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

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  • (PMID = 21205453.001).
  • [ISSN] 1559-6109
  • [Journal-full-title] Journal of the American Association for Laboratory Animal Science : JAALAS
  • [ISO-abbreviation] J. Am. Assoc. Lab. Anim. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2994055
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2. National Toxicology Program: Toxicology and carcinogenesis studies of methylene blue trihydrate (Cas No. 7220-79-3) in F344/N rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2008 May;(540):1-224
Hazardous Substances Data Bank. METHYLENE BLUE .

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

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

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  • (PMID = 19793179.001).
  • [ISSN] 1600-0684
  • [Journal-full-title] Journal of medical primatology
  • [ISO-abbreviation] J. Med. Primatol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / C06 RR016228; United States / NCRR NIH HHS / RR / P51 RR013986; United States / NCRR NIH HHS / RR / P51 RR013986-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Denmark
  • [Other-IDs] NLM/ NIHMS145553; NLM/ PMC2783813
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4. 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.
  • Magnetic resonance imaging and endoscopic ultrasonography confirmed the presence of a 2.5-cm tumor in the head of the pancreas.
  • A proinsulin-secreting islet cell tumor was diagnosed.
  • Surgical resection of the tumor was successfully accomplished, but diabetes mellitus developed 4 months postoperatively.
  • CONCLUSION: The diagnosis of a hypoglycemia-producing pancreatic adenoma can be missed when an ultraspecific insulin assay is used.
  • [MeSH-major] Insulinoma / blood. Insulinoma / diagnosis. Pancreatic Neoplasms / blood. Pancreatic Neoplasms / diagnosis. Proinsulin / blood

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  • (PMID = 20439243.001).
  • [ISSN] 1934-2403
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 9035-68-1 / Proinsulin
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5. Dombrowski F, Mathieu C, Evert M: Hepatocellular neoplasms induced by low-number pancreatic islet transplants in autoimmune diabetic BB/Pfd rats. Cancer Res; 2006 Feb 1;66(3):1833-43
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  • [Title] Hepatocellular neoplasms induced by low-number pancreatic islet transplants in autoimmune diabetic BB/Pfd rats.
  • It has been shown that combined high local hyperinsulinism and hyperglycemia after low-number islet transplantation into the livers of streptozotocin-diabetic rats lead to the development of hepatocellular neoplasms but a substantial cocarcinogenic effect of genotoxic streptozotocin could not be ruled out completely.
  • After low-number islet transplantation (n = 450), the liver acini downstream of the islets show insulin-induced alterations: massive glycogen and/or fat accumulation, translocation of the insulin receptor, decrease in glucose-6-phosphatase activity, increase in expression of insulin-like growth factor (IGF)-I, IGF-II/mannose-6-phosphate receptor, insulin receptor substrate-1, Raf-1, and Mek-1, corresponding to clear cell preneoplastic foci of altered hepatocytes known from chemical hepatocarcinogenesis and identical to that in streptozotocin-diabetic Lewis rats.
  • After 12 to 15 and 15 to 18 months, 52% and 100% of the animals showed one or multiple hepatocellular adenomas or hepatocellular carcinomas (HCCs), respectively.
  • Hepatocarcinogenesis is independent from additional genotoxic compounds (i.e., streptozotocin), but is primarily triggered by increased intracellular insulin signaling via pathways associated with cell growth and proliferation, such as the Ras-Raf-mitogen-activated protein kinase pathway and the IGF system, and secondarily involves other growth factors, such as TGF-alpha.
  • [MeSH-major] Diabetes Mellitus, Type 1 / complications. Islets of Langerhans Transplantation / adverse effects. Liver Neoplasms, Experimental / etiology


6. McElroy MK, Lowy AM, Weidner N: Case report: focal nesidioblastosis ("nesidioblastoma") in an adult. Hum Pathol; 2010 Mar;41(3):447-51
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  • [Title] Case report: focal nesidioblastosis ("nesidioblastoma") in an adult.
  • Adult nesidioblastosis is an uncommon cause of hyperinsulinemic hypoglycemia characterized by diffuse islet hyperplasia with beta-cell hypertrophy and atypia.
  • In contrast to infants, a focal form of adult nesidioblastosis (ie, "nesidioblastoma") has not been documented, although proposed.
  • [MeSH-major] Nesidioblastosis / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology

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

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  • (PMID = 16702744.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Blood Glucose; 0 / Insulin; RWM8CCW8GP / Octreotide
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8. Auerbach SS, Bristol DW, Peckham JC, Travlos GS, Hébert CD, Chhabra RS: Toxicity and carcinogenicity studies of methylene blue trihydrate in F344N rats and B6C3F1 mice. Food Chem Toxicol; 2010 Jan;48(1):169-77
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  • The incidences of pancreatic islet cell adenoma and adenoma or carcinoma (combined) were increased in all dosed groups of male rats, but increases were statistically significant in 25mg/kg bw/day males only and the dose-response was non-linear.
  • There was a corresponding increase in the incidence of pancreatic islet cell hyperplasia but statistically significant only in the 50mg/kg bw/day male rats.
  • There were no significant increases in neoplastic transformation observed in the mice; however, positive trends were noted for adenoma or carcinoma (combined) of the small intestine and malignant lymphoma.
  • [MeSH-minor] Animals. Blood Cell Count. Body Weight / drug effects. Carcinogenicity Tests. Dose-Response Relationship, Drug. Female. Hematopoietic Stem Cells / drug effects. Hyperplasia / chemically induced. Hyperplasia / pathology. Kaplan-Meier Estimate. Lung / pathology. Male. Mammary Neoplasms, Experimental / chemically induced. Mammary Neoplasms, Experimental / pathology. Mice. Mice, Inbred Strains. Neoplasms / chemically induced. Neoplasms / pathology. Rats. Rats, Inbred F344. Sex Characteristics. Species Specificity. Survival Analysis

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  • [Copyright] Published by Elsevier Ltd.
  • (PMID = 19804809.001).
  • [ISSN] 1873-6351
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Grant] United States / FDA HHS / BB / 1 Z01 ESO45004-11 BB; United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; T42P99266K / Methylene Blue
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9. Berrospi Espinoza F, Ruiz Figueroa E, Chavez Passiuri I, Celis Zapata J: [Laparoscopic treatment of insulinoma: surgical technique and perisurgical results]. Rev Gastroenterol Peru; 2005 Oct-Dec;25(4):366-70
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  • AIM: Our experience with the laparoscopic treatment of pancreatic insulinomas is reported.
  • RESULTS: All the patients were laparoscopically approached to attempt the tumor enucleation.
  • One patient developed a pancreatic fistula that closed spontaneously.
  • In all cases histological evaluation of the tumor showed benign islet cell tumor.
  • CONCLUSION: Laparoscopic enucleation of pancreatic insulinoma is a feasible and safe technique.
  • [MeSH-major] Insulinoma / surgery. Laparoscopy / methods. Pancreatic Neoplasms / surgery

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  • (PMID = 16333393.001).
  • [ISSN] 1022-5129
  • [Journal-full-title] Revista de gastroenterología del Perú : órgano oficial de la Sociedad de Gastroenterología del Perú
  • [ISO-abbreviation] Rev Gastroenterol Peru
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Peru
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10. Fedele M, Pentimalli F, Baldassarre G, Battista S, Klein-Szanto AJ, Kenyon L, Visone R, De Martino I, Ciarmiello A, Arra C, Viglietto G, Croce CM, Fusco A: Transgenic mice overexpressing the wild-type form of the HMGA1 gene develop mixed growth hormone/prolactin cell pituitary adenomas and natural killer cell lymphomas. Oncogene; 2005 May 12;24(21):3427-35
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  • [Title] Transgenic mice overexpressing the wild-type form of the HMGA1 gene develop mixed growth hormone/prolactin cell pituitary adenomas and natural killer cell lymphomas.
  • Moreover, rearrangements of this gene have been detected in several human benign tumors of mesenchymal origin.
  • To define the role of these proteins in cell transformation in vivo, we have generated transgenic mice overexpressing ubiquitously the HMGA1 gene.
  • These mice developed mixed growth hormone/prolactin cell pituitary adenomas and natural killer (NK)-T/NK cell lymphomas.
  • At odds with mice overexpressing a wild-type or a truncated HMGA2 protein, adrenal medullar hyperplasia and pancreatic islet cell hyperplasia frequently occurred and no increase in body size and weight was observed in HMGA1 mice.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Gene Expression Profiling. HMGA1a Protein / biosynthesis. HMGA1a Protein / genetics. Lymphoma / genetics. Pituitary Neoplasms / genetics. Prolactinoma / genetics
  • [MeSH-minor] Adrenal Medulla / pathology. Animals. Human Growth Hormone / secretion. Hyperplasia. Immunohistochemistry. Islets of Langerhans / pathology. Killer Cells, Natural / immunology. Mice. Mice, Transgenic. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15735694.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 124544-67-8 / HMGA1a Protein; 12629-01-5 / Human Growth Hormone
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11. Krzysztof K, Wiktor B, Tadeusz Ł, Waldemar B, Magdalena K, Janusz D: Neuroendocrine tumours--analysis of own material--a nine--year retrospective study. Hepatogastroenterology; 2010 Mar-Apr;57(98):236-41

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

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  • (PMID = 20583420.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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12. 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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  • [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.
  • 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.
  • [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


13. Loffler KA, Biondi CA, Gartside MG, Serewko-Auret MM, Duncan R, Tonks ID, Mould AW, Waring P, Muller HK, Kay GF, Hayward NK: Lack of augmentation of tumor spectrum or severity in dual heterozygous Men1 and Rb1 knockout mice. Oncogene; 2007 Jun 7;26(27):4009-17
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  • [Title] Lack of augmentation of tumor spectrum or severity in dual heterozygous Men1 and Rb1 knockout mice.
  • To identify possible genetic interactions between the mechanisms of tumor suppression of menin and pRb, we intercrossed mice with targeted deletions of Men1 and Rb1, and compared tumor development in cohorts of animals carrying single or dual mutations of these tumor-suppressor genes.
  • In mice lacking one copy of Men1, pancreatic islet and anterior pituitary adenomas are common.
  • In animals lacking one copy of Rb1, intermediate pituitary and thyroid tumors occur at high frequency, with less frequent development of pancreatic islet hyperplasia and parathyroid lesions.
  • In mice heterozygous for both Men1 and Rb1, pancreatic hyperplasia and tumors of the intermediate pituitary and thyroid occurred at high frequency.
  • Loss of heterozygosity at the Rb1 locus was common in pituitary and thyroid tumors, whereas loss of menin was observed in pancreatic and parathyroid lesions.
  • The tumor spectrum in the double heterozygotes was a combination of pathologies seen in each of the individual heterozygotes, without decrease in age of onset, indicating independent, non-additive effects of the two mutations.
  • Together with the lack of increased tumor spectrum, this suggests that menin and pRb function in a common pathway of tumor suppression.


14. Mould AW, Duncan R, Serewko-Auret M, Loffler KA, Biondi C, Gartside M, Kay GF, Hayward NK: Global expression profiling of murine MEN1-associated tumors reveals a regulatory role for menin in transcription, cell cycle and chromatin remodelling. Int J Cancer; 2007 Aug 15;121(4):776-83
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  • [Title] Global expression profiling of murine MEN1-associated tumors reveals a regulatory role for menin in transcription, cell cycle and chromatin remodelling.
  • Although the identification of menin-interacting partners and other evidence support a role for menin, the multiple endocrine neoplasia type 1 gene (MEN1) product, in regulating gene expression, little is known about the cellular pathways dysregulated by menin loss during tumorigenesis.
  • The mouse models of MEN1 accurately mimic the human syndrome and provide an opportunity to assess the transcriptional effects of Men1 deletion in different endocrine tumor types to identify common pathway aberrations underlying tumorigenesis in MEN1-affected tissues.
  • We compared the global gene expression profiles of pituitary adenomas and pancreatic islet tumors with control tissues from wild-type littermates.
  • Amongst the 551 differentially expressed genes was significant over-representation of genes associated with chromatin remodelling, transcription and cell cycling, including some genes known to encode menin-binding partners, e.g., Rhox5 and Mll1.
  • Consistent with increased cell-cycle transition from G1 to S phase was an elevation of Cdc7 expression in the tumors, which was confirmed by qRT-PCR using independent samples.
  • In support of previous findings in islet tumors, we found down-regulation of the cell-cycle regulator, p18, in both the pancreatic islet and pituitary adenomas, suggesting that reduced p18 levels may be important for Men1-related tumorigenesis in multiple tissues.
  • Surprisingly, we identified increased p16 transcript in pancreatic islet and pituitary tumors.
  • This was accompanied by increased cytoplasmic localization p16 protein in tumor cells.
  • The specific genes and general pathways we have found to be commonly dysregulated in MEN1 tumors, provide a platform for determining their roles in endocrine tumorigenesis.
  • [MeSH-major] Cell Cycle. Chromatin Assembly and Disassembly. Gene Expression Profiling. Neoplasms, Experimental / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / physiology. Transcription, Genetic
  • [MeSH-minor] Animals. Gene Expression Regulation, Neoplastic. Mice. Mice, Knockout. Models, Biological. Oligonucleotide Array Sequence Analysis. Pancreatic Neoplasms / genetics. Pituitary Neoplasms / genetics. Reproducibility of Results


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

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  • (PMID = 16444356.001).
  • [ISSN] 0004-2730
  • [Journal-full-title] Arquivos brasileiros de endocrinologia e metabologia
  • [ISO-abbreviation] Arq Bras Endocrinol Metabol
  • [Language] por
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins
  • [Number-of-references] 84
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16. Ozturk M, Chiu CY, Akdeniz N, Jenq SF, Chang SC, Hsa CY, Jap TS: Two novel mutations in the MEN1 gene in subjects with multiple endocrine neoplasia-1. J Endocrinol Invest; 2006 Jun;29(6):523-7
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  • [Title] Two novel mutations in the MEN1 gene in subjects with multiple endocrine neoplasia-1.
  • Multiple endocrine neoplasia type 1 (MEN1) is characterized by parathyroid, enteropancreatic endocrine and pituitary adenomas as well as germline mutation of the MEN1 gene.
  • This patient presented with a complaint of epigastric pain and watery diarrhea over the past 3 months, and had undergone subtotal parathyroidectomy and enucleation of pancreatic islet cell tumor about 10 yr before.
  • [MeSH-major] Multiple Endocrine Neoplasia Type 1 / genetics. Mutation, Missense. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Adenoma / genetics. Adolescent. Adult. Aged. Amino Acid Sequence. Child. Child, Preschool. DNA Mutational Analysis. Female. Humans. Hyperparathyroidism, Primary / genetics. Male. Middle Aged. Parathyroid Neoplasms / genetics. Pituitary Neoplasms / genetics. Prolactinoma / genetics. Taiwan. Turkey

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  • (PMID = 16840830.001).
  • [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 / MEN1 protein, human; 0 / Proto-Oncogene Proteins
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17. Krysiak R, Okopień B, Herman ZS: [Insulinoma]. Pol Merkur Lekarski; 2007 Jan;22(127):70-4
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  • [Transliterated title] Wyspiak wydzielajacy insuline.
  • Insulinoma is considered the most common endocrine tumour of the pancreas with an annual prevalence of 4 cases per million people.
  • Contrary to the other endocrine tumours of this organ, over 90% of the insulinomas are benign in nature.
  • Effective management requires directed biochemical testing, careful choice of preoperative imaging tests, and complete pancreatic exploration by an experienced endocrine surgeon utilising intraoperative ultrasound.
  • The only curative treatment for insulinoma is complete resection of the tumour.
  • [MeSH-major] Adenoma, Islet Cell / complications. Adenoma, Islet Cell / diagnosis. Insulinoma / complications. Insulinoma / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Endocrine Surgical Procedures / methods. Gastrinoma / complications. Gastrinoma / diagnosis. Gastrinoma / metabolism. Gastrinoma / surgery. Humans. Hypoglycemia / complications. Insulin / metabolism. Pancreatectomy / methods. Prognosis. Rare Diseases

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  • (PMID = 17477096.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Insulin
  • [Number-of-references] 34
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18. Gnacńska M, Lewczuk A, Sworczak K: [Insulinoma misdiagnosed and treated as epilepsy]. Pol Merkur Lekarski; 2008 Mar;24(141):251-3
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  • [Transliterated title] Wyspiak trzustki mylnie rozpoznany i leczony jako padaczka--opis przypadku.
  • Although insulinoma constitutes almost 90% of neuroendocrine tumors localized in the pancreas, it is a rare disease.
  • Quite commonly prior to the diagnosis there is a history of several years and misdiagnosis as neurological or cardiological disease is not infrequent.
  • The image of pancreas was normal in the acquired abdominal ultrasound and in CT a tumor was found in the tail of pancreas.
  • [MeSH-major] Epilepsy / diagnosis. Insulinoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 18634294.001).
  • [ISSN] 1426-9686
  • [Journal-full-title] Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
  • [ISO-abbreviation] Pol. Merkur. Lekarski
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
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19. Zhong L: Magnetic resonance imaging in the detection of pancreatic neoplasms. J Dig Dis; 2007 Aug;8(3):128-32
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

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  • [Title] Magnetic resonance imaging in the detection of pancreatic neoplasms.
  • Recently, with the rapid scanning time and improved image quality, outstanding advances in magnetic resonance (MR) methods have resulted in an increase in the use of MRI for patients with a variety of pancreatic neoplasms.
  • The non-invasive all-in-one MR multi-imaging techniques may provide the comprehensive information needed for the preoperative diagnosis and evaluation of pancreatic neoplasms.
  • Pancreatic neoplasms include primary tumors and pancreatic metastases.
  • Primary tumors of the pancreas may be mainly classified as ductal adenocarcinomas, cystic tumors and islet cell tumors (ICT).
  • Pancreatic adenocarcinomas can be diagnosed in a MRI study depending on direct evidence or both direct and indirect evidence.
  • The combined MRI features of a focal pancreatic mass, pancreatic duct dilatation and parenchymal atrophy are highly suggestive of a ductal adenocarcinoma.
  • Most cystic neoplasms of the pancreas are either microcystic adenomas or mucinous cystic neoplasms.
  • Intraductal papillary mucinous tumors are the uncommon low-grade malignancy of the pancreatic duct.
  • [MeSH-major] Cholangiopancreatography, Magnetic Resonance. Magnetic Resonance Angiography. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / pathology. Humans. Neoplasms, Cystic, Mucinous, and Serous / diagnosis. Neoplasms, Cystic, Mucinous, and Serous / pathology. Pancreas / pathology

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  • (PMID = 17650223.001).
  • [ISSN] 1751-2972
  • [Journal-full-title] Journal of digestive diseases
  • [ISO-abbreviation] J Dig Dis
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Australia
  • [Number-of-references] 10
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20. Alzahrani AS, Al-Khaldi N, Shi Y, Al-Rijjal RA, Zou M, Baitei EY, Amin T: Diagnosis by serendipity: Cushing syndrome attributable to cortisol-producing adrenal adenoma as the initial manifestation of multiple endocrine neoplasia type 1 due to a rare splicing site MEN1 gene mutation. Endocr Pract; 2008 Jul-Aug;14(5):595-602
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  • [Title] Diagnosis by serendipity: Cushing syndrome attributable to cortisol-producing adrenal adenoma as the initial manifestation of multiple endocrine neoplasia type 1 due to a rare splicing site MEN1 gene mutation.
  • OBJECTIVE: To report a case that highlights the potential for Cushing syndrome to be the first manifestation of multiple endocrine neoplasia type 1 (MEN 1) syndrome and to describe the rare underlying genetic mutation and the heterogeneous manifestations of the syndrome within the same family.
  • RESULTS: A 16-year-old girl who was not known to have any medical illness and had no known family history of MEN 1 syndrome presented with Cushing syndrome attributable to a cortisol-producing adrenal adenoma.
  • She did not have clinical, biochemical, or radiologic evidence of islet cell pancreatic tumors.
  • Most cases are due to corticotropin-producing pituitary adenomas.
  • [MeSH-major] Adrenocortical Adenoma / pathology. Cushing Syndrome / diagnosis. Hydrocortisone / secretion. Multiple Endocrine Neoplasia Type 1 / pathology


21. Hamir AN, Rupprecht CE: Pulmonary idiopathic alveolar ossification in a raccoon (Procyon lotor). J Am Assoc Lab Anim Sci; 2010 Sep;49(5):642-3
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  • Noteworthy microscopic findings included multifocal foci of osseous tissue within the alveoli of the lungs, bilateral thyroid adenomas, pancreatic islet cell amyloidosis, cortical kidney infarcts, cystic adenomatous hyperplasia of urinary bladder, and mineralizations (psommama bodies) of small blood vessels of meninges and choroid plexus.

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  • [Cites] Am J Respir Crit Care Med. 2002 Jun 15;165(12):1654-69 [12070068.001]
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  • (PMID = 20858368.001).
  • [ISSN] 1559-6109
  • [Journal-full-title] Journal of the American Association for Laboratory Animal Science : JAALAS
  • [ISO-abbreviation] J. Am. Assoc. Lab. Anim. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2949436
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22. Grossrubatscher E, Veronese S, Ciaramella PD, Pugliese R, Boniardi M, De Carlis L, Torre M, Ravini M, Gambacorta M, Loli P: High expression of dopamine receptor subtype 2 in a large series of neuroendocrine tumors. Cancer Biol Ther; 2008 Dec;7(12):1970-8
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  • AIM: To evaluate by immumohistochemistry the presence of DR subtype 2 (D2R) in well differentiated NETs of different sites and in normal islet cells.
  • BACKGROUND: Recent data in vitro and in vivo support that dopaminergic drugs might exert an inhibitory effect on hormone secretion and, possibly, on tumor growth in neuroendocrine tumors (NET)s.
  • Their potential therapeutic role needs the demonstration of dopamine receptors (DR) in tumor cells.
  • RESULTS: 85% of samples (100% of bronchial carcinoids and 93% of islet cell tumors) showed positivity for D2R; intensity of immunoreaction in NETs was similar or higher than in pituitary (54% and respectively 31% of cases).
  • D2R positivity in more than 70% of tumor cells was observed in 46% of samples.
  • Same intensity of D2R-immunoreactivity was found in pituitary and normal islet cells.
  • No differences in D2R expression were recorded on considering tumor grading, size, proliferative activity, presence of metastases, endocrine activity and gender.
  • A significant difference (62.5% vs 96.4%, p = 0.039) was observed in the prevalence of D2R expression between patients with more aggressive tumors and patients without recurrence/progression of disease during follow-up.
  • METHODS: 46 NET samples from 44 patients and normal endocrine pancreatic tissue were studied.
  • D2R-staining was performed on NETs and compared with six non-secreting pituitary adenomas and related to clinical-pathological data.
  • CONCLUSION: The present data demonstrate a high expression of D2R in NETs; this finding is of clinical relevance in view of the potential role of dopaminergic drugs in inhibiting secretion and/or cell proliferation in NETs.
  • [MeSH-minor] Adult. Aged. Cell Division. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Pancreas / cytology. Pancreas / physiology. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology. Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology

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  • [CommentIn] Cancer Biol Ther. 2008 Dec;7(12):1979-81 [18981728.001]
  • (PMID = 18981718.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Dopamine D2
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23. Nakahara T, Norberg SM, Shalinsky DR, Hu-Lowe DD, McDonald DM: Effect of inhibition of vascular endothelial growth factor signaling on distribution of extravasated antibodies in tumors. Cancer Res; 2006 Feb 1;66(3):1434-45
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  • Antibodies and other macromolecular therapeutics can gain access to tumor cells via leaky tumor vessels.
  • We addressed this issue by examining the distribution of extravasated antibodies in islet cell tumors of RIP-Tag2 transgenic mice and implanted Lewis lung carcinomas using fluorescence and confocal microscopic imaging.
  • Anti-E-cadherin antibody, which targets epitopes on tumor cells of RIP-Tag2 adenomas, was the only antibody to achieve detectable levels within tumor cell clusters at 6 hours after i.v. injection.
  • Treatment for 7 days with AG-013736, a potent inhibitor of VEGF signaling, reduced the tumor vascularity by 86%.
  • The overall area density of extravasated IgG/antibodies decreased after treatment but the change was less than the reduction in vascularity and actually increased when expressed per surviving tumor vessel.
  • Accumulation of anti-E-cadherin antibody in tumor cell clusters was similarly affected.
  • The patchy pattern of antibodies in stroma after treatment qualitatively resembled untreated tumors and surprisingly coincided with sleeves of basement membrane left behind after pruning of tumor vessels.
  • Together, the findings suggest that antibody transport increases from surviving tumor vessels after normalization by inhibition of VEGF signaling.
  • Antibodies preferentially distribute to tumor stroma but also accumulate on tumor cells if binding sites are accessible.

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  • (PMID = 16452199.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL 59157; United States / NHLBI NIH HHS / HL / P01 HL024136; United States / NCI NIH HHS / CA / P50 CA 90270; United States / NHLBI NIH HHS / HL / R01 HL059157; United States / NHLBI NIH HHS / HL / HL 24136; United States / NCI NIH HHS / CA / CA 82923
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Neoplasm; 0 / Cadherins; 0 / Imidazoles; 0 / Immunoglobulin G; 0 / Indazoles; 0 / Vascular Endothelial Growth Factor A; 9001-31-4 / Fibrin; C9LVQ0YUXG / axitinib
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24. Toxicology and carcinogenesis studies of androstenedione (CAS No. 63-05-8) in F344/N rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Sep;(560):1, 7-31,33-171 passim
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  • The incidences of mononuclear cell leukemia were significantly increased in 20 and 50 mg/kg females and significantly decreased in 20 and 50 mg/kg males.
  • Incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined) were significantly increased in 20 mg/kg males.
  • The incidence of testicular interstitial cell adenoma (including bilateral) was significantly decreased in 50 mg/kg males.
  • In the liver of males, the incidences of basophilic focus in all dosed groups, the incidence of clear cell focus in the 20 mg/kg group, and the incidence of eosinophilic focus in the 50 mg/kg group were significantly increased.
  • The incidences of pancreatic islet hyperplasia and atrophy of the exocrine pancreas were significantly increased in 50 mg/kg females.
  • The incidences of hepatocellular adenoma in males and females were significantly increased in the 50 mg/kg groups.
  • Incidences of hepatocellular adenoma or carcinoma (combined) in males and females were significantly increased in the 50 mg/kg groups.
  • Incidences of multiple hepatocellular adenomas and carcinomas were significantly increased in 10 and 50 mg/kg males, and there was an increased incidence of multiple hepatocellular adenomas in 50 mg/kg females.
  • The incidence of eosinophilic focus was significantly increased in 50 mg/kg males, and the incidences of mixed cell focus and cytoplasmic vacuolization were significantly increased in 50 mg/kg females.
  • There was a marginally increased incidence of pancreatic islet adenoma in 50 mg/kg males and in 10 and 50 mg/kg females, with an earlier day of first incidence in males.
  • CONCLUSIONS: under the conditions of these 2-year gavage studies, there was equivocal evidence of carcinogenic activity of androstenedione in male F344/N rats based on increased incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined).
  • There was equivocal evidence of carcinogenic activity of androstenedione in female F344/N rats based on increased incidences of mononuclear cell leukemia.
  • There was clear evidence of carcinogenic activity of androstenedione in male B6C3F1 mice based on increased incidences of multiple hepatocellular adenoma and hepatocellular carcinoma and increased incidence of hepatoblastoma.
  • There was clear evidence of carcinogenic activity of androstenedione in female B6C3F1 mice based on increased incidences of hepatocellular adenoma and hepatocellular carcinoma.
  • Increased incidences of pancreatic islet adenoma in male and female mice were also considered chemical related.
  • Androstenedione administration caused increased incidences in nonneoplastic lesions of the liver in male and female rats and mice; pancreatic islets and exocrine pancreas of female rats; and clitoral gland, kidney, and submandibular salivary gland of female mice.
  • Decreases in the incidences of testicular interstitial cell adenoma in male rats, mammary gland fibroadenoma, cysts, and hyperplasia in female rats, and malignant lymphoma in female mice were considered related to androstenedione administration.

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  • (PMID = 21037592.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Review; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Mutagens; 409J2J96VR / Androstenedione
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