with an insulinoma]. Ned Tijdschr Geneeskd; 2005 Apr 23;149(17):944-6
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  • [Title] [Missed hyperinsulinaemia in a patient with an insulinoma].
  • [Transliterated title] Gemiste hyperinsulinemie bij een patiënt met insulinoom.
  • In a 57-year-old man with symptomatic hypoglycaemias which gave cause to suspect an insulinoma, normal insulin levels were initially found.
  • Scans revealed an abnormality in the pancreas.
  • After surgical removal of the insulin-producing tumour the patient made a quick recovery.
  • The diagnosis of organic hyperinsulinaemia is established by demonstrating inappropriately high serum-insulin concentrations during fasting hypoglycaemia.
  • This new highly-specific insulin assay has no cross-reactivity with pro-insulin, which is often produced disproportionately more by an insulinoma.
  • As a result of this false-normal insulin values are found.
  • Therefore new normative values are needed for the newer insulin assays when diagnosing an insulin-producing islet cell tumour.
  • Pro-insulin and C-peptide assays may play a useful role in this.
  • [MeSH-major] Hyperinsulinism / etiology. Hypoglycemia / etiology. Insulin / blood. Insulinoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 15884409.001).
  • [ISSN] 0028-2162
  • [Journal-full-title] Nederlands tijdschrift voor geneeskunde
  • [ISO-abbreviation] Ned Tijdschr Geneeskd
  • [Language] dut
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin
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78. Grant CS: Insulinoma. Best Pract Res Clin Gastroenterol; 2005 Oct;19(5):783-98
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  • [Title] Insulinoma.
  • Although rare, insulinomas are the most common functioning islet cell tumour of the pancreas.
  • Several options are available for imaging and localizing these tumours including ultrasonography, computed tomography, and intra-arterial calcium stimulation with venous sampling.
  • The tumours are usually small, single, benign, well-circumscribed, and evenly distributed throughout the pancreas.
  • This tumour may be a part of the multiple endocrine neoplasia type 1 (MEN-1) syndrome, in which case the tumours are almost always multiple.
  • Surgical treatment is the only curative method, traditionally accomplished with enucleation or partial pancreatic resection.
  • Patients are almost invariably cured lifelong with complete excision of a benign insulinoma.
  • The most recent developments in this area are the recognition of noninsulinoma pancreatogenous hypoglycemia syndrome as a cause of organic hypoglycemia, and the development of laparoscopic techniques to excise these tumours.
  • [MeSH-major] Insulinoma / diagnosis. Insulinoma / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Aged, 80 and over. Biopsy, Needle. Endosonography / methods. Female. Humans. Immunohistochemistry. Incidence. Male. Middle Aged. Neoplasm Staging. Phlebography / methods. Prognosis. Rare Diseases. Risk Assessment. Sex Distribution. Survival Rate. Tomography, X-Ray Computed / methods. Treatment Outcome

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  • (PMID = 16253900.001).
  • [ISSN] 1521-6918
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 52
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79. Moran AE, Carothers AM, Weyant MJ, Redston M, Bertagnolli MM: Carnosol inhibits beta-catenin tyrosine phosphorylation and prevents adenoma formation in the C57BL/6J/Min/+ (Min/+) mouse. Cancer Res; 2005 Feb 1;65(3):1097-104
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  • [Title] Carnosol inhibits beta-catenin tyrosine phosphorylation and prevents adenoma formation in the C57BL/6J/Min/+ (Min/+) mouse.
  • Using the C57BL/6J/Min/+ (Min/+) mouse, a model of colonic tumorigenesis, we found that dietary administration of 0.1% carnosol decreased intestinal tumor multiplicity by 46%.
  • Previous studies showed that tumor formation in the Min/+ mouse was associated with alterations in the adherens junctions, including an increased expression of tyrosine-phosphorylated beta-catenin, dissociation of beta-catenin from E-cadherin, and strongly reduced amounts of E-cadherin located at lateral plasma membranes of histologically normal enterocytes.
  • Here, we confirm these findings and show that treatment of Min/+ intestinal tissue with carnosol restored both E-cadherin and beta-catenin to these enterocyte membranes, yielding a phenotype similar to that of the Apc(+/+) wild-type (WT) littermate.
  • Moreover, treatment of WT intestine with the phosphatase inhibitor, pervanadate, removed E-cadherin and beta-catenin from the lateral membranes of enterocytes, mimicking the appearance of the Min/+ tissue.
  • Pretreatment of WT tissue with carnosol inhibited the pervanadate-inducible expression of tyrosine-phosphorylated beta-catenin.
  • Thus, the Apc(Min) allele produces adhesion defects that involve up-regulated expression of tyrosine-phosphorylated proteins, including beta-catenin.
  • Moreover, these data suggest that carnosol prevents Apc-associated intestinal tumorigenesis, potentially via its ability to enhance E-cadherin-mediated adhesion and suppress beta-catenin tyrosine phosphorylation.
  • [MeSH-major] Adenoma / prevention & control. Colonic Neoplasms / prevention & control. Cytoskeletal Proteins / metabolism. Diterpenes, Abietane / pharmacology. Phenanthrenes / pharmacology. Trans-Activators / metabolism
  • [MeSH-minor] Animals. Cadherins / metabolism. Cell Adhesion / drug effects. Cell Membrane / drug effects. Cell Membrane / metabolism. Enterocytes / drug effects. Enterocytes / metabolism. Female. Intestine, Small / cytology. Intestine, Small / drug effects. Intestine, Small / metabolism. Mice. Mice, Inbred C57BL. Phosphorylation / drug effects. Rosmarinus / chemistry. Tyrosine / metabolism. Vanadates / antagonists & inhibitors. Vanadates / pharmacology. beta Catenin

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  • (PMID = 15705912.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R29 CA 74162; United States / NCI NIH HHS / CA / T32 CA 68971
  • [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 / CTNNB1 protein, mouse; 0 / Cadherins; 0 / Cytoskeletal Proteins; 0 / Diterpenes, Abietane; 0 / Phenanthrenes; 0 / Trans-Activators; 0 / beta Catenin; 0 / pervanadate; 3WHH0066W5 / Vanadates; 42HK56048U / Tyrosine; 5957-80-2 / carnosol
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80. Doviner V, Maly B, Kaplan V, Gingis-Velitski S, Ilan N, Vlodavsky I, Sherman Y: Spatial and temporal heparanase expression in colon mucosa throughout the adenoma-carcinoma sequence. Mod Pathol; 2006 Jun;19(6):878-88
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  • [Title] Spatial and temporal heparanase expression in colon mucosa throughout the adenoma-carcinoma sequence.
  • Heparanase is a mammalian endo-beta-D-glucuronidase that cleaves heparan sulfate side chains at a limited number of sites.
  • Such enzymatic activity is thought to participate in degradation and remodeling of the extracellular matrix and to facilitate cell invasion associated with tumor metastasis, angiogenesis and inflammation.
  • Traditionally, heparanase activity was well correlated with the metastatic potential of a large number of tumor-derived cell types.
  • More recently, heparanase upregulation has been documented in an increasing number of primary human tumors, correlating with poor postoperative survival and increased tumor vascularity.
  • Here, we employed anti-heparanase 733 polyclonal antibody that preferentially recognizes the 50 kDa active heparanase subunit over the 65 kDa proenzyme, as well as anti-heparanase 92.4 monoclonal antibody that recognizes both the latent and the active enzyme, to follow heparanase expression, processing and localization throughout the adenoma-carcinoma transition of the colon epithelium.
  • Normal (nondysplastic) mucosa of the large bowel near epithelial neoplasms, as well as areas of mild dysplasia in adenomas, exhibited a strong reactivity with antibody 733 that became even stronger in foci of moderate dysplasia.
  • Interestingly, although reactivity with antibody 733 was markedly reduced in severe dysplasia and in colorectal carcinoma, response to antibody 92.4 exhibited the opposite trend and staining intensities increased in parallel with tumor stage, the highest being in carcinoma cells.
  • Involvement of latent heparanase (detected by 92.4, but not by 733 antibody) in tumor progression was suggested by activation of the Akt/PKB signal transduction pathway upon heparanase overexpression or exogenous addition to HT29 human colon carcinoma cells.
  • These results suggest that heparanase expression is induced during colon carcinogenesis, and that its processing, conformation and localization are tightly regulated during the course of colon adenoma-carcinoma progression.
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Cell Line, Tumor / enzymology. Cell Line, Tumor / pathology. Disease Progression. Female. Fluorescent Antibody Technique, Indirect. Humans. Immunoenzyme Techniques. Mice. Mice, SCID. Neoplasm Transplantation. Transfection

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  • (PMID = 16607375.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106456
  • [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 / Biomarkers, Tumor; EC 3.2.1.- / heparanase; EC 3.2.1.31 / Glucuronidase
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81. Ciznadija D, Tothill R, Waterman ML, Zhao L, Huynh D, Yu RM, Ernst M, Ishii S, Mantamadiotis T, Gonda TJ, Ramsay RG, Malaterre J: Intestinal adenoma formation and MYC activation are regulated by cooperation between MYB and Wnt signaling. Cell Death Differ; 2009 Nov;16(11):1530-8
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  • [Title] Intestinal adenoma formation and MYC activation are regulated by cooperation between MYB and Wnt signaling.
  • Aberrant Wnt signaling mediated by mutations affecting APC (adenomatous polyposis coli) or beta-catenin initiates the majority of human colorectal cancers (CRC) and drives tumorigenesis through the activation of specific genes such as MYC.
  • We report here a novel association whereby another oncogenic transcription factor, MYB/c-Myb, is necessary for intestinal adenoma development directed by activated Wnt signaling.
  • APC(Min/+) mice in which c-myb is haploinsufficient survive longer than wild-type APC(Min/+) animals due to a delay in adenoma formation.
  • Intestinal adenomas from APC(Min/+) mice were assessed and found to have high levels of c-myc gene expression.
  • We explored the relationship between activated Wnt signaling and MYB in regulating MYC and found activated beta-catenin in combination with MYB induces robust upregulation of MYC promoter activity, as well as endogenous MYC mRNA and protein expression, in human cells.
  • This cooperation occurred through independent binding of MYB and beta-catenin to the MYC promoter.
  • [MeSH-major] Adenoma / metabolism. Colorectal Neoplasms / metabolism. Proto-Oncogene Proteins c-myb / metabolism. Proto-Oncogene Proteins c-myc / metabolism. Wnt Proteins / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / metabolism. Alleles. Animals. Cell Line. Humans. Mice. Mice, Inbred C57BL. Mice, Knockout. RNA Interference. RNA, Messenger / metabolism. RNA, Small Interfering / metabolism. Signal Transduction. Up-Regulation. beta Catenin / metabolism

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  • (PMID = 19609274.001).
  • [ISSN] 1476-5403
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Wnt Proteins; 0 / beta Catenin
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82. Bioulac-Sage P, Balabaud C, Zucman-Rossi J: Subtype classification of hepatocellular adenoma. Dig Surg; 2010;27(1):39-45
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  • [Title] Subtype classification of hepatocellular adenoma.
  • Hepatocellular adenomas (HCA) are rare benign tumours occurring mainly in women under oral contraceptives.
  • Identification of genes recurrently mutated in HCA and good genotype/phenotype correlations provided the basis of a pathomolecular classification of different HCA subgroups, characterized using immunohistochemical markers.
  • The expression of FABP1 (which is a HNF1A target gene) is downregulated and the absence of L-FABP expression diagnosed this subgroup. beta-Catenin-mutated HCA: beta-catenin mutations leading to activation of the Wnt/beta-catenin pathway represented 10-15% of HCA.
  • They are characterized by overexpression of glutamine synthetase and aberrant nuclear beta-catenin staining.
  • These beta-catenin-activated HCA are at greater risk of malignant transformation; they are difficult to differentiate from well-differentiated HCC.
  • Small in-frame deletions that target the binding site of gp130 for IL-6 have been reported in 60% of inflammatory HCA.
  • There is an overexpression of the inflammatory proteins serum amyloid A and C-reactive protein in tumour hepatocytes both at mRNA and protein levels.
  • Inflammatory HCA occurred more frequently in patients with high body mass index; they can be also mutated for beta-catenin and therefore are probably at risk of HCC.
  • [MeSH-major] Adenoma, Liver Cell / classification. Liver Neoplasms / classification
  • [MeSH-minor] Biomarkers, Tumor / analysis. Female. Hepatocyte Nuclear Factor 1 / genetics. Histocytochemistry. Humans. beta Catenin / genetics

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20357450.001).
  • [ISSN] 1421-9883
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / beta Catenin; 126548-29-6 / Hepatocyte Nuclear Factor 1
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83. Wani Y, Notohara K, Fujisawa M: Aberrant expression of an "intestinal marker" Cdx2 in pyloric gland adenoma of the gallbladder. Virchows Arch; 2008 Nov;453(5):521-7
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  • [Title] Aberrant expression of an "intestinal marker" Cdx2 in pyloric gland adenoma of the gallbladder.
  • The aim of this study was to survey Cdx2 expression in pyloric gland adenoma (PGA) of the gallbladder.
  • The immunostaining for Cdx2, beta-catenin, MUC5AC, MUC2, MUC6, and M-GGMC-1 was performed and scored (0 = negative, 1+ = <10%, 2+ = 10% to <30%, 3+ = 30% to <50%, 4+ = 50% to <70%, 5+ = 70-100%).
  • Not only goblet and/or Paneth cells were positive but also non-IM cells in PGAs, as opposed to the lack of staining in the background mucosa.
  • Furthermore, the p value of scores between Cdx2 and beta-catenin was 0.051, and both mean labeling indices (LIs) were correlated (r = 0.736).
  • Finally, we concluded that aberrant Cdx2 expression in PGAs is closely associated with nuclear beta-catenin expression and SM in contrast with IM.
  • [MeSH-major] Adenoma / metabolism. Gallbladder Neoplasms / metabolism. Gastric Mucosa / metabolism. Homeodomain Proteins / metabolism
  • [MeSH-minor] CDX2 Transcription Factor. Cell Differentiation. Gene Expression Regulation, Neoplastic. Humans. Retrospective Studies. beta Catenin / metabolism

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  • (PMID = 18843504.001).
  • [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 / CDX2 Transcription Factor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / beta Catenin
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84. Sornmayura P, Siripornpitak S, Leela-udomlipi S, Bunyaratvej S: Hepatocellular adenoma: a case report. J Med Assoc Thai; 2010 Mar;93(3):393-7
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  • [Title] Hepatocellular adenoma: a case report.
  • A case of hepatocellular adenoma (HCA) was described in a 26-year-old woman, who was a potential kidney donor for her father and denied taking the oral contraceptive pill.
  • Molecular biological studies disclosed three variants of HCAs, i.e., I) with mutation of HNF 1-alpha gene, II) with mutation of beta-catenin gene, and III) no mutation of the two genes.
  • [MeSH-major] Adenoma, Liver Cell / diagnosis. Liver Neoplasms / diagnosis

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  • (PMID = 20420118.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Thailand
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85. Zucman-Rossi J, Jeannot E, Nhieu JT, Scoazec JY, Guettier C, Rebouissou S, Bacq Y, Leteurtre E, Paradis V, Michalak S, Wendum D, Chiche L, Fabre M, Mellottee L, Laurent C, Partensky C, Castaing D, Zafrani ES, Laurent-Puig P, Balabaud C, Bioulac-Sage P: Genotype-phenotype correlation in hepatocellular adenoma: new classification and relationship with HCC. Hepatology; 2006 Mar;43(3):515-24
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  • [Title] Genotype-phenotype correlation in hepatocellular adenoma: new classification and relationship with HCC.
  • Hepatocellular adenomas are benign tumors that can be difficult to diagnose.
  • A multicentric series of 96 liver tumors with a firm or possible diagnosis of hepatocellular adenoma was reviewed by liver pathologists.
  • In all cases, the genes coding for hepatocyte nuclear factor 1alpha (HNF1alpha) and beta-catenin were sequenced.
  • No tumors were mutated in both HNF1alpha and beta-catenin enabling tumors to be classified into 3 groups, according to genotype.
  • Tumors with HNF1alpha mutations formed the most important group of adenomas (44 cases).
  • In contrast, the group of tumors defined by beta-catenin activation included 13 lesions with frequent cytological abnormalities and pseudo-glandular formation (P < 10(-5)).
  • The third group of tumors without mutation was divided into two subgroups based on the presence of inflammatory infiltrates.
  • The subgroup of tumors consisting of 17 inflammatory lesions, resembled telangiectatic focal nodular hyperplasias, with frequent cytological abnormalities (P = 10(-3)), ductular reaction (P < 10(-2)), and dystrophic vessels (P = .02).
  • In this classification, hepatocellular carcinoma associated with adenoma or borderline lesions between carcinoma and adenoma is found in 46% of the beta-catenin-mutated tumors whereas they are never observed in inflammatory lesions and are rarely found in HNF1alpha mutated tumors (P = .004).
  • In conclusion, the molecular and pathological classification of hepatocellular adenomas permits the identification of strong genotype-phenotype correlations and suggests that adenomas with beta-catenin activation have a higher risk of malignant transformation.
  • [MeSH-major] Adenoma, Liver Cell / genetics. Carcinoma, Hepatocellular / genetics. Hepatocyte Nuclear Factor 1-alpha / genetics. Liver Neoplasms / genetics. beta Catenin / genetics

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  • [CommentIn] Hepatology. 2006 Mar;43(3):401-4 [16496344.001]
  • [CommentIn] Histopathology. 2007 Dec;51(6):855-6 [17903198.001]
  • (PMID = 16496320.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / beta Catenin
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86. Yoshida A, Sen C, Asa SL, Rosenblum MK: Composite pituitary adenoma and craniopharyngioma?: an unusual sellar neoplasm with divergent differentiation. Am J Surg Pathol; 2008 Nov;32(11):1736-41
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  • [Title] Composite pituitary adenoma and craniopharyngioma?: an unusual sellar neoplasm with divergent differentiation.
  • The patient was treated with thyroid radioablation and hormone replacement and followed for 7 years, during which time the tumor grew to 4.6 cm.
  • At transsphenoidal surgery, a tumor consisting of a pituitary adenoma and adamantinomatous craniopharyngiomalike components was resected.
  • Both components were closely intermingled, but there was no evidence of an intermediate morphologic phenotype.
  • Immunohistochemically, the adenoma was not only positive for beta-thyroid stimulating hormone, alpha subunit, and pituitary transcription factor 1, but also stained for beta-follicle stimulating hormone, steroidogenic factor-1, adrenocorticotropic hormone, and pituitary-restricted transcription factor (Tpit), exhibiting an unusual plurihormonal profile.
  • This lesion may represent an unusual composite tumor attributable to divergent differentiation of a common precursor.
  • Alternatively, it may be viewed as a pituitary adenoma showing metaplastic change analogous to the development of squamous cell nests of the pars tuberalis from adenohypophyseal endocrine cells.
  • [MeSH-major] Adenoma / pathology. Craniopharyngioma / pathology. Neoplasms, Multiple Primary / pathology. Pituitary Neoplasms / pathology

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  • (PMID = 18769335.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-71-5 / Thyrotropin
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87. Owecki M, Sowiński J: [Successful pharmacological treatment of hyperinsulinemic hypoglycemia with verapamil and amlodipine--case report]. Pol Merkur Lekarski; 2005 Aug;19(110):196-8
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  • In view of the clinical picture (Whipple's triad) a suspicion of hypoglycemia due to an insulinoma of the pancreas aroused.
  • The test was terminated after 22 hours with a glucose concentration of 2.0 mmol/l (36 mg/dl) and an insulin level of 16.19 microU/ml.
  • No visual diagnostic was performed due to the lack of the patient's consent, thus no diagnosis of a tumor of the pancreas could be established.
  • Their efficacy in the medical treatment of insulinoma requires further research.
  • [MeSH-major] Amlodipine / therapeutic use. Hyperinsulinism / complications. Hypoglycemia / drug therapy. Insulinoma / complications. Pancreatic Neoplasms / complications. Verapamil / therapeutic use

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  • (PMID = 16245433.001).
  • [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
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 1J444QC288 / Amlodipine; CJ0O37KU29 / Verapamil
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88. Furuse C, Miguita L, Rosa AC, Soares AB, Martinez EF, Altemani A, de Araújo VC: Study of growth factors and receptors in carcinoma ex pleomorphic adenoma. J Oral Pathol Med; 2010 Aug 1;39(7):540-7
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  • [Title] Study of growth factors and receptors in carcinoma ex pleomorphic adenoma.
  • Carcinoma ex pleomorphic adenoma (CXPA) is a rare malignant salivary gland tumor derived from a pre-existing pleomorphic adenoma.
  • In order to investigate, by immunohistochemistry, the expression of some growth factors and its receptors [EGF receptor, fibroblast growth factor, fibroblast growth factor receptor 1, fibroblast growth factor receptor 2, hepatocyte growth factor, c-Met, transforming growth factor (TGF) beta1, TGFbetaR-II and insulin-like growth factor receptor 1] in the progression of CXPA, we have used ten cases of CXPA in several degrees of invasion- intracapsular, minimally and frankly invasive carcinoma- with only epithelial component.
  • Slides were qualitatively and semi-quantitatively evaluated according to the percentage of stained tumor cells from 0 to 3 (0 = less than 10%; 1 = 10-25%; 2 = 25-50%; 3 = more than 50% of cells).
  • Malignant epithelial cells starting with in situ areas showed stronger expression than luminal cells of pleomorphic adenoma for all antibodies.
  • In small nests of invasive carcinoma, negative cells were observed probably indicating that the proliferative process is replaced by the invasive mechanism.
  • Altogether this data infers that these factors may contribute to cell proliferation during initial phases of the tumor.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma, Pleomorphic / pathology. Intercellular Signaling Peptides and Proteins / analysis. Parotid Neoplasms / pathology. Receptors, Growth Factor / analysis
  • [MeSH-minor] Adult. Aged. Carcinoma in Situ / pathology. Cell Proliferation. Coloring Agents. Disease Progression. Epithelial Cells / pathology. Female. Fibroblast Growth Factors / analysis. Hepatocyte Growth Factor / analysis. Humans. Male. Middle Aged. Neoplasm Invasiveness. Protein-Serine-Threonine Kinases / analysis. Proto-Oncogene Proteins c-met / analysis. Receptor, Epidermal Growth Factor / analysis. Receptor, Fibroblast Growth Factor, Type 1 / analysis. Receptor, Fibroblast Growth Factor, Type 2 / analysis. Receptor, IGF Type 1 / analysis. Receptors, Transforming Growth Factor beta / analysis. Submandibular Gland Neoplasms / pathology. Transforming Growth Factor beta1 / analysis

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  • (PMID = 20149060.001).
  • [ISSN] 1600-0714
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / Intercellular Signaling Peptides and Proteins; 0 / Receptors, Growth Factor; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 62031-54-3 / Fibroblast Growth Factors; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / FGFR2 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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89. Harper J, Burns JL, Foulstone EJ, Pignatelli M, Zaina S, Hassan AB: Soluble IGF2 receptor rescues Apc(Min/+) intestinal adenoma progression induced by Igf2 loss of imprinting. Cancer Res; 2006 Feb 15;66(4):1940-8
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  • [Title] Soluble IGF2 receptor rescues Apc(Min/+) intestinal adenoma progression induced by Igf2 loss of imprinting.
  • The potent growth-promoting activity of insulin-like growth factor-II (IGF-II) is highly regulated during development but frequently up-regulated in tumors.
  • Increased expression of the normally monoallelic (paternally expressed) mouse (Igf2) and human (IGF2) genes modify progression of intestinal adenoma in the Apc(Min/+) mouse and correlate with a high relative risk of human colorectal cancer susceptibility, respectively.
  • We examined the functional consequence of Igf2 allelic dosage (null, monoallelic, and biallelic) on intestinal adenoma development in the Apc(Min/+) by breeding with mice with either disruption of Igf2 paternal allele or H19 maternal allele and used these models to evaluate an IGF-II-specific therapeutic intervention.
  • Increased allelic Igf2 expression led to elongation of intestinal crypts, increased adenoma growth independent of systemic growth, and increased adenoma nuclear beta-catenin staining.
  • By introducing a transgene expressing a soluble form of the full-length IGF-II/mannose 6-phosphate receptor (sIGF2R) in the intestine, which acts as a specific inhibitor of IGF-II ligand bioavailability (ligand trap), we show rescue of the Igf2-dependent intestinal and adenoma phenotype.
  • [MeSH-major] Adenomatous Polyposis Coli / genetics. Insulin-Like Growth Factor II / genetics. Receptor, IGF Type 2 / metabolism
  • [MeSH-minor] Alleles. Animals. Cell Growth Processes / genetics. Crosses, Genetic. Disease Progression. Female. Gene Dosage. Genomic Imprinting. Ligands. Male. Mice. Mice, Inbred C57BL. Transgenes. beta Catenin / metabolism

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  • (PMID = 16488992.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptor, IGF Type 2; 0 / beta Catenin; 67763-97-7 / Insulin-Like Growth Factor II
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90. Sillars-Hardebol AH, Carvalho B, de Wit M, Postma C, Delis-van Diemen PM, Mongera S, Ylstra B, van de Wiel MA, Meijer GA, Fijneman RJ: Identification of key genes for carcinogenic pathways associated with colorectal adenoma-to-carcinoma progression. Tumour Biol; 2010 Apr;31(2):89-96
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  • [Title] Identification of key genes for carcinogenic pathways associated with colorectal adenoma-to-carcinoma progression.
  • Colorectal adenomas form a biologically and clinically distinct intermediate stage in development of colorectal cancer (CRC) from normal colon epithelium.
  • Only 5% of adenomas progress into adenocarcinomas, indicating that malignant transformation requires other biological alterations than those involved in adenoma formation.
  • The present study aimed to explore which cancer-related biological processes are affected during colorectal adenoma-to-carcinoma progression and to identify key genes within these pathways that can serve as tumor markers for malignant transformation.
  • The activity of 12 cancer-related biological processes was compared between 37 colorectal adenomas and 31 adenocarcinomas, using the pathway analysis tool Gene Set Enrichment Analysis.
  • Expression of six gene sets was significantly increased in CRCs compared to adenomas, representing chromosomal instability, proliferation, differentiation, invasion, stroma activation, and angiogenesis.
  • For AURKA and PDGFRB, increased mRNA expression levels were verified at the protein level by immunohistochemical analysis of a series of adenomas and CRCs.
  • This study revealed cancer-related biological processes whose activities are increased during malignant transformation and identified key genes which may be used as tumor markers to improve molecular characterization of colorectal tumors.
  • [MeSH-major] Adenoma / genetics. Carcinoma / genetics. Colorectal Neoplasms / genetics
  • [MeSH-minor] Aurora Kinase A. Aurora Kinases. Cell Cycle Proteins / analysis. Cell Transformation, Neoplastic. Disease Progression. Humans. Immunohistochemistry. Protein-Serine-Threonine Kinases / analysis. Proto-Oncogene Proteins / analysis. Receptor, Platelet-Derived Growth Factor beta / analysis

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  • (PMID = 20358421.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.11.1 / AURKA protein, human; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / polo-like kinase 1
  • [Other-IDs] NLM/ PMC2848338
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91. May R, Riehl TE, Hunt C, Sureban SM, Anant S, Houchen CW: Identification of a novel putative gastrointestinal stem cell and adenoma stem cell marker, doublecortin and CaM kinase-like-1, following radiation injury and in adenomatous polyposis coli/multiple intestinal neoplasia mice. Stem Cells; 2008 Mar;26(3):630-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a novel putative gastrointestinal stem cell and adenoma stem cell marker, doublecortin and CaM kinase-like-1, following radiation injury and in adenomatous polyposis coli/multiple intestinal neoplasia mice.
  • In the gut, tumorigenesis arises from intestinal or colonic crypt stem cells.
  • Currently, no definitive markers exist that reliably identify gut stem cells.
  • Here, we used the putative stem cell marker doublecortin and CaM kinase-like-1 (DCAMKL-1) to examine radiation-induced stem cell apoptosis and adenomatous polyposis coli (APC)/multiple intestinal neoplasia (min) mice to determine the effects of APC mutation on DCAMKL-1 expression.
  • Immunoreactive DCAMKL-1 staining was demonstrated in the intestinal stem cell zone.
  • Furthermore, we observed apoptosis of the cells negative for DCAMKL-1 at 6 hours.
  • We found DNA damage in all the cells in the crypt region, including the DCAMKL-1-positive cells.
  • We also observed stem cell apoptosis and mitotic DCAMKL-1-expressing cells 24 hours after irradiation.
  • Moreover, in APC/min mice, DCAMKL-1-expressing cells were negative for proliferating cell nuclear antigen and nuclear beta-catenin in normal-appearing intestine.
  • However, beta-catenin was nuclear in DCAMKL-1-positive cells in adenomas.
  • Thus, nuclear translocation of beta-catenin distinguishes normal and adenoma stem cells.
  • [MeSH-major] Adenomatous Polyposis Coli / metabolism. Biomarkers, Tumor / metabolism. Gastrointestinal Tract / cytology. Intestinal Neoplasms / metabolism. Protein-Serine-Threonine Kinases / metabolism. Stem Cells / cytology
  • [MeSH-minor] Animals. Intestines / cytology. Intestines / metabolism. Intestines / pathology. Intestines / radiation effects. Mice. Nerve Tissue Proteins / metabolism. Protein Transport / radiation effects. RNA-Binding Proteins / metabolism. Radiation, Ionizing. Regeneration / radiation effects. beta Catenin / metabolism

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  • (PMID = 18055444.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK-002822; United States / NIDDK NIH HHS / DK / DK-066161; United States / NIDDK NIH HHS / DK / P30 DK-52574
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Msi1h protein, mouse; 0 / Nerve Tissue Proteins; 0 / RNA-Binding Proteins; 0 / beta Catenin; EC 2.7.1.- / Dcamkl1 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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92. Rebouissou S, Bioulac-Sage P, Zucman-Rossi J: Molecular pathogenesis of focal nodular hyperplasia and hepatocellular adenoma. J Hepatol; 2008 Jan;48(1):163-70
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  • [Title] Molecular pathogenesis of focal nodular hyperplasia and hepatocellular adenoma.
  • Focal nodular hyperplasia (FNH) and hepatocellular adenomas (HCAs) are benign tumors that occur in otherwise normal liver parenchyma.
  • FNH is considered to be the result of a hyperplastic response to increased blood flow secondary to vascular malformations.
  • In contrast, HCAs are consistently monoclonal tumors, which have been divided up into three subtypes of tumors depending on the molecular alteration detected in the tumors: HNF1alpha inactivation, beta-catenin activation and/or an acute inflammatory response in the tumor.
  • These molecular features are closely related to clinical and pathological characteristics, and one of the most critical correlations is the higher risk of malignant transformation for beta-catenin activated HCA cases.
  • Altogether, the recent identification of different molecular pathways that contribute to tumor development has significantly increased our knowledge of benign hepatocellular tumorigenesis.
  • [MeSH-major] Adenoma, Liver Cell / genetics. Adenoma, Liver Cell / pathology. Focal Nodular Hyperplasia / genetics. Focal Nodular Hyperplasia / pathology. Liver Neoplasms / genetics. Liver Neoplasms / pathology

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  • (PMID = 17997499.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 110
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93. Gartner W, Koc F, Nabokikh A, Daneva T, Niederle B, Luger A, Wagner L: Long-term in vitro growth of human insulin-secreting insulinoma cells. Neuroendocrinology; 2006;83(2):123-30
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  • [Title] Long-term in vitro growth of human insulin-secreting insulinoma cells.
  • OBJECTIVE: Long-term in vitro maintenance of human insulin-secreting insulinoma cells. METHODS:.
  • (1) Cell culture of ex vivo-derived insulinoma cell suspensions from 8 individual human donors, using various cell culture medium supplementations;.
  • (2) determination of insulin synthesis and secretion using immunocytochemistry and insulin and pro-insulin radioimmunoassays;.
  • (3) nestin-immunostaining of long-term in vitro grown insulinoma cell suspensions, and (4) phase-contrast light microscopy for analyzing the in vitro growth characteristics of the insulinoma cells. RESULTS:.
  • (1) Parallel persistence of in vitro insulinoma cell proliferation as well as insulin-synthesizing and -secreting capacity depended on both the co-culture of insulinoma cells with human fibroblasts and the supplementation of the cell culture medium with tissue culture supernatant derived from the rodent pituitary adenoma cell line GH-3;.
  • (2) immunostaining for insulin and secretagogin confirmed the neuroendocrine origin of the insulinoma cells grown in vitro;.
  • (3) insulin secretion capability persisted up to an observation period of 25 weeks;.
  • (4) insulin secretion rates after 6 weeks of in vitro growth ranged from 3.5 to 83.3 muU/ml/h/60,000 cells plated, and (5) after long-term in vitro growth of insulinoma-derived cell suspensions with persistent insulin-secreting capacity, nestin staining was observed predominantly in co-cultured fibroblasts.
  • CONCLUSION: Our data describe for the first time the long-term in vitro culture of insulin-secreting human insulinomas and highlight the importance of beta-cell trophic factors for insulinoma cell growth.
  • [MeSH-major] Insulin / secretion. Insulin-Secreting Cells / physiology. Insulinoma / pathology
  • [MeSH-minor] Adult. Cell Culture Techniques / methods. Cell Proliferation. Coculture Techniques / methods. Culture Media, Conditioned / pharmacology. Female. Fibroblasts / physiology. Humans. Immunohistochemistry / methods. Intermediate Filament Proteins / metabolism. Male. Middle Aged. Nerve Tissue Proteins / metabolism. Nestin. Radioimmunoassay / methods. Time Factors. Tumor Cells, Cultured

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  • (PMID = 16888402.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Insulin; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin
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94. Smith DL, Keshavan P, Avissar U, Ahmed K, Zucker SD: Sodium taurocholate inhibits intestinal adenoma formation in APCMin/+ mice, potentially through activation of the farnesoid X receptor. Carcinogenesis; 2010 Jun;31(6):1100-9
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  • [Title] Sodium taurocholate inhibits intestinal adenoma formation in APCMin/+ mice, potentially through activation of the farnesoid X receptor.
  • In light of clinical and biological evidence that bile constituents exert preventive effects against colorectal cancer, we evaluated the influence of oral bilirubin and sodium taurocholate (NaTC) on intestinal tumor formation in APC(Min/+) mice.
  • Mice received bilirubin and/or bovine serum albumin (BSA) and NaTC in the drinking water for 8 weeks, after which the number, size and location of intestinal adenomas were determined.
  • Tissue specimens were analyzed by light microscopy, TUNEL staining, immunohistochemistry for beta-catenin and Ki-67 and quantitative polymerase chain reaction for farnesoid X receptor (FXR)-dependent gene expression.
  • Colon tumor formation also was assessed in azoxymethane (AOM)-treated hyperbilirubinemic Gunn (j/j) and wild-type (+/+) rats.
  • Compared with untreated APC(Min/+) mice, the mean number of intestinal adenomas was markedly lower in both bilirubin (10.5 +/- 0.9 versus 37.0 +/- 5.2; +/-SEM; P < 0.001) and NaTC plus BSA (14.3 +/- 5.4; P = 0.01)-treated animals.
  • Both treatment groups exhibited reduced levels of cellular proliferation in the ileum (by Ki-67 staining), but no differences in TUNEL staining or the percentage of beta-catenin-positive crypts.
  • Bilirubin feeding reduced intestinal inducible nitric oxide synthase expression, but did not alter adenoma multiplicity in APC(Min/+) mice or in AOM-treated j/j versus +/+ rats.
  • Administering NaTC to APC(Min/+) mice causes a marked reduction in intestinal adenomas.

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  • (PMID = 20194350.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA119006; United States / NCI NIH HHS / CA / CA119006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Cytoplasmic and Nuclear; 0 / beta Catenin; 0 / farnesoid X-activated receptor; 5E090O0G3Z / Taurocholic Acid; RFM9X3LJ49 / Bilirubin
  • [Other-IDs] NLM/ PMC2878362
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95. Herbst A, Bommer GT, Kriegl L, Jung A, Behrens A, Csanadi E, Gerhard M, Bolz C, Riesenberg R, Zimmermann W, Dietmaier W, Wolf I, Brabletz T, Göke B, Kolligs FT: ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition. Gastroenterology; 2009 Aug;137(2):639-48, 648.e1-9
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  • [Title] ITF-2 is disrupted via allelic loss of chromosome 18q21, and ITF-2B expression is lost at the adenoma-carcinoma transition.
  • BACKGROUND & AIMS: The ubiquitously expressed basic helix-loop-helix transcription factor ITF-2B has an important role in differentiation processes, and its transcription is regulated by beta-catenin.
  • The biologic effects of ITF-2B were studied in colorectal cancer cells.
  • RESULTS: ITF-2B is strongly expressed in colon adenomas but frequently down-regulated in carcinomas because of LOH at 18q21.
  • ITF-2B induces cell cycle arrest and regulates the expression of p21(Cip1) via newly identified E-boxes in the CDKN1A gene, independently of p53.
  • This finding, along with the fact that ITF-2B is a regulator of the key cell cycle inhibitor p21(Cip1), indicates that ITF-2B is a tumor suppressor that has an important function at the adenoma to carcinoma transition.
  • [MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Basic Helix-Loop-Helix Transcription Factors / genetics. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 18 / genetics. Colorectal Neoplasms / genetics. DNA-Binding Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Basic Helix-Loop-Helix Leucine Zipper Transcription Factors. Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Genetic Predisposition to Disease. Humans. Immunohistochemistry. Loss of Heterozygosity. Mutation. Neoplasm Proteins / genetics. Precancerous Conditions / genetics. Precancerous Conditions / pathology

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  • (PMID = 19394332.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / TCF3 protein, human; 0 / TCF4 protein, human; 0 / Transcription Factors
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96. Igreja S, Chahal HS, King P, Bolger GB, Srirangalingam U, Guasti L, Chapple JP, Trivellin G, Gueorguiev M, Guegan K, Stals K, Khoo B, Kumar AV, Ellard S, Grossman AB, Korbonits M, International FIPA Consortium: Characterization of aryl hydrocarbon receptor interacting protein (AIP) mutations in familial isolated pituitary adenoma families. Hum Mutat; 2010 Aug;31(8):950-60
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  • [Title] Characterization of aryl hydrocarbon receptor interacting protein (AIP) mutations in familial isolated pituitary adenoma families.
  • Familial isolated pituitary adenoma (FIPA) is an autosomal dominant condition with variable genetic background and incomplete penetrance.
  • We describe a large cohort of FIPA families and characterize missense and silent mutations using minigene constructs, luciferase and beta-galactosidase assays, as well as in silico predictions.
  • In summary, exonic, promoter, splice-site, and large deletion mutations in AIP are implicated in 31% of families in our FIPA cohort.
  • [MeSH-minor] Adult. Alternative Splicing / genetics. Amino Acid Sequence. Animals. Cell Line. Cyclic AMP / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Family. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Molecular Sequence Data. Mutant Proteins / genetics. Mutant Proteins / metabolism. Mutation, Missense / genetics. Pedigree. Promoter Regions, Genetic / genetics. RNA Splice Sites / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Signal Transduction

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  • (PMID = 20506337.001).
  • [ISSN] 1098-1004
  • [Journal-full-title] Human mutation
  • [ISO-abbreviation] Hum. Mutat.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0701307; United Kingdom / Medical Research Council / / ; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Mutant Proteins; 0 / RNA Splice Sites; 0 / RNA, Messenger; 0 / aryl hydrocarbon receptor-interacting protein; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Other-IDs] NLM/ PMC3065644
  • [Investigator] Akker S; Atkinson B; Aylwin S; Baldeweg S; Bevan J; Cheetham T; Chew S; Choudry K; Clayton R; Damjanovic S; Darzy K; Dattani M; Davis J; Drake W; Dzeranova L; Eden B; Eguchi K; Fica S; Flanagan D; Frohman L; Gadelha M; Gallego P; Gla E; Goldman J; Goldstone T; Howlett T; Inder W; Iwata T; Kaplan F; Karavitaki N; Laws E; Lechan R; Levy M; Matsuno A; Miljic D; Modenesi S; Molitch M; Musat M; Orme S; Patocs A; Popovic V; Powell M; Quinton R; Randeva H; Ribeiro de Oliveira J R A; Schofl C; Soares B; Spada A; Strasburger C; Swords F; Tsagarakis S; Vaks V; Wass JA; Widell H; Yarman S; Yoshimoto K
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97. Oh K, Redston M, Odze RD: Support for hMLH1 and MGMT silencing as a mechanism of tumorigenesis in the hyperplastic-adenoma-carcinoma (serrated) carcinogenic pathway in the colon. Hum Pathol; 2005 Jan;36(1):101-11
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  • [Title] Support for hMLH1 and MGMT silencing as a mechanism of tumorigenesis in the hyperplastic-adenoma-carcinoma (serrated) carcinogenic pathway in the colon.
  • This mechanism has also recently been implicated in the newly postulated hyperplastic polyp-serrated adenoma-carcinoma ("serrated") pathway of carcinogenesis, although this has never been investigated thoroughly.
  • The aim of this study was to evaluate hMLH1, hMSH2, MGMT, as well as MIB-1, p53, and beta-catenin immunoexpression in an uncommon cohort of mixed colonic polyps that contain a combination of hyperplastic and adenomatous features (n = 21), and in some (n = 7), carcinoma as well.
  • DESIGN: The clinical, pathological, and immunophenotypic (hMLH1, hMSH2, MGMT, MIB-1, p53, and beta-catenin) properties of 28 mixed hyperplastic and adenomatous polyps of the colon (7 of which also contained carcinoma within the same lesion) were evaluated for the above immunopeptides in each of the different morphologic areas of the polyps, and the results were compared to traditional hyperplastic polyps, serrated adenomas, and conventional (nonserrated) adenomas.
  • Mixed polyps, particularly those with carcinoma, showed loss of hMLH1 (33%), MGMT (37%), and even hMSH2 (11%) with significantly higher frequency compared to hyperplastic polyps, conventional adenomas, and serrated adenomas.
  • However, hMSH2 loss was only present in the adenoma component and never in the hyperplastic or carcinomatous areas of these polyps.
  • However, conventional adenomas showed significantly higher rates of nuclear beta -catenin staining (100%) in comparison to the adenomatous component of mixed polyps (60%).
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Colonic Neoplasms / genetics. Colonic Polyps / genetics. Gene Silencing. Neoplasm Proteins / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Aged, 80 and over. Carcinoma / genetics. Carcinoma / metabolism. Carcinoma / pathology. Carrier Proteins. Cytoskeletal Proteins / metabolism. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Female. Humans. Hyperplasia / genetics. Hyperplasia / metabolism. Hyperplasia / pathology. Immunohistochemistry. Ki-67 Antigen / metabolism. Male. Middle Aged. MutS Homolog 2 Protein. Nuclear Proteins. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Trans-Activators / metabolism. Tumor Suppressor Protein p53 / metabolism. beta Catenin

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  • (PMID = 15712188.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / CTNNB1 protein, human; 0 / Carrier Proteins; 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / MLH1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / Tumor Suppressor Protein p53; 0 / beta Catenin; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; EC 3.6.1.3 / MSH2 protein, human; EC 3.6.1.3 / MutS Homolog 2 Protein
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98. Lourenço SV, Lima DM: Pleomorphic adenoma and adenoid cystic carcinoma: in vitro study of the impact of TGFbeta1 on the expression of integrins and cytoskeleton markers of cell differentiation. Int J Exp Pathol; 2007 Jun;88(3):191-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pleomorphic adenoma and adenoid cystic carcinoma: in vitro study of the impact of TGFbeta1 on the expression of integrins and cytoskeleton markers of cell differentiation.
  • Pleomorphic adenoma (PA) and adenoid cystic carcinoma (ACC) are the commonest benign and malignant salivary gland tumours respectively.
  • Interactions between cells and extracellular matrix of PA and ACC, partially mediated by integrins, are important in their biology.
  • Our study investigated the effects of TGFbeta1 on the expression of integrin beta subunits in vitro and on the expression of cytoskeletal proteins of cells derived from PA and ACC.
  • ELISA assays were employed to quantitate the expression integrins and MTT assays evaluated the mitochondrial activity of cells stimulated with TGFbeta1.
  • PA cells showed increased expression of integrins and de novo expression of differentiation markers upon TGFbeta1 stimulation.
  • ACC cells were less responsive to such stimulation.
  • This may reflect important differences in the biological behaviour of benign and malignant cells.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Carcinoma, Adenoid Cystic / metabolism. Integrins / metabolism. Parotid Neoplasms / metabolism. Transforming Growth Factor beta1 / pharmacology
  • [MeSH-minor] Adult. Antigens, CD29 / analysis. Antigens, CD29 / metabolism. Antigens, Differentiation / analysis. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Cytoskeleton / metabolism. Enzyme-Linked Immunosorbent Assay / methods. Female. Fluorescent Antibody Technique. Humans. Integrin beta3 / analysis. Integrin beta3 / metabolism. Integrin beta4 / analysis. Integrin beta4 / metabolism. Middle Aged. Stimulation, Chemical. Tumor Cells, Cultured

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  • (PMID = 17504449.001).
  • [ISSN] 0959-9673
  • [Journal-full-title] International journal of experimental pathology
  • [ISO-abbreviation] Int J Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD29; 0 / Antigens, Differentiation; 0 / Integrin beta3; 0 / Integrin beta4; 0 / Integrins; 0 / Transforming Growth Factor beta1
  • [Other-IDs] NLM/ PMC2517303
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99. Joo M, Shahsafaei A, Odze RD: Paneth cell differentiation in colonic epithelial neoplasms: evidence for the role of the Apc/beta-catenin/Tcf pathway. Hum Pathol; 2009 Jun;40(6):872-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Paneth cell differentiation in colonic epithelial neoplasms: evidence for the role of the Apc/beta-catenin/Tcf pathway.
  • Paneth cell differentiation may occur in colonic epithelial neoplasms.
  • Human defensin 5 is a specific marker of Paneth cells and has been shown to represent one of the target genes of the Apc/beta-catenin/Tcf pathway.
  • The aim of this study was to evaluate the frequency of Paneth cell differentiation in a variety of colonic neoplasms, and to investigate the role of human defensin 5 and beta-catenin in this process.
  • The clinical and pathologic findings, including histologic evidence of Paneth cell differentiation and immunostaining for human defensin 5 and beta-catenin, were evaluated in 29 samples of nonneoplastic colonic mucosa, 18 hyperplastic polyps, 10 sessile serrated adenomas, 12 traditional serrated adenomas, 21 mixed polyps, 39 conventional adenomas, and 40 adenocarcinomas.
  • Human defensin-5 and beta-catenin expression were evaluated for the location and degree of staining in all cell types (dysplastic and nondysplastic) and correlated with histologic areas of Paneth cell differentiation in all types of polyps.
  • Histologic evidence of Paneth cell differentiation was observed in 15 conventional adenomas (38.5%) and 1 adenocarcinoma (2.5%) but not in other types of polyps.
  • Human defensin-5 immunostaining was positive in the cytoplasm of all nonneoplastic Paneth cells and all neoplastic cells with Paneth cell differentiation.
  • Human defensin-5 expression was noted in 0% of hyperplastic polyps, 10% of sessile serrated adenomas, 25% of traditional serrated adenomas, 33.3% of mixed polyps, 82.1% of conventional adenomas, and 17.5% of adenocarcinomas: human defensin 5 expression was significantly higher in conventional adenomas compared to all other groups (P < .01).
  • Seventeen (53.1%) of 32 human defensin 5 positive conventional adenomas, 6 (86%) of 7 of human defensin 5 positive adenocarcinomas, and all human defensin 5-positive sessile serrated adenomas, traditional serrated adenomas, and mixed polyps did not show histologic evidence of Paneth cell differentiation.
  • Of the 31 conventional adenomas with nuclear beta-catenin staining, 15 (48.4%) revealed histologic evidence of Paneth cell differentiation, and all of the neoplastic cells with Paneth cell differentiation showed nuclear beta-catenin staining, whereas nonneoplastic Paneth cells consistently showed a normal pattern of membranous beta-catenin staining.
  • A strong topographical correlation was noted between human defensin 5 expression and nuclear beta-catenin expression in conventional adenomas and in conventional dysplastic epithelium of mixed polyps.
  • Paneth cell differentiation is common in early colonic neoplasms that develop via the conventional adenoma-carcinoma carcinogenic pathway.
  • Activation of Apc/beta-catenin/Tcf pathway may play a role in Paneth cell differentiation in human colonic neoplasms.
  • [MeSH-major] Adenoma / pathology. Adenoma / physiopathology. Colonic Neoplasms / pathology. Colonic Neoplasms / physiopathology. Defensins / physiology. Paneth Cells / pathology. beta Catenin / physiology
  • [MeSH-minor] Aged. Cell Differentiation. Female. Humans. Male. Middle Aged. Retrospective Studies

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  • (PMID = 19269007.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Defensins; 0 / beta Catenin
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100. Jeannot E, Wendum D, Paye F, Mourra N, de Toma C, Fléjou JF, Zucman-Rossi J: Hepatocellular adenoma displaying a HNF1alpha inactivation in a patient with familial adenomatous polyposis coli. J Hepatol; 2006 Dec;45(6):883-6
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  • [Title] Hepatocellular adenoma displaying a HNF1alpha inactivation in a patient with familial adenomatous polyposis coli.
  • Patients with familial adenomatous polyposis coli (FAP) may rarely develop hepatocellular adenoma.
  • Here we report the case of a 37-year-old FAP woman presenting a hepatocellular adenoma after oestroprogestative oral contraception use.
  • In this steatotic adenoma, we identified an inactivating biallelic mutation of HNF1alpha.
  • In addition to the known germline APC mutation Q1062fs, we did not find an inactivation of the second APC allele nor an activation of the beta-catenin target genes GLUL and GPR49.
  • Our findings contrast with two hepatocellular adenoma cases related to FAP, for which a biallelic inactivation of the APC gene was previously described.
  • Altogether, these results suggest that benign hepatocellular carcinogenesis may be dependent on or independent of the Wnt/beta-catenin pathway in patients with FAP.
  • [MeSH-minor] Adult. Alleles. Diagnosis, Differential. Female. Genes, APC. Genetic Predisposition to Disease. Humans. Immunohistochemistry. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17049664.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha
  • [Other-IDs] NLM/ HALMS130312; NLM/ PMC2121664
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