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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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  • [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. 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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5. 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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  • [Cites] BMC Cell Biol. 2007;8:38 [17727724.001]
  • [Cites] Cell Metab. 2006 Dec;4(6):491-7 [17141632.001]
  • [Cites] Cancer Res. 1996 Oct 1;56(19):4382-6 [8813130.001]
  • [Cites] Cancer Res. 1998 Apr 1;58(7):1408-16 [9537241.001]
  • [Cites] Mol Cell Biol. 2006 Dec;26(24):9517-32 [17030613.001]
  • [Cites] J Clin Invest. 2006 Oct;116(10):2610-21 [17016557.001]
  • [Cites] Cancer Biol Ther. 2006 Jul;5(7):723-8 [16861899.001]
  • [Cites] EMBO J. 2005 Oct 5;24(19):3470-81 [16148948.001]
  • [Cites] Nature. 1999 Jan 21;397(6716):271-4 [9930704.001]
  • [Cites] Int J Biochem Cell Biol. 1999 Jan;31(1):1-23 [10216939.001]
  • [Cites] Nat Genet. 2000 Aug;25(4):406-9 [10932183.001]
  • [Cites] Mol Cell. 2001 Jun;7(6):1153-63 [11430819.001]
  • [Cites] Diabetes. 2001 Oct;50(10):2260-7 [11574407.001]
  • [Cites] Endocr Relat Cancer. 2001 Dec;8(4):307-14 [11733227.001]
  • [Cites] Mol Cell Biol. 2002 Jun;22(11):3864-74 [11997520.001]
  • [Cites] Semin Oncol. 2002 Dec;29(6 Suppl 16):15-8 [12516034.001]
  • [Cites] Oncogene. 2003 Aug 14;22(34):5261-9 [12917627.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jan 1;90(1):232-6 [7678339.001]
  • [Cites] Cancer Lett. 1996 Apr 19;102(1-2):113-23 [8603359.001]
  • [Cites] Genes Dev. 1996 Sep 1;10(17):2105-16 [8804306.001]
  • [Cites] J Cell Physiol. 2008 Dec;217(3):693-707 [18683826.001]
  • (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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6. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [Cites] Lancet. 1968 Aug 3;2(7562):284 [4173718.001]
  • [Cites] Curr Opin Chem Biol. 2003 Oct;7(5):626-34 [14580568.001]
  • [Cites] Br J Surg. 1971 Mar;58(3):233-4 [4100889.001]
  • [Cites] Br J Surg. 1975 Sep;62(9):747-9 [51661.001]
  • [Cites] Diabetes. 1991 Jul;40(7):842-9 [1647994.001]
  • [Cites] Gastroenterology. 1992 Mar;102(3):1062-4 [1537497.001]
  • [Cites] Surgery. 1993 Mar;113(3):242-9 [8382841.001]
  • [Cites] Br J Surg. 1994 May;81(5):672-6 [8044542.001]
  • [Cites] Eur J Nucl Med. 1998 Jan;25(1):79-83 [9396878.001]
  • [Cites] Am J Surg. 1998 Jul;176(1):15-7 [9683125.001]
  • [Cites] Gastroenterology. 2005 May;128(6):1668-84 [15887158.001]
  • [Cites] Clin Radiol. 2005 Oct;60(10):1039-50 [16179163.001]
  • [Cites] Ann Pharmacother. 2006 Feb;40(2):299-303 [16391008.001]
  • [Cites] Br J Surg. 2006 Mar;93(3):264-75 [16498592.001]
  • [Cites] Ann Surg Oncol. 2007 Jul;14(7):2121-7 [17431724.001]
  • [Cites] Ann Surg. 2008 Jan;247(1):165-72 [18156937.001]
  • [Cites] World J Gastroenterol. 2008 Feb 7;14(5):657-65 [18205253.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Apr;94(4):1074-80 [19190102.001]
  • [Cites] J Thorac Cardiovasc Surg. 2009 Jul;138(1):133-40 [19577070.001]
  • [Cites] Mol Imaging. 2009 May-Jun;8(3):156-65 [19723473.001]
  • [Cites] Ann Surg Oncol. 2009 Oct;16(10):2943-52 [19582506.001]
  • [Cites] Br J Surg. 1969 Aug;56(8):595-7 [4183792.001]
  • (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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7. 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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8. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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9. 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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10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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11. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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12. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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13. 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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14. 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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15. 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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16. 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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17. 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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  • [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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18. 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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19. 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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20. 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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21. 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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22. 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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23. 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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  • [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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24. 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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25. 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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26. 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]
  • [Cites] Endosc Surg Allied Technol. 1994 Jun-Aug;2(3-4):181-5 [8000882.001]
  • [Cites] Br J Surg. 1994 Jan;81(1):5-6 [8313118.001]
  • [Cites] World J Surg. 1993 Jul-Aug;17(4):448-54 [8395749.001]
  • [Cites] World J Surg. 1990 May-Jun;14(3):393-8; discussion 398-9 [1973323.001]
  • [Cites] Br J Surg. 2006 Mar;93(3):264-75 [16498592.001]
  • [Cites] Arch Surg. 2007 Dec;142(12):1202-4; discussion 1205 [18086988.001]
  • (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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27. 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 / ultrasonography. Pancreatic Neoplasms / ultrasonography
  • [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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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. Cazabat L, Chanson P: [Hypoglycemia and insulinoma]. Ann Endocrinol (Paris); 2009 Sep;70 Suppl 1:S2-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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31. 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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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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  • [Cites] Gastrointest Endosc. 2004 Nov;60(5):856-8 [15557979.001]
  • [Cites] Am J Clin Oncol. 2004 Dec;27(6):576-83 [15577435.001]
  • [Cites] Am J Clin Oncol. 2004 Dec;27(6):636-7 [15577445.001]
  • [Cites] Pancreas. 2002 Jan;24(1):103-5 [11741190.001]
  • [Cites] Ann Surg Oncol. 2001 Apr;8(3):204-8 [11314935.001]
  • [Cites] Am J Gastroenterol. 1999 Jul;94(7):1955-7 [10406267.001]
  • [Cites] Cancer. 1999 Jun 15;85(12):2589-95 [10375107.001]
  • [Cites] Laryngoscope. 1992 Mar;102(3):244-9 [1545650.001]
  • [Cites] Virchows Arch. 2004 Jun;444(6):527-35 [15057558.001]
  • [Cites] JOP. 2004 Mar;5(2):92-6 [15007190.001]
  • [Cites] Radiographics. 2002 Mar-Apr;22(2):367-76 [11896226.001]
  • [Cites] Am J Clin Oncol. 2004 Oct;27(5):510-5 [15596922.001]
  • [Cites] J Clin Oncol. 2005 Apr 1;23(10):2300-9 [15800320.001]
  • [Cites] J Surg Oncol. 2005 Jan 1;89(1):1-4 [15611998.001]
  • [Cites] J Cutan Pathol. 2005 Feb;32(2):162-5 [15606676.001]
  • [Cites] Dermatol Surg. 1995 Aug;21(8):669-83 [7633811.001]
  • [Cites] J Am Acad Dermatol. 1993 Aug;29(2 Pt 1):143-56 [8335732.001]
  • [Cites] Otolaryngol Clin North Am. 1993 Apr;26(2):295-309 [8460044.001]
  • [Cites] Am J Surg. 1997 Dec;174(6):688-93 [9409598.001]
  • [Cites] Anticancer Res. 1997 Jan-Feb;17(1B):673-7 [9066600.001]
  • [Cites] AJR Am J Roentgenol. 1996 Sep;167(3):617-20 [8751663.001]
  • (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. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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34. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


35. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [Cites] Arch Surg. 2004 Mar;139(3):270-4 [15006883.001]
  • [Cites] Clin Lab. 2003;49(5-6):227-32 [15285178.001]
  • [Cites] Surgery. 2002 Dec;132(6):937-42; discussion 942-3 [12490839.001]
  • [Cites] Clin Endocrinol (Oxf). 2001 Sep;55(3):357-62 [11589679.001]
  • [Cites] J Laparoendosc Adv Surg Tech A. 2001 Aug;11(4):193-9 [11569507.001]
  • [Cites] J Am Coll Surg. 2001 Sep;193(3):281-7 [11548798.001]
  • [Cites] Surgery. 2000 Dec;128(6):937-44;discussion 944-5 [11114627.001]
  • [Cites] Surgery. 2000 Dec;128(6):903-9 [11114622.001]
  • [Cites] Arch Dis Child Fetal Neonatal Ed. 2000 Mar;82(2):F98-F107 [10685981.001]
  • [Cites] Surgery. 1999 Nov;126(5):968-73 [10568199.001]
  • [Cites] Surg Endosc. 1999 Apr;13(4):406-8 [10094758.001]
  • [Cites] World J Surg. 1998 Dec;22(12):1218-24 [9841747.001]
  • [Cites] Pancreas. 1996 Jul;13(1):55-60 [8783334.001]
  • [Cites] Surgery. 1993 Mar;113(3):242-9 [8382841.001]
  • [Cites] World J Surg. 1990 Jan-Feb;14(1):107-12; discussion 112-4 [2154901.001]
  • [Cites] Surgery. 1991 Dec;110(6):989-96; discussion 996-7 [1745987.001]
  • [Cites] World J Surg. 2004 Dec;28(12):1239-47 [15517485.001]
  • [Cites] World J Surg. 2004 Dec;28(12):1227-30 [15517495.001]
  • (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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36. Genelhu MC, Gobbi H, Arantes DC, Cardoso SV, Cassali GD: Immunolocalization of beta-catenin in pleomorphic adenomas and carcinomas ex-pleomorphic adenomas of salivary glands. Appl Immunohistochem Mol Morphol; 2007 Sep;15(3):273-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunolocalization of beta-catenin in pleomorphic adenomas and carcinomas ex-pleomorphic adenomas of salivary glands.
  • Beta-catenin plays a central role in cadherin/catenin cell-cell adhesion complex and is involved in cell signaling pathway.
  • Change in beta-catenin distribution has been associated with several human cancers including salivary gland tumors.
  • We studied the immunolocalization of beta-catenin in a series of pleomorphic adenomas (PA) and carcinomas ex-pleomorphic adenomas (Ca ex-PA).
  • Ten samples of PA and ten of Ca ex-PA were evaluated by immunohistochemistry using streptavidin-biotin-peroxidase technique and a monoclonal antibody against beta-catenin (E-5).
  • Cell membrane/cytoplasmic staining of beta-catenin was observed in normal gland parenchyma, PA, and in well-differentiated Ca ex-PA.
  • Cytoplasmic/nuclear beta-catenin staining was observed in poorly differentiated carcinomas and, interestingly, in one case of PA.
  • Our data showed decreased cell membrane beta-catenin expression in higher-grade tumors suggesting that beta-catenin may play an important role in histologic differentiation and transition to malignant phenotype of Ca ex-PA.

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  • (PMID = 17721271.001).
  • [ISSN] 1541-2016
  • [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 / beta Catenin
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37. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • [Cites] Langenbecks Arch Surg. 2005 Apr;390(2):134-40 [15609056.001]
  • [Cites] Surgery. 1996 Dec;120(6):1051-4 [8957494.001]
  • [Cites] Surg Endosc. 2004 Mar;18(3):402-6 [14735345.001]
  • [Cites] Arch Surg. 1988 May;123(5):550-3 [3358679.001]
  • [Cites] Surgery. 2005 Jun;137(6):597-605 [15962401.001]
  • [Cites] World J Surg. 2004 Dec;28(12 ):1239-47 [15517485.001]
  • [Cites] Semin Laparosc Surg. 1998 Sep;5(3):168-79 [9787203.001]
  • [Cites] Metabolism. 2003 Oct;52(10):1320-9 [14564685.001]
  • [Cites] World J Surg. 1990 May-Jun;14(3):393-8; discussion 398-9 [1973323.001]
  • [Cites] Surg Endosc. 2004 Feb;18(2):297-302 [14712388.001]
  • [Cites] Surg Endosc. 2003 Feb;17(2):201-6 [12436230.001]
  • [Cites] Arch Surg. 2004 Mar;139(3):270-4 [15006883.001]
  • [Cites] Surgery. 2000 Sep;128(3):386-91 [10965308.001]
  • [Cites] Biomed Pharmacother. 2002;56 Suppl 1:227s-230s [12487288.001]
  • [Cites] World J Surg. 2005 Jun;29(6):789-93 [15880279.001]
  • [Cites] Surg Clin North Am. 2004 Jun;84(3):775-85 [15145234.001]
  • [Cites] World J Surg. 2002 Oct;26(10):1297-300 [12205557.001]
  • [Cites] J Gastrointest Surg. 2004 May-Jun;8(4):493-501 [15120376.001]
  • (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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38. Fontanière S, Casse H, Bertolino P, Zhang CX: Analysis of p27(Kip1) expression in insulinomas developed in pancreatic beta-cell specific Men1 mutant mice. Fam Cancer; 2006;5(1):49-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of p27(Kip1) expression in insulinomas developed in pancreatic beta-cell specific Men1 mutant mice.
  • Multiple Endocrine Neoplasia type 1 (MEN1) is a hereditary disease characterised by the occurrence of multiple endocrine tumours.
  • Interestingly, it has been recently reported that p27(Kip1) expression is regulated by menin and that decreased p27(Kip1) expression can be found in MEN1 insulinomas and parathyroid adenomas.
  • In order to address whether and when p27(Kip1) expression alters during insulinoma development in pancreatic beta-cell-specific Men1 mutant mice, we analysed p27(Kip1) expression in islet lesions from mutant mice at different ages.
  • Our data revealed that p27(Kip1) protein expression was reduced in 40 out of 52 (77%) insulinomas analysed, whereas the remaining 12 insulinomas (23%) did not show altered p27(Kip1) expression.
  • No difference between the insulinomas with and without decreased p27(Kip1) expression could be observed in terms of histological features or menin inactivation.
  • Furthermore, our analysis on hyperplastic and dysplastic islets developed in young mutant mice showed the lack of detectable alteration in p27(Kip1) expression, despite evident loss of menin expression in a substantial proportion of islet cells.
  • Our work confirms the altered p27(Kip1) expression reported in tumours from MEN1 patients, whereas it suggests that other molecular events may also participate in the tumorigenesis process initiated by the Men1 gene inactivation.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p27 / genetics. Gene Expression Regulation, Neoplastic. Insulinoma / genetics. Multiple Endocrine Neoplasia Type 1 / genetics. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Animals. Blotting, Western. Cell Survival. Disease Models, Animal. Down-Regulation. Gene Deletion. Immunohistochemistry. Islets of Langerhans / cytology. Mice. Mice, Mutant Strains. Probability. Proto-Oncogene Proteins / genetics. Sensitivity and Specificity. Tumor Cells, Cultured


39. 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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40. Chanson P, Brochier S: Non-functioning pituitary adenomas. J Endocrinol Invest; 2005;28(11 Suppl International):93-9
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  • [Title] Non-functioning pituitary adenomas.
  • The vast majority (>80%) of clinically non-functioning pituitary adenomas (NFPAs) are gonadotroph-cell adenomas, as demonstrated by immunocytochemistry.
  • Increased levels of uncombined subunits (free alpha-subunit mainly, LH-beta subunit more rarely) are more frequently encountered, but are generally modest.
  • The main problems raised by NFPA are mass effects problems, responsible for optic chiasm compression or deficient hormone secretion resulting from compression of normal anterior pituitary cells.
  • The strategy of observation only for patients with incidentally discovered pituitary adenomas may be appropriate, provided that the tumor is well-delimited, small, has no extension with risk of neurological or visual chiasm compression, and that a meticulous hormonal work-up has ruled out the possibility of a minimal hormonal hypersecretion.
  • Transsphenoidal surgery allows improvement in visual disturbances due to chiasmal syndrome in most patients, and sometimes, in pituitary function.
  • Prolonged administration of GnRH antagonist in a small number of patients with a secreting gonadotroph cell adenoma has been reported to reduce supranormal gonadotropins levels but not to produce any change in tumoral size.
  • [MeSH-major] Adenoma. Pituitary Neoplasms

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  • (PMID = 16625856.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
  • [Number-of-references] 66
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41. 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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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. Cetani F, Pardi E, Banti C, Collecchi P, Viacava P, Borsari S, Fanelli G, Naccarato AG, Saponaro F, Berti P, Miccoli P, Pinchera A, Marcocci C: Beta-catenin activation is not involved in sporadic parathyroid carcinomas and adenomas. Endocr Relat Cancer; 2010 Mar;17(1):1-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Beta-catenin activation is not involved in sporadic parathyroid carcinomas and adenomas.
  • Aberrant accumulation of beta-catenin has been found in various types of human tumors.
  • The aim of this study was to evaluate whether Wnt/beta-catenin signaling is activated in parathyroid carcinomas and adenomas.
  • We studied 154 parathyroid tumors (18 carcinomas (13 with distant metastases), six atypical adenomas, and 130 adenomas).
  • Direct sequencing of exon 3 of the CTNNB1 gene showed absence of stabilizing mutations in all the tumors.
  • Immunostaining of beta-catenin was performed in all carcinomas and in 66 adenomas (including three atypical).
  • Normal parathyroid showed a homogeneous distinct outer cell membrane staining in the majority of cells and no nuclear staining.
  • All tumors showed negative nuclear staining.
  • With the exception of one carcinoma, which had a negative membrane staining, all other samples showed a membrane staining which was similar to that of the normal parathyroid. beta-Catenin expression was heterogeneous with a range of positive cells between 5 and 80%, independently of tumor type.
  • Our results suggest that the Wnt/beta-catenin signaling pathway is not involved in the development of parathyroid carcinomas and adenomas.
  • [MeSH-major] Adenoma / physiopathology. Carcinoma / physiopathology. Neoplasm Proteins / physiology. Parathyroid Neoplasms / physiopathology. Signal Transduction / physiology. Wnt Proteins / physiology. beta Catenin / physiology
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Cytoplasm / chemistry. DNA Mutational Analysis. Exons / genetics. Humans. Membrane Proteins / analysis

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  • (PMID = 19755524.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Wnt Proteins; 0 / beta Catenin
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44. 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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45. Tadjine M, Lampron A, Ouadi L, Bourdeau I: Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas. Clin Endocrinol (Oxf); 2008 Feb;68(2):264-70

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Frequent mutations of beta-catenin gene in sporadic secreting adrenocortical adenomas.
  • OBJECTIVE: Molecular alterations remain largely unknown in most sporadic adrenocortical tumours and hyperplasias.
  • In our previous work, we demonstrated the differential expression of several Wnt/beta-catenin signalling-related genes implicated in ACTH-independent macronodular adrenal hyperplasias (AIMAH).
  • To better understand the role of Wnt/beta-catenin signalling in adrenocortical tumours, we performed mutational analysis of the beta-catenin gene.
  • METHODS: We studied 53 human adrenocortical samples (33 adenomas, 4 carcinomas, 13 AIMAH, 3 ACTH-dependent adrenal hyperplasias) and the human adrenocortical cancer cell line NCI-H295R.
  • All samples were screened for somatic mutations in exons 3 and 5 of the beta-catenin gene.
  • Eleven and six samples were analysed for beta-catenin protein expression by Western blotting and immunohistochemistry, respectively.
  • Genetic alterations were found in 5 (15%) out of 33 adenomas: three cortisol-secreting adenomas, one aldosterone-secreting adenoma and one nonfunctional adenoma.
  • The remaining three tumours contained deletions of 6, 55 and 271 bp.
  • H295R cells carry an activating S45P mutation.
  • Western blot analysis of samples with 55- and 271-bp deletions showed an additional shorter and more intense band representing an accumulation of the mutated form of beta-catenin protein.
  • In addition, cytoplasmic and/or nuclear accumulation of beta-catenin was observed in mutated adenomas by immunohistochemistry.
  • CONCLUSIONS: Activating mutations of exon 3 of the beta-catenin gene are frequent in adrenocortical adenomas, and further characterization of the Wnt/beta-catenin signalling pathway should lead to a better understanding of adrenal tumourigenesis.
  • [MeSH-major] Adrenocortical Adenoma / genetics. Adrenocortical Adenoma / metabolism. beta Catenin / genetics. beta Catenin / metabolism

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  • (PMID = 17854394.001).
  • [ISSN] 1365-2265
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / beta Catenin
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46. Micchelli ST, Vivekanandan P, Boitnott JK, Pawlik TM, Choti MA, Torbenson M: Malignant transformation of hepatic adenomas. Mod Pathol; 2008 Apr;21(4):491-7
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  • [Title] Malignant transformation of hepatic adenomas.
  • Hepatic adenomas are benign neoplasms of the liver that occur in several well-defined clinical settings, but principally that of excess hormone exposure.
  • The clinical presentation and pathological findings were reviewed for all hepatic adenomas resected between January 1, 2003 and July 1, 2006.
  • Immunohistochemistry for p53, beta-catenin and alpha-fetoprotein (AFP) were performed on those cases with malignant transformation and exon 3 of beta-catenin was amplified and sequenced.
  • A total of 17 hepatic adenomas were resected and 3 showed malignant transformation.
  • Histologically, the malignant transformation occurred within otherwise typical hepatic adenomas.
  • Two of three cases showed patchy atypia throughout the hepatic adenoma.
  • The hepatocellular carcinoma arose as distinct nodules directly within the adenomas, effectively ruling out synchronous lesions.
  • Immunostains for AFP and beta-catenin were negative in both the hepatic adenomas and areas of hepatocellular carcinoma. p53 immunostaining was positive within the areas of malignant transformation in one case.
  • No mutations or deletions were seen in exon 3 of the beta-catenin gene for either the adenomas or the carcinoma.
  • In conclusion, two of the cases that developed hepatocellular carcinomas showed cytological atypia in the background adenoma.
  • The hepatocellular carcinomas arose as distinct nodules within the adenomas.
  • No common molecular pathway of hepatocellular carcinogenesis was observed by examining AFP, beta-catenin, and p53 immunostains and no beta-catenin mutations or deletions were found.
  • [MeSH-major] Adenoma, Liver Cell / pathology. Carcinoma, Hepatocellular / pathology. Cell Transformation, Neoplastic / pathology. Liver Neoplasms / pathology
  • [MeSH-minor] Adult. Contraceptives, Oral, Hormonal / adverse effects. Female. Humans. Immunohistochemistry. Tumor Suppressor Protein p53 / biosynthesis. alpha-Fetoproteins / biosynthesis. beta Catenin / genetics

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  • (PMID = 18246041.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contraceptives, Oral, Hormonal; 0 / Tumor Suppressor Protein p53; 0 / alpha-Fetoproteins; 0 / beta Catenin
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47. 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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  • [Cites] Dig Dis Sci. 2003 Aug;48(8):1665-7 [12924666.001]
  • [Cites] Cancer. 1993 Sep 1;72(5):1547-50 [8348490.001]
  • [Cites] Gastroenterology. 1995 Jun;108(6):1637-49 [7768367.001]
  • [Cites] Surgery. 1995 Dec;118(6):973-9; discussion 979-80 [7491542.001]
  • [Cites] Surgery. 1997 Dec;122(6):1176-82 [9426435.001]
  • [Cites] Wien Klin Wochenschr. 2007;119(19-20):602-8 [17985096.001]
  • [Cites] J Surg Oncol. 2005 Mar 1;89(3):143-50 [15719382.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2006;13(5):477-81 [17013727.001]
  • [Cites] Br J Surg. 2007 Nov;94(11):1331-41 [17939142.001]
  • [Cites] Wien Klin Wochenschr. 2007;119(19-20):573-8 [17985090.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):615-30 [10080607.001]
  • (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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48. 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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49. 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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  • [Cites] Yonsei Med J. 2000 Jun;41(3):426-9 [10957903.001]
  • [Cites] Am J Gastroenterol. 2000 Sep;95(9):2271-7 [11007228.001]
  • [Cites] Surg Clin North Am. 2001 Jun;81(3):511-25 [11459268.001]
  • [Cites] Am Surg. 2002 Aug;68(8):660-5; discussion 665-6 [12206598.001]
  • [Cites] J Laparoendosc Adv Surg Tech A. 2003 Feb;13(1):33-6 [12676019.001]
  • [Cites] Ann Chir. 2004 Feb;129(1):2-7; discussion 8-10 [15019845.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):615-30 [10080607.001]
  • [Cites] Hum Pathol. 1982 Mar;13(3):263-71 [7076209.001]
  • [Cites] Arch Surg. 1988 Jul;123(7):843-8 [2838008.001]
  • [Cites] Am J Surg. 1990 Feb;159(2):258-64 [2154144.001]
  • [Cites] J Am Coll Surg. 1994 Feb;178(2):187-211 [8173736.001]
  • [Cites] Surgery. 1994 Dec;116(6):1131-8 [7985098.001]
  • [Cites] J Gastrointest Surg. 1998 Sep-Oct;2(5):472-82 [9843608.001]
  • [Cites] Neuroendocrinology. 2004;80 Suppl 1:62-6 [15477720.001]
  • (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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50. 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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51. Di Leo A, Barone M, Maiorano E, Tanzi S, Piscitelli D, Marangi S, Lofano K, Ierardi E, Principi M, Francavilla A: ER-beta expression in large bowel adenomas: implications in colon carcinogenesis. Dig Liver Dis; 2008 Apr;40(4):260-6
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  • [Title] ER-beta expression in large bowel adenomas: implications in colon carcinogenesis.
  • BACKGROUND: A pivotal role of oestrogen receptor-beta has been suggested in colon carcinogenesis in humans.
  • However, few data are available on oestrogen receptor-beta in colorectal pre-cancerous lesions.
  • AIM: In the present study, we evaluated oestrogen receptor-beta expression and its possible correlation with proliferative activity and apoptosis in colorectal adenomas and normal colon tissue.
  • Oestrogen receptor-beta expression, colonocyte proliferation (expressed as PCNA positivity) and apoptosis were evaluated.
  • RESULTS: In adenomatous tissue, a significant reduction of oestrogen receptor-beta was observed compared to normal mucosa (10.1+/-5.5% vs. 44.2+/-13.7; p<0.03), while the expression of oestrogen receptor-alpha remained unvaried.
  • Cell proliferative activity significantly increased in adenomatous tissue compared to normal mucosa (59.3+/-7.1 vs. 18.5+/-8.8; p<0.0001), doubling the PCNA/apoptosis ratio.
  • An inverse correlation was found between oestrogen receptor-beta and PCNA expression in adenomas (r=-0.81), a datum confirmed by confocal microscopy evaluation.
  • CONCLUSIONS: Our data demonstrate, for the first time, a significant reduction of oestrogen receptor-beta expression already in the pre-cancerous phase of colon carcinogenesis.
  • This suggests a role of selective oestrogen receptor-beta agonists in the prevention of colorectal cancer.
  • [MeSH-major] Adenoma / metabolism. Estrogen Receptor beta / metabolism. Intestinal Neoplasms / metabolism

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  • (PMID = 18093886.001).
  • [ISSN] 1590-8658
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Estrogen Receptor beta
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52. Sabates-Bellver J, Van der Flier LG, de Palo M, Cattaneo E, Maake C, Rehrauer H, Laczko E, Kurowski MA, Bujnicki JM, Menigatti M, Luz J, Ranalli TV, Gomes V, Pastorelli A, Faggiani R, Anti M, Jiricny J, Clevers H, Marra G: Transcriptome profile of human colorectal adenomas. Mol Cancer Res; 2007 Dec;5(12):1263-75
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  • [Title] Transcriptome profile of human colorectal adenomas.
  • Colorectal cancers are believed to arise predominantly from adenomas.
  • To characterize the molecular processes underlying the transformation of normal colonic epithelium, we compared the transcriptomes of 32 prospectively collected adenomas with those of normal mucosa from the same individuals.
  • Important differences emerged not only between the expression profiles of normal and adenomatous tissues but also between those of small and large adenomas.
  • In normal mucosa, KIAA1199 expression was confined to cells in the lower portion of intestinal crypts, where Wnt signaling is physiologically active, but it was markedly increased in all adenomas, where it was expressed in most of the epithelial cells, and in colon cancer cell lines, it was markedly reduced by inactivation of the beta-catenin/T-cell factor(s) transcription complex, the pivotal mediator of Wnt signaling.
  • Our transcriptomic profiles of normal colonic mucosa and colorectal adenomas shed new light on the early stages of colorectal tumorigenesis and identified KIAA1199 as a novel target of the Wnt signaling pathway and a putative marker of colorectal adenomatous transformation.
  • [MeSH-major] Adenoma / genetics. Biomarkers, Tumor / genetics. Colorectal Neoplasms / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic / genetics. Female. Genetic Markers. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Phylogeny. RNA, Messenger / metabolism. Transcription, Genetic

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  • (PMID = 18171984.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / RNA, Messenger
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53. 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
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  • [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


54. Pantelis A, Wenghoefer M, Haas S, Merkelbach-Bruse S, Pantelis D, Jepsen S, Bootz F, Winter J: Down regulation and nuclear localization of human beta-defensin-1 in pleomorphic adenomas of salivary glands. Oral Oncol; 2009 Jun;45(6):526-30
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  • [Title] Down regulation and nuclear localization of human beta-defensin-1 in pleomorphic adenomas of salivary glands.
  • Although antimicrobial peptides (AMPs) appear to have diverse functional activities in innate immunity, a few reports suggest a potential role of human beta-defensin (hBD)-1 in tumor suppression.
  • The aim of the present study was to compare the expression patterns of hBD-1, -2 and -3 in various features of human salivary gland tissues, such as healthy parenchyma, chronic sialadenitis and intraglandular pleomorphic adenomas, with their adjacent normal tissues.
  • Twenty human salivary gland specimens (five healthy, five chronic sialadenitis, five pleomorphic adenomas and five adenoma adjacent normal tissues (AANTs)) were investigated for mRNA expression levels of hBD-1, -2 and -3 by quantitative real-time RT-PCR.
  • In pleomorphic adenomas hBD-2 expression levels were lower, but hBD-1 expression levels were significant decreased (p=0.03) compared to healthy parenchyma.
  • Immunohistochemistry of the tumors showed nuclear hBD-1 localization.
  • For the first time, it was shown that hBD-1 gene expression is significantly decreased in pleomorphic adenomas, while simultaneously the protein is localized in the nucleus.
  • These data support the hypothesis that hBD-1 might be a potential tumor suppressor also in benign salivary gland tumors in addition to other genetic alterations.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Neoplasm Proteins / metabolism. Salivary Gland Neoplasms / metabolism. beta-Defensins / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Case-Control Studies. Cell Nucleus / metabolism. Chronic Disease. Down-Regulation. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction / methods. RNA, Messenger. Sialadenitis / metabolism. Sialadenitis / pathology. Young Adult

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  • (PMID = 18805729.001).
  • [ISSN] 1879-0593
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DEFB1 protein, human; 0 / DEFB4A protein, human; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / beta-Defensins; 0 / beta-defensin 3, human
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55. 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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  • [Cites] N Engl J Med. 2005 Jul 21;353(3):249-54 [16034010.001]
  • [Cites] Diabetes Care. 2006 Jul;29(7):1554-9 [16801578.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2003 May;30(5):781-93 [12707737.001]
  • [Cites] J Nucl Med. 2007 May;48(5):736-43 [17475961.001]
  • [Cites] Physiol Rev. 2007 Oct;87(4):1409-39 [17928588.001]
  • [Cites] N Engl J Med. 2008 Aug 14;359(7):766-8 [18703486.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Nov;94(11):4398-405 [19820010.001]
  • [Cites] Am J Pathol. 1998 Jul;153(1):233-45 [9665484.001]
  • [Cites] Nat Med. 2009 Jun;15(6):616-7 [19498374.001]
  • [Cites] Diabetologia. 2005 Nov;48(11):2236-40 [16195867.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Dec;92(12):4678-85 [17895322.001]
  • (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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56. Manoranjan B, Salehi F, Scheithauer BW, Rotondo F, Kovacs K, Cusimano MD: Estrogen receptors alpha and beta immunohistochemical expression: clinicopathological correlations in pituitary adenomas. Anticancer Res; 2010 Jul;30(7):2897-904
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  • [Title] Estrogen receptors alpha and beta immunohistochemical expression: clinicopathological correlations in pituitary adenomas.
  • AIM: We investigated the immunohistochemical expression of estrogen receptors alpha (ERalpha) and beta (ERbeta) in pituitary adenoma subtypes combined with clinicopathological factors.
  • MATERIALS AND METHODS: Pituitary adenomas (n=75) were immunostained for ERalpha and ERbeta using the streptavidin-biotin-peroxidase complex method with a monoclonal ERalpha antibody and polyclonal ERbeta antibody.
  • RESULTS: Nuclear immunoreactivity for both receptors was highest among PRL, FSH/LH, null cell, and GH adenomas.
  • ACTH, silent subtypes I and II corticotrophs, and subtype III adenomas were the least immunoreactive for both receptors.
  • ACTH adenomas expressed significantly less ERalpha than FSH-LH, GH, and null cell adenomas.
  • A significantly elevated ERalpha expression was observed in macroadenomas compared to microadenomas and non-invasive compared to invasive tumors.
  • CONCLUSION: ERalpha and ERbeta are differentially expressed in the various pituitary adenoma subtypes suggesting a cell-specific function for these receptors.
  • To elucidate the role of ERalpha in tumor size and invasiveness, additional studies are required.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Estrogen Receptor alpha / biosynthesis. Estrogen Receptor beta / biosynthesis. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology
  • [MeSH-minor] Cell Nucleus / metabolism. Cytoplasm / metabolism. Female. Humans. Immunohistochemistry. Male. Neoplasm Invasiveness

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  • (PMID = 20683030.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta
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57. 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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  • [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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58. Miyakoshi T, Takei M, Kajiya H, Egashira N, Takekoshi S, Teramoto A, Osamura RY: Expression of Wnt4 in human pituitary adenomas regulates activation of the beta-catenin-independent pathway. Endocr Pathol; 2008;19(4):261-73
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  • [Title] Expression of Wnt4 in human pituitary adenomas regulates activation of the beta-catenin-independent pathway.
  • A member of the Wnt family of genes, Wnt4, has been known to regulate proliferation of anterior pituitary cell types in the mouse during embryonic development.
  • In order to elucidate the roles of Wnt signaling in human pituitary adenomas, we examined the expression of Wnt4 and its putative receptor Frizzled6 (Fzd6) by immunohistochemistry in pituitary adenomas and normal pituitaries.
  • Expression of Wnt4 was higher in growth hormone-producing adenomas (GHomas), prolactin-producing adenomas (PRLomas), and thyroid-stimulating hormone-producing adenomas (TSHomas) than in the normal pituitary.
  • Fzd6 was widely expressed in GHomas, PRLomas, TSHomas, and gonadotropin subunit (GnSU)-positive adenomas.
  • In normal pituitary glands, Wnt4 and Fzd6 were colocalized predominantly in follicle-stimulating hormone-, luteinizing hormone-, and alpha-subunits of glycoprotein hormone-positive cells.
  • The canonical Wnt/beta-catenin signaling pathway was analyzed by beta-catenin immunohistochemistry. beta-Catenin was localized at the cell membrane in all pituitary adenomas, but not in the nuclei.
  • These results suggested that activation of Wnt4/Fzd6 signaling through a "beta-catenin-independent" pathway played a role in proliferation and survival of the pituitary adenoma cells.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / metabolism. Pituitary Neoplasms / metabolism. Wnt Proteins / metabolism. beta Catenin / metabolism

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  • (PMID = 19034702.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / FZD6 protein, human; 0 / Frizzled Receptors; 0 / Receptors, G-Protein-Coupled; 0 / WNT4 protein, human; 0 / Wnt Proteins; 0 / Wnt4 Protein; 0 / Wnt4 protein, mouse; 0 / beta Catenin
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59. 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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  • [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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60. 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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61. Nucera C, Mazzon E, Caillou B, Violi MA, Moleti M, Priolo C, Sturniolo G, Puzzolo D, Cavallari V, Trimarchi F, Vermiglio F: Human galectin-3 immunoexpression in thyroid follicular adenomas with cell atypia. J Endocrinol Invest; 2005 Feb;28(2):106-12
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  • [Title] Human galectin-3 immunoexpression in thyroid follicular adenomas with cell atypia.
  • Human galectin-3 (hgal-3) is a beta-galactoside binding protein involved in a number of physiological and pathological processes.
  • Increasing hgal-3 immunoexpression has been reported in several human tumors, including thyroid carcinomas, but not in benign thyroid lesions.
  • We analyzed the immunolocalization of hgal-3 in cell compartments of benign and malignant thyroid lesions.
  • Hgal-3 immunoperoxidase reaction was carried out on 133 thyroid tissue samples obtained from 113 patients; 20 of these were normal (NT), 85 were benign thyroid lesions [20 colloid nodules (CN), 21 nodular hyperplasias (NH), 7 focal lymphocytic thyroiditis (FLT), 15 Hashimoto's thyroiditis (HT), 22 follicular adenomas (FA)], 25 differentiated carcinomas [15 papillary carcinomas (PC), 6 follicular carcinomas (FC) and 4 Hürthle cell carcinomas (HC)] and 3 anaplastic carcinomas (AC).
  • [MeSH-major] Adenoma / chemistry. Adenoma / pathology. Galectin 3 / analysis. Thyroid Neoplasms / chemistry. Thyroid Neoplasms / pathology

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  • (PMID = 15887854.001).
  • [ISSN] 0391-4097
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Galectin 3
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62. Dadan J, Wojskowicz P, Wojskowicz A: Neuroendocrine tumors of the pancreas. Wiad Lek; 2008;61(1-3):43-7
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  • [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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63. 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
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  • [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


64. Misikangas M, Tanayama H, Rajakangas J, Lindén J, Pajari AM, Mutanen M: Inulin results in increased levels of beta-catenin and cyclin D1 as the adenomas increase in size from small to large in the Min/+ mouse. Br J Nutr; 2008 May;99(5):963-70
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  • [Title] Inulin results in increased levels of beta-catenin and cyclin D1 as the adenomas increase in size from small to large in the Min/+ mouse.
  • The mechanism that drives the growth of some colonic adenomas towards malignancy, while permitting others to remain for decades in quiescence, remains unknown.
  • Diets can alter the growth rate of intestinal tumours but it is still unknown whether diets are able to alter the molecular biology of these adenomas in a way that predicts further outcome.
  • To address this issue we fed Min/+ mice with two diets known to lead to different adenoma outcomes: a high-fat control diet (n 15) or a high-fat inulin-enriched (10 % w/w) diet (n 13).
  • To study the effect of diet on cell signalling during adenoma growth, the adenomas of each Min/+ mouse were divided into three size-categories, and the levels of beta-catenin, E-cadherin, cyclin D1 and matrix metalloproteinase-9, which are known to be involved in colon tumorigenesis, were determined.
  • The growth-promoting inulin diet resulted in more large adenomas than the control feeding (P = 0.003) and doubled the total area of the adenomas (P = 0.008).
  • The inulin diet increased the expression of nuclear beta-catenin (P = 0.004) and its target cyclin D1 (P = 0.017) as the adenomas increased in size from small to large, indicating the presence of an accelerated cancerous process.
  • Neither phenomenon was seen in the control group during adenoma growth.
  • Our results suggest that in addition to the number, size, and growth rate of adenomatous polyps, the signalling pattern of the adenomas should also be considered when evaluating preventive dietary strategies.
  • [MeSH-major] Adenomatous Polyposis Coli / pathology. Cyclin D1 / metabolism. Diet. Inulin / pharmacology. beta Catenin / metabolism
  • [MeSH-minor] Animals. Cadherins / metabolism. Dietary Fats / administration & dosage. Disease Models, Animal. Disease Progression. Mice. Mice, Inbred C57BL. Neoplasm Proteins / metabolism. Signal Transduction / drug effects

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  • (PMID = 17977470.001).
  • [ISSN] 0007-1145
  • [Journal-full-title] The British journal of nutrition
  • [ISO-abbreviation] Br. J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cadherins; 0 / Dietary Fats; 0 / Neoplasm Proteins; 0 / beta Catenin; 136601-57-5 / Cyclin D1; 9005-80-5 / Inulin
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65. Rajakangas J, Misikangas M, Päivärinta E, Mutanen M: Chemoprevention by white currant is mediated by the reduction of nuclear beta-catenin and NF-kappaB levels in Min mice adenomas. Eur J Nutr; 2008 Apr;47(3):115-22
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  • [Title] Chemoprevention by white currant is mediated by the reduction of nuclear beta-catenin and NF-kappaB levels in Min mice adenomas.
  • AIMS OF THE STUDY: To study if white currant is chemopreventive in an experimental model for intestinal tumorigenesis and further study the effects on beta-catenin and NF-kappaB signaling pathways.
  • Cell signaling parameters were analysed from intestinal adenomas and surrounding mucosa by Western blotting and immunohistochemistry.
  • RESULTS: The white currant diet reduced the number of adenomas from 81 (min-max 47-114) to 51 (36-84) in the total small intestine of Min mice (P<0.02).
  • Most of the adenomas develop in the distal part of the small intestine, and in this area white currant reduced the number from 49 to 29.5 (P<0.01) and also the size of the adenomas from 0.88 mm to 0.70 mm (P<0.02).
  • In the colon white currant increased the number of adenomas (0.3+/-0.6 vs. 0.8+/-0.6, mean +/- SD, P<0.05), but did not affect the size.
  • White currant reduced nuclear beta-catenin and NF-kappaB protein levels in the adenomas (P<0.05 and P<0.02, respectively).
  • They were correlated with the size of adenomas (P<0.01).
  • [MeSH-major] Adenoma / prevention & control. Antineoplastic Agents, Phytogenic / pharmacology. Fruit / chemistry. Intestinal Mucosa / pathology. Intestinal Neoplasms / prevention & control. NF-kappa B / metabolism. beta Catenin / metabolism

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  • [Cites] Curr Cancer Drug Targets. 2004 Dec;4(8):653-71 [15578921.001]
  • [Cites] J Agric Food Chem. 2007 Feb 21;55(4):1612-9 [17261015.001]
  • [Cites] Trends Mol Med. 2005 Nov;11(11):496-502 [16214417.001]
  • [Cites] Annu Rev Immunol. 2000;18:621-63 [10837071.001]
  • [Cites] Curr Opin Cell Biol. 2007 Apr;19(2):150-8 [17306971.001]
  • [Cites] Nat Rev Cancer. 2007 Feb;7(2):139-47 [17218951.001]
  • [Cites] J Agric Food Chem. 2004 Oct 6;52(20):6122-8 [15453676.001]
  • [Cites] Br J Cancer. 1999 Jun;80(7):1046-51 [10362114.001]
  • [Cites] Am J Pathol. 1997 Jun;150(6):1977-84 [9176391.001]
  • [Cites] Mol Nutr Food Res. 2007 Jun;51(6):684-91 [17492800.001]
  • [Cites] Nutr Cancer. 2006;54(1):84-93 [16800776.001]
  • [Cites] Nutr Cancer. 2006;56(1):86-94 [17176222.001]
  • [Cites] Gastroenterology. 1996 Mar;110(3):669-74 [8608874.001]
  • [Cites] J Agric Food Chem. 2004 Jul 14;52(14):4477-86 [15237955.001]
  • [Cites] Cancer Lett. 2003 May 8;194(1):13-9 [12706854.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7613-8 [14633677.001]
  • [Cites] Oncogene. 1999 Nov 22;18(49):6853-66 [10602461.001]
  • [Cites] Science. 1992 May 1;256(5057):668-70 [1350108.001]
  • [Cites] J Nutr Biochem. 2005 Jul;16(7):402-9 [15992678.001]
  • [Cites] Biochim Biophys Acta. 2006 Jan;1765(1):14-24 [16226380.001]
  • [Cites] Virchows Arch. 1997 Sep;431(3):167-72 [9334837.001]
  • [Cites] Anticancer Drugs. 2003 Nov;14(10):845-50 [14597880.001]
  • [Cites] J Biol Chem. 1999 Sep 17;274(38):27307-14 [10480951.001]
  • [Cites] Antioxid Redox Signal. 2001 Dec;3(6):981-93 [11813993.001]
  • [Cites] Br J Cancer. 2004 Jan 12;90(1):224-9 [14710233.001]
  • [Cites] J Agric Food Chem. 2003 Jan 1;51(1):68-75 [12502387.001]
  • [Cites] Nat Rev Immunol. 2005 Oct;5(10):749-59 [16175180.001]
  • [Cites] Nutr Cancer. 2006;54(1):79-83 [16800775.001]
  • [Cites] Breast Dis. 2006-2007;26:27-54 [17473364.001]
  • [Cites] Nature. 1998 Nov 5;396(6706):77-80 [9817203.001]
  • [Cites] J Agric Food Chem. 2004 May 5;52(9):2512-7 [15113149.001]
  • [Cites] J Agric Food Chem. 2006 Feb 8;54(3):980-5 [16448212.001]
  • [Cites] Anticancer Res. 2007 Mar-Apr;27(2):937-48 [17465224.001]
  • [Cites] Mol Nutr Food Res. 2007 Jun;51(6):665-74 [17487926.001]
  • [Cites] AAPS J. 2006 Jul 07;8(3):E443-9 [17025261.001]
  • [Cites] Science. 1990 Jan 19;247(4940):322-4 [2296722.001]
  • [Cites] Am J Pathol. 2000 Mar;156(3):865-70 [10702403.001]
  • [Cites] J Nutr. 2007 Oct;137(10):2285-90 [17885012.001]
  • [Cites] Nutr Cancer. 2001;40(2):125-33 [11962247.001]
  • [Cites] Am J Pathol. 1996 Jan;148(1):39-46 [8546224.001]
  • [Cites] J Nutr. 1993 Nov;123(11):1939-51 [8229312.001]
  • [Cites] Cell. 2006 Nov 3;127(3):469-80 [17081971.001]
  • [Cites] Nat Rev Drug Discov. 2004 Jan;3(1):17-26 [14708018.001]
  • [Cites] Carcinogenesis. 2004 Dec;25(12):2443-9 [15297372.001]
  • [Cites] J Agric Food Chem. 2005 Sep 7;53(18):7320-9 [16131149.001]
  • [Cites] Oncogene. 2006 Oct 30;25(51):6887-99 [17072334.001]
  • [Cites] Int J Cancer. 2006 Nov 1;119(9):2213-20 [16823841.001]
  • (PMID = 18389329.001).
  • [ISSN] 1436-6207
  • [Journal-full-title] European journal of nutrition
  • [ISO-abbreviation] Eur J Nutr
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / NF-kappa B; 0 / beta Catenin
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66. Wang Y, Giel-Moloney M, Rindi G, Leiter AB: Enteroendocrine precursors differentiate independently of Wnt and form serotonin expressing adenomas in response to active beta-catenin. Proc Natl Acad Sci U S A; 2007 Jul 3;104(27):11328-33
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  • [Title] Enteroendocrine precursors differentiate independently of Wnt and form serotonin expressing adenomas in response to active beta-catenin.
  • Wnt signaling is required for the maintenance of intestinal stem cells and self-renewal of the intestinal epithelium.
  • Here, we show that specification of enteroendocrine but not Paneth cells occurs independently of Wnt signals by conditional deletion of beta-catenin in immature cells expressing the transcription factor, neurogenin 3.
  • In addition, we determined whether neurogenin 3-expressing cells respond to abnormal Wnt signaling.
  • Activation of the Wnt pathway by conditionally deleting exon 3 of the beta-catenin gene at an early stage of enteroendocrine cell differentiation induced small-intestinal adenomas expressing serotonin, a feature not previously described in other tumors induced by Wnt in mice.
  • In contrast, excision of exon 3 of beta-catenin at a later stage of enteroendocrine differentiation did not produce tumors.
  • These results provide direct evidence that some intestinal lineages are specified independently of the Wnt pathway and may lead to a better understanding of the spectrum of neuroendocrine differentiation frequently seen in human gastrointestinal cancer.

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  • [Cites] Nat Genet. 2000 Jan;24(1):36-44 [10615124.001]
  • [Cites] Virchows Arch. 2006 Nov;449(5):499-506 [17033797.001]
  • [Cites] Development. 2001 Apr;128(8):1253-64 [11262227.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6656-9 [11559529.001]
  • [Cites] Science. 2001 Dec 7;294(5549):2155-8 [11739954.001]
  • [Cites] Genes Dev. 2002 Jun 15;16(12):1488-97 [12080087.001]
  • [Cites] EMBO J. 2002 Dec 2;21(23):6338-47 [12456641.001]
  • [Cites] Genes Dev. 2003 Jul 15;17(14):1709-13 [12865297.001]
  • [Cites] Dev Biol. 2004 Jun 15;270(2):443-54 [15183725.001]
  • [Cites] Genes Dev. 2004 Jun 15;18(12):1385-90 [15198980.001]
  • [Cites] Pathol Res Pract. 1988 Apr;183(2):119-28 [2968544.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 9;92(10):4482-6 [7753829.001]
  • [Cites] Genes Dev. 1998 Mar 15;12(6):820-30 [9512516.001]
  • [Cites] Nat Genet. 1998 Aug;19(4):379-83 [9697701.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):70-1 [9916792.001]
  • [Cites] Mol Cell Biol. 1999 Jun;19(6):4503-15 [10330189.001]
  • [Cites] Development. 2005 Mar;132(6):1443-51 [15716339.001]
  • [Cites] Nat Cell Biol. 2005 Apr;7(4):381-6 [15778706.001]
  • [Cites] Genes Dev. 2005 Apr 15;19(8):877-90 [15833914.001]
  • [Cites] Neuroendocrinology. 2004;80(6):394-424 [15838182.001]
  • [Cites] EMBO J. 1999 Nov 1;18(21):5931-42 [10545105.001]
  • [Cites] Nature. 2005 Jun 23;435(7045):1126-30 [15973414.001]
  • [Cites] Gastroenterology. 2005 Aug;129(2):626-38 [16083717.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12443-8 [16107537.001]
  • [Cites] Genes Dev. 2005 Oct 15;19(20):2412-7 [16230531.001]
  • [Cites] Diabetes. 2000 Feb;49(2):163-76 [10868931.001]
  • (PMID = 17592150.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32-DK007542; United States / NIDDK NIH HHS / DK / P30 DK034928; United States / NIDDK NIH HHS / DK / DK67166; United States / NIDDK NIH HHS / DK / DK52870; United States / NIDDK NIH HHS / DK / P30-DK34928; United States / NIDDK NIH HHS / DK / DK43673; United States / NIDDK NIH HHS / DK / T32 DK007542; United States / NIDDK NIH HHS / DK / R01 DK067166; United States / NIDDK NIH HHS / DK / R01 DK043673
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / CTNNB1 protein, human; 0 / NEUROG3 protein, human; 0 / Nerve Tissue Proteins; 0 / Wnt Proteins; 0 / beta Catenin; 333DO1RDJY / Serotonin
  • [Other-IDs] NLM/ PMC2040898
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67. 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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68. 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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69. Morris DG, Musat M, Czirják S, Hanzély Z, Lillington DM, Korbonits M, Grossman AB: Differential gene expression in pituitary adenomas by oligonucleotide array analysis. Eur J Endocrinol; 2005 Jul;153(1):143-51
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  • [Title] Differential gene expression in pituitary adenomas by oligonucleotide array analysis.
  • OBJECTIVES: Microarray technology allows for the expression profile of many thousands of genes to be quantified at the same time, and has resulted in novel discoveries about the tumour biology of a number of cancers.
  • We sought to do this in pituitary adenomas, the most common intracranial neoplasm.
  • METHODS: Affymetrix GeneChip HG-U133A oligonucleotide arrays covering 14 500 well-characterised genes from the human genome were used to study pooled RNA for each of the four major pituitary adenoma subtypes.
  • Individual gene-expression levels in the tumours were compared relative to the expression profile in normal pooled pituitary RNA.
  • Three differentially expressed genes with potential importance in tumourigenesis were chosen for validation by real-time quantitative PCR on the original tumours and on an additional 26 adenomas.
  • RESULTS: Bioinformatic analysis showed that 3906 genes and 351 expressed sequence tags were differentially expressed among all pituitary tumour subtypes.
  • Lysosomal-associated protein transmembrane- 4-beta (LAPTM4B), a novel gene upregulated in hepatocellular carcinoma, was significantly over-expressed in adrenocorticotrophin (ACTH)-secreting adenomas and non-functioning pituitary adenomas (NFPAs).
  • Bcl-2-associated athanogene (BAG1), an anti-apoptotic protein found at high levels in a number of human cancers, was significantly over-expressed in growth hormone-secreting and prolactin-secreting adenomas and NFPAs.
  • The cyclin-dependent kinase inhibitor p18, in which murine gene deletion has been shown to produce pituitary ACTH cell hyperplasia and adenomas, was significantly under-expressed in ACTH-secreting adenomas.
  • CONCLUSIONS: Expression array analysis of pituitary adenomas using the Affymetrix GeneChip HG-U133A arrays appears to be a valid method of identifying genes that may be important in tumour pathogenesis.

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  • (PMID = 15994756.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL2-associated athanogene 1 protein; 0 / CDKN2C protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p18; 0 / DNA-Binding Proteins; 0 / LAPTM4B protein, human; 0 / Membrane Proteins; 0 / Oncogene Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
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70. 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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  • [Cites] Am J Pathol. 1991 Jun;138(6):1335-47 [1711288.001]
  • [Cites] Cell Struct Funct. 1986 Sep;11(3):245-52 [3768962.001]
  • [Cites] Eur J Cancer. 1996 Dec;32A(14):2451-60 [9059333.001]
  • [Cites] Anticancer Res. 1997 Mar-Apr;17(2B):1227-30 [9137477.001]
  • [Cites] Science. 1997 Jul 11;277(5323):242-5 [9211853.001]
  • [Cites] Am J Surg. 1997 Sep;174(3):251-7 [9324132.001]
  • [Cites] Nat Med. 1999 Mar;5(3):286-91 [10086383.001]
  • [Cites] Curr Top Pathol. 1999;93:27-33 [10339896.001]
  • [Cites] Development. 1999 Jun;126(14):3047-55 [10375497.001]
  • [Cites] Cancer Res. 2004 Dec 1;64(23):8630-8 [15574770.001]
  • [Cites] Science. 2005 Jan 7;307(5706):58-62 [15637262.001]
  • [Cites] Curr Opin Genet Dev. 2005 Feb;15(1):102-11 [15661540.001]
  • [Cites] Expert Rev Mol Diagn. 2005 Mar;5(2):221-30 [15833051.001]
  • [Cites] Tumour Biol. 2005 Mar-Apr;26(2):103-12 [15897690.001]
  • [Cites] Circ Res. 2005 Sep 16;97(6):512-23 [16166562.001]
  • [Cites] Oncology. 2005;69(2):159-66 [16127287.001]
  • [Cites] Brain Res Bull. 2000 Mar 15;51(5):363-9 [10715555.001]
  • [Cites] Am J Pathol. 2000 Apr;156(4):1363-80 [10751361.001]
  • [Cites] Dev Dyn. 2001 Jan;220(1):60-73 [11146508.001]
  • [Cites] EMBO J. 2001 Feb 15;20(4):672-82 [11179212.001]
  • [Cites] Pancreas. 2001 Mar;22(2):122-5 [11249065.001]
  • [Cites] J Cell Biol. 2001 Apr 30;153(3):543-53 [11331305.001]
  • [Cites] Cells Tissues Organs. 2001;169(1):1-11 [11340256.001]
  • [Cites] Nature. 2001 May 17;411(6835):375-9 [11357145.001]
  • [Cites] Bioessays. 2001 Jun;23(6):494-507 [11385629.001]
  • [Cites] Cancer Res. 2001 Oct 15;61(20):7627-34 [11606404.001]
  • [Cites] Circulation. 2002 Jan 1;105(1):112-7 [11772885.001]
  • [Cites] Glycobiology. 2002 Jan;12(1):47-63 [11825886.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):801-13 [11891179.001]
  • [Cites] Am J Pathol. 2002 Mar;160(3):985-1000 [11891196.001]
  • [Cites] Physiol Rev. 2002 Jul;82(3):673-700 [12087132.001]
  • [Cites] EMBO J. 2002 Aug 15;21(16):4307-16 [12169633.001]
  • [Cites] Nat Rev Cancer. 2002 Jun;2(6):442-54 [12189386.001]
  • [Cites] Nat Genet. 2003 Jan;33(1):49-54 [12469122.001]
  • [Cites] J Clin Invest. 2003 May;111(9):1287-95 [12727920.001]
  • [Cites] Nat Med. 2003 Jun;9(6):685-93 [12778167.001]
  • [Cites] Br J Dermatol. 2003 May;148(5):971-80 [12786828.001]
  • [Cites] Genes Dev. 2003 Aug 1;17(15):1835-40 [12897053.001]
  • [Cites] J Clin Invest. 2003 Oct;112(8):1142-51 [14561699.001]
  • [Cites] J Cell Biol. 2003 Oct 27;163(2):209-13 [14581448.001]
  • [Cites] Clin Chem. 2004 Mar;50(3):509-15 [14726469.001]
  • [Cites] PLoS Biol. 2003 Nov;1(2):E52 [14624252.001]
  • [Cites] Cancer Res. 2004 Apr 15;64(8):2725-33 [15087386.001]
  • [Cites] Circ Res. 2004 Apr 30;94(8):1067-74 [15031262.001]
  • [Cites] Nature. 1985 May 9-15;315(6015):115-22 [2986015.001]
  • [Cites] Nature. 1994 Feb 3;367(6462):455-9 [8107803.001]
  • (PMID = 16470244.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecules
  • [Other-IDs] NLM/ PMC1361347
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71. Lorentzen A, Vogel LK, Lewinsky RH, Saebø M, Skjelbred CF, Godiksen S, Hoff G, Tveit KM, Lothe IM, Ikdahl T, Kure EH, Mitchelmore C: Expression of NDRG2 is down-regulated in high-risk adenomas and colorectal carcinoma. BMC Cancer; 2007 Oct 12;7:192
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  • [Title] Expression of NDRG2 is down-regulated in high-risk adenomas and colorectal carcinoma.
  • BACKGROUND: It has recently been shown that NDRG2 mRNA is down-regulated or undetectable in several human cancers and cancer cell-lines.
  • By examining affected and normal tissue from individuals with colorectal adenomas and carcinomas, as well as in healthy individuals, we aim to determine whether and at which stages NDRG2 down-regulation occurs during colonic carcinogenesis.
  • METHODS: Using quantitative RT-PCR, we have determined the mRNA levels for NDRG2 in low-risk (n = 15) and high-risk adenomas (n = 57), colorectal carcinomas (n = 50) and corresponding normal tissue, as well as control tissue from healthy individuals (n = 15).
  • NDRG2 levels were normalised to beta-actin.
  • When comparing adenomas/carcinomas with adjacent normal tissue from the same individual, NDRG2 expression levels were significantly reduced in both high-risk adenoma (p < 0.001) and in colorectal carcinoma (p < 0.001).
  • Future studies are needed to address whether NDRG2 down-regulation is a cause or consequence of the progression of colorectal adenomas to carcinoma.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Down-Regulation. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Female. Humans. Male. Middle Aged. Neoplasm Staging. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • [Cites] Oncogene. 1999 May 13;18(19):3004-16 [10378696.001]
  • [Cites] J Mol Diagn. 2006 May;8(2):193-201 [16645205.001]
  • [Cites] Anal Biochem. 2000 Feb 15;278(2):175-84 [10660460.001]
  • [Cites] Proteins. 2002 May 1;47(2):163-8 [11933063.001]
  • [Cites] Mol Cell Biochem. 2002 Jan;229(1-2):35-44 [11936845.001]
  • [Cites] Scand J Gastroenterol. 2003 Jun;38(6):635-42 [12825872.001]
  • [Cites] Int J Cancer. 2003 Sep 1;106(3):342-7 [12845671.001]
  • [Cites] FEBS Lett. 2003 Oct 23;553(3):413-8 [14572661.001]
  • [Cites] Neurobiol Dis. 2004 Jun;16(1):48-58 [15207261.001]
  • [Cites] Mech Dev. 1999 May;83(1-2):39-52 [10381566.001]
  • [Cites] World J Gastroenterol. 2004 Dec 1;10(23):3518-21 [15526377.001]
  • [Cites] Biochem Soc Trans. 2005 Aug;33(Pt 4):672-5 [16042571.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7121-6 [16103061.001]
  • [Cites] Oncogene. 2006 Jan 5;25(1):111-21 [16247483.001]
  • [Cites] Cancer Cell. 2006 Mar;9(3):157-73 [16530701.001]
  • [Cites] J Biol Chem. 2006 Dec 22;281(51):39159-68 [17050536.001]
  • (PMID = 17935612.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NDRG2 protein, human; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2099434
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72. Yachida S, Mudali S, Martin SA, Montgomery EA, Iacobuzio-Donahue CA: Beta-catenin nuclear labeling is a common feature of sessile serrated adenomas and correlates with early neoplastic progression after BRAF activation. Am J Surg Pathol; 2009 Dec;33(12):1823-32
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  • [Title] Beta-catenin nuclear labeling is a common feature of sessile serrated adenomas and correlates with early neoplastic progression after BRAF activation.
  • Recent observations indicate that some sessile serrated adenomas (SSAs) have aberrant beta-catenin nuclear labeling, implicating the Wnt pathway in the molecular progression of SSAs to colorectal carcinoma.
  • We sought to expand upon this finding by characterizing beta-catenin expression in the full spectrum of serrated colorectal polyps, and correlating these findings with the genetic status of BRAF, KRAS and CTNNB1.
  • Immunolabeling for beta-catenin confirmed the presence of abnormal nuclear accumulation in SSAs, with 35/54 (67%) SSAs showing nuclear labeling compared with 0/12 hyperplastic polyps.
  • Abnormal nuclear labeling was also identified in 4/11 (36%) traditional serrated adenomas (TSAs) (P=0.00001).
  • When SSAs were further analyzed with respect to the presence or absence of conventional epithelial dysplasia, nuclear beta-catenin labeling was seen in 8/27 (29%) SSAs without dysplasia (SSA) but in 27/27 (100%) of SSAs with dysplasia (P=0.000001).
  • Sequencing of genomic DNA extracted from a subset of hyperplastic polyps, SSAs, SSAs with dysplasia, TSAs and tubular adenomas failed to identify any CTNNB1 mutations to account for abnormal beta-catenin nuclear labeling.
  • However, abnormal nuclear labeling always occurred in the setting of a BRAF V600E mutation, indicating aberrant nuclear labeling occurs on a background of BRAF activation.

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  • [Cites] Nat Genet. 2000 Mar;24(3):245-50 [10700176.001]
  • [Cites] Int J Cancer. 2008 Dec 1;123(11):2587-93 [18798261.001]
  • [Cites] Br J Cancer. 2003 Jul 7;89(1):152-7 [12838317.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):4878-81 [12941809.001]
  • [Cites] Nat Genet. 2004 Apr;36(4):417-22 [15034581.001]
  • [Cites] Gut. 2004 Aug;53(8):1137-44 [15247181.001]
  • [Cites] J Clin Pathol. 2004 Oct;57(10):1089-93 [15452166.001]
  • [Cites] Am J Surg Pathol. 2004 Nov;28(11):1452-9 [15489648.001]
  • [Cites] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597.001]
  • [Cites] Am J Surg Pathol. 1990 Jun;14(6):524-37 [2186644.001]
  • [Cites] Cell. 1990 Jun 1;61(5):759-67 [2188735.001]
  • [Cites] Science. 1991 Mar 15;251(4999):1366-70 [1848370.001]
  • [Cites] Tohoku J Exp Med. 1992 Oct;168(2):141-7 [1339098.001]
  • [Cites] Science. 1997 Mar 21;275(5307):1787-90 [9065402.001]
  • [Cites] Cancer Res. 1999 Jul 15;59(14):3346-51 [10416591.001]
  • [Cites] Gut. 2005 Feb;54(2):264-7 [15647192.001]
  • [Cites] Am J Clin Pathol. 2006 Jan;125(1):132-45 [16483002.001]
  • [Cites] Nat Genet. 2006 Jul;38(7):787-93 [16804544.001]
  • [Cites] Histopathology. 2006 Aug;49(2):121-31 [16879389.001]
  • [Cites] Am J Clin Pathol. 2006 Oct;126(4):564-71 [16938659.001]
  • [Cites] Cell. 2006 Nov 3;127(3):469-80 [17081971.001]
  • [Cites] Am J Surg Pathol. 2006 Dec;30(12):1491-501 [17122504.001]
  • [Cites] Am J Surg Pathol. 2007 Aug;31(8):1238-45 [17667549.001]
  • [Cites] Am J Surg Pathol. 2008 Jan;32(1):21-9 [18162766.001]
  • [Cites] Am J Clin Pathol. 2008 Mar;129(3):416-23 [18285264.001]
  • [Cites] Am J Surg Pathol. 2008 Mar;32(3):407-12 [18300810.001]
  • [Cites] Fam Cancer. 2008;7(2):157-62 [17929199.001]
  • [Cites] World J Gastroenterol. 2008 Jun 14;14(22):3461-3 [18567071.001]
  • [Cites] Curr Gastroenterol Rep. 2008 Oct;10(5):490-8 [18799125.001]
  • [Cites] Am J Surg Pathol. 2003 Jan;27(1):65-81 [12502929.001]
  • (PMID = 19745699.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA106610; United States / NCI NIH HHS / CA / K08 CA106610-05; United States / NCI NIH HHS / CA / CA106610
  • [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 / CTNNB1 protein, human; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / beta Catenin; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS139736; NLM/ PMC2788075
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73. 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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  • [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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74. 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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75. Caldwell GM, Jones CE, Taniere P, Warrack R, Soon Y, Matthews GM, Morton DG: The Wnt antagonist sFRP1 is downregulated in premalignant large bowel adenomas. Br J Cancer; 2006 Mar 27;94(6):922-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Wnt antagonist sFRP1 is downregulated in premalignant large bowel adenomas.
  • Our previous studies have implicated the Wnt antagonist, sFRP1, as a tumour suppressor gene in advanced colorectal cancer.
  • In this study, we set out to investigate the relationship between sFRP1 expression and large bowel adenomas, a precursor of colorectal cancer.
  • The induction of beta-catenin/TCF mediated transcription is both a frequent early event in colorectal neoplasia, and a key downstream effect of wnt growth factor signalling.
  • Lithium treatment of a small bowel mucosal cell line (FHs 74 int) induced sFRP1 within 8 h, indicating that this gene is positively regulated by beta-catenin, contrasting with the suppression of sFRP1 expression, we saw previously in advanced colorectal cancers.
  • We therefore investigated a series of 12 adenomas and matched large bowel mucosa samples.
  • Real-time RT-PCR analysis showed a reduction in sFRP1 expression in all 12 dysplastic lesions (median 485-fold, IQR 120- to 1500-fold), indicating factors other than beta-catenin influence sFRP1 levels.
  • In a second series of 11 adenomas, we identified methylation of the sFRP1 promotor region in all 11 samples, and this was increased compared with the surrounding normal mucosa in seven cases.
  • Immunohistochemical analysis using a polyclonal antibody supported these findings, with sFRP1 expression reduced in many of the adenoma samples examined. sFRP1 staining in normal mucosa adjacent to the dysplastic tissue was also reduced compared with the normal controls, suggesting that sFRP1 expression may be suppressed in a field of mucosa rather than in individual cells.
  • This study identifies sFRP1 inactivation at the premalignant stage of colorectal cancer development, indicating that these pathways may be useful targets for chemoprevention strategies in this common solid tumour.
  • [MeSH-major] Adenoma / genetics. Colorectal Neoplasms / genetics. Intercellular Signaling Peptides and Proteins / biosynthesis. Membrane Proteins / biosynthesis
  • [MeSH-minor] Cell Transformation, Neoplastic. Chemoprevention. DNA Methylation. Down-Regulation. Humans. Immunohistochemistry. Intestinal Mucosa. Intestine, Large / physiology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Tumor Cells, Cultured. Wnt Proteins / physiology

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  • [Cites] Nucleic Acids Res. 2001 Jul 1;29(13):E65-5 [11433041.001]
  • [Cites] Oncogene. 2005 Nov 24;24(53):7946-52 [16007117.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):14973-8 [11752446.001]
  • [Cites] Cancer Res. 2002 Mar 1;62(5):1296-9 [11888894.001]
  • [Cites] Gut. 2002 Apr;50(4):513-9 [11889072.001]
  • [Cites] J Pathol. 2003 Oct;201(2):204-12 [14517837.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):883-8 [14871816.001]
  • [Cites] Lab Invest. 2004 Apr;84(4):465-78 [14968126.001]
  • [Cites] Nat Genet. 2004 Apr;36(4):417-22 [15034581.001]
  • [Cites] Genes Dev. 2004 Jun 15;18(12):1385-90 [15198980.001]
  • [Cites] Cancer Res. 2004 Jul 15;64(14):4717-20 [15256437.001]
  • [Cites] Int J Oncol. 2004 Sep;25(3):641-9 [15289865.001]
  • [Cites] Oncogene. 2004 Aug 26;23(39):6672-6 [15221014.001]
  • [Cites] Arch Pathol Lab Med. 2004 Sep;128(9):967-73 [15335268.001]
  • [Cites] Cancer Sci. 2004 Sep;95(9):741-4 [15471560.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8455-9 [8710892.001]
  • [Cites] Science. 1997 Mar 21;275(5307):1787-90 [9065402.001]
  • [Cites] Nucleic Acids Res. 1997 Jun 15;25(12):2532-4 [9171110.001]
  • [Cites] FASEB J. 2005 Jan;19(1):144-6 [15507471.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):1098-103 [15592505.001]
  • [Cites] Oncogene. 2005 Apr 21;24(18):3054-8 [15735684.001]
  • [Cites] J Clin Pathol. 2005 May;58(5):515-9 [15858124.001]
  • [Cites] Cancer Res. 2005 May 15;65(10):4218-27 [15899813.001]
  • [Cites] Int J Cancer. 2005 Sep 10;116(4):584-91 [15825175.001]
  • [Cites] Gastroenterology. 2005 Aug;129(2):626-38 [16083717.001]
  • [Cites] Nature. 2005 Sep 8;437(7056):281-5 [16007074.001]
  • [Cites] Oncogene. 2001 Sep 13;20(41):5810-7 [11593386.001]
  • (PMID = 16523202.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / SFRP1 protein, human; 0 / Wnt Proteins
  • [Other-IDs] NLM/ PMC2361362
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76. 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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  • [Cites] J Cell Biol. 2001 Oct 1;155(1):41-51 [11571310.001]
  • [Cites] J Mol Biol. 2009 Jun 26;389(5):907-20 [19427320.001]
  • [Cites] Nature. 2002 Apr 4;416(6880):535-9 [11932745.001]
  • [Cites] Diabetes. 2003 Jan;52(1):102-10 [12502499.001]
  • [Cites] J Cell Physiol. 2003 May;195(2):158-67 [12652643.001]
  • [Cites] Science. 2003 Apr 18;300(5618):486-9 [12702875.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10132-6 [15220483.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Apr 28;160(2):961-7 [2655598.001]
  • [Cites] FEBS Lett. 1989 Jul 17;251(1-2):261-4 [2666169.001]
  • [Cites] Diabetes. 1990 Jun;39(6):752-6 [2189768.001]
  • [Cites] Diabetes. 1994 Feb;43(2):329-36 [8288058.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):7283-8 [8692984.001]
  • [Cites] Diabetes. 1996 Aug;45(8):1094-101 [8690157.001]
  • [Cites] Diabetologia. 1996 May;39(5):530-6 [8739912.001]
  • [Cites] Biochem J. 1998 May 1;331 ( Pt 3):809-13 [9560308.001]
  • [Cites] Diabetes. 1998 May;47(5):743-50 [9588445.001]
  • [Cites] Diabetes. 1999 Mar;48(3):491-8 [10078548.001]
  • [Cites] Diabetologia. 1999 Apr;42(4):427-34 [10230646.001]
  • [Cites] J Clin Invest. 1999 Sep;104(6):787-94 [10491414.001]
  • [Cites] J Biol Chem. 2004 Nov 5;279(45):46363-6 [15385542.001]
  • [Cites] ILAR J. 2006;47(3):225-33 [16804197.001]
  • [Cites] Diabetes. 2007 Jan;56(1):65-71 [17192466.001]
  • [Cites] Mol Genet Metab. 2007 Apr;90(4):393-401 [17185018.001]
  • [Cites] Diabetes. 2007 May;56(5):1324-32 [17353506.001]
  • [Cites] Autophagy. 2007 Jul-Aug;3(4):387-9 [17438364.001]
  • [Cites] Biochim Biophys Acta. 2007 Aug;1768(8):2002-9 [17349968.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2007 Dec;293(6):E1656-62 [17911343.001]
  • [Cites] Endocr Rev. 2008 May;29(3):303-16 [18314421.001]
  • [Cites] Endocr Rev. 2008 May;29(3):317-33 [18436705.001]
  • [Cites] Mol Neurobiol. 2008 Feb;37(1):39-43 [18446451.001]
  • [Cites] Genes Dev. 2008 Jun 1;22(11):1427-38 [18519635.001]
  • [Cites] Mol Neurobiol. 2008 Aug;38(1):78-100 [18686046.001]
  • [Cites] Ann N Y Acad Sci. 2008 Dec;1147:221-32 [19076444.001]
  • [Cites] J Gerontol A Biol Sci Med Sci. 2009 Feb;64(2):167-70 [19228787.001]
  • [Cites] Mol Biol Cell. 2009 Jun;20(11):2744-54 [19357194.001]
  • [Cites] Nature. 2001 Dec 13;414(6865):807-12 [11742413.001]
  • (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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77. Declercq J, Van Dyck F, Van Damme B, Van de Ven WJ: Upregulation of Igf and Wnt signalling associated genes in pleomorphic adenomas of the salivary glands in PLAG1 transgenic mice. Int J Oncol; 2008 May;32(5):1041-7
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  • [Title] Upregulation of Igf and Wnt signalling associated genes in pleomorphic adenomas of the salivary glands in PLAG1 transgenic mice.
  • The Pleomorphic adenoma gene 1 (PLAG1) is involved in various human neoplasias, including pleomorphic adenomas of the salivary glands.
  • MMTV-Cre-mediated targeted overexpression of PLAG1 in the salivary glands of double transgenic offspring mice, referred to as P1-MCre and P2-MCre mice, induced pleomorphic adenomas in this organ.
  • Igf2, a genuine PLAG1 target gene, was highly upregulated in those tumours as well as in human pleomorphic adenomas of the salivary glands.
  • These and previous observations in other PLAG1-induced tumours e.g. breast adenomyoepitheliomas emphasize the importance of Igf upregulation in such tumours.
  • Inactivation of Igf2 in P1-MCre mice leads to a significant delay in tumour development.
  • Since tumour development is not fully abrogated by inactivation of Igf2, other signalling pathways are likely to contribute to PLAG1-induced tumourigenesis as well.
  • Further studies revealed that several genes such as H19, Dlk1, Gtl2, Igfbp2, Igfbp3 and genes involved in Wnt signalling, such as Wnt6, Cyclin D1 and beta-catenin are upregulated in P1-MCre mice in which Igf2 is inactivated.
  • In conclusion, we clearly demonstrate upregulation of several genes associated with Igf and Wnt signalling in PLAG1-induced pleomorphic adenomas.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Neoplastic. Insulin-Like Growth Factor II / metabolism. Salivary Gland Neoplasms / metabolism. Signal Transduction / genetics. Wnt Proteins / metabolism
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Mice. Mice, Knockout. Mice, Transgenic. Time Factors

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  • (PMID = 18425330.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / IGF2 protein, mouse; 0 / Plag1 protein, mouse; 0 / Wnt Proteins; 67763-97-7 / Insulin-Like Growth Factor II
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78. Wasko R, Jaskuła M, Plewa R, Komarowska H, Poreba E, Goździcka-Józefiak A, Liebert W, Bednarek J, Sowiński J: The evaluation of ghrelin mRNA expression in human somatotroph adenomas. Neuro Endocrinol Lett; 2006 Feb-Apr;27(1-2):169-73
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  • [Title] The evaluation of ghrelin mRNA expression in human somatotroph adenomas.
  • The ghrelin peptide and ghrelin mRNA have been detected in several regions of hypothalamus, in normal pituitary, as well as in various types of pituitary adenoma, with different levels of expression in different tumour types.
  • We decided to determine the expression of ghrelin in somatotroph adenomas.
  • Human pituitary somatotroph adenoma tissues were obtained at the time of transsphenoidal surgery from 3 acromegalic patients and studied for ghrelin mRNA expression.
  • We wished to determine the number of copies of ghrelin gene within the single cell.
  • We used the beta-actin, and the GAPDH genes as a reference molecules for standard curve calculation.
  • [MeSH-major] Adenoma / metabolism. Human Growth Hormone / metabolism. Peptide Hormones / biosynthesis. Pituitary Neoplasms / metabolism

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  • (PMID = 16648773.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Actins; 0 / DNA, Complementary; 0 / Ghrelin; 0 / Peptide Hormones; 0 / RNA, Messenger; 12629-01-5 / Human Growth Hormone; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
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79. 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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  • [Cites] J Clin Oncol. 2005 May 20;23(15):3465-74 [15908655.001]
  • [Cites] Eur J Radiol. 2009 Dec;72(3):517-28 [18829195.001]
  • [Cites] World J Surg. 2005 Jun;29(6):789-93 [15880279.001]
  • [Cites] Cardiovasc Intervent Radiol. 2005 Jul-Aug;28(4):409-21 [16041556.001]
  • [Cites] Cancer. 2005 Oct 15;104(8):1590-602 [16134179.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Oct;19(5):783-98 [16253900.001]
  • [Cites] Surgery. 2005 Dec;138(6):1003-8; discussion 1008 [16360384.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):401-6 [16421420.001]
  • [Cites] Ann Surg Oncol. 2006 Apr;13(4):572-81 [16511671.001]
  • [Cites] Liver Transpl. 2006 Mar;12(3):448-56 [16498656.001]
  • [Cites] J Vasc Interv Radiol. 2006 Aug;17(8):1235-49; quiz 1250 [16923972.001]
  • [Cites] J Pharm Pharmacol. 2006 Dec;58(12):1623-8 [17331326.001]
  • [Cites] Clin Cancer Res. 2000 Aug;6(8):3062-70 [10955785.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Sep;85(9):3222-6 [10999812.001]
  • [Cites] Am J Gastroenterol. 2000 Sep;95(9):2271-7 [11007228.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Oct;85(10):3628-30 [11061513.001]
  • [Cites] Semin Oncol. 2002 Apr;29(2):192-5 [11951217.001]
  • [Cites] J Am Coll Surg. 2002 Jun;194(6):761-4 [12081066.001]
  • [Cites] World J Surg. 2002 Aug;26(8):985-90 [12016479.001]
  • [Cites] Expert Opin Pharmacother. 2002 Jun;3(6):643-56 [12472080.001]
  • [Cites] Surgery. 2002 Dec;132(6):976-82; discussion 982-3 [12490844.001]
  • [Cites] Surg Oncol Clin N Am. 2003 Jan;12(1):231-42 [12735141.001]
  • [Cites] J Am Coll Surg. 2003 Jul;197(1):29-37 [12831921.001]
  • [Cites] AJR Am J Roentgenol. 2003 Sep;181(3):775-80 [12933480.001]
  • [Cites] Surgery. 2003 Dec;134(6):1057-63; discussion 1063-5 [14668741.001]
  • [Cites] J Gastrointest Surg. 2004 Feb;8(2):208-12 [15036197.001]
  • [Cites] Dig Liver Dis. 2004 Feb;36 Suppl 1:S106-20 [15077919.001]
  • [Cites] Surg Clin North Am. 2004 Jun;84(3):775-85 [15145234.001]
  • [Cites] Surgery. 1984 Dec;96(6):1027-37 [6095477.001]
  • [Cites] Ann Surg. 1988 Feb;207(2):160-8 [2829761.001]
  • [Cites] Ann Intern Med. 1989 Jan 1;110(1):35-50 [2535688.001]
  • [Cites] Radiology. 1991 Jun;179(3):709-12 [2027979.001]
  • [Cites] Surgery. 1991 Dec;110(6):989-96; discussion 996-7 [1745987.001]
  • [Cites] Surgery. 1991 Dec;110(6):998-1004; discussion 1004-5 [1684067.001]
  • [Cites] N Engl J Med. 1992 Feb 20;326(8):519-23 [1310159.001]
  • [Cites] Am J Surg. 1993 Feb;165(2):243-8 [8427405.001]
  • [Cites] World J Surg. 1994 Jul-Aug;18(4):488-93; discussion 493-4 [7725733.001]
  • [Cites] J Clin Endocrinol Metab. 1995 Oct;80(10):2884-7 [7559869.001]
  • [Cites] Gut. 1996 Mar;38(3):430-8 [8675099.001]
  • [Cites] Surgery. 1997 Dec;122(6):1189-93; discussion 1193-4 [9426437.001]
  • [Cites] West J Med. 1998 Aug;169(2):98-104 [9735690.001]
  • [Cites] Transplantation. 1998 Nov 27;66(10):1307-12 [9846513.001]
  • [Cites] Surgery. 1998 Dec;124(6):1056-61; discussion 1061-2 [9854583.001]
  • [Cites] Cancer. 1999 Sep 15;86(6):944-8 [10491519.001]
  • [Cites] Endocrinol Metab Clin North Am. 1999 Sep;28(3):519-32, vi [10500929.001]
  • [Cites] J Am Coll Surg. 1999 Oct;189(4):368-73 [10509462.001]
  • [Cites] J Clin Oncol. 2004 Dec 1;22(23):4762-71 [15570077.001]
  • [Cites] Am J Clin Oncol. 2004 Oct;27(5):485-8 [15596916.001]
  • [Cites] Surgery. 2004 Dec;136(6):1176-82 [15657573.001]
  • [Cites] J Clin Oncol. 2005 Apr 20;23(12):2754-62 [15837990.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2007 Mar;21(1):111-29 [17382268.001]
  • [Cites] Endocr Relat Cancer. 2007 Jun;14(2):207-19 [17639038.001]
  • [Cites] Arch Surg. 2007 Dec;142(12):1202-4; discussion 1205 [18086988.001]
  • [Cites] Ann Surg. 2008 Jan;247(1):165-72 [18156937.001]
  • [Cites] World J Surg. 2008 May;32(5):904-17 [18264824.001]
  • [Cites] Surg Clin North Am. 2008 Aug;88(4):863-95, viii [18672144.001]
  • [Cites] Surg Oncol Clin N Am. 2008 Oct;17(4):857-76, x [18722923.001]
  • [Cites] Cancer. 2008 Sep 1;113(5):921-9 [18618495.001]
  • [Cites] Gastroenterology. 2008 Nov;135(5):1469-92 [18703061.001]
  • [Cites] Surgery. 2008 Dec;144(6):885-93; discussion 893-4 [19040993.001]
  • [Cites] Surgery. 2008 Dec;144(6):895-8 [19040994.001]
  • [Cites] J Clin Endocrinol Metab. 2009 Apr;94(4):1074-80 [19190102.001]
  • [Cites] Cancer. 2005 Jul 15;104(2):264-72 [15937909.001]
  • (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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80. 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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81. Will OC, Leedham SJ, Elia G, Phillips RK, Clark SK, Tomlinson IP: Location in the large bowel influences the APC mutations observed in FAP adenomas. Fam Cancer; 2010 Sep;9(3):389-93

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Location in the large bowel influences the APC mutations observed in FAP adenomas.
  • In both sporadic colorectal cancer and Familial Adenomatous Polyposis (FAP), polyp density and cancer susceptibility vary markedly by colonic site.
  • Adenomas in FAP have a different mutational spectrum in small intestine versus colon.
  • 127 1-2 mm mildly dysplastic adenomas from 5 patients with a codon 1309 germline mutation, and 41 from 3 patients with mutations proximal to codon 1265, were analysed to assess the frequency of loss of heterozygosity (LOH).
  • Immunohistochemistry for beta-catenin, caspase-3 and Ki-67 was performed to assess Wnt pathway activation, apoptosis and proliferation.
  • Beta-catenin and caspase-3 expression showed no significant variation by colonic region, but Ki-67 expression decreased from ascending colon to rectum in tumours and normal tissue.
  • Colonic site alters the mutational spectrum of APC, and crypt cell proliferation.
  • The higher frequency of LOH in rectal polyps from patients with codon 1309 mutations may help to explain their increased polyp burden at this site compared with patients who have other germline APC mutations.
  • [MeSH-minor] Caspase 3 / biosynthesis. Humans. Immunohistochemistry. Ki-67 Antigen / biosynthesis. Lasers. Loss of Heterozygosity. Microdissection. Mutation. Polymerase Chain Reaction. beta Catenin / biosynthesis

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  • (PMID = 20229069.001).
  • [ISSN] 1573-7292
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / beta Catenin; EC 3.4.22.- / Caspase 3
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82. Souazé F, Viardot-Foucault V, Roullet N, Toy-Miou-Leong M, Gompel A, Bruyneel E, Comperat E, Faux MC, Mareel M, Rostène W, Fléjou JF, Gespach C, Forgez P: Neurotensin receptor 1 gene activation by the Tcf/beta-catenin pathway is an early event in human colonic adenomas. Carcinogenesis; 2006 Apr;27(4):708-16
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  • [Title] Neurotensin receptor 1 gene activation by the Tcf/beta-catenin pathway is an early event in human colonic adenomas.
  • Alterations in the Wnt/APC (adenomatous polyposis coli) signalling pathway, resulting in beta-catenin/T cell factor (Tcf)-dependent transcriptional gene activation, are frequently detected in familial and sporadic colon cancers.
  • NT1 receptor is not expressed in normal colon epithelial cells, but is over expressed in a number of cancer cells and tissues suggesting a link to the outgrowth of human colon cancer.
  • Consequently, we observed the activation of NT1 receptor gene by agents causing beta-catenin cytosolic accumulation, as well as a strong decline of endogenous receptor when wt-APC was restored.
  • We corroborated the Wnt/APC signalling pathway on the NT1 receptor promoter activation with human colon carcinogenesis, and showed that NT1 receptor gene activation was perfectly correlated with nuclear or cytoplasmic beta-catenin localization while NT1 receptor was absent when beta-catenin was localized at the cell-cell junction in early adenomas of patients with familial adenomatous polyposis, hereditary non-polyposis colorectal cancer and loss of heterozygosity tumours.
  • In this report we establish a novel link in vitro between the Tcf/beta-catenin pathway and NT1 receptor promoter activation.
  • [MeSH-major] Adenoma / genetics. Colonic Neoplasms / genetics. Receptors, Neurotensin / biosynthesis. TCF Transcription Factors / physiology. beta Catenin / physiology
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / physiology. Cell Proliferation. Cell Survival. Cell Transformation, Neoplastic. Humans. Loss of Heterozygosity. Promoter Regions, Genetic. Signal Transduction. Up-Regulation. Wnt Proteins / physiology

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  • (PMID = 16299383.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Receptors, Neurotensin; 0 / TCF Transcription Factors; 0 / Wnt Proteins; 0 / beta Catenin; 0 / neurotensin type 1 receptor
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83. Bowden NA, Croft A, Scott RJ: Gene expression profiling in familial adenomatous polyposis adenomas and desmoid disease. Hered Cancer Clin Pract; 2007;5(2):79-96
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  • [Title] Gene expression profiling in familial adenomatous polyposis adenomas and desmoid disease.
  • The disease familial adenomatous polyposis (FAP) is associated with germline mutations in the APC gene, which result in aberrant beta-catenin control.
  • The molecular mechanisms underlying colorectal cancer development in FAP are being characterised but limited information is available about other symptoms that occur in this disorder.
  • Although extremely rare in the general population, desmoid tumours in approximately 10% of FAP patients.
  • The aim of this study was to determine the similarities and differences in gene expression profiles in adenomas and compare them to those observed in desmoid tumours.
  • Illumina whole genome gene expression BeadChips were used to measure gene expression in FAP adenomas and desmoid tumours.
  • Similarities between gene expression profiles and mechanisms important in regulating formation of FAP adenomas and desmoid tumours were identified.
  • This study furthers our understanding of the mechanisms underlying FAP and desmoid tumour formation.

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  • [Cites] Dig Liver Dis. 2000 Jun-Jul;32(5):426-39 [11030190.001]
  • [Cites] PLoS Biol. 2005 Dec;3(12):e416 [16292982.001]
  • [Cites] BMC Cancer. 2005;5:66 [15982419.001]
  • [Cites] Clin Cancer Res. 2005 Jul 15;11(14):5181-7 [16033834.001]
  • [Cites] Dis Colon Rectum. 2005 Jun;48(6):1275-81 [15793634.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Jul 15;332(4):1146-52 [15949466.001]
  • [Cites] Clin Cancer Res. 2005 Jun 1;11(11):4090-6 [15930344.001]
  • [Cites] Cell Biol Int. 1995 May;19(5):357-71 [7640653.001]
  • [Cites] Am J Hum Genet. 1996 Dec;59(6):1193-201 [8940264.001]
  • [Cites] World J Gastroenterol. 2005 Apr 7;11(13):1937-45 [15800983.001]
  • [Cites] Breast Cancer Res Treat. 1994;31(2-3):309-14 [7533562.001]
  • [Cites] Am J Surg. 1986 Feb;151(2):230-7 [3946757.001]
  • [Cites] Int J Colorectal Dis. 2004 Sep;19(5):438-45 [14986031.001]
  • [Cites] Wound Repair Regen. 2004 May-Jun;12(3):320-6 [15225210.001]
  • [Cites] J Cell Biol. 2004 Jul 5;166(1):37-47 [15240568.001]
  • [Cites] Oncogene. 2004 Jun 3;23(26):4584-93 [15077158.001]
  • [Cites] J Invest Dermatol. 2004 Jul;123(1):229-36 [15191565.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3179-85 [15126357.001]
  • [Cites] Pathol Oncol Res. 2004;10(1):26-33 [15029258.001]
  • [Cites] J Lab Clin Med. 2004 Feb;143(2):89-98 [14966464.001]
  • [Cites] Oncogene. 2004 Jan 22;23(3):654-64 [14737101.001]
  • [Cites] Gastrointest Endosc. 2003 Dec;58(6):885-94 [14652558.001]
  • [Cites] Cancer Res. 2003 Jul 1;63(13):3819-25 [12839979.001]
  • [Cites] Cell. 2002 Oct 18;111(2):251-63 [12408869.001]
  • [Cites] J Pathol. 2002 Sep;198(1):69-76 [12210065.001]
  • [Cites] Br J Surg. 2002 Jul;89(7):845-60 [12081733.001]
  • [Cites] Oncogene. 2002 Jun 13;21(26):4120-8 [12037668.001]
  • [Cites] Pathol Int. 2002 Apr;52(4):272-6 [12031082.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6973-8 [11983872.001]
  • [Cites] Clin Biochem. 2002 Mar;35(2):87-92 [11983341.001]
  • [Cites] Scand J Gastroenterol. 2001 Aug;36(8):865-9 [11495083.001]
  • [Cites] Oncogene. 2002 Mar 27;21(13):2051-7 [11960377.001]
  • [Cites] Eur J Surg Oncol. 2001 Dec;27(8):701-6 [11735163.001]
  • [Cites] Gastroenterology. 2001 Jul;121(1):198-213 [11438509.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3034-9 [11248027.001]
  • [Cites] FEBS Lett. 2000 Jul 7;476(3):203-7 [10913614.001]
  • [Cites] Cancer Res. 2000 Jul 1;60(13):3584-91 [10910072.001]
  • [Cites] Clin Genet. 2000 Mar;57(3):205-12 [10782927.001]
  • [Cites] Am J Pathol. 2000 Mar;156(3):865-70 [10702403.001]
  • [Cites] Lancet. 2000 Feb 26;355(9205):716-9 [10703804.001]
  • [Cites] Hepatology. 2006 May;43(5):1042-52 [16628636.001]
  • [Cites] Ann N Y Acad Sci. 2004 Dec;1028:28-37 [15650229.001]
  • [Cites] Oncogene. 2004 Dec 16;23(58):9336-47 [15531928.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Nat Genet. 1999 Jan;21(1 Suppl):38-41 [9915499.001]
  • [Cites] Br J Surg. 1998 Jul;85(7):965-9 [9692574.001]
  • [Cites] Am J Pathol. 1997 Aug;151(2):329-34 [9250146.001]
  • [Cites] Int J Biochem Cell Biol. 1997 Jan;29(1):63-78 [9076942.001]
  • [Cites] Br J Cancer. 2006 Jun 5;94(11):1672-7 [16705313.001]
  • [Cites] Hepatology. 2006 Jun;43(6):1267-75 [16628605.001]
  • [Cites] J Plast Reconstr Aesthet Surg. 2006;59(3):221-9 [16676428.001]
  • [Cites] Oncol Rep. 2006 May;15(5):1391-5 [16596216.001]
  • [Cites] Carcinogenesis. 2006 Mar;27(3):454-64 [16272170.001]
  • [Cites] Mol Med Today. 2000 Dec;6(12):462-9 [11099951.001]
  • (PMID = 19725988.001).
  • [ISSN] 1897-4287
  • [Journal-full-title] Hereditary cancer in clinical practice
  • [ISO-abbreviation] Hered Cancer Clin Pract
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Other-IDs] NLM/ PMC2736996
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84. 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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85. Obrador-Hevia A, Chin SF, González S, Rees J, Vilardell F, Greenson JK, Cordero D, Moreno V, Caldas C, Capellá G: Oncogenic KRAS is not necessary for Wnt signalling activation in APC-associated FAP adenomas. J Pathol; 2010 May;221(1):57-67

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  • [Title] Oncogenic KRAS is not necessary for Wnt signalling activation in APC-associated FAP adenomas.
  • Recent studies have suggested that APC loss alone may be insufficient to promote aberrant Wnt/beta-catenin signalling.
  • Our aim was to comprehensively characterize Wnt signalling components in a set of APC-associated familial adenomatous polyposis (FAP) tumours.
  • Sixty adenomas from six FAP patients with known pathogenic APC mutations were included.
  • Somatic APC and KRAS mutations, beta-catenin immunostaining, and qRT-PCR of APC, MYC, AXIN2 and SFRP1 were analysed.
  • Array-comparative genomic hybridization (aCGH) was also assessed in 26 FAP adenomas and 24 paired adenoma-carcinoma samples.
  • A somatic APC alteration was present in 15 adenomas (LOH in 11 and four point mutations).
  • APC mRNA was overexpressed in adenomas.
  • Increased cytoplasmic and/or nuclear beta-catenin staining was seen in 94% and 80% of the adenomas. beta-Catenin nuclear staining was strongly associated with MYC levels (p value 0.03) but not with KRAS mutations.
  • Based on beta-catenin staining and Wnt pathway target genes alterations the Wnt pathway appears to be constitutively activated in all APC-FAP tumours, with alterations occurring both upstream and downstream of APC.
  • Somatic profiling of APC-FAP tumours provides new insights into the role of APC in tumourigenesis.
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / biosynthesis. Adenomatous Polyposis Coli Protein / genetics. Adult. Cell Nucleus / metabolism. Comparative Genomic Hybridization. Female. Gene Expression Regulation, Neoplastic. Genetic Predisposition to Disease. Germ-Line Mutation. Humans. Loss of Heterozygosity. Male. Signal Transduction / physiology. Young Adult. beta Catenin / metabolism

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  • [Copyright] Copyright (c) 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • [CommentIn] J Pathol. 2010 Jul;221(3):239-41 [20527017.001]
  • (PMID = 20196079.001).
  • [ISSN] 1096-9896
  • [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 / Adenomatous Polyposis Coli Protein; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Wnt Proteins; 0 / beta Catenin; EC 3.6.5.2 / ras Proteins
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86. Jin L, Riss D, Ruebel K, Kajita S, Scheithauer BW, Horvath E, Kovacs K, Lloyd RV: Galectin-3 Expression in Functioning and Silent ACTH-Producing Adenomas. Endocr Pathol; 2005;16(2):107-14
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  • [Title] Galectin-3 Expression in Functioning and Silent ACTH-Producing Adenomas.
  • Galectin-3 (Gal-3), a beta galactoside-binding protein, has been implicated in a variety of biological functions including cell growth, differentiation, tumor cell adhesion, angiogenesis, tumor progression, and metastasis.
  • We recently reported that Gal-3 was expressed in a subset of normal pituitary cells and tumors including PRL, ACTH, and in folliculo-stellate (FS) cells and tumors and that Gal-3 had an important regulatory role in pituitary cell proliferation.
  • We further investigated the expression of Gal-3 protein in ACTH- and PRL-producing tumors and the expression of various galectin mRNAs by RT-PCR in pituitary adenomas and normal pituitary.
  • Most silent ACTH subtypes 1 and 2 adenomas were negative or only focally positive for Gal-3 expression compared to functioning ACTH tumors from patients with Cushing's disease and Nelson's syndrome.
  • In the normal pituitary, Gal-3 was expressed in less than 1% of the basophil-invading cells (ACTH cells present in the posterior pituitary) and in a subset of the anterior lobe ACTH-positive cells.
  • RT-PCR analyses showed that many members of the galectin family including galectins 1, 2, 3, 4, 5, 6, 7, 8, and 9 were expressed in normal pituitary and in functioning ACTH- and PRL-producing tumors.
  • These results indicate that Gal-3 is associated with functioning ACTH and PRL tumors and is expressed infrequently in silent ACTH adenomas, suggesting that Gal-3 protein and/or gene is altered in non-functioning ACTH tumors.
  • The use of ACTH and Gal-3 immunostaining should help in the diagnosis of silent ACTH adenomas.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Adrenocorticotropic Hormone / secretion. Galectin 3 / biosynthesis. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism

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  • (PMID = 16199895.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA90249
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Galectin 3; 0 / RNA, Messenger; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
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87. Luciani P, Gelmini S, Ferrante E, Lania A, Benvenuti S, Baglioni S, Mantovani G, Cellai I, Ammannati F, Spada A, Serio M, Peri A: Expression of the antiapoptotic gene seladin-1 and octreotide-induced apoptosis in growth hormone-secreting and nonfunctioning pituitary adenomas. J Clin Endocrinol Metab; 2005 Nov;90(11):6156-61
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  • [Title] Expression of the antiapoptotic gene seladin-1 and octreotide-induced apoptosis in growth hormone-secreting and nonfunctioning pituitary adenomas.
  • CONTEXT: Seladin-1 (from selective Alzheimer's disease indicator-1) is a recently discovered gene that has been found to be down-regulated in brain regions affected by Alzheimer's disease.
  • Seladin-1 effectively protects neurons against beta-amyloid-mediated toxicity and prevents apoptosis via inhibition of the activation of caspase-3, a key mediator of the apoptotic cascade.
  • Although seladin-1 is expressed in the pituitary gland, no study addressed the expression or the function of this gene in pituitary adenomas.
  • OBJECTIVE: The aim of the present study was to determine the expression level of the seladin-1 gene in pituitary tumors, i.e.
  • GH-secreting and nonfunctioning pituitary adenomas (NFPA), and to determine whether differential expression might be associated with different somatostatin (sst)-induced apoptosis.
  • RESULTS: We found by quantitative real-time RT-PCR that the expression level of seladin-1 was significantly higher in NFPA (n = 21) than in GH-secreting adenomas (n = 30; mean +/- se, 25.69 +/- 6.39 vs. 8.02 +/- 2.68 pg/microg total RNA; P = 0.006).
  • Although the amount of activated caspase-3 did not differ between the two groups of tumors, in primary cell cultures, octreotide was able to increase apoptosis, evaluated by the level of cleaved cytokeratin 18 and the presence of apoptotic nuclei, in GH-secreting adenomas, but not in NFPA.
  • This different response was not attributable to differences in the amount of transcript of sst receptors 2 and 5, which was similar in the two groups of tumors.
  • CONCLUSIONS: Our results suggest that differential seladin-1 expression in pituitary adenomas may be associated with a different apoptotic response to sst analogs.
  • [MeSH-major] Adenoma / metabolism. Apoptosis / drug effects. Human Growth Hormone / secretion. Nerve Tissue Proteins / genetics. Octreotide / pharmacology. Oxidoreductases Acting on CH-CH Group Donors / genetics. Pituitary Neoplasms / metabolism

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  • (PMID = 16091489.001).
  • [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 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 12629-01-5 / Human Growth Hormone; EC 1.3.- / Oxidoreductases Acting on CH-CH Group Donors; EC 1.3.1.- / DHCR24 protein, human; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; RWM8CCW8GP / Octreotide
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88. Obari A, Sano T, Ohyama K, Kudo E, Qian ZR, Yoneda A, Rayhan N, Mustafizur Rahman M, Yamada S: Clinicopathological features of growth hormone-producing pituitary adenomas: difference among various types defined by cytokeratin distribution pattern including a transitional form. Endocr Pathol; 2008;19(2):82-91
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  • [Title] Clinicopathological features of growth hormone-producing pituitary adenomas: difference among various types defined by cytokeratin distribution pattern including a transitional form.
  • Pituitary adenomas producing almost exclusively growth hormones (GH) have been ultrastructurally classified into two distinct types: densely granulated somatotroph (DG) adenomas and sparsely granulated (SG) adenomas.
  • Fibrous body (FB), an intracytoplasmic globular aggregation of cytokeratin (CK) filaments, is a hallmark of SG adenomas.
  • Under light microscope, FB could be identified by CK immunohistochemistry as a dot-pattern immunoreaction versus a perinuclear pattern for cells without FB.
  • However, it has been noted that numerous adenomas contain mixed populations of the two patterns.
  • To clarify clinicopathological characteristics of the adenomas with mixed populations ("intermediate type" adenomas) and to confirm clinicopathological differences between strictly defined DG-type and SG-type adenomas, we performed this study on 104 GH cell adenomas.
  • Having segregated "intermediate-type" adenomas (26 cases), we found significant differences between typical DG-type (47 cases) and SG-type adenomas (31 cases); SG-type adenomas had younger ages (44 vs. 50), higher frequency of macroadenomas (86% vs. 58%), invasiveness (65% vs. 38%), advanced grades (3 or 4) in Knosp's classification (50% vs. 24%), and weaker immunoreaction for GH, beta-TSH, alpha-subunit, E-cadherin, and beta-catenin.
  • Clinicopathological characteristics of "intermediate-type" adenomas were identical to those of DG-type adenomas.
  • These findings confirm that SG-type adenoma is a distinct section of GH cell adenomas with special properties and biological behavior, and suggest that intermediate-phenotype adenomas are enrolled in DG-type adenomas.
  • Special properties and biological behavior of SG-type adenomas may appear after the majority of tumor cells possess a fully developed fibrous body.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / pathology. Keratins / metabolism. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology
  • [MeSH-minor] Acromegaly / pathology. Adolescent. Adult. Aged. Aging / pathology. Cadherins / metabolism. Cell Count. Cytoplasm / metabolism. Female. Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Thyrotropin / metabolism. Tissue Fixation. beta Catenin / metabolism

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  • (PMID = 18629656.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / beta Catenin; 12629-01-5 / Human Growth Hormone; 68238-35-7 / Keratins; 9002-71-5 / Thyrotropin
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89. Rishi A, Sharma MC, Sarkar C, Jain D, Singh M, Mahapatra AK, Mehta VS, Das TK: A clinicopathological and immunohistochemical study of clinically non-functioning pituitary adenomas: a single institutional experience. Neurol India; 2010 May-Jun;58(3):418-23
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  • [Title] A clinicopathological and immunohistochemical study of clinically non-functioning pituitary adenomas: a single institutional experience.
  • BACKGROUND: Non-functioning pituitary adenomas (NFPA) are characterized by the lack of clinical syndrome as compared to functioning adenomas (FA) but not all functioning adenomas have clinical effects.
  • RESULTS: Of the 151 pituitary adenomas diagnosed during a period of one and half years, 77 (51%) were NFPA with a male predominance.
  • On the basis of immunohistochemistry, NFPA were classified into three subtypes; gonadotroph adenomas, silent adenomas, and null cell adenomas.
  • Gonadotroph adenomas were the commonest subtype.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adrenocorticotropic Hormone / metabolism. Adult. Age Factors. Aged. Female. Follicle Stimulating Hormone / metabolism. Humans. Ki-67 Antigen / metabolism. Luteinizing Hormone, beta Subunit / metabolism. Male. Middle Aged. Receptor, Epidermal Growth Factor / metabolism. Sex Factors. Young Adult

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  • (PMID = 20644271.001).
  • [ISSN] 0028-3886
  • [Journal-full-title] Neurology India
  • [ISO-abbreviation] Neurol India
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Luteinizing Hormone, beta Subunit; 9002-60-2 / Adrenocorticotropic Hormone; 9002-68-0 / Follicle Stimulating Hormone; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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90. 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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91. van den Broek FJ, de Graaf EJ, Dijkgraaf MG, Reitsma JB, Haringsma J, Timmer R, Weusten BL, Gerhards MF, Consten EC, Schwartz MP, Boom MJ, Derksen EJ, Bijnen AB, Davids PH, Hoff C, van Dullemen HM, Heine GD, van der Linde K, Jansen JM, Mallant-Hent RC, Breumelhof R, Geldof H, Hardwick JC, Doornebosch PG, Depla AC, Ernst MF, van Munster IP, de Hingh IH, Schoon EJ, Bemelman WA, Fockens P, Dekker E: Transanal endoscopic microsurgery versus endoscopic mucosal resection for large rectal adenomas (TREND-study). BMC Surg; 2009;9:4
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  • [Title] Transanal endoscopic microsurgery versus endoscopic mucosal resection for large rectal adenomas (TREND-study).
  • BACKGROUND: Recent non-randomized studies suggest that extended endoscopic mucosal resection (EMR) is equally effective in removing large rectal adenomas as transanal endoscopic microsurgery (TEM).
  • Furthermore, EMR appears to be associated with fewer complications.The aim of this study is to compare the cost-effectiveness and cost-utility of TEM and EMR for the resection of large rectal adenomas.
  • Patients with a rectal adenoma > or = 3 cm, located between 1-15 cm ab ano, will be randomized to a TEM- or EMR-treatment strategy.
  • For TEM, patients will be treated under general anesthesia, adenomas will be dissected en-bloc by a full-thickness excision, and patients will be admitted to the hospital.
  • Residual adenoma that is visible during the first surveillance endoscopy at 3 months will be removed endoscopically in both treatment strategies and is considered as part of the primary treatment.
  • 4) disease specific and general quality of life;.
  • A cost-effectiveness and cost-utility analysis of EMR against TEM for large rectal adenomas will be performed from a societal perspective with respectively the costs per recurrence free patient and the cost per quality adjusted life year as outcome measures.
  • Based on comparable recurrence rates for TEM and EMR of 3.3% and considering an upper-limit of 10% for EMR to be non-inferior (beta-error 0.2 and one-sided alpha-error 0.05), 89 patients are needed per group.
  • DISCUSSION: The TREND study is the first randomized trial evaluating whether TEM or EMR is more cost-effective for the treatment of large rectal adenomas.
  • [MeSH-major] Adenoma / surgery. Endoscopy / economics. Rectal Neoplasms / surgery

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  • [Cites] Ned Tijdschr Geneeskd. 2006 Dec 16;150(50):2739-44 [17225784.001]
  • [Cites] Br J Surg. 2007 May;94(5):627-33 [17335125.001]
  • [Cites] Colorectal Dis. 2007 Jul;9(6):553-8 [17573752.001]
  • [Cites] Endoscopy. 2007 Aug;39(8):701-5 [17661244.001]
  • [Cites] Clin Gastroenterol Hepatol. 2007 Aug;5(8):982-90 [17553754.001]
  • [Cites] Colorectal Dis. 2006 Sep;8(7):581-5 [16919110.001]
  • [Cites] Dis Colon Rectum. 2006 Sep;49(9):1384-92 [16897333.001]
  • [Cites] Endoscopy. 2006 Sep;38(9):902-6 [16981107.001]
  • [Cites] Colorectal Dis. 2006 Nov;8(9):795-9 [17032328.001]
  • [Cites] N Engl J Med. 2006 Nov 2;355(18):1863-72 [17079760.001]
  • [Cites] Z Gastroenterol. 2002 Feb;40(2):67-72 [11857100.001]
  • [Cites] Gastrointest Endosc. 2002 Mar;55(3):371-5 [11868011.001]
  • [Cites] World J Gastroenterol. 2002 Jun;8(3):488-92 [12046076.001]
  • [Cites] Gastroenterology. 2003 Feb;124(2):544-60 [12557158.001]
  • [Cites] Endoscopy. 2003 Oct;35(10):845-9 [14551863.001]
  • [Cites] Ann Surg Oncol. 2003 Nov;10(9):1106-11 [14597451.001]
  • [Cites] Dis Colon Rectum. 2003 Dec;46(12):1626-32 [14668587.001]
  • [Cites] J Clin Oncol. 2004 Jan 15;22(2):244-53 [14665610.001]
  • [Cites] Scand J Gastroenterol Suppl. 2003;(239):34-9 [14743881.001]
  • [Cites] BMJ. 2004 Feb 14;328(7436):360-1 [14962852.001]
  • [Cites] Surg Endosc. 2003 Sep;17(9):1461-3 [12739115.001]
  • [Cites] JSLS. 2004 Apr-Jun;8(2):123-6 [15119655.001]
  • [Cites] Hong Kong Med J. 2004 Aug;10(4):239-43 [15299168.001]
  • [Cites] Gut. 2004 Sep;53(9):1334-9 [15306595.001]
  • [Cites] Chirurg. 1984 Oct;55(10):677-80 [6510078.001]
  • [Cites] Surg Endosc. 1988;2(2):71-5 [3413659.001]
  • [Cites] Gastrointest Endosc. 1991 Mar-Apr;37(2):128-32 [2032596.001]
  • [Cites] Dis Colon Rectum. 1992 Dec;35(12):1183-91 [1473424.001]
  • [Cites] N Engl J Med. 1993 Dec 30;329(27):1977-81 [8247072.001]
  • [Cites] Surg Endosc. 1995 Jan;9(1):56-60 [7725216.001]
  • [Cites] Tumori. 1995 May-Jun;81(3 Suppl):50-6 [7571054.001]
  • [Cites] Surg Endosc. 1995 Oct;9(10):1106-12 [8553213.001]
  • [Cites] Semin Surg Oncol. 1995 Nov-Dec;11(6):399-405 [8607008.001]
  • [Cites] Dis Colon Rectum. 1996 Aug;39(8):886-92 [8756844.001]
  • [Cites] Dis Colon Rectum. 1996 Sep;39(9):969-76 [8797643.001]
  • [Cites] Gastrointest Endosc. 1996 Mar;43(3):189-95 [8857132.001]
  • [Cites] Hepatogastroenterology. 1997 May-Jun;44(15):698-702 [9222674.001]
  • [Cites] Dis Colon Rectum. 1997 Oct;40(10 Suppl):S80-5 [9378018.001]
  • [Cites] Med Care. 1997 Nov;35(11):1095-108 [9366889.001]
  • [Cites] Praxis (Bern 1994). 1998 Aug 12;87(33):1014-8 [9747130.001]
  • [Cites] Ned Tijdschr Geneeskd. 1998 Nov 21;142(47):2577-81 [10028355.001]
  • [Cites] J Gastrointest Surg. 2004 Dec;8(8):1032-9; discussion 1039-40 [15585391.001]
  • [Cites] J Gastroenterol Hepatol. 2005 Jan;20(1):51-5 [15610446.001]
  • [Cites] Int J Colorectal Dis. 2005 Mar;20(2):126-36 [15449078.001]
  • [Cites] Cell Oncol. 2005;27(1):17-29 [15750204.001]
  • [Cites] Surg Endosc. 2004 Dec;18(12):1730-7 [15809779.001]
  • [Cites] Dis Colon Rectum. 2005 Feb;48(2):270-84 [15711865.001]
  • [Cites] Hepatogastroenterology. 2005 Mar-Apr;52(62):429-32 [15816450.001]
  • [Cites] J Surg Oncol. 2007 Dec 15;96(8):644-50 [18081069.001]
  • [Cites] Dis Colon Rectum. 2008 Jan;51(1):38-42 [18038181.001]
  • [Cites] Gastroenterology. 2000 Apr;118(4):670-7 [10734018.001]
  • [Cites] Dis Colon Rectum. 2000 May;43(5):662-7; discussion 667-8 [10826428.001]
  • [Cites] Health Econ. 2001 Mar;10(2):179-84 [11252048.001]
  • [Cites] Endoscopy. 2001 Apr;33(4):367-73 [11315901.001]
  • [Cites] Gastrointest Endosc. 2001 Jul;54(1):62-6 [11427843.001]
  • [Cites] Gastrointest Endosc Clin N Am. 2001 Jul;11(3):519-35 [11778753.001]
  • [Cites] Dis Colon Rectum. 2002 Feb;45(2):200-6 [11852333.001]
  • [Cites] Dig Surg. 2005;22(3):182-9; discussion 189-90 [16137996.001]
  • [Cites] Ann R Coll Surg Engl. 2005 Nov;87(6):432-6 [16263010.001]
  • [Cites] Cochrane Database Syst Rev. 2006;(1):CD004276 [16437481.001]
  • [Cites] Dig Liver Dis. 2006 Mar;38(3):202-7 [16461025.001]
  • [Cites] Endoscopy. 2006 Mar;38(3):231-5 [16528648.001]
  • [Cites] Int J Colorectal Dis. 2006 Sep;21(6):533-7 [16133003.001]
  • [Cites] Colorectal Dis. 2005 Jul;7(4):339-44 [15932555.001]
  • [Cites] Dis Colon Rectum. 2005 Jun;48(6):1182-92 [15793641.001]
  • [Cites] Ned Tijdschr Geneeskd. 2005 Jul 9;149(28):1574-8 [16038162.001]
  • [Cites] J Clin Oncol. 2005 Sep 1;23(25):6199-206 [16135487.001]
  • [Cites] Asian J Surg. 2006 Oct;29(4):227-32 [17098653.001]
  • [Cites] Ned Tijdschr Geneeskd. 2006 Nov 11;150(45):2490-6 [17137098.001]
  • (PMID = 19284647.001).
  • [ISSN] 1471-2482
  • [Journal-full-title] BMC surgery
  • [ISO-abbreviation] BMC Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2664790
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92. 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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93. Ruebel KH, Leontovich AA, Jin L, Stilling GA, Zhang H, Qian X, Nakamura N, Scheithauer BW, Kovacs K, Lloyd RV: Patterns of gene expression in pituitary carcinomas and adenomas analyzed by high-density oligonucleotide arrays, reverse transcriptase-quantitative PCR, and protein expression. Endocrine; 2006 Jun;29(3):435-44
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  • [Title] Patterns of gene expression in pituitary carcinomas and adenomas analyzed by high-density oligonucleotide arrays, reverse transcriptase-quantitative PCR, and protein expression.
  • Very few of the genes that are important in pituitary tumor initiation, progression, and metastasis have been identified to date.
  • To identify potential genes that may be important in pituitary tumor progression and carcinoma development, we used Affymetrix GeneChip HGU-133A-oligonucleotide arrays, which contain more than 15,000 characterized genes from the human genome to study gene expression in an ACTH pituitary carcinoma metastatic to the liver and four pituitary adenomas.
  • Reverse-transcriptase real-time quantitative- PCR (RT-qPCR) was then used to analyze 4 nonneoplastic pituitaries, 19 adenomas, and the ACTH carcinoma.
  • A larger series of pituitary adenomas and carcinomas were also analyzed for protein expression using tissue microarrays (TMA) (n = 233) and by Western blotting (n = 18).
  • There were 4298 genes that were differentially expressed among the adenomas compared to the carcinoma, with 2057 genes overexpressed and 2241 genes underexpressed in the adenomas.
  • The beta-galactoside binding protein galactin-3 was underexpressed in some adenomas compared to the carcinomas.
  • Prolactin (PRL) and ACTH tumors had the highest levels of expression of galectin-3.
  • The human achaetescute homolog-1 ASCL1 (hASH-1) gene was also underexpressed in some adenomas compared to the carcinoma.
  • Prolactin and ACTH tumors had the highest levels of expression of hASH-1.
  • ID2, which has an important role in cell development and tumorigenesis, was underexpressed in some adenomas compared to the carcinomas.
  • Transducin-like enhancer of split four/ Groucho (TLE-4) was over-expressed in adenomas compared to the ACTH carcinoma.
  • [MeSH-major] Adenoma / genetics. Carcinoma / genetics. Gene Expression Profiling / methods. Oligonucleotide Array Sequence Analysis / methods. Pituitary Neoplasms / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. Blotting, Western. DNA-Binding Proteins / metabolism. Follicle Stimulating Hormone / secretion. GRB2 Adaptor Protein / metabolism. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Humans. Immunohistochemistry. Inhibitor of Differentiation Protein 2 / metabolism. Luteinizing Hormone / secretion. Nuclear Proteins / metabolism. Prolactinoma / metabolism. Repressor Proteins / metabolism

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  • (PMID = 16943582.001).
  • [ISSN] 1355-008X
  • [Journal-full-title] Endocrine
  • [ISO-abbreviation] Endocrine
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 90249
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / GRB2 Adaptor Protein; 0 / GRB2 protein, human; 0 / ID2 protein, human; 0 / Inhibitor of Differentiation Protein 2; 0 / Nuclear Proteins; 0 / Repressor Proteins; 0 / TLE4 protein, human; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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94. Bao Y, Yoshida D, Morimoto D, Teramoto A: Expression of laminin beta2: a novel marker of hypoxia in pituitary adenomas. Endocr Pathol; 2006;17(3):251-61
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  • [Title] Expression of laminin beta2: a novel marker of hypoxia in pituitary adenomas.
  • Some studies indicate that pituitary adenoma tissues are hypovascular and have lower oxygen saturation relative to the normal pituitary gland and suggest that this may induce hypoxia.
  • Our previous study showed that laminin beta2 mRNA is upregulated under hypoxic conditions (1% oxygen) but not under normoxic conditions (21% oxygen) in the HP-75 cell line.
  • In the present study, we further investigated the expression of laminin beta1, 2, or 3 chain, under hypoxic and normoxic conditions in HP-75 cells using Western blotting.
  • We found that only laminin beta2 had a significantly higher expression under hypoxia than under normoxia in the HP-75 cell line.
  • The expression of laminin beta chains was investigated by fluorescent immunohistochemistry of paraffin-embedded sections of tissue from pituitary adenomas of 42 cases (30 cases without apoplexy and 12 with apoplexy) categorized according to Knosp grading and tumor size.
  • We found that only laminin beta2 expression correlated significantly with tumor size, but did not correlate with apoplexy and invasiveness.
  • [MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / analysis. Cell Hypoxia / physiology. Laminin / biosynthesis. Pituitary Neoplasms / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Blotting, Western. Cell Line, Tumor. Female. Humans. Immunohistochemistry. Male. Middle Aged

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  • (PMID = 17308362.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Laminin; 124148-86-3 / laminin beta2
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95. Shan L, Yu M, Snyderwine EG: Global gene expression profiling of chemically induced rat mammary gland carcinomas and adenomas. Toxicol Pathol; 2005;33(7):768-75
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  • [Title] Global gene expression profiling of chemically induced rat mammary gland carcinomas and adenomas.
  • Chemical carcinogens induce both benign and malignant mammary gland tumors in female Sprague-Dawley rats.
  • To identify gene expression profiles associated with malignancy, cDNA microarray analysis was used to compare gene expression profiles in rat mammary gland carcinomas, adenomas, and normal mammary gland.
  • Tumors were induced with various chemical carcinogens including 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), 7-12-dimethylbenz[a]anthracene (DMBA), N-nitrosomethylurea (NMU), and 4-aminobiphenyl.
  • The global gene expression profiles in carcinomas and adenomas were distinguishable by hierarchical clustering and multi-dimensional scaling analyses.
  • Permutation analysis revealed 110 clones statistically differentially expressed between benign and malignant tumors (p < 0.0005).
  • Carcinomas showed relatively high expression of several genes associated with mammary epithelial cell growth and proliferation (e.g., cyclin D1, PDGFalpha) and relatively low expression of differentiation marker genes (e.g., beta -casein, whey acidic protein, transferrin).
  • Other categories of genes showing differential expression between carcinomas and adenomas were associated with protein homeostasis, cytoskeleton, extracellular matrix, and cell metabolism (fatty acid metabolism, oxidative phosphorylation, and glycolysis).
  • [MeSH-major] Adenoma / chemically induced. Adenoma / genetics. Carcinoma / chemically induced. Carcinoma / genetics. Gene Expression Regulation, Neoplastic / genetics. Mammary Neoplasms, Experimental / chemically induced. Mammary Neoplasms, Experimental / genetics

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  • (PMID = 16316942.001).
  • [ISSN] 0192-6233
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary
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96. Kishnani PS, Chuang TP, Bali D, Koeberl D, Austin S, Weinstein DA, Murphy E, Chen YT, Boyette K, Liu CH, Chen YT, Li LH: Chromosomal and genetic alterations in human hepatocellular adenomas associated with type Ia glycogen storage disease. Hum Mol Genet; 2009 Dec 15;18(24):4781-90
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  • [Title] Chromosomal and genetic alterations in human hepatocellular adenomas associated with type Ia glycogen storage disease.
  • Hepatocellular adenoma (HCA) is a frequent long-term complication of glycogen storage disease type I (GSD I) and malignant transformation to hepatocellular carcinoma (HCC) is known to occur in some cases.
  • However, the molecular pathogenesis of tumor development in GSD I is unclear.
  • The sizes of GSD Ia adenomas with chromosome 6 aberrations were larger than the sizes of adenomas without the changes (P = 0.012).
  • Expression of IGF2R and LATS1 candidate tumor suppressor genes at 6q was reduced in more than 50% of GSD Ia HCA that were examined (n = 7).
  • [MeSH-major] Adenoma, Liver Cell / genetics. Chromosome Aberrations. Chromosomes, Human, Pair 6 / genetics. Glycogen Storage Disease Type I / genetics. Liver Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Female. Gene Dosage. Gene Expression. Hepatocyte Nuclear Factor 1-alpha / genetics. Humans. Male. Polymorphism, Single Nucleotide. Protein-Serine-Threonine Kinases / genetics. Receptor, IGF Type 2 / genetics. Young Adult. beta Catenin / genetics

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  • (PMID = 19762333.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Receptor, IGF Type 2; 0 / beta Catenin; EC 2.7.1.- / LATS1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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97. Laumonier H, Bioulac-Sage P, Laurent C, Zucman-Rossi J, Balabaud C, Trillaud H: Hepatocellular adenomas: magnetic resonance imaging features as a function of molecular pathological classification. Hepatology; 2008 Sep;48(3):808-18
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  • [Title] Hepatocellular adenomas: magnetic resonance imaging features as a function of molecular pathological classification.
  • Hepatocellular adenomas (HCAs) are a group of benign tumors forming three molecular pathological subgroups:.
  • (1) hepatocyte nuclear factor 1alpha (HNF-1alpha)-inactivated, (2) beta-catenin-activated, and (3) inflammatory.
  • Some HCAs present both beta-catenin activation and inflammation.
  • [MeSH-major] Adenoma, Liver Cell / classification. Adenoma, Liver Cell / pathology. Liver Neoplasms / classification. Liver Neoplasms / pathology. Magnetic Resonance Imaging
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. Fatty Liver / pathology. Female. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Inflammation / pathology. Liver / pathology. Male. Middle Aged. Predictive Value of Tests. Retrospective Studies. Sensitivity and Specificity. beta Catenin / metabolism

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  • [ErratumIn] Hepatology. 2008 Oct;48(4):1356
  • (PMID = 18688875.001).
  • [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 / Biomarkers, Tumor; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / beta Catenin
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98. Paun BC, Kukuruga D, Jin Z, Mori Y, Cheng Y, Duncan M, Stass SA, Montgomery E, Hutcheon D, Meltzer SJ: Relation between normal rectal methylation, smoking status, and the presence or absence of colorectal adenomas. Cancer; 2010 Oct 1;116(19):4495-501
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  • [Title] Relation between normal rectal methylation, smoking status, and the presence or absence of colorectal adenomas.
  • CRC develops from premalignant lesions, chiefly colorectal adenomas.
  • Currently, the most accurate and recommended screening method for finding colorectal adenomas is colonoscopy performed on all individuals aged>50 years.
  • The objectives of the current study were to correlate epigenetic alterations that occur in normal rectal mucosa, smoking status, and age with the presence or absence of concomitant colorectal adenomas and to assess the potential clinical value of methylation in normal rectal biopsies as a screening assay for the presence of polyps and, hence, the need for a full colonoscopy.
  • DNA was extracted, modified with sodium bisulfite, and subjected to real-time quantitative, methylation-specific polymerase chain reaction analysis for the following genes: adenomatous polyposis coli (APC); cadherin 1, type 1, E-cadherin (epithelial) (CDH1); estrogen receptor 1 (ESR1); cytokine high in normal 1 (HIN1); hyperplastic polyposis protein 1 (HPP1); O-6 methylguanine-DNA methyltransferase (MGMT); neural epidermal growth factor-like 1 (NELL1); splicing factor 3B, 14-kDa subunit (p14); cyclin-dependent kinase (CDK) inhibitor 2B (inhibits CDK4) (p15); retinoic acid receptor beta (RARβ); somatostatin (SST); tachykinin, precursor 1 (TAC1); and tissue inhibitor of metalloproteinase (TIMP) metallopeptidase inhibitor 3 (TIMP3).
  • RESULTS: By using several sets of genes, clinical characteristics, and multivariate analyses, the authors developed a prediction model for the presence of concomitant colorectal adenomas at the time of rectal biopsy.
  • They also observed strong correlations between smoking status and rectal methylation pattern and between smoking status and the presence or risk of concomitant adenomas.
  • CONCLUSIONS: A prediction model was developed for the presence of colorectal adenomas based on gene methylation patterns in the normal rectum.
  • The results indicated that these genes may be involved in early stages of adenoma formation.

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  • [Copyright] Copyright © 2010 American Cancer Society.
  • [Cites] J Natl Cancer Inst. 2000 Sep 20;92(18):1460-1 [10995795.001]
  • [Cites] Curr Opin Clin Nutr Metab Care. 2009 Sep;12(5):539-43 [19512917.001]
  • [Cites] J Gastroenterol. 2000;35(10):727-34 [11063215.001]
  • [Cites] Am J Pathol. 2003 Apr;162(4):1361-71 [12651628.001]
  • [Cites] Cancer Res. 2003 Apr 15;63(8):1727-30 [12702551.001]
  • [Cites] Rom J Gastroenterol. 2004 Sep;13(3):187-93 [15470530.001]
  • [Cites] Dis Colon Rectum. 1977 Nov-Dec;20(8):661-8 [923394.001]
  • [Cites] Nature. 1983 Jan 6;301(5895):89-92 [6185846.001]
  • [Cites] Biochem Biophys Res Commun. 1983 Feb 28;111(1):47-54 [6187346.001]
  • [Cites] Science. 1985 Apr 12;228(4696):187-90 [2579435.001]
  • [Cites] Cell. 1990 Jun 1;61(5):759-67 [2188735.001]
  • [Cites] N Engl J Med. 1993 Apr 1;328(13):901-6 [8446136.001]
  • [Cites] Gastroenterology. 1993 May;104(5):1445-51 [8482454.001]
  • [Cites] Eur J Cancer Prev. 1993 Jun;2 Suppl 2:83-7 [8364377.001]
  • [Cites] N Engl J Med. 1993 Dec 30;329(27):1977-81 [8247072.001]
  • [Cites] Nat Genet. 1994 Aug;7(4):536-40 [7951326.001]
  • [Cites] Cancer Res. 1995 Dec 15;55(24):6063-70 [8521394.001]
  • [Cites] Mol Cancer. 2004 Oct 11;3:28 [15476557.001]
  • [Cites] CA Cancer J Clin. 2005 Jan-Feb;55(1):10-30 [15661684.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):740-3 [15767361.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13580-5 [16174748.001]
  • [Cites] J Nutr. 2006 Nov;136(11):2748-53 [17056795.001]
  • [Cites] Dig Dis Sci. 2007 Jun;52(6):1462-70 [17372834.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Oct;16(10):2128-35 [17932361.001]
  • [Cites] BMC Cancer. 2008;8:87 [18380902.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1801-6 [18772397.001]
  • [Cites] Gastroenterology. 2009 Jan;136(1):227-235.e3 [18992744.001]
  • [Cites] Gut. 2000 Nov;47(5):689-93 [11034586.001]
  • (PMID = 20572039.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA077057-06; United States / NCI NIH HHS / CA / CA095323-09A2; United States / NIDDK NIH HHS / DK / R01 DK047717; United States / NCI NIH HHS / CA / CA077057-06; United States / NIDDK NIH HHS / DK / DK047717-07; United States / NCI NIH HHS / CA / R01 CA095323-09A2; United States / NCI NIH HHS / CA / R01 CA077057; United States / NCI NIH HHS / CA / R01 CA095323; United States / NIDDK NIH HHS / DK / R01 DK047717-07
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS251065; NLM/ PMC2988654
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99. Cassiman D, Libbrecht L, Verslype C, Meersseman W, Troisi R, Zucman-Rossi J, Van Vlierberghe H: An adult male patient with multiple adenomas and a hepatocellular carcinoma: mild glycogen storage disease type Ia. J Hepatol; 2010 Jul;53(1):213-7
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  • [Title] An adult male patient with multiple adenomas and a hepatocellular carcinoma: mild glycogen storage disease type Ia.
  • The development of hepatocellular adenomas and - more rarely - carcinoma in the liver of patients with Glycogen Storage Disease type Ia (GSDIa) is a well-known complication of the disease.
  • The pathophysiology of adenoma and carcinoma development in these patients is, however, hitherto largely unknown and is thought to be related to the metabolic control of the patient and/or the type of mutations in the G6PC gene.
  • We report here on a very illustrative case of adenoma and carcinoma formation in a previously undiagnosed 42 year old male GSDIa patient (enzymatically and genetically proven).
  • To gain a better view on the type of adenoma formed in this patient, molecular studies were performed.
  • We show here that in this patient with mild GSDIa without recurrent hypoglycaemic episodes, adenoma and carcinoma formation still occurred and that malignant transformation of adenoma here is associated with CTNNB1 mutations and a typical mRNA profile of a beta-catenin activated lesion.
  • [MeSH-major] Adenoma, Liver Cell / etiology. Carcinoma, Hepatocellular / etiology. Glycogen Storage Disease Type I / complications. Liver Neoplasms / etiology. Neoplasms, Multiple Primary / etiology
  • [MeSH-minor] Adult. Glucose-6-Phosphatase / genetics. Humans. Male. Mutation. RNA, Messenger / genetics. RNA, Neoplasm / genetics. beta Catenin / genetics

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  • [Copyright] Copyright 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20447711.001).
  • [ISSN] 1600-0641
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / beta Catenin; EC 3.1.3.9 / Glucose-6-Phosphatase
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100. Hanson PL, Aylwin SJ, Monson JP, Burrin JM: FSH secretion predominates in vivo and in vitro in patients with non-functioning pituitary adenomas. Eur J Endocrinol; 2005 Mar;152(3):363-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FSH secretion predominates in vivo and in vitro in patients with non-functioning pituitary adenomas.
  • OBJECTIVE: Non-functioning pituitary adenomas (NFPAs) are characterised by the lack of symptoms of hormone hypersecretory syndromes but in vitro studies have demonstrated that tumour cells may stain for gonadotrophins and/or their alpha- or beta-subunits.
  • In this study, we aimed to examine the pattern of secretion of LH and FSH from a series of pituitary adenomas cultured in vitro and where data were available to relate the results to pre-operative serum gonadotrophin levels.
  • Peritumorous 'normal' pituitary cell cultures from 20 additional pituitary tumour patients were used for comparison with the NFPA group.
  • Peritumorous 'normal' pituitary cells released LH and FSH in a reversed ratio (median LH:FSH ratio = 3.6:1, P < 0.01 compared with NFPAs).
  • By demonstrating that NFPAs cultured in vitro reflect the in vivo situation of preferential secretion of FSH, it may be possible in future to perform functional studies using this system to elucidate the cellular and molecular mechanisms involved in the development of an imbalance in gonadotroph cells preferentially overproducing FSH in NFPAs.

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  • (PMID = 15757852.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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