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1. Poggi G, Villani L, Bernardo G: Multimodality treatment of unresectable hepatic metastases from pancreatic glucagonoma. Rare Tumors; 2009;1(1):e6

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  • [Title] Multimodality treatment of unresectable hepatic metastases from pancreatic glucagonoma.
  • Glucagonomas are pancreatic islet cell tumors arising from the alpha cells which belong to neuroendocrine tumors.
  • We report the case of a 52- year old man with a pancreatic glucagonoma with synchronous multiple liver metastases treated by surgery, transarterial chemoembolization, percutaneous radiofrequency thermal ablation and long-acting octreotide.
  • Our report confirms that a multimodal approach is very effective in patients with unresectable liver metastases from pancreatic endocrine tumors providing long-lasting palliation and probably prolonging survival.

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  • [Cites] Cancer. 1993 Jul 1;72(1):244-8 [8389666.001]
  • [Cites] Cancer. 1993 Apr 15;71(8):2624-30 [8384072.001]
  • [Cites] Ann Intern Med. 1994 Feb 15;120(4):302-9 [8291824.001]
  • [Cites] Anticancer Res. 2008 Nov-Dec;28(6B):3835-42 [19192637.001]
  • [Cites] J Vasc Interv Radiol. 2008 Jun;19(6):855-61 [18503899.001]
  • [Cites] J Hepatol. 2008 Aug;49(2):217-22 [18486261.001]
  • [Cites] J Vasc Interv Radiol. 2006 Aug;17(8):1335-43 [16923981.001]
  • [Cites] World J Gastroenterol. 2005 Dec 28;11(48):7676-83 [16437698.001]
  • [Cites] J Am Coll Surg. 2000 Apr;190(4):432-45 [10757381.001]
  • [Cites] N Engl J Med. 1982 Mar 11;306(10):580-90 [6120456.001]
  • [Cites] Eur J Radiol. 2009 Dec;72(3):517-28 [18829195.001]
  • [Cites] J Hepatol. 2007 Mar;46(3):474-81 [17239480.001]
  • [Cites] Neuroendocrinology. 2004;80(6):394-424 [15838182.001]
  • [Cites] Cancer. 1990 May 15;65(10):2227-32 [2161278.001]
  • [Cites] Dig Surg. 1999;16(1):32-8 [9949265.001]
  • [Cites] Lancet. 1974 Jul 6;2(7871):1-5 [4134714.001]
  • [Cites] Abdom Imaging. 2005 Jul-Aug;30(4):435-41 [15759207.001]
  • [Cites] Surg Oncol Clin N Am. 2003 Jan;12(1):231-42 [12735141.001]
  • [Cites] Eur Radiol. 2003 Jan;13(1):136-40 [12541121.001]
  • [Cites] Radiology. 2000 Oct;217(1):119-26 [11012432.001]
  • (PMID = 21139900.001).
  • [ISSN] 2036-3613
  • [Journal-full-title] Rare tumors
  • [ISO-abbreviation] Rare Tumors
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2994425
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2. Okauchi Y, Nammo T, Iwahashi H, Kizu T, Hayashi I, Okita K, Yamagata K, Uno S, Katsube F, Matsuhisa M, Kato K, Aozasa K, Kim T, Osuga K, Nakamori S, Tamaki Y, Funahashi T, Miyagawa J, Shimomura I: Glucagonoma diagnosed by arterial stimulation and venous sampling (ASVS). Intern Med; 2009;48(12):1025-30
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  • [Title] Glucagonoma diagnosed by arterial stimulation and venous sampling (ASVS).
  • To identify the location of pancreatic endocrine tumors, arterial stimulation and venous sampling (ASVS) is known to be useful for insulinoma and gastrinoma, but its usefulness for glucagonoma has not been verified to date.
  • Here we report a case of glucagonoma that was diagnosed by ASVS with calcium loading, in which an approximately 6-fold increase of glucagon was observed in the splenic artery territory.
  • MEN1 gene analysis verified the presence of a mutation and the glucagonoma was confirmed after operation.
  • In conclusion, ASVS could be useful for the diagnosis of glucagonoma.
  • [MeSH-major] Glucagon / blood. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 19525592.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 9007-92-5 / Glucagon; SY7Q814VUP / Calcium
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3. 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.
  • [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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4. Yoshida M, Hayashi K, Ohara H, Miyabe K, Okumura F, Naitoh I, Tanaka H, Ando T, Nakazawa T, Takahashi S, Joh T: A case of pancreatic glucagonoma with erythema. Nihon Shokakibyo Gakkai Zasshi; 2010 Jun;107(6):930-6
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  • [Title] A case of pancreatic glucagonoma with erythema.
  • Full-body computed tomography (CT) scanning revealed a tumor mass in the tail of the pancreas; CT and magnetic resonance imaging (MRI) scans confirmed the presence of a spherical mass.
  • In contrast CT scans, although the contrast was gradually increased, no strong contrast differences were observed between the tumor and the surrounding tissue.
  • Blood test results revealed that the patient had a high glucagon level.
  • We diagnosed glucagonoma syndrome on the basis of the above results and resected the tail of the pancreas.
  • Pathological analysis revealed that the tumor cells had proliferated in ribbon-like, cord-like structures.
  • Immunostaining results were positive for glucagon, which confirmed our diagnosis.
  • [MeSH-major] Erythema / etiology. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20530930.001).
  • [ISSN] 0446-6586
  • [Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
  • [ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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5. Colović R, Matić S, Micev M, Grubor N, Latincić S: [Glucagonoma without glucagonoma syndrome]. Srp Arh Celok Lek; 2010 Mar-Apr;138(3-4):244-7
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  • [Title] [Glucagonoma without glucagonoma syndrome].
  • INTRODUCTION: Glucagonomas are rare, frequently malignant tumours, arising from the Langerhans' islets of the pancreas.
  • They usually secrete large amounts of glucagon that can cause a characteristic "glucagonoma syndrome", which includes necrolytic migratory erythema, glucose intolerance or diabetes, weight loss and sometimes, normochromic normocytic anaemia, stomatitis or cheilitis, diarrhoea or other digestive symptoms, thoromboembolism, hepatosplenomegaly, depression or other psychiatric and paraneoplastic symptoms.
  • In certain cases, some or all glucagonoma symptoms may appear late, or even may be completely absent.
  • CASE OUTLINE: The authors present a 43-year-old woman in whom an investigation for abdominal pain revealed a tumour of the body of the pancreas.
  • During operation, the tumour of the body of the pancreas extending to the mesentery measuring 85 x 55 x 55 mm was excised.
  • Histology and immunohistochemistry showed malignant glucagonoma, with co-expression of somatostatin in about 5% and pancreatic polypeptide in a few tumour cells.
  • CONCLUSION: Glucagonoma syndrome may be absent in glucagonoma tumour patients so that in unclear pancreatic tumours the clinician should frequently request the serum hormone level (including glucagon) measurement by radioimmunoassay and the pathologist should perform immunohistochemistry investigation.
  • Those two would probably result in discovery of more glucagonomas and other neuroendocrine tumours without characteristic clinical syndromes.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 20499510.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia
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6. Lobo I, Carvalho A, Amaral C, Machado S, Carvalho R: Glucagonoma syndrome and necrolytic migratory erythema. Int J Dermatol; 2010 Jan;49(1):24-9
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  • [Title] Glucagonoma syndrome and necrolytic migratory erythema.
  • The glucagonoma syndrome is a rare disorder, characterized by necrolytic migratory erythema, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia in association with a glucagon-secreting alpha-cell tumor of the pancreas.
  • The clinical investigation revealed a pancreatic glucagonoma with resolution of the cutaneous and systemic features after surgical removal.
  • The dermatologic and endocrine approach to this syndrome is discussed here.
  • Early recognition and treatment may prevent metastatic disease and ensure its cure with resolution of the cutaneous and catabolic manifestations.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Skin / pathology
  • [MeSH-minor] Aged. Biopsy. Glucagon / blood. Humans. Male. Necrosis. Pancreatectomy. Tomography, X-Ray Computed

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  • (PMID = 20465606.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-92-5 / Glucagon
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7. Kim S, Keku TO, Martin C, Galanko J, Woosley JT, Schroeder JC, Satia JA, Halabi S, Sandler RS: Circulating levels of inflammatory cytokines and risk of colorectal adenomas. Cancer Res; 2008 Jan 1;68(1):323-8
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  • [Title] Circulating levels of inflammatory cytokines and risk of colorectal adenomas.
  • Circulating levels of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) are elevated in the obese.
  • We examined circulating levels of CRP, IL-6, and TNF-alpha in relation to risk factors and the prevalence of colorectal adenomas.
  • Plasma levels of CRP, IL-6, and TNF-alpha were quantified in 873 participants (242 colorectal adenoma cases and 631 controls) in a colonoscopy-based cross-sectional study conducted between 1998 and 2002.
  • Multivariable logistic regression was used to estimate associations between known risk factors for colorectal neoplasia and circulating levels of inflammatory cytokines and associations between inflammatory cytokines and colorectal adenomas.
  • The prevalence of colorectal adenomas was associated with higher concentrations of IL-6 and TNF-alpha and, to a lesser degree, with CRP.
  • For IL-6, adjusted odds ratios (OR) for colorectal adenomas were 1.79 [95% confidence interval (CI), 1.19-2.69] for the second highest plasma level and 1.85 (95% CI, 1.24-2.75) for the highest level compared with the reference level.
  • A similar association was found with TNF-alpha, with adjusted ORs of 1.56 (95% CI, 1.03-2.36) and 1.66 (95% CI, 1.10-2.52), respectively.

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  • [Cites] JAMA. 2003 Apr 9;289(14):1799-804 [12684358.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Jun;15(6):1126-31 [16775170.001]
  • [Cites] J Clin Invest. 2003 Dec;112(12):1796-808 [14679176.001]
  • [Cites] JAMA. 2004 Feb 4;291(5):585-90 [14762037.001]
  • [Cites] Nat Rev Cancer. 2004 Aug;4(8):579-91 [15286738.001]
  • [Cites] Obes Res. 2004 Jul;12(7):1094-103 [15292473.001]
  • [Cites] Annu Rev Med. 2000;51:245-70 [10774463.001]
  • [Cites] Lancet. 2001 Feb 17;357(9255):539-45 [11229684.001]
  • [Cites] Clin Chem. 2001 Mar;47(3):426-30 [11238292.001]
  • [Cites] J Am Coll Cardiol. 2001 Jun 15;37(8):2036-41 [11419884.001]
  • [Cites] Proc Nutr Soc. 2001 Aug;60(3):329-39 [11681807.001]
  • [Cites] Am J Epidemiol. 2001 Dec 15;154(12):1089-99 [11744511.001]
  • [Cites] Nutrition. 2001 Nov-Dec;17(11-12):953-66 [11744348.001]
  • [Cites] Am J Epidemiol. 2002 Jan 15;155(2):176-84 [11790682.001]
  • [Cites] Am J Cardiol. 2002 May 1;89(9):1117-9 [11988205.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2002 Oct 1;22(10):1668-73 [12377747.001]
  • [Cites] J Pathol. 2002 Dec;198(4):428-34 [12434411.001]
  • [Cites] Br J Nutr. 2004 Sep;92(3):347-55 [15469638.001]
  • [Cites] J Gerontol A Biol Sci Med Sci. 2004 Sep;59(9):M924-9 [15472157.001]
  • [Cites] Proc Natl Acad Sci U S A. 1975 Sep;72(9):3666-70 [1103152.001]
  • [Cites] Am J Epidemiol. 1986 Sep;124(3):453-69 [3740045.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Jul;82(7):2182-91 [9215292.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 1997 Oct;17(10):2167-76 [9351386.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4601-6 [9539784.001]
  • [Cites] Circulation. 1999 Aug 24;100(8):793-8 [10458713.001]
  • [Cites] J Biol Chem. 2004 Nov 19;279(47):48487-90 [15337754.001]
  • [Cites] Nutr Rev. 2005 Jan;63(1):22-8 [15730232.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2294-9 [15572589.001]
  • [Cites] Ann Intern Med. 2005 Mar 15;142(6):425-32 [15767620.001]
  • [Cites] Cancer Cell. 2005 Mar;7(3):211-7 [15766659.001]
  • [Cites] J Allergy Clin Immunol. 2005 May;115(5):911-9; quiz 920 [15867843.001]
  • [Cites] J Epidemiol. 2005 Jun;15 Suppl 2:S185-9 [16127232.001]
  • [Cites] Psychosom Med. 2005 Sep-Oct;67(5):679-87 [16204423.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):2413-8 [16214925.001]
  • [Cites] Nat Rev Cancer. 2006 Jan;6(1):24-37 [16397525.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2483-7 [16489056.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Apr;15(4):690-5 [16614110.001]
  • [Cites] Mech Ageing Dev. 2003 Apr;124(4):487-93 [12714257.001]
  • (PMID = 18172326.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA044684; United States / NCI NIH HHS / CA / R01 CA044684-17; United States / NCI NIH HHS / CA / R01 CA 44684; United States / NIDDK NIH HHS / DK / P30 DK034987; United States / NCI NIH HHS / CA / CA044684-17; United States / NIDDK NIH HHS / DK / P30 DK034987-23; United States / NIDDK NIH HHS / DK / P30 DK34987
  • [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 / Cytokines; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ NIHMS92897; NLM/ PMC2675825
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8. Simonenko VB, Dulin PA, Beliaev LB, Makanin MA, Dem'ianenko AV, Zykova AA, Zhuravleva SI, Kolesnikova VN: [A case of pancreatic glucagonoma]. Klin Med (Mosk); 2007;85(8):67-70
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  • [Title] [A case of pancreatic glucagonoma].
  • Neuroendocrine tumor consisting of pancreatic alpha-cells -- glucagonoma -- is a very rare finding (one case per two million people a year).
  • This functionally active, usually malignant tumor has typical clinical manifestations.
  • Glucagonoma syndrome is a disease that has an original clinical picture that includes necrolytic migrating erythema with secondary bullous dermatitis, glucose tolerance disorder or diabetes mellitus, weight loss, anemia, hypoaminoacidemia, venous thrombosis, and alimentary and mental disturbances.
  • By the time diagnosis is made, 60 to 70% of glucagonomas already give metastases, and even small glucagonomas should be considered tumors with unknown malignant potential or malignant tumors.
  • Glucagonomas grow slowly, and patients live long (the survival median is approximately 15 years).
  • [MeSH-major] Glucagonoma / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 17926496.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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9. Technau K, Renkl A, Norgauer J, Ziemer M: Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma. Eur J Dermatol; 2005 Mar-Apr;15(2):110-2
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  • [Title] Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma.
  • Necrolytic migratory erythema is a cutaneous paraneoplastic manifestation, which is usually associated with a glucagon-secreting pancreatic tumor.
  • However, it also may occur in other circumstances in which serum glucagon is elevated, as in hepatic cirrhosis.
  • Rarely, necrolytic migratory erythema is reported in association with a jejunal and rectal adenocarcinoma or villous atrophy of the small intestine without any evidence for increased serum glucagon levels.
  • In this context we report the case of an 85-year-old male with myelodysplastic syndrome who developed typical necrolytic migratory erythema without glucagonoma syndrome or evidence for other pancreatic or liver disease.
  • We suggest that, in addition to the diseases listed, myelodysplastic syndrome might be able to cause necrolytic migratory erythema.
  • [MeSH-major] Erythema / complications. Glucagonoma / complications. Myelodysplastic Syndromes / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / complications


10. Cruz-Bautista I, Lerman I, Perez-Enriquez B, Padilla LS, Torres CL, Lopez A, Cabrera T, Mehta RP, Gómez-Pérez FJ, Rull JA, Orozco-Topete R: Diagnostic challenge of glucagonoma: case report and literature review. Endocr Pract; 2006 Jul-Aug;12(4):422-6
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  • [Title] Diagnostic challenge of glucagonoma: case report and literature review.
  • OBJECTIVE: To report the diagnostic difficulties encountered in a case of glucagonoma.
  • METHODS: We provide a literature review and present the clinical findings, pertinent laboratory data, and results of related studies in a patient with a glucagonoma.
  • The patient was hospitalized, and because of the dermatologic findings suggestive of necrolytic migratory erythema, the presence of a glucagonoma was suspected.
  • Glucagon levels were found to be elevated, and imaging studies confirmed the presence of an enlarged mass in the pancreatic tail, without evidence of extension to surrounding structures.
  • After surgical removal of the tumor, the skin and oral mucosal lesions disappeared spontaneously.
  • The histologic appearance and immunohistochemical staining results confirmed the diagnosis of a glucagonoma.
  • Subsequently, all related symptoms resolved, and the glucagon levels normalized.
  • CONCLUSION: The diagnosis of glucagonoma is often delayed.
  • Clinicians should be aware of the unusual initial manifestations of this tumor and the potential for less than a full spectrum of the characteristic features of the glucagonoma syndrome.
  • [MeSH-major] Glucagonoma / diagnosis
  • [MeSH-minor] Erythema / etiology. Humans. Hyperpigmentation / etiology. Male. Middle Aged. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / ultrasonography. Pancreatic Neoplasms / ultrastructure. Regional Blood Flow. Tomography, X-Ray Computed. Wound Healing

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  • (PMID = 16901799.001).
  • [ISSN] 1530-891X
  • [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
  • [Publication-country] United States
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11. Caron P: [Clinically non functioning pituitary adenomas and gonadotroph-cell adenomas]. Presse Med; 2009 Jan;38(1):103-6
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  • [Title] [Clinically non functioning pituitary adenomas and gonadotroph-cell adenomas].
  • Clinically non-functioning pituitary adenomas and gonadotroph-cell adenomas are relatively common: microadenomas (< 1cm) are usually pituitary incidentalomas while most macroadenomas are revealed by mass effect and/or hypopituitarism.
  • They are rarely associated with high gonadotropin (Luteinizing hormone, LH; Follicle-stimulating hormone FSH) levels while increased alpha-subunit levels are more frequent.
  • Immunocytochemistry of pituitary tumor confirms the diagnosis of clinically non-functioning or gonadotroph-cell adenoma.
  • Treatment of macroadenoma with visual field defect or hypopituitarism is transphenoidal surgery, but cure is rarely obtained and tumor recurrence is significant during follow-up.
  • [MeSH-major] Adenoma / diagnosis. Pituitary Neoplasms / diagnosis

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  • (PMID = 18990542.001).
  • [ISSN] 2213-0276
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Follicle Stimulating Hormone, Human; 9002-67-9 / Luteinizing Hormone
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12. Oberkirchner U, Linder KE, Zadrozny L, Olivry T: Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide. Vet Dermatol; 2010 Oct;21(5):510-6
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  • [Title] Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide.
  • Necrolytic migratory erythema (NME; also known as superficial necrolytic dermatitis) is a syndrome most often associated with certain chronic liver diseases or pancreatic glucagonomas.
  • In humans with glucagonoma-associated NME, skin lesions usually respond to octreotide, a somatostatin analogue that inhibits glucagon release.
  • In this report an 11-year-old golden retriever dog with pancreatic glucagonoma and metastasis to the regional lymph nodes, spleen and liver was diagnosed with NME.
  • The dog was later euthanized because of progressive metastatic disease.
  • In conclusion, subcutaneous octreotide injections were beneficial in this dog with glucagonoma-associated NME.
  • This somatostatin analogue could be a valuable option to treat canine patients with non-resectable or relapsing pancreatic glucagonoma-associated NME.
  • [MeSH-major] Dog Diseases / drug therapy. Glucagonoma / veterinary. Necrolytic Migratory Erythema / veterinary. Octreotide / therapeutic use. Pancreatic Neoplasms / veterinary
  • [MeSH-minor] Animals. Anorexia / chemically induced. Anorexia / veterinary. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Hormonal / adverse effects. Antineoplastic Agents, Hormonal / therapeutic use. Dogs. Dose-Response Relationship, Drug. Lymph Nodes / pathology. Male. Paraneoplastic Syndromes / pathology. Paraneoplastic Syndromes / veterinary

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  • [Copyright] © 2010 The Authors. Journal compilation © 2010 ESVD and ACVD.
  • (PMID = 20500495.001).
  • [ISSN] 1365-3164
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
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13. 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.
  • Dopamine agonist bromocriptine decreases gonadotropin and alpha-subunit in vitro and in vivo, but, in clinical studies, was poorly effective in reducing supranormal gonadotropins and free subunits levels, and rarely produced a minimal tumoral shrinkage.
  • 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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14. Suzuki M, Egashira N, Kajiya H, Minematsu T, Takekoshi S, Tahara S, Sanno N, Teramoto A, Osamura RY: ACTH and alpha-subunit are co-expressed in rare human pituitary corticotroph cell adenomas proposed to originate from ACTH-committed early pituitary progenitor cells. Endocr Pathol; 2008;19(1):17-26
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  • [Title] ACTH and alpha-subunit are co-expressed in rare human pituitary corticotroph cell adenomas proposed to originate from ACTH-committed early pituitary progenitor cells.
  • The functional differentiation of pituitary cells and adenomas follows the combination of transcription factors and co-factors in three cell lineages [growth hormone-prolactin-thyroid-stimulating hormone lineage, adrenocorticotrophic hormone (ACTH)/pro-opiomelanocortin (POMC) lineage, and follicular stimulating hormone (FSH)/luteinizing hormone (LH) lineage], which include Pit-1, GATA-2, SF-1, NeuroD1/beta2, Tpit, ERalpha, and others.
  • Only rarely are hormones from different lineages co-expressed in the same adenoma cells.
  • Most corticotroph cell adenomas belonging to the ACTH/POMC lineage are mono-hormonal.
  • In our study of 89 corticotroph cell adenomas, 5 cases expressed both ACTH and alpha-subunit; these adenomas did not express any other anterior pituitary hormones or subunits.
  • To clarify the mechanism involved, we studied the transcription factors that regulate pituitary cell differentiation.
  • NeuroD1 and T-pit, markers of the ACTH/POMC lineage, and SF-1 and DAX-1, related to the LH/FSH cell lineage were expressed in all cases.
  • GATA2, a synergistic factor in the gonadotroph cell lineage with SF-1, was also expressed in three of five cases.
  • As ACTH and alpha-subunit are the earliest hormones to appear during development, we speculate that these particular adenomas are derived from committed ACTH progenitor cells.
  • The molecular process governing functional differentiation of these adenomas requires further investigation.
  • [MeSH-major] Adenoma / genetics. Adrenocorticotropic Hormone / genetics. Gene Expression Regulation, Neoplastic. Glycoprotein Hormones, alpha Subunit / genetics. Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology

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  • (PMID = 18228160.001).
  • [ISSN] 1559-0097
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Glycoprotein Hormones, alpha Subunit; 0 / NEUROD1 protein, human; 0 / Transcription Factor Pit-1; 0 / Transcription Factors; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
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15. Kindmark H, Sundin A, Granberg D, Dunder K, Skogseid B, Janson ET, Welin S, Oberg K, Eriksson B: Endocrine pancreatic tumors with glucagon hypersecretion: a retrospective study of 23 cases during 20 years. Med Oncol; 2007;24(3):330-7
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  • [Title] Endocrine pancreatic tumors with glucagon hypersecretion: a retrospective study of 23 cases during 20 years.
  • BACKGROUND: Glucagon-secreting endocrine pancreatic tumor is a rare disease, hence controlled studies on clinical management are lacking.
  • In an attempt to assess the efficacy of diagnostic and therapeutic measures in patients with glucagonoma, a retrospective study was performed using the archives of a tertiary care center.
  • PATIENTS AND METHODS: Records from 340 patients with endocrine pancreatic tumors were reassessed and 23 patients with malignant endocrine pancreatic tumor and elevated plasma glucagon levels were identified.
  • RESULTS: About 7% of patients with histologically verified tumors fullfilled our criteria for glucagonoma.
  • Only 22% of these patients had developed diabetes prior to the diagnosis of glucagonoma.
  • Seventy eight percent had metastatic disease to the liver at diagnosis.
  • During the study period, 11 patients died at a median of 80 months from diagnosis whereas 11 patients are still alive after a median follow up of 52 months.
  • CONCLUSIONS: Glucagonomas represent 7% of our comprehensive referral material of endocrine pancreatic tumors.
  • Necrolytic migratory erythema was a common finding (52%) and diabetes less frequent at presentation than previously reported.
  • Tumors were positive on somatostatin receptor scintigraphy and objective responses were seen to chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Erythema / complications. Glucagonoma / therapy. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Female. Glucagon / blood. Humans. Interferons. Liver Neoplasms / secondary. Male. Middle Aged. Receptors, Somatostatin / metabolism. Retrospective Studies. Sex Factors. Survival Analysis. Treatment Outcome

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  • (PMID = 17873310.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Somatostatin; 9007-92-5 / Glucagon; 9008-11-1 / Interferons
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16. Peros G, Sakorafas GH, Konstantoudakis G, Giannopoulos GA, Petropoulou K, Parasi A: Duodeno-pancreatic neuroendocrine tumours. Eur J Cancer Care (Engl); 2010 May;19(3):393-402
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  • [Title] Duodeno-pancreatic neuroendocrine tumours.
  • Duodeno-pancreatic neuroendocrine tumours (DP-ETs) are increasingly diagnosed today due to the widespread use of modern imaging methods.
  • Duodeno-pancreatic endocrine tumours should be treated by radical surgical resection, which offers a high chance for cure when the disease is localized.
  • A high index of suspicion is required in these patients for the presence of a multiple endocrine neoplasia type syndrome.
  • Histological/immunohistochemical diagnosis was somatostatin-producing tumour in the first patient, oncocytic endocrine tumour positive for neurone-specific enolase and focally for chromogranin in the second patient, glucagonoma and pancreatic polypeptide-producing endocrine pancreatic tumour in the third patient, and gastrin, somatostatin, calcitonin, insulin and adrenocorticotropic hormone (ACTH)-producing tumour in the fourth.
  • The second patient died 6.5 years following surgery due to disseminated disease.
  • [MeSH-major] Duodenal Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Biopsy. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Proteins / metabolism. Treatment Outcome

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  • (PMID = 19708940.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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17. Kovács RK, Korom I, Dobozy A, Farkas G, Ormos J, Kemény L: Necrolytic migratory erythema. J Cutan Pathol; 2006 Mar;33(3):242-5
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  • The classical symptoms are associated with alpha-cell pancreatic islet cell tumor or 'glucagonoma'.
  • Generally, extracutaneous hallmarks of this disease include weight loss, diabetes, anaemia and diarrhoea.
  • OBSERVATION: We report a case of a 39-year-old woman with a 3-year history of recalcitrant psoriasiform eruption, who had no other associated symptoms on routine examination.
  • Abdominal computer tomography was performed, which revealed a tumor in the tail of the pancreas.
  • After distal resection of the pancreas her skin symptoms resolved in a few days time.
  • Histology was consistent with glucagonoma.
  • CONCLUSIONS: It is infrequent to have only necrolytic migratory erythema, hyperglucagonaemia and islet-cell tumor but no other extracutaneous symptoms in glucagonoma syndrome.
  • Skin symptoms are important, often they are the clue to the diagnosis of glucagonoma syndrome.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Glucagonoma / pathology. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Female. Humans. Necrosis. Paraneoplastic Syndromes. Treatment Outcome

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  • (PMID = 16466513.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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18. 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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19. van Rijn SJ, Grinwis GC, Penning LC, Meij BP: Expression of Ki-67, PCNA, and p27kip1 in canine pituitary corticotroph adenomas. Domest Anim Endocrinol; 2010 May;38(4):244-52
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  • [Title] Expression of Ki-67, PCNA, and p27kip1 in canine pituitary corticotroph adenomas.
  • Pituitary-dependent hypercortisolism (PDH), which is caused by adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas, is a common endocrinopathy in dogs.
  • The aim of this study was to investigate the expression of the proliferation markers Ki-67 and proliferating cell nuclear antigen (PCNA) and the cell-cycle inhibitor p27kip1 in corticotroph adenomas in enlarged and non-enlarged pituitaries.
  • The expression of Ki-67, PCNA, and p27kip1 was analyzed by immunohistochemical staining of 17 pituitary adenoma samples harvested during pituitary surgery in dogs with PDH.
  • The labeling index was calculated by counting the number of immunopositive cells per 1,000 cells.
  • It is concluded that Ki-67 and PCNA are not useful as proliferative markers for studying the pathobiology of pituitary corticotroph adenomas in dogs.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Cyclin-Dependent Kinase Inhibitor p27 / analysis. Dog Diseases / metabolism. Ki-67 Antigen / analysis. Pituitary Neoplasms / veterinary. Proliferating Cell Nuclear Antigen / analysis
  • [MeSH-minor] Adrenocorticotropic Hormone / analysis. Animals. Dogs. Female. Immunohistochemistry. Male. alpha-MSH / analysis

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  • [Copyright] Copyright (c) 2009 Elsevier Inc. All rights reserved.
  • (PMID = 20022446.001).
  • [ISSN] 1879-0054
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Proliferating Cell Nuclear Antigen; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone
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20. Mendoza-Guil F, Hernández-Jurado I, Burkhardt P, Linares J, Naranjo R: [Necrolytic migratory erythema associated with glucagonoma]. Actas Dermosifiliogr; 2005 Apr;96(3):175-8
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  • [Title] [Necrolytic migratory erythema associated with glucagonoma].
  • [Transliterated title] Eritema necrolítico migratorio asociado a glucagonoma.
  • Glucagonoma is a rare pancreatic tumor that is usually associated with a syndrome that includes diabetes, anemia, weight loss and skin lesions in the form of necrolytic migratory erythema.
  • We present the case of a patient with malignant glucagonoma treated with surgery and octreotide, which manifested with skin lesions.
  • The discussion will review the physiopathology, other causes of necrolytic erythema, diagnosis and differential diagnosis and treatment.
  • [MeSH-major] Erythema / complications. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications

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  • (PMID = 16476361.001).
  • [ISSN] 0001-7310
  • [Journal-full-title] Actas dermo-sifiliográficas
  • [ISO-abbreviation] Actas Dermosifiliogr
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Spain
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21. Spada A, Lania A, Mantovani G: Hormonal signaling and pituitary adenomas. Neuroendocrinology; 2007;85(2):101-9
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  • [Title] Hormonal signaling and pituitary adenomas.
  • In recent years the demonstration that human pituitary adenomas are monoclonal in origin provides further evidence that pituitary neoplasia arise from the replication of a single mutated cell in which growth advantage results from either activation of proto-oncogenes or inactivation of tumor suppressor genes.
  • Mutations in common oncogenes and tumor suppressor genes are only exceptionally involved in pituitary tumors.
  • Since pituicytes may proliferate in response to hypothalamic neurohormones, locally produced growth factors and peripheral hormones, it has been speculated that dysregulation of the signaling molecules that constitute these pathways may confer growth advantage to the target cell, finally resulting in tumor formation.
  • The only mutational change so far recognized to be unequivocally associated with pituitary tumors occur in the Gs alpha gene (GNAS1) and cause constitutive activation of the cAMP-dependent pathway.
  • [MeSH-major] Adenoma / etiology. Hormones / physiology. Pituitary Neoplasms / etiology. Signal Transduction / physiology

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  • (PMID = 17337884.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Hormones; 0 / Hypothalamic Hormones; 0 / Intercellular Signaling Peptides and Proteins; 0 / Receptors, G-Protein-Coupled
  • [Number-of-references] 66
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22. Abreu Velez AM, Howard MS: Diagnosis and treatment of cutaneous paraneoplastic disorders. Dermatol Ther; 2010 Nov-Dec;23(6):662-75
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  • [Title] Diagnosis and treatment of cutaneous paraneoplastic disorders.
  • Cutaneous signs of these disorders afford clinicians opportunities for early diagnosis and treatment.
  • We aim to succinctly review the recognition, diagnosis, and treatment of selected cutaneous paraneoplastic diseases.
  • Skin disorders that may be associated with paraneoplastic syndromes include: cutaneous metastases, tripe palms, Sweet's syndrome, glucagonoma, Paget's disease and extramammary Paget's disease, acanthosis nigricans, Birt-Hogg-Dube syndrome, basal cell nevus syndrome, Bazex syndrome (acrokeratosis paraneoplastica), carcinoid syndrome, Cowden's disease(multiple hamartoma syndrome), dermatomyositis, erythema gyratum repens, ichthyosis aquisita, von Recklinghausen's disease, pityriasis rotunda, pyoderma gangrenosum, Quincke's edema (angioedema and paraneoplastic uricaria), paraneoplastic pemphigus, Degos' disease, superior vena cava syndrome, Werner's syndrome, diffuse normolipemic plane xanthomas, and yellow nail syndrome.
  • [MeSH-major] Paraneoplastic Syndromes / diagnosis. Paraneoplastic Syndromes / therapy. Skin Diseases / diagnosis. Skin Diseases / therapy

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  • [Copyright] © 2010 Wiley Periodicals, Inc.
  • (PMID = 21054710.001).
  • [ISSN] 1529-8019
  • [Journal-full-title] Dermatologic therapy
  • [ISO-abbreviation] Dermatol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
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23. Rotondo F, Kovacs K, Scheithauer BW, Horvath E, Bell CD, Lloyd RV, Cusimano M: Immunohistochemical expression of SNAP-25 protein in adenomas of the human pituitary. Appl Immunohistochem Mol Morphol; 2008 Oct;16(5):477-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical expression of SNAP-25 protein in adenomas of the human pituitary.
  • SNAP-25, a synaptosome-associated exocytosis protein of 25 kd mw, plays an important role in the secretory activity of several endocrine cells.
  • In the present study, we investigated surgically removed pituitary adenomas including 40 prolactin (PRL), 31 growth hormone, 5 adrenocorticotropic hormone, 5 thyroid-stimulating hormone, 14 follicle-stimulating hormone/luteinizing hormone/alpha-subunit-producing tumors, and 5 null cell adenomas.
  • Among the 40 patients with PRL-producing pituitary adenoma, 16 had been preoperatively treated with the dopamine agonist bromocriptine.
  • Similarly, of the 31 patients with GH-producing pituitary adenomas, 15 had been treated with the long-acting somatostatin analog, octreotide.
  • All tumors were subjected to transsphenoidal surgery, formalin-fixed, routinely processed, and paraffin-embedded.
  • Immunostaining for SNAP-25 (streptavidin-biotin peroxidase complex method) showed that 10 PRL-producing adenomas were strongly immunoreactive.
  • Immunopositivity was mainly cell membrane in distribution but several cells showed mild cytoplasmic staining.
  • Among GH-producing adenomas, SNAP-25 was seen in 5 cases; reactivity being mild-to-moderate, membrane-bound, and cytoplasmic.
  • Other adenoma types were virtually immunonegative.
  • It is conceivable that SNAP-25 plays an important role in PRL release and is involved in the bromocriptine-induced suppression of PRL secretion from PRL-producing adenoma cells.

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  • (PMID = 18633321.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SNAP25 protein, human; 0 / Synaptosomal-Associated Protein 25; 12629-01-5 / Human Growth Hormone; 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide
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24. Rotondo F, Oniya K, Kovacs K, Bell CD, Scheithauer BW: MAP-2 expression in the human adenohypophysis and in pituitary adenomas. An immunohistochemical study. Pituitary; 2005;8(2):75-9
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  • [Title] MAP-2 expression in the human adenohypophysis and in pituitary adenomas. An immunohistochemical study.
  • MAP-2, a well characterized member of the microtubule associated protein (MAP) family, binds to and stabilizes microtubules and is involved in cell proliferation as well as neuronal differentiation.
  • The aim of the present work was to study MAP-2 expression in human adenohypophyses and pituitary adenomas.
  • Nine non-tumorous adenohypophyses and 77 adenomas (GH-, PRL-, ACTH-, TSH-, FSH/LH- and/or alpha subunit- producing or immunonegative tumors) were investigated.
  • The results show that MAP-2 is expressed in the cytoplasm of non-tumorous adenohypophysial cells as well as of various pituitary adenoma types.
  • Thus MAP-2 expression cannot be used to estimate cell proliferation rate, growth potential, endocrine activity or biologic behaviour of an adenoma.
  • Immunopositivity appeared to be stronger in the cytoplasm of adenoma cells than in that of non-tumorous adenohypophysial cells, implying that the adenoma cells contain larger quantities of MAP-2.
  • It can be concluded that the functional activity of MAP-2 is not associated with the manufacture of any specific adenohypophysial hormone(s) and is not limited to one specific cell type.
  • [MeSH-major] Adenoma / metabolism. Microtubule-Associated Proteins / biosynthesis. Pituitary Gland, Anterior / metabolism. Pituitary Neoplasms / metabolism

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  • (PMID = 16195780.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MAP2 protein, human; 0 / Microtubule-Associated Proteins
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25. Cooper O, Ben-Shlomo A, Bonert V, Bannykh S, Mirocha J, Melmed S: Silent corticogonadotroph adenomas: clinical and cellular characteristics and long-term outcomes. Horm Cancer; 2010 Apr;1(2):80-92

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  • [Title] Silent corticogonadotroph adenomas: clinical and cellular characteristics and long-term outcomes.
  • Silent corticotrophins adenomas (SCAs) are clinically silent and non-secreting but immunostain positively for ACTH.
  • We compared preoperative and postoperative clinical results and tumor cytogenesis in 25 SCAs and 84 nonfunctioning adenomas in 109 consecutive patients diagnosed pre-operatively with nonfunctioning pituitary adenomas.
  • Preoperative SCA presentation was similar to that observed for nonfunctioning adenomas.
  • However, SCAs recurred postoperatively at a median of 3 years vs. 8 years for nonfunctioning adenomas (p<0.0001).
  • Fifty-four percent of patients with SCAs had new onset postoperative hypopituitarism vs. 17% of nonfunctioning adenomas (p<0.025).
  • SCAs (n=18) were immunopositive for ACTH, cytoplasmic and nuclear SF-1, NeuroD1, DAX-1, and alpha-gonadotropin subunit, but Tpit negative, and co-expression of tumor ACTH with either SF-1 or LH was detected.
  • In contrast, functional corticotroph adenomas (n=11) were immunopositive for ACTH, nuclear SF-1, NeuroD1, and Tpit, but negative for DAX-1, a gonadotroph cell transcription factor.
  • Gonadotroph adenomas (n=23) were immunonegative for ACTH and Tpit but positive for nuclear SF-1, NeuroD1, and DAX-1.
  • SCA electron microscopy demonstrated ultrastructural features consistent with corticotroph and gonadotroph cells.
  • As SCAs exhibit features consistent with both corticotroph and gonadotroph cytologic origin, we propose a pathologic and clinically distinct classification of SCAs as silent corticogonadotroph adenomas.

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  • [Cites] J Clin Endocrinol Metab. 2000 Jul;85(7):2537-42 [10902805.001]
  • [Cites] Clin Endocrinol (Oxf). 1998 May;48(5):647-54 [9666878.001]
  • [Cites] Cell. 2001 Mar 23;104(6):849-59 [11290323.001]
  • [Cites] J Clin Endocrinol Metab. 2001 Jun;86(6):2476-83 [11397843.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8674-9 [11447259.001]
  • [Cites] Mod Pathol. 2001 Sep;14(9):892-9 [11557786.001]
  • [Cites] Acta Neuropathol. 2001 Oct;102(4):398-403 [11603817.001]
  • [Cites] Neuropathology. 2001 Dec;21(4):288-93 [11837535.001]
  • [Cites] Endocr Pathol. 2002 Summer;13(2):125-30 [12165660.001]
  • [Cites] Endocr J. 2002 Jun;49(3):285-92 [12201210.001]
  • [Cites] Clin Endocrinol (Oxf). 2003 Jan;58(1):59-64 [12519413.001]
  • [Cites] Genes Dev. 2003 Mar 15;17(6):738-47 [12651892.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3050-6 [12843142.001]
  • [Cites] Pituitary. 2002;5(4):221-3 [14558669.001]
  • [Cites] Neurosurgery. 2003 Nov;53(5):1076-84; discussion 1084-5 [14580274.001]
  • [Cites] J Clin Invest. 2003 Dec;112(11):1603-18 [14660734.001]
  • [Cites] Endocr Pathol. 2003 Winter;14(4):363-8 [14739492.001]
  • [Cites] Hum Pathol. 2004 Sep;35(9):1137-47 [15343517.001]
  • [Cites] Am J Pathol. 1980 Mar;98(3):617-38 [6244736.001]
  • [Cites] J Pathol. 1985 Jan;145(1):59-62 [3881578.001]
  • [Cites] J Neurosurg. 1987 Feb;66(2):244-50 [3543255.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1988;413(1):61-8 [2453972.001]
  • [Cites] Acta Endocrinol (Copenh). 1988 Aug;118(4):533-7 [2840793.001]
  • [Cites] Pathol Res Pract. 1988 Sep;183(5):601-5 [2467268.001]
  • [Cites] Pathol Res Pract. 1988 Sep;183(5):610-2 [2467270.001]
  • [Cites] Neurosurgery. 1990 Mar;26(3):397-403 [1690866.001]
  • [Cites] Am J Pathol. 1990 Aug;137(2):479-88 [2167013.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1990;417(4):361-7 [2173251.001]
  • [Cites] Hum Pathol. 1991 Jul;22(7):719-21 [1649119.001]
  • [Cites] Pathol Res Pract. 1991 Jun;187(5):637-41 [1717963.001]
  • [Cites] Neurol Med Chir (Tokyo). 1992;32(7 Spec No):381-547 [1381065.001]
  • [Cites] Ultrastruct Pathol. 1999 May-Jun;23(3):141-8 [10445280.001]
  • [Cites] Mol Endocrinol. 1999 Aug;13(8):1267-84 [10446902.001]
  • [Cites] Br J Neurosurg. 2005 Feb;19(1):38-42 [16147581.001]
  • [Cites] Endocr Pathol. 2005 Fall;16(3):239-44 [16299407.001]
  • [Cites] Pathol Res Pract. 2006;202(6):457-64 [16497445.001]
  • [Cites] Neurosurgery. 2006 Aug;59(2):341-53; discussion 341-53 [16883174.001]
  • [Cites] Clin Genet. 2007 Sep;72(3):175-82 [17718852.001]
  • [Cites] Neurosurgery. 2007 Sep;61(3):580-4; discussion 584-5 [17881972.001]
  • [Cites] Exp Clin Endocrinol Diabetes. 2007 Oct;115(9):610-5 [17943697.001]
  • [Cites] Eur J Endocrinol. 2007 Dec;157(6):717-24 [18057378.001]
  • [Cites] Endocr J. 2007 Dec;54(6):961-8 [18079591.001]
  • [Cites] J Clin Endocrinol Metab. 2008 May;93(5):1526-40 [18334580.001]
  • [Cites] Mol Endocrinol. 2008 Jul;22(7):1647-57 [18388149.001]
  • [Cites] Neuro Endocrinol Lett. 2008 Jun;29(3):347-50 [18580839.001]
  • [Cites] Endocr Pathol. 2008 Spring;19(1):17-26 [18228160.001]
  • [Cites] Clin Endocrinol (Oxf). 2010 May;72(5):648-53 [19650787.001]
  • [Cites] Pathol Int. 1994 Sep;44(9):697-703 [7804432.001]
  • [Cites] Eur J Endocrinol. 1995 Jul;133(1):25-32 [7542980.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Jun;81(6):2165-70 [8964846.001]
  • [Cites] J Clin Endocrinol Metab. 1997 Mar;82(3):818-24 [9062489.001]
  • [Cites] Endocr J. 1997 Apr;44(2):329-33 [9228470.001]
  • [Cites] Clin Endocrinol (Oxf). 1997 Jun;46(6):669-79 [9274697.001]
  • [Cites] Mol Cell Biol. 1997 Nov;17(11):6673-82 [9343431.001]
  • [Cites] Endocrinol Metab Clin North Am. 1997 Dec;26(4):741-62 [9429858.001]
  • [Cites] Neurosurgery. 2000 Sep;47(3):723-9; discussion 729-30 [10981760.001]
  • (PMID = 20717480.001).
  • [ISSN] 1868-8500
  • [Journal-full-title] Hormones & cancer
  • [ISO-abbreviation] Horm Cancer
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / T32 DK007770-08; United States / NCI NIH HHS / CA / R01 CA075979-08; United States / NIDDK NIH HHS / DK / T32 DK007770; United States / NIDDK NIH HHS / DK / T32 DK07770; United States / NIDDK NIH HHS / DK / DK007770-08; United States / NCI NIH HHS / CA / CA 075979; United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA075979-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gonadotropins
  • [Keywords] NOTNLM ; Corticotroph adenoma / Gonadotroph adenoma / Nonfunctioning adenoma / Pituitary adenoma
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26. Pawlikowski M, Winczyk K: Immunohistochemical detection of prothymosin alpha in pituitary adenomas--a new marker of tumor recurrence? Folia Histochem Cytobiol; 2009;47(4):559-62
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  • [Title] Immunohistochemical detection of prothymosin alpha in pituitary adenomas--a new marker of tumor recurrence?
  • Forty pituitary adenomas were immunostained with an antibody raised against the C-terminal fragment (101-109) of human prothymosin alpha (PT alpha).
  • The strong positive immunostaining was found in the subpopulation of cell nuclei and intratumoral vessel walls, while the cytoplasm of adenoma cells was slightly immunopositive.
  • The significantly higher percentage of PT alpha-positive cell nuclei was found in recurrent pituitary adenomas as compared with primary tumors.
  • However, there was no correlation between the percentage of PT alpha-positive cell nuclei and Ki-67 indices.
  • Gonadotropinomas were characterized by higher nuclear PT alpha expression in comparison to other pituitary adenomas, which is probably linked with the high recurrence rate of these tumors.
  • It is suggested that PT alpha immunostaining may be helpful in predicting the pituitary tumor recurrence.
  • Moreover, PT alpha may be also useful as an immunohistochemical marker of the intratumoral microvasculature.

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  • (PMID = 20430720.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Protein Precursors; 0 / prothymosin alpha; 61512-21-8 / Thymosin
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27. Marko PB, Miljković J, Zemljic TG: Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors. Acta Dermatovenerol Alp Pannonica Adriat; 2005 Dec;14(4):161-4, 166
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  • [Title] Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors.
  • The computed tomographic scan of the abdomen revealed multiple hepatic tumors.
  • Histopathological examination of ultrasound-guided needle biopsy from a hepatic lesion demonstrated a neuroendocrine tumor.
  • Somatostatin-receptor scintigraphy with radio-labelled octreotide confirmed the likelihood of the neuroendocrine nature of the hepatic tumors and excluded the presence of other such lesions throughout the rest of the body, including the pancreas.
  • The serum glucagon level was markedly increased.
  • The diagnosis of necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors was made and therapy with the long-acting somatostatin analogue octreotide was started.
  • Having reached the final stage of the disease, which was further complicated by congestive heart failure, the patient died one year later.
  • As no autopsy was performed, we were unable to establish whether the hepatic tumors represented a metastatic process of previously undetected pancreatic glucagonoma or if they were extra-pancreatic glucagon-secreting tumors.
  • The correct diagnosis of necrolytic migratory erythema is important, since it might be the clue for early detection of glucagonoma or of extra-pancreatic glucagon-secreting tumors.
  • [MeSH-major] Dermatitis / etiology. Erythema / etiology. Liver Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Paraneoplastic Syndromes / diagnosis
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Glucagon / blood. Humans. Male. Middle Aged. Octreotide / therapeutic use

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  • (PMID = 16435046.001).
  • [ISSN] 1318-4458
  • [Journal-full-title] Acta dermatovenerologica Alpina, Pannonica, et Adriatica
  • [ISO-abbreviation] Acta Dermatovenerol Alp Pannonica Adriat
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Slovenia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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28. Docherty HM, Hay CW, Ferguson LA, Barrow J, Durward E, Docherty K: Relative contribution of PDX-1, MafA and E47/beta2 to the regulation of the human insulin promoter. Biochem J; 2005 Aug 1;389(Pt 3):813-20
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  • Of these, the homoeodomain protein PDX-1 (pancreatic duodenal homeobox factor-1), the basic leucine zipper protein MafA and the basic helix-loop-helix heterodimer E47/BETA2 (beta-cell E box transactivator 2; referred to here as beta2) bind to important regulatory sites.
  • Mutagenesis of the PDX-1, MafA and E47/beta2 binding sites reduced promoter activity by 60, 74 and 94% respectively, in INS-1 beta-cells.
  • In the islet glucagonoma cell line alphaTC1.6, overexpression of PDX-1 and MafA separately increased promoter activity approx.
  • In HeLa cells, PDX-1 stimulated the basal promoter by approx.
  • PDX-1 was shown further to activate the endogenous insulin 1 gene in alphaTC1.6 cells, whereas MafA activated the insulin 2 gene.

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  • [Cites] Mol Endocrinol. 1994 Dec;8(12):1798-806 [7708065.001]
  • [Cites] J Biol Chem. 2005 Mar 25;280(12):11887-94 [15665000.001]
  • [Cites] Diabetes. 1990 Apr;39(4):406-14 [2156740.001]
  • [Cites] J Biol Chem. 1990 May 15;265(14):8285-96 [2186040.001]
  • [Cites] Mol Endocrinol. 1991 Jun;5(6):836-43 [1922098.001]
  • [Cites] Endocrinology. 1992 Jan;130(1):167-78 [1370150.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Feb 1;89(3):1045-9 [1310538.001]
  • [Cites] Mol Cell Biol. 1992 Apr;12(4):1777-88 [1549125.001]
  • [Cites] EMBO J. 1993 Nov;12(11):4251-9 [7901001.001]
  • [Cites] Mol Endocrinol. 1993 Oct;7(10):1275-83 [7505393.001]
  • [Cites] EMBO J. 1994 Mar 1;13(5):1145-56 [7907546.001]
  • [Cites] Nature. 1994 Oct 13;371(6498):606-9 [7935793.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 6;91(25):12203-7 [7991607.001]
  • [Cites] Genes Dev. 1995 Apr 15;9(8):1009-19 [7774807.001]
  • [Cites] Diabetes. 1995 Aug;44(8):1002-4 [7621988.001]
  • [Cites] Development. 1996 Mar;122(3):983-95 [8631275.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Aug 20;93(17):9015-20 [8799146.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 24;93(26):15057-62 [8986763.001]
  • [Cites] Mol Cell Biol. 1997 Jul;17(7):3987-96 [9199333.001]
  • [Cites] Mol Cell Biol. 2000 Feb;20(3):900-11 [10629047.001]
  • [Cites] J Biol Chem. 2000 Jan 21;275(3):2199-204 [10636926.001]
  • [Cites] J Biol Chem. 2001 Jan 5;276(1):104-13 [11024035.001]
  • [Cites] Mol Cell Biol. 2001 May;21(9):3234-43 [11287626.001]
  • [Cites] J Biol Chem. 2001 Sep 21;276(38):35751-60 [11457839.001]
  • [Cites] Diabetologia. 2001 Oct;44(10):1203-14 [11692168.001]
  • [Cites] Mol Cell Biol. 2002 Jan;22(2):412-20 [11756538.001]
  • [Cites] J Endocrinol. 2002 Mar;172(3):653-72 [11874714.001]
  • [Cites] Diabetologia. 2002 Mar;45(3):309-26 [11914736.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6737-42 [12011435.001]
  • [Cites] Mol Biol Evol. 2002 Jul;19(7):1114-21 [12082130.001]
  • [Cites] J Biol Chem. 2002 Dec 20;277(51):49903-10 [12368292.001]
  • [Cites] Curr Biol. 2003 Jan 21;13(2):105-15 [12546783.001]
  • [Cites] J Biol Chem. 2003 Jun 27;278(26):23617-23 [12711597.001]
  • [Cites] Mol Cell Biol. 2003 Sep;23(17):6049-62 [12917329.001]
  • [Cites] Mol Biol Evol. 2003 Sep;20(9):1377-419 [12777501.001]
  • [Cites] Mol Cell Biol. 2003 Oct;23(19):6713-24 [12972592.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Dec 19;312(3):831-42 [14680841.001]
  • [Cites] J Mol Endocrinol. 2004 Feb;32(1):9-20 [14765989.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):2930-3 [14973194.001]
  • [Cites] J Biol Chem. 2004 May 21;279(21):22228-35 [15028719.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 1;101(22):8319-24 [15148392.001]
  • [Cites] Nature. 1980 Mar 6;284(5751):26-32 [6243748.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Dec;84(24):8819-23 [3321054.001]
  • [Cites] Nature. 1988 Mar 3;332(6159):87-90 [2831456.001]
  • [Cites] Mol Cell Biol. 1989 Aug;9(8):3253-9 [2552288.001]
  • [Cites] Genes Dev. 1997 Sep 15;11(18):2323-34 [9308961.001]
  • [Cites] J Biol Chem. 1999 Jul 23;274(30):21095-103 [10409662.001]
  • [Cites] Biochem J. 1989 Nov 15;264(1):233-9 [2690822.001]
  • (PMID = 15862113.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / HMGB Proteins; 0 / Homeodomain Proteins; 0 / Insulin; 0 / MAFA protein, human; 0 / Maf Transcription Factors, Large; 0 / NEUROD1 protein, human; 0 / TCF Transcription Factors; 0 / TCF7L1 protein, human; 0 / Tcf7l1 protein, rat; 0 / Trans-Activators; 0 / Transcription Factor 7-Like 1 Protein; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein
  • [Other-IDs] NLM/ PMC1180732
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29. Buurman H, Saeger W: Subclinical adenomas in postmortem pituitaries: classification and correlations to clinical data. Eur J Endocrinol; 2006 May;154(5):753-8
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  • [Title] Subclinical adenomas in postmortem pituitaries: classification and correlations to clinical data.
  • OBJECTIVE: The aim of this study was to examine pituitary adenomas in a series of postmortem pituitaries by use of modern technologies of immunostaining, to classify the adenomas according to the current WHO classification and to analyse the possible associations to the available clinical data.
  • RESULTS: A total of 334 pituitary adenomas were found in 316 pituitaries.
  • One hundred and thirty-two sparsely granulated prolactin cell adenomas (39.5%), 75 null cell adenomas (22.5%) and 31 oncocytomas were diagnosed.
  • Forty-six ACTH cell adenomas (13.8%, 27 densely granulated, 19 sparsely granulated) and one adenoma composed of Crooke's cells were detected.
  • Twenty-two gonadotroph cell adenomas (6.6%), seven GH cell adenomas (four sparsely granulated, three densely granulated), one mixed GH cell-PRL cell adenoma, two TSH cell adenomas, five plurihormonal adenoma type I, four plurihormonal adenoma type II and two alpha-subunit-only adenomas were seen.
  • Six adenomas remained unclassified because the tissue was not contained in all sections for immunohistochemistry.
  • The overall tumour size ranged from 0.1 to 20 mm in diameter.
  • Among 76 adenomas (22.7%), which had a tumour size of > or = 3 mm, only three tumours were macroadenomas corresponding to a tumour size of more than 10 mm.
  • CONCLUSIONS: Adenomas in postmortem pituitaries differ from those in surgical series in proportion of adenoma types and biological behaviour.

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  • (PMID = 16645024.001).
  • [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] 0 / Glycoprotein Hormones, alpha Subunit; 0 / Gonadotropins; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin
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30. Heliövaara E, Raitila A, Launonen V, Paetau A, Arola J, Lehtonen H, Sane T, Weil RJ, Vierimaa O, Salmela P, Tuppurainen K, Mäkinen M, Aaltonen LA, Karhu A: The expression of AIP-related molecules in elucidation of cellular pathways in pituitary adenomas. Am J Pathol; 2009 Dec;175(6):2501-7
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  • [Title] The expression of AIP-related molecules in elucidation of cellular pathways in pituitary adenomas.
  • Germline mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene predispose to the development of pituitary adenomas.
  • Here, we characterized AIP mutation positive (AIPmut+) and AIP mutation negative (AIPmut-) pituitary adenomas by immunohistochemistry.
  • The expressions of the AIP-related proteins aryl hydrocarbon receptor (AHR), AHR nuclear translocator (ARNT), cyclin-dependent kinase inhibitor 1B encoding p27(Kip1), and hypoxia-inducible factor 1-alpha were examined in 14 AIPmut+ and 53 AIPmut- pituitary adenomas to detect possible expression differences.
  • In addition, the expression of CD34, an endothelial and hematopoietic stem cell marker, was analyzed.
  • We found ARNT to be less frequently expressed in AIPmut+ pituitary adenomas (P = 0.001), suggesting that AIP regulates the ARNT levels.
  • AIP small interfering RNA-treated HeLa, HEK293, or Aip-null mouse embryonic fibroblast cells did not show lowered expression of ARNT.
  • Instead, in the pituitary adenoma cell line GH3, Aip silencing caused a partial reduction of Arnt and a clear increase in cell proliferation.
  • The expressions of p27(Kip1), hypoxia-inducible factor 1-alpha, or CD34 did not differ between tumor types.
  • The present study shows that the expression of ARNT protein is significantly reduced in AIPmut+ tumors.
  • [MeSH-minor] Animals. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Blotting, Western. Cyclin-Dependent Kinase Inhibitor p27. Down-Regulation. Gene Expression. Gene Expression Profiling. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Immunohistochemistry. Mice. Mutation. RNA, Small Interfering. Receptors, Aryl Hydrocarbon / biosynthesis. Receptors, Aryl Hydrocarbon / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • [Cites] J Biol Chem. 2006 May 26;281(21):14654-62 [16567799.001]
  • [Cites] J Cell Biochem. 2005 Dec 15;96(6):1174-84 [16211578.001]
  • [Cites] J Biol Chem. 2006 Aug 25;281(34):24721-7 [16807248.001]
  • [Cites] EMBO Rep. 2006 Oct;7(10):1035-9 [16936638.001]
  • [Cites] Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R80-7 [17613552.001]
  • [Cites] FEBS Lett. 2007 Jul 31;581(19):3608-15 [17412325.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Aug;92(8):3321-5 [17519308.001]
  • [Cites] Endocr Relat Cancer. 2007 Sep;14(3):901-6 [17914118.001]
  • [Cites] Nature. 2007 Dec 6;450(7171):893-8 [17982442.001]
  • [Cites] Cell Death Differ. 2008 Apr;15(4):678-85 [18259193.001]
  • [Cites] J Clin Endocrinol Metab. 2008 Jun;93(6):2390-401 [18381572.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 17;103(42):15558-63 [17030811.001]
  • [Cites] J Biol Chem. 2006 Dec 8;281(49):37507-16 [17023418.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4101-5 [17360484.001]
  • [Cites] J Biol Chem. 2007 May 4;282(18):13656-63 [17329248.001]
  • [Cites] Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R73-9 [17613551.001]
  • [Cites] Endocr Relat Cancer. 2009 Sep;16(3):1029-43 [19556287.001]
  • [Cites] EMBO Rep. 2009 Jun;10(6):622-8 [19390533.001]
  • [Cites] Mol Pharmacol. 1999 Dec;56(6):1127-37 [10570039.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2000;40:519-61 [10836146.001]
  • [Cites] Mol Endocrinol. 2000 Oct;14(10):1674-81 [11043581.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6692-7 [11381139.001]
  • [Cites] J Histochem Cytochem. 2003 Jan;51(1):41-54 [12502753.001]
  • [Cites] Nucleic Acids Res. 2003 Jan 1;31(1):278-81 [12520002.001]
  • [Cites] J Biol Chem. 2003 Feb 14;278(7):4467-73 [12482853.001]
  • [Cites] J Biol Chem. 2003 Aug 29;278(35):33351-63 [12810716.001]
  • [Cites] J Cell Biol. 2003 Oct 13;163(1):45-56 [14557246.001]
  • [Cites] Nat Rev Cancer. 2004 Apr;4(4):285-95 [15057288.001]
  • [Cites] Science. 1992 May 22;256(5060):1193-5 [1317062.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 1995;35:307-40 [7598497.001]
  • [Cites] J Biol Chem. 1997 Apr 25;272(17):11452-6 [9111057.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 25;96(11):6382-7 [10339596.001]
  • [Cites] Genes Dev. 1999 Jul 1;13(13):1742-53 [10398686.001]
  • [Cites] Biochemistry. 1999 Jul 13;38(28):8907-17 [10413464.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Oct;84(10):3823-30 [10523037.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 28;102(26):9218-23 [15972329.001]
  • [Cites] Endocr Pathol. 2005 Spring;16(1):53-62 [16000847.001]
  • [Cites] Cell. 2005 Aug 12;122(3):337-49 [16096055.001]
  • [Cites] Science. 2006 May 26;312(5777):1228-30 [16728643.001]
  • (PMID = 19850893.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARNT protein, human; 0 / Antigens, CD34; 0 / CDKN1B protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; 0 / Receptors, Aryl Hydrocarbon; 0 / aryl hydrocarbon receptor-interacting protein; 138391-32-9 / Aryl Hydrocarbon Receptor Nuclear Translocator; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
  • [Other-IDs] NLM/ PMC2789606
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31. Greijer AE, Delis-van Diemen PM, Fijneman RJ, Giles RH, Voest EE, van Hinsbergh VW, Meijer GA: Presence of HIF-1 and related genes in normal mucosa, adenomas and carcinomas of the colorectum. Virchows Arch; 2008 May;452(5):535-44
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  • [Title] Presence of HIF-1 and related genes in normal mucosa, adenomas and carcinomas of the colorectum.
  • Expression of the transcription factor hypoxia-inducible factor 1 (HIF-1), which plays a key role in cellular adaptation to hypoxia, was investigated in normal colorectal mucosa (ten), adenomas (61), and carcinomas (23).
  • Tissue samples were analyzed for HIF-1 alpha, its upstream regulators, von Hippel-Lindau factor, AKT, and mammalian target of rapamycin (mTOR) and its downstream targets glucose transporter 1 (GLUT1), carbonic anhydrase IX, stromal-cell-derived factor 1 (SDF-1) by immunohistochemistry.
  • In normal colorectal mucosa, HIF-1 alpha was observed in almost all nuclei of surface epithelial cells, probably secondary to a gradient of oxygenation, as indicated by pimonidazole staining.
  • The same staining pattern was present in 87% of adenomas.
  • In carcinomas, HIF-1 alpha was present predominantly around areas of necrosis (78%).
  • Active AKT and mTOR, were present in all adenomas, carcinomas, and in normal colorectal mucosa.
  • GLUT1 and SDF-1 were present in the normal surface epithelium of all adenoma cases, whereas in the carcinoma GLUT1 was located around necrotic regions and SDF-1 was present in all epithelial cells.
  • In conclusion, HIF-1 alpha appears to be physiologically expressed in the upper part of the colorectal mucosa.
  • The present observations support that upregulation of HIF-1 alpha and its downstream targets GLUT1 and SDF-1 in colorectal adenomas and carcinomas may be due to hypoxia, in close interaction with an active phosphatidylinositol 3-kinases-AKT-mTOR pathway.
  • [MeSH-major] Adenoma / metabolism. Chemokine CXCL12 / metabolism. Colorectal Neoplasms / metabolism. Glucose Transporter Type 1 / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Intestinal Mucosa / metabolism

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  • [Cites] Cancer Res. 1999 Nov 15;59(22):5830-5 [10582706.001]
  • [Cites] Cancer Res. 2000 Mar 15;60(6):1541-5 [10749120.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):7075-83 [11156414.001]
  • [Cites] J Natl Cancer Inst. 2001 Feb 21;93(4):309-14 [11181778.001]
  • [Cites] Genes Dev. 2001 Apr 1;15(7):807-26 [11297505.001]
  • [Cites] Science. 2001 Apr 20;292(5516):464-8 [11292862.001]
  • [Cites] Science. 2001 Apr 20;292(5516):468-72 [11292861.001]
  • [Cites] Mol Cell Biol. 2001 Jun;21(12):3995-4004 [11359907.001]
  • [Cites] J Natl Cancer Inst. 2001 Sep 5;93(17):1337-43 [11535709.001]
  • [Cites] Cancer Res. 2001 Dec 15;61(24):8924-9 [11751418.001]
  • [Cites] Carcinogenesis. 2002 Jan;23(1):201-5 [11756242.001]
  • [Cites] Br J Cancer. 2002 Apr 22;86(8):1250-6 [11953881.001]
  • [Cites] Cancer. 2002 Jun 15;94(12):3127-34 [12115344.001]
  • [Cites] Cancer Res. 2002 Dec 1;62(23):7066-74 [12460928.001]
  • [Cites] Int J Cancer. 2003 Mar 10;104(1):85-91 [12532423.001]
  • [Cites] Cancer Res. 2003 Mar 1;63(5):917-22 [12615703.001]
  • [Cites] Cancer. 2003 Mar 15;97(6):1573-81 [12627523.001]
  • [Cites] Int J Cancer. 2003 Jun 10;105(2):176-81 [12673675.001]
  • [Cites] Nat Rev Cancer. 2003 Oct;3(10):721-32 [13130303.001]
  • [Cites] Nat Genet. 2003 Dec;35(4):323-30 [14625550.001]
  • [Cites] Cancer Sci. 2004 Feb;95(2):149-53 [14965365.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Jun;286(6):G1059-68 [14764445.001]
  • [Cites] Nat Med. 2004 Aug;10(8):858-64 [15235597.001]
  • [Cites] J Clin Invest. 2004 Oct;114(8):1098-106 [15489957.001]
  • [Cites] Hum Pathol. 1996 Feb;27(2):152-6 [8617456.001]
  • [Cites] Am J Pathol. 1998 Jul;153(1):279-85 [9665489.001]
  • [Cites] Nature. 1999 May 20;399(6733):271-5 [10353251.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8554-60 [15623639.001]
  • [Cites] Blood. 2005 Jan 15;105(2):659-69 [15374877.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2005 Feb;288(2):G316-26 [15358596.001]
  • [Cites] J Clin Oncol. 2005 Apr 20;23(12):2744-53 [15837989.001]
  • [Cites] Cell. 2005 May 6;121(3):335-48 [15882617.001]
  • [Cites] J Pathol. 2005 Jul;206(3):291-304 [15906272.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6178-88 [16024619.001]
  • [Cites] Oncogene. 2005 Nov 14;24(50):7465-74 [16288293.001]
  • [Cites] Cell. 2006 Jan 13;124(1):175-89 [16413490.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2006 May 1;65(1):246-54 [16618579.001]
  • [Cites] Oncogene. 2006 May 18;25(21):3065-70 [16407833.001]
  • [Cites] Oncogene. 2006 Oct 5;25(45):6123-7 [16682946.001]
  • [Cites] Cell Oncol. 2007;29(3):229-40 [17452775.001]
  • (PMID = 18351386.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Chemokine CXCL12; 0 / Glucose Transporter Type 1; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / SLC2A1 protein, human; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Oncogene Protein v-akt; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2329727
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32. Shigematsu K, Nishida N, Sakai H, Igawa T, Toriyama K, Nakatani A, Takahara O, Kawai K: Synaptophysin immunoreactivity in adrenocortical adenomas: a correlation between synaptophysin and CYP17A1 expression. Eur J Endocrinol; 2009 Dec;161(6):939-45
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  • [Title] Synaptophysin immunoreactivity in adrenocortical adenomas: a correlation between synaptophysin and CYP17A1 expression.
  • DESIGN AND METHODS: The adrenal cortex is not considered to be an intrinsic part of the diffuse neuroendocrine system, but adrenocortical neoplasms possess neuroendocrine properties.
  • In this study, we examined synaptophysin (SYP) and neural cell adhesion molecule (NCAM) expression in adrenocortical adenomas in relation to adrenal function.
  • RESULTS: Immunohistochemical analysis showed that 50.7 and 98.6% of the cortical adenomas showed SYP and NCAM immunoreactivities respectively.
  • There was no apparent difference in NCAM immunoreactivity among the adenomas.
  • However, the immunostaining for SYP was significantly stronger in cortisol-producing adenomas (CPA) than in aldosterone-producing adenomas (APA), nonfunctioning adenomas (NFA), showing no clinical or endocrinological abnormality, or adenomas associated with preclinical Cushing's syndrome (preCS).
  • It was unexpected that the ratio of positive cells for SYP in preCS was less than that in APA and NFA.
  • CONCLUSIONS: We propose that SYP expression in adrenocortical cells may be involved in some aspect of adrenal function such as transport or secretion of glucocorticoids.

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  • (PMID = 19755404.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecules; 0 / RNA, Messenger; 0 / Synaptophysin; EC 1.14.99.9 / CYP17A1 protein, human; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase
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33. Pertuit M, Barlier A, Enjalbert A, Gérard C: Signalling pathway alterations in pituitary adenomas: involvement of Gsalpha, cAMP and mitogen-activated protein kinases. J Neuroendocrinol; 2009 Nov;21(11):869-77
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  • [Title] Signalling pathway alterations in pituitary adenomas: involvement of Gsalpha, cAMP and mitogen-activated protein kinases.
  • Despite extensive research on sporadic pituitary adenomas, it is not yet possible to assign one protein alteration to one specific type of pituitary adenomas.
  • Nevertheless, alterations of the cAMP pathway appear to be molecular hallmarks of most growth hormone (GH)-secreting adenomas.
  • In this review, we summarise the literature regarding signalling alterations observed in GH-secreting adenomas.
  • In the light of results obtained on human somatotroph adenoma cells in primary culture and on models of murine somatotroph cell lines, we postulate a crucial role for ERK1/2 in GH-secreting adenomas downstream of cAMP pathway alterations that might impact the tumoural phenotype.
  • [MeSH-major] Adenoma / metabolism. Cyclic AMP / metabolism. GTP-Binding Protein alpha Subunits, Gs / metabolism. Mitogen-Activated Protein Kinases / metabolism. Pituitary Neoplasms / metabolism. Signal Transduction

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  • (PMID = 19732293.001).
  • [ISSN] 1365-2826
  • [Journal-full-title] Journal of neuroendocrinology
  • [ISO-abbreviation] J. Neuroendocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 9002-72-6 / Growth Hormone; E0399OZS9N / Cyclic AMP; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Number-of-references] 95
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34. Ritz-Laser B, Mamin A, Brun T, Avril I, Schwitzgebel VM, Philippe J: The zinc finger-containing transcription factor Gata-4 is expressed in the developing endocrine pancreas and activates glucagon gene expression. Mol Endocrinol; 2005 Mar;19(3):759-70
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  • [Title] The zinc finger-containing transcription factor Gata-4 is expressed in the developing endocrine pancreas and activates glucagon gene expression.
  • We show here that Gata-4 and/or Gata-6 are not only expressed in the adult exocrine pancreas but also in glucagonoma and insulinoma cell lines, whereas Gata-5 is restricted to the exocrine pancreas.
  • During pancreas development, Gata-4 is expressed already at embryonic d 10.5 and colocalizes with early glucagon+ cells at embryonic d 12.5.
  • Gata-4 was able to transactivate the glucagon gene both in heterologous BHK-21 (nonislet Syrian baby hamster kidney) and in glucagon-producing InR1G9 cells.
  • Using gel-mobility shift assays, we identified a complex formed with nuclear extracts from InR1G9 cells on the G5 control element (-140 to -169) of the glucagon gene promoter as Gata-4.
  • Mutation of the GATA binding site on G5 abrogated the transcriptional activation mediated by Gata-4 and reduced basal glucagon gene promoter activity in glucagon-producing cells by 55%.
  • Furthermore, Gata-4 acted more than additively with Forkhead box A (hepatic nuclear factor-3) to trans-activate the glucagon gene promoter.
  • We conclude that, besides its role in endoderm differentiation, Gata-4 might be implicated in the regulation of glucagon gene expression in the fetal pancreas and that Gata activity itself may be modulated by interactions with different cofactors.
  • [MeSH-major] DNA-Binding Proteins / chemistry. Gene Expression Regulation. Glucagon / metabolism. Islets of Langerhans / metabolism. Transcription Factors / chemistry. Zinc Fingers
  • [MeSH-minor] Animals. Base Sequence. Binding Sites. Cell Differentiation. Cell Line. Cell Nucleus / metabolism. Chloramphenicol O-Acetyltransferase / metabolism. Cricetinae. Dose-Response Relationship, Drug. GATA4 Transcription Factor. GATA6 Transcription Factor. Humans. Mice. Microscopy, Fluorescence. Molecular Sequence Data. Mutation. Pancreas / embryology. Promoter Regions, Genetic. Protein Binding. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tissue Distribution. Transcriptional Activation. Transfection


35. La Rosa S, Uccella S, Dainese L, Marchet S, Placidi C, Vigetti D, Capella C: Characterization of c-kit (CD117) expression in human normal pituitary cells and pituitary adenomas. Endocr Pathol; 2008;19(2):104-11
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  • [Title] Characterization of c-kit (CD117) expression in human normal pituitary cells and pituitary adenomas.
  • c-kit (CD117) is a tyrosine kinase receptor involved in the proliferation, differentiation, and secretory functions of various cells.
  • In experimental animal models, c-kit has been detected in the pars intermedia of the normal pituitary gland and in alpha-melanocyte-stimulating-hormone-positive adenomas and it has been suggested that it plays a role in regulating adrenocorticotropic hormone (ACTH) secretion.
  • To the best of our knowledge, the expression of c-kit in normal human pituitary cells and in pituitary adenomas has never been reported, so the possible biological role of this receptor in the control of pituitary hormone secretion remains unclear.
  • The aim of this study was to evaluate the immunohistochemical expression of c-kit in normal human pituitary glands and in a series of 62 well-characterized pituitary adenomas.
  • In normal adenohypophyses, several cells, mainly located in the central mucoid wedge, showed a c-kit immunoreactivity (IR).
  • Double label immunostaining procedures showed that the c-kit-IR cells corresponded to ACTH cells.
  • Out of 62 adenomas, 15 (24%) were c-kit-IR, including 7/16 (44%) ACTH cell, 3/7 (42%) null cell, 4/11 (36%) alpha-subunit cell, and 1/11 (10%) follicle-stimulating hormone-luteinizing hormone cell adenomas.
  • By contrast, all ten prolactin cell and seven growth hormone cell adenomas were c-kit negative.
  • [MeSH-major] Adenoma / metabolism. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adolescent. Adult. Aged. Blotting, Western. Child. Female. Follicle Stimulating Hormone / blood. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / pathology. Humans. Immunohistochemistry. Luteinizing Hormone / blood. Male. Middle Aged. Paraffin Embedding. Prolactinoma / metabolism. Prolactinoma / pathology. Tissue Fixation

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  • (PMID = 18568298.001).
  • [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] 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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36. Dinc B, Sahin C: Metastatic glucagonoma. Eurasian J Med; 2009 Apr;41(1):70-2

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  • [Title] Metastatic glucagonoma.
  • We report a case of a very rare endocrine tumor of the pancreas.
  • Because the CA 19-9 and glucagon levels were high, and abdominal dynamic CT showed a mass in the pancreas body and metastatic lesions in the liver, the decision was made to operate.
  • The histopathology of the tumor was reported as a neuroendocrine tumor, which was concordant with glucagonoma.

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  • (PMID = 25610069.001).
  • [ISSN] 1308-8734
  • [Journal-full-title] The Eurasian journal of medicine
  • [ISO-abbreviation] Eurasian J Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  • [Other-IDs] NLM/ PMC4261651
  • [Keywords] NOTNLM ; Glucagonoma / Liver / Metastases
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37. 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.
  • 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.
  • 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.
  • [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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38. Mizokami Y, Egashira N, Takekoshi S, Itoh J, Itoh Y, Osamura RY, Matsumae M: Expression of MSX1 in human normal pituitaries and pituitary adenomas. Endocr Pathol; 2008;19(1):54-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of MSX1 in human normal pituitaries and pituitary adenomas.
  • Transcription factors play specific roles in the development and differentiation of normal pituitary tissues and pituitary adenoma.
  • The transcription factor, muscle segment homeobox 1 (MSX1), which belongs to the homeobox gene family, binds the promoter region of the glycoprotein hormone alpha-subunit (SU) in TSH-producing cells in the mouse pituitary and regulates alpha-SU expression.
  • In addition, 50 pituitary adenomas were examined using immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) to clarify the role of MSX1 in the development and functional differentiation of pituitary adenoma cells.
  • In the normal pituitary, MSX1 was predominantly expressed in the cytoplasm of GH-producing cells.
  • Furthermore, MSX1 immunoreactivity was observed in the cytoplasm of some alpha-SU-producing cells.
  • It is interesting to note that, in the pituitary adenoma, MSX1 was expressed in the nucleus of GH- and TSH-producing adenomas.
  • RT-PCR using RNA extracted and purified from formalin-fixed paraffin-embedded pituitary adenoma specimens revealed MSX1 mRNA expressed in GH- and TSH-producing adenomas.
  • These results suggest that MSX1 plays a specific role in human pituitary adenoma.
  • [MeSH-major] Adenoma / genetics. MSX1 Transcription Factor / genetics. Pituitary Gland / physiology. Pituitary Neoplasms / genetics
  • [MeSH-minor] Animals. Autopsy. Blotting, Western. Cell Differentiation. DNA Primers. Humans. Immunohistochemistry. Mice. Microscopy, Immunoelectron. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18379900.001).
  • [ISSN] 1559-0097
  • [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 / DNA Primers; 0 / MSX1 Transcription Factor; 0 / MSX1 protein, human; 0 / Msx1 protein, mouse; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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39. Evans CO, Yao C, Laborde D, Oyesiku NM: Folate receptor expression in pituitary adenomas cellular and molecular analysis. Vitam Horm; 2008;79:235-66
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  • [Title] Folate receptor expression in pituitary adenomas cellular and molecular analysis.
  • Clinically nonfunctional pituitary adenomas cause hypopituitarism or compression of regional structures.
  • Unlike functional tumors, there is no available medical treatment or specific imaging technique for these tumors.
  • We have recently discovered that both folate receptor (FR)alpha mRNA and protein are uniquely overexpressed in nonfunctional pituitary tumors, but not in functional adenomas.
  • Here, we used murine pituitary tumor cell line alphaT3-1 as a model to investigate the biological significance of FRalpha and its mutant FR67.
  • We demonstrate that overexpression of FR facilitated tumor cell growth and anchorage-independent growth in soft agar.
  • More colonies were observed in FR overexpressing cells than in mutant FR67 clones in soft agar.
  • Cell proliferation rate was increased, the percentage of cells in S-phase was increased, and high PCNA staining was detected in cells overexpressing the receptor.
  • In alphaT3-1 cells transfected with mutant FR67, cell proliferation rate was reduced, the percentage of cells residing in S-phase was slightly decreased, and low PCNA staining was observed.
  • By real-time quantitative PCR, the genes involved in NOTCH3 pathway including NOTCH3, HES-1, and TLE2 were altered; the mRNA expression of FGFR1 was upregulated, and ERbeta mRNA was downregulated in FR overexpressing cells.
  • Our findings suggest that FRalpha plays a role in pituitary tumor formation, and this effect may in part be due to its regulation of the NOTCH3 pathway.
  • [MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Cell Line. Cell Proliferation. Female. Folate Receptor 1. Folic Acid / metabolism. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Male. Mice. Middle Aged. Mutation. Protein Binding. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Notch / metabolism

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  • (PMID = 18804697.001).
  • [ISSN] 0083-6729
  • [Journal-full-title] Vitamins and hormones
  • [ISO-abbreviation] Vitam. Horm.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01-NS5143901
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Folate Receptor 1; 0 / Folr1 protein, mouse; 0 / Notch3 protein, mouse; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Receptors, Notch; 935E97BOY8 / Folic Acid
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40. Karpac J, Ostwald D, Li GY, Bui S, Hunnewell P, Brennan MB, Hochgeschwender U: Proopiomelanocortin heterozygous and homozygous null mutant mice develop pituitary adenomas. Cell Mol Biol (Noisy-le-grand); 2006;52(2):47-52
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  • [Title] Proopiomelanocortin heterozygous and homozygous null mutant mice develop pituitary adenomas.
  • Mice lacking all pro-opiomelanocortin (POMC)-derived peptides have been created by gene targeting of the POMC locus in embryonic stem cells.
  • Here, we report that both POMC null homozygous and heterozygous mutants also develop pituitary gland tumors, which result in their premature death.
  • The tumors occur with 100% penetrance in both POMC heterozygous and homozygous genotypes.
  • Histological examinations reveal that tumors start from hyperplastic focal points of melanotrophic cells within the intermediate lobe.
  • Based on the morphological and immunohistological features, we have classified the tumors as non-invasive, non-secreting, intermediate lobe adenomas.
  • These findings uncover potential novel roles of melanocortins in the regulation of cell proliferation.
  • [MeSH-major] Adenoma / genetics. Pituitary Neoplasms / genetics. Pro-Opiomelanocortin / genetics
  • [MeSH-minor] Adrenocorticotropic Hormone / analysis. Animals. Disease Progression. Heterozygote. Homozygote. Immunohistochemistry. In Situ Hybridization. Mice. Mice, Knockout. Survival Analysis. Survival Rate. alpha-MSH / analysis

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  • (PMID = 16914086.001).
  • [ISSN] 1165-158X
  • [Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)
  • [ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 581-05-5 / alpha-MSH; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone
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41. 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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42. 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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43. Winczyk K, Kunert-Radek J, Gruszka A, Radek M, Ławnicka H, Pawlikowski M: Effects of rosiglitazone--peroxisome proliferators-activated receptor gamma (PPARgamma) agonist on cell viability of human pituitary adenomas in vitro. Neuro Endocrinol Lett; 2009 Mar;30(1):107-10
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  • [Title] Effects of rosiglitazone--peroxisome proliferators-activated receptor gamma (PPARgamma) agonist on cell viability of human pituitary adenomas in vitro.
  • It was shown that tumoral tissue, including the pituitary adenomas, posses PPARgamma receptors.
  • The activation of PPARgamma receptors inhibits tumour growth in rodents and induces the oncostatic effect on human cancer cell lines.
  • The aim of the present study was to examine the anti-tumour effect of RGZ on human pituitary adenomas in vitro.
  • MATERIALS AND METHODS: Cells of eight pituitary adenomas removed neurosurgically were used to our experiment.
  • Before the operation, the hormonal secretion of the tumour was estimated.
  • After the surgery, the histological diagnosis and immunohistochemical detection of pituitary hormones and PPARgamma receptors were performed.
  • The cells of pituitary tumours were exposed in the primary culture to RGZ at the concentrations of 10(-9)-10(-4) M for 24 hours.
  • To measure the cell growth the modified colorimetric Mossman method detecting the cells viability was applied.
  • RESULTS: On the basis of the pre-operative diagnosis the 6 clinically non-functioning adenomas (CNFPA), one case of acromegaly and one case of Cushing's disease were recognized.
  • In 5 out of 6 CNFPA the immunopositive reaction for different pituitary hormones such as: LH, HGH, PRL, FSH and alpha-subunit was detected.
  • Rosiglitazone decreased the cell viability of all CNFPA and corticotropinoma for 20% or more.
  • In somatotropinoma inhibition of the cell growth was about 13%.
  • THE MAIN FINDING: The obtained results indicate that RZG exerts a suppressive effect on the cell viability in non-functioning pituitary adenomas.
  • CONCLUSION: Our data suggest that rosiglitazone may be useful in the treatment of non-functioning pituitary adenomas, but its efficacy in Cushing's disease and acromegaly requires further study.
  • [MeSH-major] Adenoma / pathology. PPAR gamma / agonists. Pituitary Neoplasms / pathology. Thiazolidinediones / pharmacology
  • [MeSH-minor] Acromegaly / etiology. Acromegaly / pathology. Adrenocorticotropic Hormone / secretion. Adult. Aged. Cell Proliferation / drug effects. Cell Survival / drug effects. Drug Evaluation, Preclinical. Female. Human Growth Hormone / secretion. Humans. Hypoglycemic Agents / pharmacology. Male. Middle Aged. Pituitary ACTH Hypersecretion / etiology. Pituitary ACTH Hypersecretion / pathology. Tumor Cells, Cultured

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  • (PMID = 19300395.001).
  • [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 / Hypoglycemic Agents; 0 / PPAR gamma; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone
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44. 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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45. 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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46. Yoshida D, Kim K, Yamazaki M, Teramoto A: Expression of hypoxia-inducible factor 1alpha and cathepsin D in pituitary adenomas. Endocr Pathol; 2005;16(2):123-31
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  • [Title] Expression of hypoxia-inducible factor 1alpha and cathepsin D in pituitary adenomas.
  • Hypoxia-inducible factor (HIF)-1alpha is a crucial transcription factor involved in the adaptive response to hypoxia, whereas cathepsin D, which regulates angiostatin in several cancer cell lines, has been reported to be upregulated by HIF-1alpha.
  • In order to determine the involvement of angiogenesis in pituitary adenomas, we studied the expression of both HIF-1alpha and cathepsin D in tissues from 58 patients (39 women, 19 men, ranging in age from 20 to 78 yr), sorted by histological group, and assayed by double immunohistochemistry.
  • HIF-1alpha immunoreactivity, confined to the nucleoplasm, was present in both tumor and vascular endothelial cells.
  • ACTH-producing adenomas showed the lowest level of HIF-1alpha, whereas prolactin (PRL)-producing adenomas and HIF-1alpha-positive microvessels showed the highest (p < 0.001).
  • In contrast, the lowest expression of cathepsin D was observed in PRL-producing adenomas, whereas the highest expression was detected in ACTH-producing adenomas (p < 0.0001).
  • Imaging analysis with fluorescence double immunohistochemistry showed that HIF-1alpha-negative tumor cells did not express significantly higher levels of cathepsin D.
  • In these poorly vascularized tumors, the hypoxic marker HIF-1alpha may not downregulate cathepsin D.
  • The mechanisms of tumor angiogenesis and cell invasion in pituitary adenomas may differ from those in other tumor cells.
  • [MeSH-major] Adenoma / metabolism. Cathepsin D / biosynthesis. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Pituitary Neoplasms / metabolism

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  • (PMID = 16199897.001).
  • [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 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 3.4.23.5 / Cathepsin D
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47. Ho GY, Xue X, Cushman M, McKeown-Eyssen G, Sandler RS, Ahnen DJ, Barry EL, Saibil F, Bresalier RS, Rohan TE, Baron JA: Antagonistic effects of aspirin and folic acid on inflammation markers and subsequent risk of recurrent colorectal adenomas. J Natl Cancer Inst; 2009 Dec 02;101(23):1650-4
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  • [Title] Antagonistic effects of aspirin and folic acid on inflammation markers and subsequent risk of recurrent colorectal adenomas.
  • The Aspirin/Folate Polyp Prevention Trial found that aspirin, but not folic acid, reduced recurrence of colorectal adenomas.
  • There were 884 subjects who had colonoscopic evaluation for adenomas at year 3 and plasma levels of C-reactive protein (CRP), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), soluble TNF receptor type II (sTNF-R2), and IL-1 receptor antagonist (IL-1Ra) measured at baseline and year 3.
  • Changes in inflammation markers were not associated with adenoma recurrence.
  • Nevertheless, inflammation markers do not mediate the chemopreventive effect of aspirin on colorectal adenomas.
  • [MeSH-major] Adenoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Aspirin / pharmacology. C-Reactive Protein / metabolism. Colorectal Neoplasms / blood. Folic Acid / pharmacology. Inflammation / blood
  • [MeSH-minor] Aged. Biomarkers / blood. Drug Administration Schedule. Drug Antagonism. Female. Humans. Interleukin-6 / blood. Male. Middle Aged. Risk Assessment. Risk Factors. Tumor Necrosis Factor-alpha / blood

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  • [Cites] J Lab Clin Med. 1984 Jun;103(6):944-8 [6726059.001]
  • [Cites] Blood. 1971 Oct;38(4):405-16 [5571429.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jun 1;89(11):4845-9 [1317575.001]
  • [Cites] Gut. 1998 May;42(5):643-9 [9659157.001]
  • [Cites] Circulation. 1999 Aug 24;100(8):793-8 [10458713.001]
  • [Cites] Immunol Rev. 2004 Dec;202:275-93 [15546400.001]
  • [Cites] Arch Intern Med. 2005 Jun 27;165(12):1388-94 [15983288.001]
  • [Cites] Thromb Haemost. 2005 Jul;94(1):96-100 [16113791.001]
  • [Cites] Int J Obes (Lond). 2006 Aug;30(8):1197-202 [16491109.001]
  • [Cites] Clin Chem Lab Med. 2007;45(1):54-8 [17243915.001]
  • [Cites] JAMA. 2007 Jun 6;297(21):2351-9 [17551129.001]
  • [Cites] Mutat Res. 2007 Sep 1;622(1-2):42-57 [17628614.001]
  • [Cites] Gastroenterology. 2008 Jan;134(1):29-38 [18022173.001]
  • [Cites] J Thromb Thrombolysis. 2000 Jan;9(1):37-41 [10590187.001]
  • [Cites] Hepatogastroenterology. 2000 Jan-Feb;47(31):57-70 [10690586.001]
  • [Cites] Clin Chem. 2000 Jul;46(7):934-8 [10894836.001]
  • [Cites] Ann Rheum Dis. 2000 Nov;59 Suppl 1:i60-4 [11053091.001]
  • [Cites] Cell Mol Life Sci. 1999 Oct 15;56(3-4):305-12 [11212358.001]
  • [Cites] J Am Coll Cardiol. 2001 Jun 15;37(8):2036-41 [11419884.001]
  • [Cites] Trends Mol Med. 2002 Jan;8(1):10-6 [11796261.001]
  • [Cites] Oncology (Williston Park). 2002 Feb;16(2):217-26, 229; discussion 230-2 [11866137.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):883-90 [12621132.001]
  • [Cites] N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133.001]
  • [Cites] Eur J Clin Invest. 2003 Mar;33(3):209-15 [12641538.001]
  • [Cites] Am J Cardiol. 2003 Jul 15;92(2):236-9 [12860235.001]
  • [Cites] Thromb Res. 2003 Apr 15;110(1):13-7 [12877903.001]
  • [Cites] Gastroenterology. 2003 Aug;125(2):328-36 [12891533.001]
  • [Cites] Semin Cancer Biol. 2004 Dec;14(6):433-9 [15489136.001]
  • [Cites] Biochem J. 1992 Feb 15;282 ( Pt 1):197-202 [1540135.001]
  • (PMID = 19822838.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA108841; United States / NCI NIH HHS / CA / U54 CA100971; United States / NCI NIH HHS / CA / U54-CA100971; United States / NCI NIH HHS / CA / R01 CA059005; United States / PHS HHS / / R01-108841; United States / NCI NIH HHS / CA / R01-CA059005
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Biomarkers; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 9007-41-4 / C-Reactive Protein; 935E97BOY8 / Folic Acid; R16CO5Y76E / Aspirin
  • [Other-IDs] NLM/ PMC2786916
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48. Hanson JM, Mol JA, Meij BP: Expression of leukemia inhibitory factor and leukemia inhibitory factor receptor in the canine pituitary gland and corticotrope adenomas. Domest Anim Endocrinol; 2010 May;38(4):260-71
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  • [Title] Expression of leukemia inhibitory factor and leukemia inhibitory factor receptor in the canine pituitary gland and corticotrope adenomas.
  • Leukemia inhibitory factor (LIF) is a pleiotropic cytokine of the IL-6 family that activates the hypothalamic-pituitary-adrenal axis and promotes corticotrope cell differentiation during development.
  • The aim of this study was to investigate the expression of LIF and its receptor (LIFR) in the canine pituitary gland and in corticotrope adenomas, and to perform a mutation analysis of LIFR.
  • Using immunohistochemistry, immunofluorescence, and quantitative expression analysis, LIF and LIFR expression were studied in pituitary glands of control dogs and in specimens of corticotrope adenoma tissue collected through hypophysectomy in dogs with pituitary-dependent hypercortisolism (PDH, Cushing's disease).
  • In the control pituitary tissues and corticotrope adenomas, there was a low magnitude of LIF expression.
  • Cytoplasmatic immunoreactivity of LIFR was preserved in corticotrope adenomas and adjacent nontumorous cells of pars intermedia.
  • Surprisingly, nuclear to perinuclear immunoreactivity for LIFR was present in nontumorous pituitary cells of the pars distalis in 10 of 12 tissue specimens from PDH dogs.
  • These data show that LIFR is highly co-expressed with adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) in the canine pituitary gland and in corticotrope adenomas.
  • Nuclear immunoreactivity for LIFR in nontumorous cells of the pars distalis may indicate the presence of a corticotrope adenoma.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Dog Diseases / metabolism. Leukemia Inhibitory Factor / analysis. Pituitary Gland / chemistry. Pituitary Neoplasms / veterinary. Receptors, OSM-LIF / analysis
  • [MeSH-minor] Animals. Cell Nucleus / chemistry. Cosyntropin / analysis. Cytoplasm / chemistry. DNA, Complementary / analysis. Dogs. Female. Fluorescent Antibody Technique. Immunohistochemistry. Male. Mutation. Polymerase Chain Reaction. Sequence Analysis, DNA. alpha-MSH / analysis

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  • [Copyright] Copyright (c) 2009 Elsevier Inc. All rights reserved.
  • (PMID = 20036483.001).
  • [ISSN] 1879-0054
  • [Journal-full-title] Domestic animal endocrinology
  • [ISO-abbreviation] Domest. Anim. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Leukemia Inhibitory Factor; 0 / Receptors, OSM-LIF; 16960-16-0 / Cosyntropin; 581-05-5 / alpha-MSH
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49. de Mestier L, Hammel P, Hentic O, Dove P, Lévy P, Ruszniewski P: [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency]. Gastroenterol Clin Biol; 2010 Jan;34(1):106-10
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  • [Title] [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency].
  • [Transliterated title] Efficacité spectaculaire d'une chimiothérapie par 5-fluoro-uracile et dacarbazine chez un malade atteint de glucagonome métastatique avec insuffisance cardiaque.
  • Malignant glucagonoma is an exceptional pancreatic endocrine tumour, with frequent dermatologic symptoms, diabetes and degradation of the general health status.
  • We report here an observation of a patient who was treated for a glucagonoma with multiple liver metastases, migratory necrolytic erythema, dilated cardiomypathy and diabetes that dramatically improved after a dacarbazin-based chemotherapy, allowing subsequent surgical resection of the primary.
  • The patient was still alive and asymptomatic without progressive disease nearly two years after surgery.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cardiomyopathy, Dilated / complications. Glucagonoma / drug therapy. Liver Neoplasms / drug therapy
  • [MeSH-minor] Adult. Dacarbazine / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery

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  • [Copyright] Copyright 2009. Published by Elsevier Masson SAS.
  • (PMID = 19875259.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 7GR28W0FJI / Dacarbazine; U3P01618RT / Fluorouracil
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50. Yao C, Evans CO, Stevens VL, Owens TR, Oyesiku NM: Folate receptor alpha regulates cell proliferation in mouse gonadotroph alphaT3-1 cells. Exp Cell Res; 2009 Nov 1;315(18):3125-32
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  • [Title] Folate receptor alpha regulates cell proliferation in mouse gonadotroph alphaT3-1 cells.
  • We have previously found that the mRNA and protein levels of the folate receptor alpha (FRalpha) are uniquely over-expressed in clinically human nonfunctional (NF) pituitary adenomas, but the mechanistic role of FRalpha has not fully been determined.
  • We investigated the effect of FRalpha over-expression in the mouse gonadotroph alphaT3-1 cell line as a model for NF pituitary adenomas.
  • Furthermore, we found a higher cell growth rate, an enhanced percentage of cells in S-phase by BrdU assay, and a higher PCNA staining.
  • These observations indicate that over-expression of FRalpha promotes cell proliferation.
  • These effects were abrogated in the same alphaT3-1 cells when transfected with a mutant FRalpha cDNA that confers a dominant-negative phenotype by inhibiting folic acid binding.
  • Finally, by real-time quantitative PCR, we found that mRNA expression of NOTCH3 was up-regulated in FRalpha over-expressing cells.
  • In summary, our data suggests that FRalpha regulates pituitary tumor cell proliferation and mechanistically may involve the NOTCH pathway.
  • Potentially, this finding could be exploited to develop new, innovative molecular targeted treatment for human NF pituitary adenomas.
  • [MeSH-major] Carrier Proteins / metabolism. Folic Acid / metabolism. Gonadotrophs / metabolism. Receptors, Cell Surface / metabolism. Receptors, Notch / metabolism
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Animals. Cell Line. Cell Proliferation. Disease Models, Animal. Folate Receptors, GPI-Anchored. Humans. Mice. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology. Proliferating Cell Nuclear Antigen / metabolism. Transfection. Up-Regulation / genetics. Up-Regulation / physiology

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  • (PMID = 19446551.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01-NS5143901
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Folate Receptors, GPI-Anchored; 0 / Notch3 protein, mouse; 0 / Proliferating Cell Nuclear Antigen; 0 / Receptors, Cell Surface; 0 / Receptors, Notch; 935E97BOY8 / Folic Acid
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51. Mizuno T, Hiraoka H, Yoshioka C, Takeda Y, Matsukane Y, Shimoyama N, Morimoto M, Hayashi T, Okuda M: Superficial necrolytic dermatitis associated with extrapancreatic glucagonoma in a dog. Vet Dermatol; 2009 Feb;20(1):72-9

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  • [Title] Superficial necrolytic dermatitis associated with extrapancreatic glucagonoma in a dog.
  • Based on histopathological findings, blood examinations and necropsy findings, the condition was diagnosed as superficial necrolytic dermatitis associated with a glucagon-secreting extrapancreatic neuroendocrine tumour.
  • Gross necropsy revealed tumour invasion into the spleen, liver, adrenal glands and mesenteric lymph nodes.
  • Immunohistochemical analysis of the neoplastic cells revealed that the tumour was a glucagonoma, consistent with earlier findings of persistent glucagonaemia and hypoaminoacidaemia.
  • [MeSH-major] Dermatitis / veterinary. Dog Diseases / pathology. Glucagonoma / veterinary

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  • (PMID = 19152590.001).
  • [ISSN] 1365-3164
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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52. Zatelli MC, Piccin D, Vignali C, Tagliati F, Ambrosio MR, Bondanelli M, Cimino V, Bianchi A, Schmid HA, Scanarini M, Pontecorvi A, De Marinis L, Maira G, degli Uberti EC: Pasireotide, a multiple somatostatin receptor subtypes ligand, reduces cell viability in non-functioning pituitary adenomas by inhibiting vascular endothelial growth factor secretion. Endocr Relat Cancer; 2007 Mar;14(1):91-102
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  • [Title] Pasireotide, a multiple somatostatin receptor subtypes ligand, reduces cell viability in non-functioning pituitary adenomas by inhibiting vascular endothelial growth factor secretion.
  • Somatostatin (SRIF) analogs have been employed in medical therapy of non-functioning pituitary adenomas (NFA), with contrasting results.
  • Previous evidence showed that SRIF can exert its antiproliferative effects by reducing vascular endothelial growth factor (VEGF) secretion and action, and that VEGF expression may be related to pituitary tumor growth.
  • The aim of our study was to clarify the possible effects of a multireceptor SRIF ligand on VEGF secretion and cell proliferation in human NFA primary cultures.
  • We assessed the expression of SRIF receptors (SSTR1-5), the in vitro effects on VEGF secretion, and on cell viability of SRIF and of the stable SRIF analog pasireotide (SOM230), which activates SSTR1, 2, 3, and 5.
  • Twenty-five NFA were examined by RT-PCR for expression of alpha-subunit, SSTR, VEGF, and VEGF receptors 1 (VEGF-R1) and 2 (VEGF-R2).
  • All NFA samples expressed alpha-sub, VEGF and VEGFR-1 and 2, while SSTR expression pattern was highly variable.
  • VEGF secretion and cell viability were reduced by SRIF and pasireotide in the 'responder' group, but not in the 'non-responder' group, including NFA expressing SSTR5.
  • In addition, SRIF and pasireotide completely abrogated the promoting effects of VEGF on NFA cell viability.
  • Our data demonstrate that pasireotide can inhibit NFA cell viability by inhibiting VEGF secretion, and suggest that the multireceptor-SSTR agonist pasireotide might be useful in medical therapy of selected NFA.
  • [MeSH-major] Adenoma / secretion. Oligopeptides / pharmacology. Pituitary Neoplasms / secretion. Somatostatin / pharmacology. Vascular Endothelial Growth Factor A / secretion
  • [MeSH-minor] Adult. Aged. Cell Survival / drug effects. Female. Hormones / pharmacology. Humans. Ligands. Male. RNA, Messenger / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism

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  • (PMID = 17395978.001).
  • [ISSN] 1351-0088
  • [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 / Hormones; 0 / Ligands; 0 / Oligopeptides; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / Vascular Endothelial Growth Factor A; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide
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53. Fernando MA, Heaney AP: Alpha1-adrenergic receptor antagonists: novel therapy for pituitary adenomas. Mol Endocrinol; 2005 Dec;19(12):3085-96
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  • [Title] Alpha1-adrenergic receptor antagonists: novel therapy for pituitary adenomas.
  • Pituitary tumors are common and cause considerable morbidity due to local invasion and altered hormone secretion.
  • Doxazosin (dox), a selective alpha(1)-adrenergic receptor antagonist, used to treat hypertension, also inhibits prostate cancer cell proliferation.
  • We examined the effects of dox on murine and human pituitary tumor cell proliferation in vitro and in vivo. dox treatment inhibited proliferation of murine pituitary tumor cells, induced G(0)-G(1) cell cycle arrest, and reduced phosphorylated retinoblastoma levels.
  • In addition, increased annexin-fluorescein isothiocyanate immunoreactivity and cleaved caspase-3 levels, in keeping with dox-mediated apoptosis, were observed in the human and murine pituitary tumor cells, and dox administration to mice, harboring corticotroph tumors, decreased tumor growth and reduced plasma ACTH levels. dox-mediated antiproliferative and proapoptotic actions were not confined to alpha-adrenergic receptor-expressing pituitary tumor cells and were unaffected by cotreatment with the alpha-adrenergic receptor blocker, phenoxybenzamine. dox treatment led to reduced phosphorylated inhibitory kappaB (IkappaB)-alpha expression, and nuclear factor-kappaB transcription and decreased basal and TNFalpha-induced proopiomelanocortin transcriptional activation.
  • These results demonstrate that the selective alpha(1)-adrenergic receptor antagonist dox inhibits pituitary tumor cell growth in vitro and in vivo by mechanisms that are in part independent of its alpha-adrenergic receptor-blocking actions and involve down-regulation of nuclear factor-kappaB signaling. dox is proposed as a possible novel medical therapy for pituitary tumors.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Adenoma / drug therapy. Adrenergic alpha-1 Receptor Antagonists. Adrenergic alpha-Antagonists / therapeutic use. Antineoplastic Agents / therapeutic use. Doxazosin / therapeutic use
  • [MeSH-minor] Adrenocorticotropic Hormone / blood. Animals. Apoptosis. Caspase 3. Caspases / metabolism. Cell Cycle / drug effects. Cell Proliferation / drug effects. Humans. I-kappa B Proteins / metabolism. Mice. Mice, Nude. NF-kappa B / metabolism. Neoplasm Transplantation. Pro-Opiomelanocortin / genetics. Receptors, Adrenergic, alpha-1 / genetics. Receptors, Adrenergic, alpha-1 / metabolism. Transcriptional Activation. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16020484.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Antineoplastic Agents; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Receptors, Adrenergic, alpha-1; 0 / Tumor Necrosis Factor-alpha; 139874-52-5 / NF-kappaB inhibitor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; NW1291F1W8 / Doxazosin
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54. Matthiessen MW, Pedersen G, Albrektsen T, Adamsen S, Fleckner J, Brynskov J: Peroxisome proliferator-activated receptor expression and activation in normal human colonic epithelial cells and tubular adenomas. Scand J Gastroenterol; 2005 Feb;40(2):198-205
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  • [Title] Peroxisome proliferator-activated receptor expression and activation in normal human colonic epithelial cells and tubular adenomas.
  • OBJECTIVE: Peroxisome proliferator-activated receptor (PPAR) ligands, widely used in type 2 diabetes treatment, have variably been shown to promote or prevent colon tumor formation in animal models and cell lines, but their role in normal human colon is unknown.
  • The aim of this study was to determine PPAR expression and function in normal human colonic epithelial cells and tubular adenomas.
  • MATERIAL AND METHODS: Short-term cultures of normal human colonic epithelial cells were established from biopsies obtained in 42 patients with normal colonoscopy.
  • PPARs were activated by ligands for PPAR alpha (Wy-14643), PPAR delta (GW-501516) and PPAR gamma (rosiglitazone or troglitazone).
  • Cell viability was measured using the methyltetrazoleum assay, proliferation by thymidine incorporation, and DNA profiles by flow cytometry.
  • PPAR mRNA levels in tubular adenomas or metaplastic polyps (n=12) were compared with those in controls.
  • RESULTS: PPAR alpha and gamma were consistently expressed in normal colonocytes while no PPAR delta expression could be detected.
  • PPAR gamma activation had no effect on viability or DNA profiles, but led to a 25% significant decrease in cell proliferation.
  • Finally, a selective and significant 2.5-fold decrease in PPAR alpha expression was observed in tubular adenomas, but not in metaplastic polyps, compared to controls.
  • Moreover, they raise interest in investigation of PPAR alpha as a therapeutic target to prevent adenoma formation.
  • [MeSH-major] Adenoma / metabolism. Colonic Neoplasms / metabolism. Epithelial Cells / metabolism. Peroxisome Proliferator-Activated Receptors / biosynthesis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Proliferation. Cell Survival / physiology. Colon. Female. Humans. Male. Middle Aged

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  • (PMID = 15764152.001).
  • [ISSN] 0036-5521
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Peroxisome Proliferator-Activated Receptors
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55. Hussaini IM, Trotter C, Zhao Y, Abdel-Fattah R, Amos S, Xiao A, Agi CU, Redpath GT, Fang Z, Leung GK, Lopes MB, Laws ER Jr: Matrix metalloproteinase-9 is differentially expressed in nonfunctioning invasive and noninvasive pituitary adenomas and increases invasion in human pituitary adenoma cell line. Am J Pathol; 2007 Jan;170(1):356-65
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  • [Title] Matrix metalloproteinase-9 is differentially expressed in nonfunctioning invasive and noninvasive pituitary adenomas and increases invasion in human pituitary adenoma cell line.
  • The complete resection of pituitary adenomas (PAs) is unlikely when there is an extensive local dural invasion and given that the molecular mechanisms remain primarily unknown.
  • Gene clustering revealed a robust eightfold increase in matrix metalloproteinase (MMP)-9 expression in surgically resected human invasive PAs and in the (nonfunctioning) HP75 human pituitary tumor-derived cell line treated with phorbol-12-myristate-13-acetate; these results were confirmed by real-time polymerase chain reaction, gelatin zymography, reverse transcriptase-polymerase chain reaction, Western blot, immunohistochemistry, and Northern blot analyses.
  • The activation of protein kinase C (PKC) increased both MMP-9 activity and expression, which were blocked by some PKC inhibitors (Gö6976, bisindolylmaleimide, and Rottlerin), PKC-alpha, and PKC-delta small interfering (si)RNAs but not by hispidin (PKC-beta inhibitor).
  • In a transmembrane invasion assay, phorbol-12-myristate-13-acetate (100 nmol/L) increased the number of invaded HP75 cells, a process that was attenuated by PKC inhibitors, MMP-9 antibody, PKC-alpha siRNA, or PKC-delta siRNA.
  • These results demonstrate that MMP-9 and PKC-alpha or PKC-delta may provide putative therapeutic targets for the control of PA dural invasion.

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  • [Cites] Neuroendocrinology. 2005;82(3-4):208-14 [16601360.001]
  • [Cites] Endocrinology. 1994 Jul;135(1):416-22 [8013379.001]
  • [Cites] J Biol Chem. 2000 Jul 21;275(29):22348-54 [10806212.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Aug;85(8):2931-5 [10946906.001]
  • [Cites] Neurosci Lett. 2000 Sep 1;290(3):201-4 [10963898.001]
  • [Cites] Neurosurgery. 2001 Oct;49(4):857-62; discussion 862-3 [11564246.001]
  • [Cites] Exp Cell Res. 2001 Dec 10;271(2):344-55 [11716547.001]
  • [Cites] J Neurosurg. 2002 Feb;96(2):195-208 [11838791.001]
  • [Cites] J Clin Endocrinol Metab. 2002 Mar;87(3):1262-7 [11889197.001]
  • [Cites] Int J Oncol. 2003 Jan;22(1):137-43 [12469196.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1034-9 [12552124.001]
  • [Cites] J Biol Chem. 2003 Apr 25;278(17):15056-64 [12586837.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2251-5 [12727847.001]
  • [Cites] J Biol Chem. 2003 May 16;278(20):18140-5 [12642591.001]
  • [Cites] Biochem Biophys Res Commun. 2003 May 30;305(2):428-33 [12745093.001]
  • [Cites] Cancer Res. 2003 Jul 15;63(14):4218-24 [12874029.001]
  • [Cites] Glia. 2003 Sep;43(3):254-64 [12898704.001]
  • [Cites] Acta Neuropathol. 2003 Nov;106(5):471-8 [12904990.001]
  • [Cites] Mol Cell Biochem. 2003 Nov;253(1-2):269-85 [14619979.001]
  • [Cites] J Pathol. 2006 May;209(1):15-24 [16463268.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Nov;88(11):5119-26 [14602737.001]
  • [Cites] J Biol Chem. 2004 May 21;279(21):22118-23 [15037605.001]
  • [Cites] Cancer Res. 2004 Aug 15;64(16):5693-701 [15313909.001]
  • [Cites] J Clin Endocrinol Metab. 1993 Nov;77(5):1125-9 [8077302.001]
  • [Cites] FASEB J. 1995 Apr;9(7):484-96 [7737456.001]
  • [Cites] Cell Signal. 1995 Nov;7(8):793-801 [8593248.001]
  • [Cites] J Clin Endocrinol Metab. 1996 Feb;81(2):656-62 [8636285.001]
  • [Cites] J Neurosurg. 1996 Aug;85(2):329-34 [8755764.001]
  • [Cites] Acta Neurochir (Wien). 1996;138(4):390-5 [8738388.001]
  • [Cites] Cancer. 1997 Feb 15;79(4):804-12 [9024719.001]
  • [Cites] Mol Endocrinol. 1997 Apr;11(4):433-41 [9092795.001]
  • [Cites] J Endocrinol. 1997 Apr;153(1):131-7 [9135578.001]
  • [Cites] Horm Res. 1997;47(4-6):227-34 [9167956.001]
  • [Cites] Cancer Res. 1997 Jun 1;57(11):2209-15 [9187123.001]
  • [Cites] J Endocrinol. 1998 Sep;158(3):425-33 [9846172.001]
  • [Cites] Mol Pharm. 2004 Jan 12;1(1):9-22 [15832497.001]
  • [Cites] Eur J Endocrinol. 2005 Jul;153(1):143-51 [15994756.001]
  • [Cites] Cancer Res. 2005 Sep 15;65(18):8366-71 [16166314.001]
  • [Cites] J Med Invest. 2005 Aug;52(3-4):151-8 [16167532.001]
  • [Cites] J Clin Neurosci. 2005 Sep;12(7):791-4 [16198918.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10214-22 [16288009.001]
  • [Cites] Int J Cancer. 1982 Nov 15;30(5):669-73 [6295970.001]
  • [Cites] J Neurosurg. 1986 Mar;64(3):402-7 [3950720.001]
  • [Cites] Biochim Biophys Acta. 1987 Nov 25;907(3):191-217 [2823896.001]
  • [Cites] Endocrinology. 1990 May;126(5):2567-76 [2109689.001]
  • [Cites] Int J Cancer. 1992 Mar 12;50(5):724-30 [1347514.001]
  • [Cites] J Biol Chem. 1992 Jul 25;267(21):14543-6 [1378833.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Aug 15;89(16):7427-31 [1502154.001]
  • [Cites] Neurosurgery. 1993 Apr;32(4):635-42 [8097303.001]
  • [Cites] Neurosurgery. 1999 Dec;45(6):1432-40; discussion 1440-1 [10598711.001]
  • (PMID = 17200207.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS035122; United States / NCI NIH HHS / CA / R01 CA090851; United States / NINDS NIH HHS / NS / R29 NS035122; United States / NINDS NIH HHS / NS / NS35122; United States / NCI NIH HHS / CA / CA90851
  • [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 / Enzyme Inhibitors; 0 / Pyrones; 0 / RNA, Small Interfering; 56937-68-9 / phorbolol myristate acetate; EC 2.7.11.13 / Protein Kinase C; EC 3.4.24.35 / Matrix Metalloproteinase 9; NI40JAQ945 / Tetradecanoylphorbol Acetate; SSJ18CG55E / hispidin
  • [Other-IDs] NLM/ PMC1762693
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56. Mantovani G, Bondioni S, Ferrero S, Gamba B, Ferrante E, Peverelli E, Corbetta S, Locatelli M, Rampini P, Beck-Peccoz P, Spada A, Lania AG: Effect of cyclic adenosine 3',5'-monophosphate/protein kinase a pathway on markers of cell proliferation in nonfunctioning pituitary adenomas. J Clin Endocrinol Metab; 2005 Dec;90(12):6721-4
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  • [Title] Effect of cyclic adenosine 3',5'-monophosphate/protein kinase a pathway on markers of cell proliferation in nonfunctioning pituitary adenomas.
  • In particular, activating mutations of the G(s)alpha gene and protein kinase A (PKA) overactivity due to low expression of PKA regulatory subunit 1A (R1A) have been implicated in somatotroph proliferation.
  • OBJECTIVE: The objective of this study was to evaluate the effects of cAMP-PKA cascade activation in nonfunctioning pituitary adenomas (NFPA).
  • DESIGN AND METHODS: By immunohistochemistry, R1A, R2A, and R2B expression was evaluated in cells obtained from eight surgically removed NFPA positive for gonadotropins.
  • CONCLUSIONS: These data show that in contrast with what was previously observed in transformed somatotrophs, activation of the cAMP-PKA pathway did not generate proliferative signals in tumoral cells of the gonadotroph lineage, and in a subset of tumors even exerted a tonic inhibitory effect, thus confirming a different role for the cAMP-mediated pathway in promoting proliferation in the pituitary.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Biomarkers, Tumor / metabolism. Cyclic AMP / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology
  • [MeSH-minor] Base Sequence. Cell Proliferation. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit. Cyclin D1 / metabolism. Enzyme Activation. Humans. In Vitro Techniques. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Proteins / genetics. Proteins / metabolism. Receptors, Cell Surface / metabolism

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  • (PMID = 16204369.001).
  • [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 / Biomarkers, Tumor; 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Proteins; 0 / Receptors, Cell Surface; 136601-57-5 / Cyclin D1; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
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57. 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:.
  • For the diagnosis of HNF-1alpha-inactivated HCA, the positive predictive value of homogeneous signal dropout on chemical shift images was 100%, the negative predictive value was 94.7%, the sensitivity was 86.7%, and the specificity was 100%.
  • Marked hypersignal on T2W sequences associated with delayed persistent enhancement had a positive predictive value of 88.5%, a negative predictive value of 84%, a sensitivity of 85.2%, and a specificity of 87.5% for the diagnosis of inflammatory HCA.
  • [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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58. Mikkelsen CS, Mikkelsen DB, Vestergaard V, Clemmensen O, Nielsen HO, Bygum A: [Glucagonoma syndrome without diabetes mellitus]. Ugeskr Laeger; 2008 Nov 17;170(47):3876
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  • [Title] [Glucagonoma syndrome without diabetes mellitus].
  • Computerised tomography and endoscopic ultrasound showed a solid tumour of the pancreas.
  • A blood sample showed an increased level of glucagon without diabetes.
  • Glucagonoma syndrome is characterized by glucagon overproduction, diabetes, depression, deep venous thrombosis and necrolytic migrating erythema.
  • Glucagonoma is frequently diagnosed late which increases the risk of metastases.
  • It is important not to rule out glucagonoma in patients with a relevant clinical picture but without diabetes.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • [CommentIn] Ugeskr Laeger. 2008 Dec 15;170(51):4241; author reply 4241 [19160469.001]
  • (PMID = 19014744.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Denmark
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59. 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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  • [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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60. Shibata H, Takano H, Ito M, Shioya H, Hirota M, Matsumoto H, Kakudo Y, Ishioka C, Akiyama T, Kanegae Y, Saito I, Noda T: Alpha-catenin is essential in intestinal adenoma formation. Proc Natl Acad Sci U S A; 2007 Nov 13;104(46):18199-204
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  • [Title] Alpha-catenin is essential in intestinal adenoma formation.
  • Although the molecular mechanism of tumor initiation is complex, several modifier genes have been identified using mouse models, including the ApcMin mouse.
  • Among the familial adenomatous polyposis mouse lines carrying a truncation mutation at codon 580 in Apc (Apc580D), one line (line19-Apc(580D/+)) showed a remarkably reduced incidence of intestinal adenomas (<5% compared with other lines).
  • Extensive genetic analysis identified a deletion in the alpha-catenin (Ctnna1) gene as the cause of this suppression.
  • In all adenomas generated in line19-Apc(580D/+), somatic recombination between the Apc and Ctnna1 loci retained the wild-type Ctnna1 allele.
  • These data strongly indicate that simultaneous inactivation of alpha-catenin and Apc during tumor initiation suppresses adenoma formation in line19-Apc(580D/+), suggesting that alpha-catenin plays an essential role in the initiation of intestinal adenomas.
  • Although accumulating evidence obtained from human colon tumors with invasive or metastatic potential has established a tumor-suppressive role for alpha-catenin in late-stage tumorigenesis, the role of alpha-catenin in the initiation of intestinal tumorigenesis is not well documented, especially compared with that of beta-catenin.
  • A mouse model used in this study focused on the early stage of tumor initiation and clearly indicated an essential role for alpha-catenin.
  • Thus, alpha-catenin has dual roles in intestinal tumorigenesis, a supporting role in tumor initiation, and a suppressive role in tumor progression.
  • [MeSH-major] Adenoma / pathology. Intestinal Neoplasms / pathology. alpha Catenin / physiology

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  • [Cites] J Biol Chem. 2004 Oct 8;279(41):43061-9 [15292248.001]
  • [Cites] Cancer Cell. 2006 Nov;10(5):437-49 [17097565.001]
  • [Cites] Cell. 1991 Aug 9;66(3):601-13 [1678319.001]
  • [Cites] Science. 1991 Aug 9;253(5020):665-9 [1651563.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 1;90(7):2846-50 [8385345.001]
  • [Cites] Hum Mol Genet. 1992 Jul;1(4):229-33 [1338904.001]
  • [Cites] Cell. 1995 Jun 16;81(6):957-66 [7781071.001]
  • [Cites] Cancer Res. 1995 Oct 15;55(20):4722-8 [7553655.001]
  • [Cites] Science. 1996 May 17;272(5264):1023-6 [8638126.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Feb 4;94(3):901-6 [9023354.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1402-7 [9037065.001]
  • [Cites] Science. 1997 Mar 21;275(5307):1787-90 [9065402.001]
  • [Cites] Nat Genet. 1997 Sep;17(1):88-91 [9288104.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):1070-6 [10706126.001]
  • [Cites] J Biol Chem. 2000 Jul 21;275(29):21883-8 [10896949.001]
  • [Cites] Cancer Res. 2000 Jul 15;60(14):3965-70 [10919675.001]
  • [Cites] Cell. 2001 Feb 23;104(4):605-17 [11239416.001]
  • [Cites] Nat Genet. 2001 Jun;28(2):169-72 [11381266.001]
  • [Cites] J Biol Chem. 2001 Oct 19;276(42):39094-102 [11483600.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):297-302 [11756652.001]
  • [Cites] Curr Biol. 2002 Jan 22;12(2):95-104 [11818059.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Feb 5;99(3):1521-6 [11818567.001]
  • [Cites] Jpn J Cancer Res. 2002 Sep;93(9):1020-8 [12359056.001]
  • [Cites] Nat Genet. 2003 Jan;33(1):33-9 [12447373.001]
  • [Cites] Nat Rev Mol Cell Biol. 2004 Aug;5(8):614-25 [15366705.001]
  • [Cites] Science. 1997 Oct 3;278(5335):120-3 [9311916.001]
  • [Cites] J Biol Chem. 1997 Oct 3;272(40):24735-8 [9312064.001]
  • [Cites] J Cell Biol. 1997 Nov 17;139(4):1033-46 [9362521.001]
  • [Cites] Annu Rev Cell Dev Biol. 1997;13:119-46 [9442870.001]
  • [Cites] Science. 1998 Apr 24;280(5363):596-9 [9554852.001]
  • [Cites] J Surg Oncol. 1998 Jun;68(2):92-9 [9624037.001]
  • [Cites] Science. 1998 Sep 4;281(5382):1509-12 [9727977.001]
  • [Cites] J Cell Biol. 1999 Mar 22;144(6):1311-22 [10087272.001]
  • [Cites] Nature. 1999 Apr 1;398(6726):422-6 [10201372.001]
  • [Cites] J Cell Biol. 1999 Sep 6;146(5):967-80 [10477752.001]
  • [Cites] Science. 1989 Apr 14;244(4901):207-11 [2565047.001]
  • (PMID = 17989230.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / alpha Catenin
  • [Other-IDs] NLM/ PMC2084320
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61. Salehi F, Kovacs K, Scheithauer BW, Cantelmi D, Horvath E, Lloyd RV, Cusimano M: Immunohistochemical expression of pituitary tumor transforming gene (PTTG) in pituitary adenomas: a correlative study of tumor subtypes. Int J Surg Pathol; 2010 Feb;18(1):5-13
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  • [Title] Immunohistochemical expression of pituitary tumor transforming gene (PTTG) in pituitary adenomas: a correlative study of tumor subtypes.
  • OBJECTIVE: We investigated the correlation between immunohistochemical expression of the pituitary tumor transforming gene (PTTG) and pituitary adenoma subtype.
  • METHODS: Pituitary adenomas (n = 89) were stained for PTTG using the streptavidin-biotin-peroxidase complex method and a monoclonal PTTG antibody.
  • Reactivity was highest in growth hormone (GH) adenomas as compared with other tumors, including prolactin (PRL), follicle-stimulating hormone/luteinizing hormone/alpha subunit, as well as adrenocorticotrophic hormone-secreting adenomas.
  • PRL adenomas exhibited the lowest expression levels.
  • Among GH adenomas, untreated tumors demonstrated significantly higher PTTG levels than octreotide-treated examples.
  • Although dopamine agonist-treated PRL adenomas tended to show lower expression levels, statistical significance was not reached.
  • CONCLUSIONS: Our finding that PTTG was differentially expressed in pituitary adenoma subtypes suggests a cell-specific function for PTTG.
  • Moreover, treatment of GH adenomas with somatostatin analogues lowered PTTG expression.
  • Further investigation into mechanisms mediating cell-specific expression of PTTG is warranted.
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Biomarkers, Tumor / metabolism. Bromocriptine / therapeutic use. Hormone Antagonists / therapeutic use. Humans. Immunoenzyme Techniques. Octreotide / therapeutic use. Securin

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  • (PMID = 20106827.001).
  • [ISSN] 1940-2465
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Hormone Antagonists; 0 / Neoplasm Proteins; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human; 3A64E3G5ZO / Bromocriptine; RWM8CCW8GP / Octreotide
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62. Pelletier L, Rebouissou S, Paris A, Rathahao-Paris E, Perdu E, Bioulac-Sage P, Imbeaud S, Zucman-Rossi J: Loss of hepatocyte nuclear factor 1alpha function in human hepatocellular adenomas leads to aberrant activation of signaling pathways involved in tumorigenesis. Hepatology; 2010 Feb;51(2):557-66
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  • [Title] Loss of hepatocyte nuclear factor 1alpha function in human hepatocellular adenomas leads to aberrant activation of signaling pathways involved in tumorigenesis.
  • Hepatocellular adenomas (HCAs) are benign liver tumors that usually develop in women who are taking oral contraceptives.
  • Among these tumors, biallelic inactivating mutations of the hepatocyte nuclear factor 1alpha (HNF1A) transcription factor have been frequently identified and in rare cases of hepatocellular carcinomas developed in noncirrhotic liver.
  • Because HNF1A meets the genetic criteria of a tumor suppressor gene, we aimed to elucidate the tumorigenic mechanisms related to HNF1alpha inactivation in hepatocytes.
  • Then, we assessed the role of HNF1alpha in the observed deregulations in hepatocellular cell models (HepG2 and Hep3B) by silencing its endogenous expression using small interfering RNA.
  • Along with the previously described induction of glycolysis and lipogenesis, H-HCA also displayed overexpression of several genes encoding growth factor receptors, components of the translation machinery, cell cycle, and angiogenesis regulators, with, in particular, activation of the mammalian target of rapamycin (mTOR) pathway.
  • In the cell model, inhibition of HNF1alpha recapitulated most of these identified transcriptional deregulations, demonstrating that they were related to HNF1alpha inhibition.
  • CONCLUSION: H-HCA showed a combination of alterations related to HNF1alpha inactivation that may cooperate to promote tumor development.
  • [MeSH-major] Adenoma, Liver Cell / etiology. Hepatocyte Nuclear Factor 1-alpha / physiology. Liver Neoplasms / etiology. Signal Transduction
  • [MeSH-minor] Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Humans. Tumor Cells, Cultured

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  • (PMID = 20041408.001).
  • [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 / Hepatocyte Nuclear Factor 1-alpha
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63. Lee TY, Kim KT, Han SY: Expression of ErbB receptor proteins and TGF-alpha during diethylnitrosamine-induced hepatocarcinogenesis in the rat liver. Korean J Hepatol; 2007 Mar;13(1):70-80
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  • [Title] Expression of ErbB receptor proteins and TGF-alpha during diethylnitrosamine-induced hepatocarcinogenesis in the rat liver.
  • In this study the expression of ErbB receptors and TGF-alpha were investigated using an experimental cirrhosis rat model giving rise to hepatocellular neoplasms, similar to human liver diseases.
  • Antibodies for GSTp, TGF-alpha, EGF-R, ErbB2, ErbB3 and ErbB4 were used for immunohistochemistry.
  • Preneoplastic foci, hepatocellular adenomas (HCA) and hepatocellular carcinomas (HCC) were noted from the second, eleventh and fifteenth week, respectively.
  • TGF-alpha was expressed in 92.4% of RN, 91.3% HCA and 93.2% HCC.
  • Sixty eight percent of TGF-alpha expressing nodules showed concurrent EGF-R expression.
  • CONCLUSIONS: Increased expression of EGF-R and decreased expression of ErbB4, might be related with tumor progression during DEN-induced hepatocarcinogenesis.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Liver Neoplasms, Experimental / metabolism. Receptor, Epidermal Growth Factor / metabolism. Receptor, ErbB-2 / metabolism. Transforming Growth Factor alpha / metabolism
  • [MeSH-minor] Adenoma, Liver Cell / chemically induced. Adenoma, Liver Cell / metabolism. Adenoma, Liver Cell / pathology. Animals. Diethylnitrosamine. Glutathione Transferase / metabolism. Immunohistochemistry. Male. Rats. Rats, Wistar. Receptor, ErbB-4


64. Simiantonaki N, Taxeidis M, Jayasinghe C, Kurzik-Dumke U, Kirkpatrick CJ: Hypoxia-inducible factor 1 alpha expression increases during colorectal carcinogenesis and tumor progression. BMC Cancer; 2008;8:320
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  • [Title] Hypoxia-inducible factor 1 alpha expression increases during colorectal carcinogenesis and tumor progression.
  • BACKGROUND: Hypoxia-inducible factor 1 alpha (HIF-1alpha) is involved in processes promoting carcinogenesis of many tumors.
  • METHODS: Immunohistochemistry and Western blot is used to analyse HIF-1alpha expression in normal colonic mucosa, hyperplastic polyps (HPP), sessile serrated adenomas (SSA), low-grade (TA-LGD) and high-grade (TA-HGD) traditional adenomas as well as in non-metastatic and metastatic colorectal adenocarcinomas.
  • Eight colorectal carcinoma cell lines are tested for their HIF-1alpha inducibility after lipopolysaccharide (LPS) stimulation using western blot and immunocytochemistry.
  • In these cases HIF-1alpha activation was seen in viable cohesive tumor epithelia surrounding necrosis and in dissociated tumor cells, which subsequently die.
  • In additional in vitro studies, treatment of diverse colorectal carcinoma cell lines with the potent pro-inflammatory factor lipopolysaccharide (LPS) led to HIF-1alpha expression and nuclear translocation.
  • Perinecrotic activation of HIF-1alpha in invasive tumors underlines a dual role of HIF-1alpha by regulating both pro-survival and pro-death processes.
  • These patterns of HIF-1alpha inducibility could contribute indirectly to the acquisition of a metastatic phenotype.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Colorectal Neoplasms / metabolism. Colorectal Neoplasms / pathology. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Precancerous Conditions / metabolism
  • [MeSH-minor] Cell Line, Tumor. Colonic Polyps / metabolism. Colonic Polyps / pathology. Disease Progression. Humans. Immunohistochemistry. Lipopolysaccharides / pharmacology. Neoplasm Metastasis

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  • [Cites] Clin Colorectal Cancer. 2006 Jan;5(5):350-3 [16512994.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):632-7 [16423989.001]
  • [Cites] Biochem J. 2006 Jun 15;396(3):517-27 [16533170.001]
  • [Cites] Histopathology. 2006 Aug;49(2):121-31 [16879389.001]
  • [Cites] Cancer Res. 1999 Nov 15;59(22):5830-5 [10582706.001]
  • [Cites] Genes Dev. 2000 Jan 1;14(1):34-44 [10640274.001]
  • [Cites] Am J Pathol. 2000 Aug;157(2):411-21 [10934146.001]
  • [Cites] Am J Surg. 2000 Jul;180(1):65-72 [11036145.001]
  • [Cites] J Natl Cancer Inst. 2001 Feb 21;93(4):309-14 [11181778.001]
  • [Cites] Lancet. 2001 Feb 17;357(9255):539-45 [11229684.001]
  • [Cites] J Natl Cancer Inst. 2001 Aug 1;93(15):1175-7 [11481392.001]
  • [Cites] Am J Pathol. 2001 Dec;159(6):2107-16 [11733361.001]
  • [Cites] Nat Rev Cancer. 2002 Jan;2(1):38-47 [11902584.001]
  • [Cites] Exp Mol Pathol. 2002 Aug;73(1):46-53 [12127053.001]
  • [Cites] J Mol Diagn. 2002 Nov;4(4):191-200 [12411586.001]
  • [Cites] J Biol Chem. 2002 Dec 20;277(51):50081-6 [12401798.001]
  • [Cites] World J Gastroenterol. 2006 Aug 7;12(29):4660-4 [16937436.001]
  • [Cites] Br J Cancer. 2007 Jan 15;96(1):95-103 [17179985.001]
  • [Cites] J Mol Med (Berl). 2007 Feb;85(2):139-48 [17180667.001]
  • [Cites] Pathol Oncol Res. 2007;13(1):15-20 [17387384.001]
  • [Cites] Cancer Res. 2007 Apr 1;67(7):3177-84 [17409425.001]
  • [Cites] Cell Oncol. 2007;29(3):219-27 [17452774.001]
  • [Cites] Int J Mol Med. 2007 Jul;20(1):21-9 [17549384.001]
  • [Cites] J Immunol. 2007 Jun 15;178(12):7516-9 [17548584.001]
  • [Cites] Int J Oncol. 2007 Aug;31(2):269-75 [17611682.001]
  • [Cites] World J Gastroenterol. 2007 Jul 28;13(28):3784-91 [17657831.001]
  • [Cites] Methods Enzymol. 2007;435:405-19 [17998066.001]
  • [Cites] Int J Oncol. 2008 Mar;32(3):585-92 [18292935.001]
  • [Cites] Cancer Res. 2003 Mar 1;63(5):1138-43 [12615733.001]
  • [Cites] World J Gastroenterol. 2003 Mar;9(3):491-4 [12632503.001]
  • [Cites] Int J Cancer. 2003 Jun 10;105(2):176-81 [12673675.001]
  • [Cites] Mol Cell Biol. 2003 May;23(9):3265-73 [12697826.001]
  • [Cites] Am J Pathol. 2003 Jun;162(6):1789-806 [12759237.001]
  • [Cites] Nat Rev Cancer. 2003 Oct;3(10):721-32 [13130303.001]
  • [Cites] Blood. 2004 Feb 1;103(3):1124-30 [14525767.001]
  • [Cites] Cancer Detect Prev. 2004;28(2):88-93 [15068831.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):3082-90 [15131047.001]
  • [Cites] Shock. 2004 Sep;22(3):270-7 [15316398.001]
  • [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] Immunobiology. 1993 Apr;187(3-5):212-26 [7687233.001]
  • [Cites] Oncologist. 2004;9 Suppl 5:10-7 [15591418.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8554-60 [15623639.001]
  • [Cites] Am J Pathol. 2005 Apr;166(4):1069-75 [15793287.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4690-7 [15930287.001]
  • [Cites] Nat Clin Pract Oncol. 2005 Aug;2(8):398-405 [16130936.001]
  • [Cites] Cancer Lett. 2006 Jun 8;237(1):10-21 [16002209.001]
  • (PMID = 18983642.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Lipopolysaccharides
  • [Other-IDs] NLM/ PMC2584660
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65. Furuse C, Sousa SO, Nunes FD, Magalhães MH, Araújo VC: Myoepithelial cell markers in salivary gland neoplasms. Int J Surg Pathol; 2005 Jan;13(1):57-65
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  • [Title] Myoepithelial cell markers in salivary gland neoplasms.
  • We compared the immunoexpression of 5 myoepithelial cell (MEC) markers (alpha-smooth-muscle actin, calponin, h-caldesmon, vimentin, and S-100-protein) using 16 pleomorphic adenomas (PA), 15 adenoid cystic carcinomas (ACC), and 3 epithelial-myoepithelial carcinomas (EMC) of salivary glands.
  • The alpha-smooth-muscle actin was useful for identification of MECs, especially in cribriform and tubular ACC, followed by EMC.
  • Calponin was similar to alpha-smooth-muscle actin, except for polygonal and plasmacytoid cells of PA and for solid ACC, which showed alpha-smooth-muscle actin negative and calponin positive.
  • Vimentin immunostained all MEC types, and was negative in luminal cells.
  • S-100 protein was expressed both in the nuclei and cytoplasm of MECs and luminal cells, especially in PA.
  • The best way to identify MEC is using alpha-smooth-muscle actin or calponin, plus vimentin, since in tumors MECs are hardly ever fully differentiated.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Biomarkers, Tumor / metabolism. Carcinoma, Adenoid Cystic / metabolism. Myoepithelioma / metabolism. Salivary Gland Neoplasms / metabolism

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  • (PMID = 15735856.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / Microfilament Proteins; 0 / S100 Proteins; 0 / Vimentin; 0 / calponin
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66. Raverot G, Arnous W, Calender A, Trouillas J, Sassolas G, Bournaud C, Pugeat M, Borson-Chazot F: Familial pituitary adenomas with a heterogeneous functional pattern: clinical and genetic features. J Endocrinol Invest; 2007 Oct;30(9):787-90
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  • [Title] Familial pituitary adenomas with a heterogeneous functional pattern: clinical and genetic features.
  • Familial pituitary adenoma is a rare syndrome which may present either as isolated lesions, or in association with other endocrine tumors, for example in the frame of multiple endocrine neoplasia (MEN-1) or Carney complex (CNC).
  • The most frequently described forms of familial isolated pituitary adenoma (FIPA) are familial somatotropinomas or prolactinomas.
  • The present report shows heterogeneous FIPA with 3 subtypes of tumor in 3 individuals of the same family: somatotropinoma in the proband, giant prolactinoma in a brother, and gonadotroph cell macroadenoma in the father.
  • A prospective survey also suggested the occurrence of a silent microadenoma in the proband's sister.
  • Genetic screening for germline mutation of the MEN-1, the gene encoding the protein kinase A (PKA) type 1 alpha regulatory subunit (R1 alpha) (PRKAR1alpha) and AIP gene was negative in 2 affected members.
  • In conclusion, these data suggest that familial pituitary adenomas can occur with a heterogeneous functional pattern that is distinguished from MEN-1 or CNC.
  • [MeSH-major] Adenoma / genetics. Adenoma / physiopathology. Pituitary Neoplasms / genetics. Pituitary Neoplasms / physiopathology
  • [MeSH-minor] Female. Genetic Predisposition to Disease / genetics. Genetic Testing. Humans. Male. Middle Aged. Pedigree. Polymorphism, Single Nucleotide / genetics. Proto-Oncogene Proteins / genetics. Receptors, Aryl Hydrocarbon / genetics

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  • (PMID = 17993773.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Aryl Hydrocarbon
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67. Florio T, Barbieri F, Spaziante R, Zona G, Hofland LJ, van Koetsveld PM, Feelders RA, Stalla GK, Theodoropoulou M, Culler MD, Dong J, Taylor JE, Moreau JP, Saveanu A, Gunz G, Dufour H, Jaquet P: Efficacy of a dopamine-somatostatin chimeric molecule, BIM-23A760, in the control of cell growth from primary cultures of human non-functioning pituitary adenomas: a multi-center study. Endocr Relat Cancer; 2008 Jun;15(2):583-96
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  • [Title] Efficacy of a dopamine-somatostatin chimeric molecule, BIM-23A760, in the control of cell growth from primary cultures of human non-functioning pituitary adenomas: a multi-center study.
  • Dopamine D2 and somatostatin receptors (sstrs) were reported to affect non-functioning pituitary adenoma (NFPA) proliferation in vitro.
  • We established an experimental protocol allowing reproducible evaluation of NFPA cell proliferation in vitro, to test and compare the antiproliferative effects of dopamine and somatostatin analogs (alone or in combination) with the activity of the dopamine-somatostatin chimeric molecule BIM-23A760.
  • The protocol was utilized by four independent laboratories, studying 38 fibroblast-deprived NFPA cell cultures.
  • Cells were characterized for GH, POMC, sstr1-sstr5, total dopamine D2 receptor (D2R) (in all cases), and D2 receptor long and short isoforms (in 15 out of 38 cases) mRNA expression and for alpha-subunit, LH, and FSH release.
  • BIM-23A760 effects were similar to those induced by the selective D2R agonist cabergoline that showed a statistically significant inhibition in 18 out of 27 tumors (compared with a significant inhibition obtained in 17 out of 27 tumors using BIM-23A760, in the same subgroup of adenomas analyzed), while octreotide was effective in 13 out of 27 cases.
  • In conclusion, superimposable data generated in four independent laboratories using a standardized protocol demonstrate that, in vitro, chimeric dopamine/sstr agonists are effective in inhibiting cell proliferation in two-thirds of NFPAs.
  • [MeSH-major] Adenoma / drug therapy. Adenoma / pathology. Dopamine / analogs & derivatives. Pituitary Neoplasms / drug therapy. Pituitary Neoplasms / pathology. Somatostatin / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents, Hormonal / pharmacology. Cell Division / drug effects. Dopamine Antagonists / pharmacology. Dose-Response Relationship, Drug. Ergolines / pharmacology. Female. Fibroblasts / cytology. Humans. Male. Middle Aged. Octreotide / pharmacology. RNA, Messenger / metabolism. Receptors, Dopamine D2 / genetics. Receptors, Somatostatin / genetics. Sulpiride / pharmacology. Thymidine / metabolism. Tritium. Tumor Cells, Cultured

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  • (PMID = 18509006.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / BIM 23A760; 0 / Dopamine Antagonists; 0 / Ergolines; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 3; 10028-17-8 / Tritium; 51110-01-1 / Somatostatin; 7MNE9M8287 / Sulpiride; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide; VC2W18DGKR / Thymidine; VTD58H1Z2X / Dopamine
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68. Krysiak R, Okopień B, Herman ZS: [Rare pancreatic endocrine tumors]. Przegl Lek; 2008;65(4):209-16
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  • [Title] [Rare pancreatic endocrine tumors].
  • [Transliterated title] Rzadkie guzy endokrynne trzustki.
  • Functional pancreatic endocrine tumors other than gastrinoma and insulinoma are quite rare.
  • Some of these tumors may be part of multiple endocrine neoplasia type one (MEN-1) syndrome or phakomatoses.
  • Depending on their cell type, functional pancreatic endocrine tumors may cause distinct clinical endocrine syndromes, such as the 'glucagonoma syndrome', Verner-Morrison syndrome and the 'somatostatinoma syndrome'.
  • Currently, the only curative treatment for islet cell tumors is complete surgical resection.
  • The medical treatment of endocrine pancreatic tumours consists of somatostatin analogues, chemotherapy, and interferon-alpha.
  • The purpose of this manuscript is to provide an overview of the contemporary etiopathogenesis, diagnosis and treatment of rare pancreatic endocrine tumors.
  • [MeSH-major] Glucagonoma / diagnosis. Glucagonoma / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy. Somatostatinoma / diagnosis. Somatostatinoma / therapy. Vipoma / diagnosis. Vipoma / therapy
  • [MeSH-minor] Humans. Rare Diseases / diagnosis. Rare Diseases / therapy

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  • (PMID = 18724549.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 47
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69. Nakashima H, Komine M, Sasaki K, Mitsui H, Fujimoto M, Ihn H, Asahina A, Kikuchi K, Tamaki K: Necrolytic migratory erythema without glucagonoma in a patient with short bowel syndrome. J Dermatol; 2006 Aug;33(8):557-62
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  • [Title] Necrolytic migratory erythema without glucagonoma in a patient with short bowel syndrome.
  • While it is typically associated with glucagonoma, some cases of NME without glucagonoma have been reported.
  • Her laboratory data revealed essential amino acid deficiency and a slightly decreased serum zinc level, while her plasma glucagon level was low.
  • With diagnosis of non-glucagonoma-associated NME with malabsorption due to short-bowel syndrome, she was treated and improved by i.v. amino acid supplement.
  • Histological findings of NME include necrotic changes of keratinocytes in the upper epidermis, proliferation of those in the lower epidermis and inflammatory cell infiltration of upper dermis.
  • [MeSH-major] Erythema / etiology. Short Bowel Syndrome / complications
  • [MeSH-minor] Cell Differentiation. Cell Proliferation. Female. Humans. Keratinocytes / pathology. Keratinocytes / physiology. Keratins / metabolism. Middle Aged


70. Gutiérrez V, Cobo M, Olea D, García J, Ramírez C, Bautista D, Alcalde J: Glucagonoma with two pancreatic masses and pulmonary metastases as debut of MEN-1. Clin Transl Oncol; 2007 Oct;9(10):674-7
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  • [Title] Glucagonoma with two pancreatic masses and pulmonary metastases as debut of MEN-1.
  • This is a rare case of a patient with type 1 multiple endocrine neoplasia (MEN-1) syndrome.
  • The case is further unusual in that the glucagonoma debuted with two synchronic pancreatic masses at the time of diagnosis and with pulmonary metastases as the primary site of metastasis and not the more usual site of the liver.
  • [MeSH-major] Glucagonoma / radionuclide imaging. Lung Neoplasms / radionuclide imaging. Multiple Endocrine Neoplasia Type 1 / radionuclide imaging. Pancreatic Neoplasms / radionuclide imaging

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  • (PMID = 17974529.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Spain
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71. Tannehill-Gregg SH, Sanderson TP, Minnema D, Voelker R, Ulland B, Cohen SM, Arnold LL, Schilling BE, Waites CR, Dominick MA: Rodent carcinogenicity profile of the antidiabetic dual PPAR alpha and gamma agonist muraglitazar. Toxicol Sci; 2007 Jul;98(1):258-70
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  • [Title] Rodent carcinogenicity profile of the antidiabetic dual PPAR alpha and gamma agonist muraglitazar.
  • The carcinogenic potential of muraglitazar, a dual human peroxisome proliferator-activated receptor alpha/gamma agonist, was evaluated in 2-year studies in mice (1, 5, 20, and 40 mg/kg) and rats (1, 5, 30, and 50 mg/kg).
  • Benign gallbladder adenomas occurred at low incidences in male mice at 20 and 40 mg/kg (area under the curve [AUC] exposures > or = 62 times human exposure at 5 mg/day) and were considered drug related due to an increased incidence of gallbladder mucosal hyperplasia at these doses.
  • There was a dose-related increased incidence of transitional cell papilloma and carcinoma of the urinary bladder in male rats at 5, 30, and 50 mg/kg (AUC exposures > or = 8 times human exposure at 5 mg/day).
  • At 30 and 50 mg/kg, the urinary bladder tumors were accompanied by evidence of increased urine solids.
  • Considering that muraglitazar is nongenotoxic, the observed tumorigenic effects in mice and rats have no established clinical relevance since they occurred at either clinically nonrelevant exposures (gallbladder and adipose tumors) or by a species-specific mechanism (urinary bladder tumors).
  • [MeSH-major] Carcinogens. Glycine / analogs & derivatives. Hypoglycemic Agents / toxicity. Oxazoles / toxicity. PPAR alpha / agonists. PPAR gamma / agonists

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  • (PMID = 17426106.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Hypoglycemic Agents; 0 / Oxazoles; 0 / PPAR alpha; 0 / PPAR gamma; TE7660XO1C / Glycine; W1MKM70WQI / muraglitazar
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72. Stark I, Mensing CH, Sander CA: [Necrolytic migratory erythema in glucagonoma syndrome]. Hautarzt; 2008 Jan;59(1):50-3
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  • [Title] [Necrolytic migratory erythema in glucagonoma syndrome].
  • The glucagonoma syndrome is a rare disease in which a typical skin lesion, necrolytic migratory erythema, is often one of the presenting symptoms.
  • Skin biopsies, laboratory studies and imaging confirmed the diagnosis of necrolytic migratory erythema as part of a glucagonoma syndrome.
  • [MeSH-major] Ciprofloxacin / administration & dosage. Erythema / diagnosis. Erythema / drug therapy. Glucagonoma / diagnosis. Glucagonoma / drug therapy
  • [MeSH-minor] Administration, Oral. Aged. Anti-Infective Agents / administration & dosage. Female. Humans. Necrosis / diagnosis. Necrosis / drug therapy. Syndrome. Treatment Outcome

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  • [Cites] J Clin Oncol. 2003 Jul 15;21(14 ):2689-96 [12860945.001]
  • [Cites] Med Oncol. 2002;19(1):35-42 [12025889.001]
  • [Cites] Proc R Soc Med. 1971 Dec;64(12):1197-8 [5131260.001]
  • [Cites] J Exp Clin Cancer Res. 2006 Mar;25(1):135-9 [16761630.001]
  • [Cites] Medicine (Baltimore). 1996 Mar;75(2):53-63 [8606627.001]
  • [Cites] JOP. 2004 Jul;5(4):179-85 [15254346.001]
  • [Cites] J Am Acad Dermatol. 1995 Apr;32(4):604-9 [7896950.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2005 Oct;19(5):753-81 [16253899.001]
  • (PMID = 17549440.001).
  • [ISSN] 1432-1173
  • [Journal-full-title] Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete
  • [ISO-abbreviation] Hautarzt
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 5E8K9I0O4U / Ciprofloxacin
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73. Romano D, Magalon K, Pertuit M, Rasolonjanahary R, Barlier A, Enjalbert A, Gerard C: Conditional overexpression of the wild-type Gs alpha as the gsp oncogene initiates chronic extracellularly regulated kinase 1/2 activation and hormone hypersecretion in pituitary cell lines. Endocrinology; 2007 Jun;148(6):2973-83
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  • [Title] Conditional overexpression of the wild-type Gs alpha as the gsp oncogene initiates chronic extracellularly regulated kinase 1/2 activation and hormone hypersecretion in pituitary cell lines.
  • In pituitary cells, activation of the cAMP pathway by specific G protein-coupled receptors controls differentiative functions and proliferation.
  • Constitutively active forms of the alpha subunit of the heterotrimeric G(s) protein resulting from mutations at codon 201 or 227 (gsp oncogene) were first identified in 30-40% of human GH-secreting pituitary adenomas.
  • This rate of occurrence suggests that the gsp oncogene is not responsible for initiating the majority of these tumors.
  • Moreover, there is a large overlap between the clinical phenotypes observed in patients with tumors bearing the gsp oncogene and those devoid of this oncogene.
  • To explore the role of G(s)alpha in GH-secreting adenomas, we obtained somatolactotroph GH4C1 cell lines by performing doxycycline-dependent conditional overexpression of the wild-type G(s)alpha protein and expression of the gsp oncogene.
  • Although the resulting adenylyl cyclase and cAMP levels were 10-fold lower in the wild-type G(s)alpha-overexpressing cell line, a sustained MAPK ERK1/2 activation was observed in both cell lines.
  • Overexpression of the wild-type G(s)alpha protein as the gsp oncogene initiated chronic activation of endogenous prolactin synthesis and release, as well as chronic activation of ERK1/2-sensitive human prolactin and GH promoters.
  • [MeSH-major] GTP-Binding Protein alpha Subunits, Gs / genetics. Gene Expression Regulation, Enzymologic. Growth Hormone / secretion. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Prolactin / secretion. Somatotrophs / metabolism
  • [MeSH-minor] Adenylyl Cyclases / metabolism. Animals. Cell Line. Cyclic AMP / metabolism. Doxycycline / pharmacology. Enzyme Activation. Oncogene Proteins / genetics. Rats. Time Factors. Transfection. Transgenes / drug effects

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  • (PMID = 17363453.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone; E0399OZS9N / Cyclic AMP; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.6.1.- / Gnas protein, rat; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs; EC 4.6.1.1 / Adenylyl Cyclases; N12000U13O / Doxycycline
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74. Hays T, Rusyn I, Burns AM, Kennett MJ, Ward JM, Gonzalez FJ, Peters JM: Role of peroxisome proliferator-activated receptor-alpha (PPARalpha) in bezafibrate-induced hepatocarcinogenesis and cholestasis. Carcinogenesis; 2005 Jan;26(1):219-27
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  • [Title] Role of peroxisome proliferator-activated receptor-alpha (PPARalpha) in bezafibrate-induced hepatocarcinogenesis and cholestasis.
  • Peroxisome proliferator-activated receptor-alpha (PPARalpha) is required to mediate alterations in PPARalpha target gene expression, repress apoptosis, enhance replicative DNA synthesis, oxidative stress to DNA and hepatocarcinogenesis induced by the relatively specific PPARalpha agonist, Wy-14,643.
  • Increased levels of mRNA encoding cell cycle regulatory proteins and DNA repair enzymes were found in (+/+) mice fed bezafibrate, and this effect was not found in (-/-) mice.
  • In mice fed bezafibrate for 1 year, preneoplastic foci, adenomas and a hepatocellular carcinoma were found in (+/+) mice, while only a single microscopic adenoma was found in one (-/-) mouse.
  • [MeSH-major] Bezafibrate / metabolism. Cholestasis / chemically induced. Liver Neoplasms / metabolism. PPAR alpha / deficiency. Peroxisome Proliferators / toxicity
  • [MeSH-minor] Acyl-CoA Oxidase / drug effects. Acyl-CoA Oxidase / metabolism. Animals. Bile Acids and Salts / metabolism. Blotting, Northern. Cell Cycle Proteins / drug effects. Cell Cycle Proteins / metabolism. Cytochrome P-450 CYP4A / drug effects. Cytochrome P-450 CYP4A / metabolism. DNA Repair Enzymes / drug effects. DNA Repair Enzymes / metabolism. DNA-Binding Proteins / drug effects. DNA-Binding Proteins / metabolism. Disease Models, Animal. Male. Mice. RNA, Messenger / analysis. Receptors, Cytoplasmic and Nuclear. Transcription Factors / drug effects. Transcription Factors / metabolism

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  • (PMID = 15447978.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA89607; United States / NCI NIH HHS / CA / CA97999
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / PPAR alpha; 0 / Peroxisome Proliferators; 0 / RNA, Messenger; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Transcription Factors; 0 / farnesoid X-activated receptor; EC 1.14.15.3 / Cytochrome P-450 CYP4A; EC 1.3.3.6 / Acyl-CoA Oxidase; EC 6.5.1.- / DNA Repair Enzymes; Y9449Q51XH / Bezafibrate
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75. Obi N, Katabami T, Obi R, Odanaka M, Sasano K, Tanaka Y: Primary malignant hepatic glucagonoma: an autopsy case. Endocr J; 2009;56(5):715-9
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  • [Title] Primary malignant hepatic glucagonoma: an autopsy case.
  • She displayed the signs and symptoms of glucagonoma syndrome, including necrolytic migratory erythema (NME), low aminoacidemia, and a marked increase of the serum glucagon level (4,940 pg/ ml).
  • Thus, we suspected a glucagonoma causing secondary diabetes.
  • However, we could not detect any mass in the pancreas or the gastrointestinal tract, and only found a liver lesion resembling a hemangioma.
  • At autopsy, the only tumor detected was the liver mass.
  • This was a large solid tumor (8 x 6 x 5 cm) with a pattern of white and dark brown stripes located in the left lobe, while two white nodules were also found in the right lobe.
  • Based on the histopathological and immunohistochemical findings, the liver lesion was shown to be a malignant glucagonoma with intrahepatic metastases.
  • Since primary malignant hepatic glucagonoma has not been reported before, we present this extremely rare case of primary malignant glucagonoma of the liver.
  • [MeSH-major] Diabetes Mellitus, Type 2 / etiology. Glucagonoma / pathology. Liver Neoplasms / pathology

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  • (PMID = 19367016.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Amino Acids
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76. Muinelo-Romay L, Vázquez-Martín C, Villar-Portela S, Cuevas E, Gil-Martín E, Fernández-Briera A: Expression and enzyme activity of alpha(1,6)fucosyltransferase in human colorectal cancer. Int J Cancer; 2008 Aug 1;123(3):641-6
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  • [Title] Expression and enzyme activity of alpha(1,6)fucosyltransferase in human colorectal cancer.
  • Changes in enzyme activity and the expression levels of alpha(1,6)fucosyltransferase [alpha(1,6)FT] have been reported in certain types of malignant transformations.
  • To develop a better understanding of the role of alpha(1,6)FT in human colorectal carcinoma (CRC), we analysed the enzyme activity in healthy and tumour tissues. alpha(1,6)FT activity was considerably higher in tumour tissue than in healthy tissue and was related to gender, lymph node metastasis, type of growth and tumour stage.
  • We also observed a significant increase in the alpha(1,6)FT expression in tumour tissues as compared to healthy and transitional tissues, inflammatory lesions and adenomas.
  • The immunohistochemical expression in tumour tissues was correlated with the degree of infiltration through the intestinal wall.
  • All these findings demonstrate an alteration of alpha(1,6)FT activity and expression in CRC.
  • [MeSH-major] Adenocarcinoma / enzymology. Biomarkers, Tumor / metabolism. Colorectal Neoplasms / enzymology. Fucosyltransferases / metabolism
  • [MeSH-minor] Adenoma / enzymology. Aged. Blotting, Western. Cell Transformation, Neoplastic. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male

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  • (PMID = 18491404.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.4.1.- / Fucosyltransferases; EC 2.4.1.68 / Glycoprotein 6-alpha-L-fucosyltransferase
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77. Radny P, Eigentler TK, Soennichsen K, Overkamp D, Raab HR, Viebahn R, Mueller-Horvart C, Sotlar K, Rassner G: Metastatic glucagonoma: treatment with liver transplantation. J Am Acad Dermatol; 2006 Feb;54(2):344-7
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  • [Title] Metastatic glucagonoma: treatment with liver transplantation.
  • Glucagonoma is a rare pancreatic endocrine tumor that is often both well developed and malignant at detection.
  • We hope to familiarize dermatologists and other specialists with this rare and potentially fatal disorder because early recognition of necrolytic migratory erythema, a clinical feature that may appear in patients with glucagonoma, can lead to possible cure, whereas delayed identification of the disease is associated with metastatic disease and a poor prognosis.
  • We report the case of a 57-year-old patient with a metastatic glucagon-producing tumor; necrolytic migratory erythema was diagnosed and was successfully treated by a multimodal intervention including liver transplantation.
  • Currently, 72 months after transplantation, our patient is in complete remission, which has been verified by somatostatin receptor scintigraphy monitoring, computed tomographic scanning and glucagon serum control.
  • Increased awareness of the clinical symptoms and visible polymorphic mucocutaneous and nonspecific histopathologic features of glucagonoma syndrome is needed to avoid unnecessary delay in the diagnosis of this syndrome.
  • [MeSH-major] Glucagonoma / secondary. Glucagonoma / surgery. Liver Neoplasms / secondary. Liver Neoplasms / surgery. Liver Transplantation. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Glucagon / blood. Humans. Immunohistochemistry. Male. Middle Aged. Octreotide / administration & dosage. Pancreatectomy. Receptors, Somatostatin / metabolism. Splenectomy


78. Letsas KP, Vartholomatos G, Tsepi C, Tsatsoulis A, Frangou-Lazaridis M: Fine-needle aspiration biopsy-RT-PCR expression analysis of prothymosin alpha and parathymosin in thyroid: novel proliferation markers? Neoplasma; 2007;54(1):57-62
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  • [Title] Fine-needle aspiration biopsy-RT-PCR expression analysis of prothymosin alpha and parathymosin in thyroid: novel proliferation markers?
  • Genetic analysis of the aspirates by RT-PCR may contribute, in parallel to the cytology report, to a more precise diagnosis.
  • Prothymosin alpha and parathymosin are two homologous chromatin remodeling proteins essential for cell cycle progression and proliferation of either normal or malignant cells.
  • A semi-quantitative RT-PCR assay was developed to determine prothymosin alpha and parathymosin mRNA expression patterns in thyroid follicular cells obtained from the fine-needle aspiration biopsy specimens of patients diagnosed with simple nodular goitre, follicular adenoma, papillary and follicular well-differentiated carcinomas.
  • Prothymosin alpha and parathymosin mRNA levels were found significantly elevated in well-differentiated carcinomas in relation to adenomas (p<0.05) and goitres (p<0.05), an event possibly linked to the proliferation activity of thyroid follicular cells.
  • Further studies are required to establish prothymosin alpha and parathymosin as diagnostic proliferation markers in thyroid cancer, especially in cases of undetermined cellular morphology of follicular origin which reflect the most common cytohistopathological discrepancies.
  • [MeSH-minor] Adenocarcinoma, Follicular / genetics. Adenocarcinoma, Follicular / pathology. Adult. Aged. Biomarkers / analysis. Biopsy, Fine-Needle / methods. Carcinoma, Papillary / genetics. Carcinoma, Papillary / pathology. Cell Proliferation. Diagnosis, Differential. Female. Humans. Male. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reproducibility of Results. Reverse Transcriptase Polymerase Chain Reaction / methods. Thyroid Nodule / genetics. Thyroid Nodule / pathology

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  • (PMID = 17203893.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Protein Precursors; 0 / RNA, Messenger; 0 / prothymosin alpha; 61512-21-8 / Thymosin; 95328-48-6 / parathymosin alpha
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79. Ludvíková M, Holubec L Jr, Ryska A, Topolcan O: Proliferative markers in diagnosis of thyroid tumors: a comparative study of MIB-1 and topoisomerase II-a immunostaining. Anticancer Res; 2005 May-Jun;25(3A):1835-40
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  • [Title] Proliferative markers in diagnosis of thyroid tumors: a comparative study of MIB-1 and topoisomerase II-a immunostaining.
  • BACKGROUND: The differential diagnosis of well-differentiated tumors of follicular cell origin remains a most problematic task in thyroid pathology.
  • The aim of our study was to evaluate the proliferative MIB-1 and topoisomerase II-alpha markers in both oncocytic and non-oncocytic epithelial thyroid tumors.
  • MATERIALS AND METHODS: Proliferative activity was analyzed by means of immunohistochemistry in 215 thyroid tumors and the evaluated proliferative indices (PI) were correlated with morphological diagnosis.
  • RESULTS: Carcinomas generally showed significantly higher PI than adenomas, irrespective of their oncocytic or non-oncocytic features.
  • Moreover, PI in oncocytic adenomas was significantly higher than in non-oncocytic ones.
  • CONCLUSION: PI can help the differential diagnosis of morphologically difficult cases of thyroid tumors.
  • Oncocytic adenomas have higher malignant potential and should be promptly surgically removed.
  • Both MIB-1 and topoisomerase II-alpha are recommended for the evaluation of thyroid tumor cell proliferation.
  • [MeSH-major] Antigens, Neoplasm. DNA Topoisomerases, Type II. DNA-Binding Proteins. Ki-67 Antigen. Thyroid Neoplasms / diagnosis
  • [MeSH-minor] Cell Division. Humans. Immunohistochemistry

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  • (PMID = 16033110.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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80. Candolfi M, Jaita G, Pisera D, Ferrari L, Barcia C, Liu C, Yu J, Liu G, Castro MG, Seilicovich A: Adenoviral vectors encoding tumor necrosis factor-alpha and FasL induce apoptosis of normal and tumoral anterior pituitary cells. J Endocrinol; 2006 Jun;189(3):681-90
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  • [Title] Adenoviral vectors encoding tumor necrosis factor-alpha and FasL induce apoptosis of normal and tumoral anterior pituitary cells.
  • Our previous work showed that tumor necrosis factor (TNF)-alpha and FasL induce apoptosis of anterior pituitary cells.
  • To further analyze the effect of these proapoptotic factors, we infected primary cultures from rat anterior pituitary, GH3 and AtT20 cells with first-generation adenoviral vectors encoding TNF-alpha, FasL or, as a control, beta-galactosidase (beta-Gal), under the control of the human cytomegalovirus promoter.
  • Although we observed basal expression of TNF-alpha and FasL in control cultures of anterior pituitary cells, fluorescence-activated cell sorting (FACS) cell cycle analysis showed that the overexpression of TNF-alpha or FasL increases the percentage of hypodiploid lactotropes and somatotropes.
  • Nuclear morphology and TUNEL staining revealed that the cells undergo an apoptotic death process.
  • We detected strong immunoreactivity for TNFR1 and Fas in the somatolactotrope cell line GH3.
  • TNF-alpha, but not FasL, was expressed in control cultures of GH3 cells.
  • The infection of GH3 cells with adenovirus encoding TNF-alpha or FasL increased the percentages of hypodiploid and TUNEL-positive cells.
  • TNF-alpha or FasL immunoreactivity was not observed in the corticotrope cell line AtT20.
  • However, adenovirus encoding TNF-alpha or FasL efficiently transduced these cells and increased the percentages of hypodiploid and TUNEL-positive cells.
  • The expression of beta-Gal was detected in all these cultures but did not affect cell viability.
  • In conclusion, these results suggest that death signaling cascades triggered by TNF receptor 1 (TNFR1) and Fas are present in both normal and tumoral pituitary cells.
  • Therefore, overexpression of proapoptotic factors could be a useful tool in the therapy of pituitary adenomas.
  • [MeSH-major] Adenoviridae / genetics. Genetic Vectors / administration & dosage. Membrane Glycoproteins / genetics. Pituitary Gland, Anterior / cytology. Pituitary Neoplasms / pathology. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factors / genetics
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Fas Ligand Protein. Female. Flow Cytometry. Gene Expression. Immunohistochemistry / methods. Rats. Rats, Sprague-Dawley. Rats, Wistar

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  • (PMID = 16731798.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Grant] United States / FIC NIH HHS / TW / 1R03 TW006273-01; United States / NINDS NIH HHS / NS / 1R21 NS047298-01; United States / NINDS NIH HHS / NS / NS 42893-01; United States / NINDS NIH HHS / NS / U54 NS045309-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Tnfsf6 protein, rat; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Necrosis Factors
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81. Vaiman M, Olevson Y, Habler L, Kessler A, Zehavi S, Sandbank J: Diagnostic value of estrogen receptors in thyroid lesions. Med Sci Monit; 2010 Jul;16(7):BR203-7
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  • BACKGROUND: The objective of this study was to evaluate the presence of estrogen receptors (ER) alpha and beta in various thyroid lesions and to assess the practicality of this test.
  • MATERIAL/METHODS: Immunohistochemical stains were performed for both ERalpha and ERbeta, for evaluation of immunoreactivity in 296 thyroid tissue samples that consisted of 150 goiters, 90 papillary carcinomas, 19 follicular adenomas, 15 Hurtle cell adenomas, 6 Hashimoto thyroiditis, 5 anaplastic carcinomas, 4 medullary carcinomas, 4 follicular carcinomas, 2 Hurtle cell carcinomas, and 1 squamous cell carcinoma of the thyroid.
  • [MeSH-major] Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Goiter, Nodular / diagnosis. Thyroid Gland / metabolism. Thyroid Gland / pathology. Thyroid Neoplasms / diagnosis

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  • (PMID = 20581768.001).
  • [ISSN] 1643-3750
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta
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82. Fendrich V, Bartsch DK: [Diagnosis and surgical management of neureondocrine pancreatic tumours]. Zentralbl Chir; 2010 Jun;135(3):210-7
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  • [Title] [Diagnosis and surgical management of neureondocrine pancreatic tumours].
  • [Transliterated title] Diagnostik und operative Therapie des Gastrinoms, Vipoms, Glukagonoms, Somatostatinoms und nichtfunktioneller endokriner Pankreastumoren.
  • The only chance of cure for patients with pancreatic endocrine tumours (PETs) is complete surgical removal not only of the primary tumour, but also of local or distant metastases.
  • This is true for gastrinomas, vipomas, glucagonomas, somatostatinomas and non-functional pancreatic endocrine tumours.
  • [MeSH-major] Hyperinsulinism / surgery. Insulinoma / surgery. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Laparoscopy. Lymph Node Excision. Male. Middle Aged. Minimally Invasive Surgical Procedures. Neoplasm Staging. Pancreas / pathology. Pancreas / surgery. Young Adult

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  • [Copyright] Georg Thieme Verlag Stuttgart, New York.
  • (PMID = 20549584.001).
  • [ISSN] 1438-9592
  • [Journal-full-title] Zentralblatt für Chirurgie
  • [ISO-abbreviation] Zentralbl Chir
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
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83. Bioulac-Sage P, Blanc JF, Rebouissou S, Balabaud C, Zucman-Rossi J: Genotype phenotype classification of hepatocellular adenoma. World J Gastroenterol; 2007 May 21;13(19):2649-54
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  • [Title] Genotype phenotype classification of hepatocellular adenoma.
  • Studies that compare tumor genotype with phenotype have provided the basis of a new histological/molecular classification of hepatocellular adenomas.
  • Based on two molecular criteria (presence of a TCF1/HNF1 alpha or beta-catenin mutation), and an additional histological criterion (presence or absence of an inflammatory infiltrate), subgroups of hepatocellular adenoma can be defined and distinguished from focal nodular hyperplasia.
  • Analysis of 96 hepatocellular adenomas performed by a French collaborative network showed that they can be divided into four broad subgroups: the first one is defined by the presence of mutations in TCF1 gene inactivating the hepatocyte nuclear factor 1 (HNF1 alpha); the second by the presence of beta-catenin activating mutations; the category without mutations of HNF1 alpha or beta-catenin is further divided into 2 subgroups depending on the presence or absence of inflammation.
  • Therefore, the approach to the diagnosis of problematic benign hepatocytic nodules may be entering a new era directed by new molecular information.
  • It is hoped that immunohistological tools will improve significantly diagnosis of liver biopsy in our ability to distinguish hepatocellular adenoma from focal nodular hyperplasia (FNH), and to delineate clinically meaningful entities within each group to define the best clinical management.
  • [MeSH-major] Adenoma, Liver Cell / classification. Genotype. Liver Neoplasms / classification. Phenotype
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Focal Nodular Hyperplasia / diagnosis. Hepatocyte Nuclear Factor 1-alpha / genetics. Humans. Liver / pathology. Mutation / genetics. beta Catenin / genetics

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  • [Cites] Hepatology. 2002 Oct;36(4 Pt 1):927-35 [12297840.001]
  • [Cites] J Hepatol. 2004 Jun;40(6):1036-9 [15158349.001]
  • [Cites] J Hepatol. 2003 Jul;39(1):77-85 [12821047.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Oct;41(2):93-8 [15287021.001]
  • [Cites] Am J Hematol. 2004 Nov;77(3):257-67 [15495253.001]
  • [Cites] N Engl J Med. 1976 Feb 26;294(9):470-2 [173996.001]
  • [Cites] N Engl J Med. 1978 Aug 3;299(5):239-41 [207987.001]
  • [Cites] Hepatology. 1995 Sep;22(3):983-93 [7657307.001]
  • [Cites] Gastroenterology. 1997 Mar;112(3):919-22 [9041254.001]
  • [Cites] Hepatology. 1997 Oct;26(4):891-5 [9328310.001]
  • [Cites] J Inherit Metab Dis. 2005;28(2):153-62 [15877204.001]
  • [Cites] Gastroenterology. 2005 May;128(5):1211-8 [15887105.001]
  • [Cites] Hepatology. 2006 Mar;43(3):515-24 [16496320.001]
  • [Cites] J Hepatol. 2006 Dec;45(6):883-6 [17049664.001]
  • [Cites] J Hepatol. 2007 Mar;46(3):521-7 [17239484.001]
  • [Cites] Gut. 2007 Feb;56(2):307-9 [17303609.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2611-6 [17363580.001]
  • [Cites] Hepatology. 2007 Sep;46(3):740-8 [17663417.001]
  • [Cites] Gastroenterology. 2003 Nov;125(5):1470-5 [14598263.001]
  • [Cites] J Clin Endocrinol Metab. 2004 Mar;89(3):1476-80 [15001650.001]
  • [Cites] Gastroenterology. 2004 May;126(5):1323-9 [15131793.001]
  • [Cites] Nat Genet. 2002 Oct;32(2):312-5 [12355088.001]
  • (PMID = 17569132.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / beta Catenin
  • [Number-of-references] 23
  • [Other-IDs] NLM/ PMC4147112
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84. Marcus NY, Brunt EM, Blomenkamp K, Ali F, Rudnick DA, Ahmad M, Teckman JH: Characteristics of hepatocellular carcinoma in a murine model of alpha-1-antitrypsin deficiency. Hepatol Res; 2010 Jun;40(6):641-53
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  • [Title] Characteristics of hepatocellular carcinoma in a murine model of alpha-1-antitrypsin deficiency.
  • AIM: Individuals with homozygous (ZZ) alpha-1-antitrypsin (alpha1AT) deficiency are at an increased risk for liver damage, cirrhosis and hepatocellular carcinoma (HCC).
  • The transgenic PiZ mouse, expressing the human alpha1AT mutant Z gene, is a valuable model for this disease.
  • METHODS: Tumor incidence and histology were studied, gene expression levels were surveyed with microarrays, RNA quantified with quantitative real time polymerase chain reaction and protein levels determined with immunoblots and immunohistochemistry.
  • RESULTS: By 16-19 months of age, approximately 69% of the PiZ mice had developed tumors.
  • HCC was present with no evidence of benign adenomas as pre-cancerous lesions.
  • Tumors showed abnormal mitochondria, variable levels of steatosis, globular inclusions of alpha1AT mutant Z protein and metastases.
  • PiZ mice that subsequently developed liver tumors had higher serum levels of alpha1AT mutant Z protein than those that did not develop tumors.
  • Cyclin D1, a cell cycle protein, was upregulated in PiZ livers without tumors compared to Wt. cFOS, a component of AP-1 that may be involved in transforming cells and MCAM, an adhesion molecule likely involved in tumorigenesis and metastases, were elevated in tumors compared with livers without tumors.
  • CONCLUSION: In the PiZ model, many of the histological characteristics of HCC recapitulated features seen in human HCC, whether from individuals with homozygous ZZ liver disease or from unrelated causes in individuals that were not homozygous ZZ.

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  • [Cites] J Cell Sci. 2008 Dec 1;121(Pt 23):3853-7 [19020303.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1796-801 [10677536.001]
  • [Cites] Hepatology. 2007 Oct;46(4):1228-35 [17886264.001]
  • [Cites] J Biol Chem. 2007 Sep 21;282(38):27769-80 [17635928.001]
  • [Cites] Science. 2007 Jul 6;317(5834):121-4 [17615358.001]
  • [Cites] Hepatology. 2007 Apr;45(4):968-76 [17393506.001]
  • [Cites] Clin Cancer Res. 2007 Mar 1;13(5):1362-6 [17332277.001]
  • [Cites] Hepatology. 2006 Oct;44(4):976-82 [17006946.001]
  • [Cites] Pediatr Res. 2006 Aug;60(2):233-8 [16864711.001]
  • [Cites] Gastroenterology. 2006 Jul;131(1):179-93 [16831601.001]
  • [Cites] Nat Med. 2006 Apr;12(4):410-6 [16532004.001]
  • [Cites] Hepatology. 2006 Feb;43(2 Suppl 1):S145-50 [16447291.001]
  • [Cites] Hepatology. 2006 Jan;43(1):194 [16374862.001]
  • [Cites] J Biol Chem. 2005 Nov 25;280(47):39002-15 [16183649.001]
  • [Cites] Hepatology. 2005 Sep;42(3):514-21 [16044402.001]
  • [Cites] Hepatology. 2005 Jan;41(1):160-7 [15619240.001]
  • [Cites] J Biol Chem. 2005 Jan 7;280(1):768-76 [15509582.001]
  • [Cites] Kidney Int. 2005 Jan;67(1):94-102 [15610232.001]
  • [Cites] Endocrinology. 2004 Dec;145(12):5439-47 [15331580.001]
  • [Cites] Hepatology. 1996 Dec;24(6):1504-16 [8938188.001]
  • [Cites] J Hepatol. 1994 Dec;21(6):1006-11 [7699220.001]
  • [Cites] Hepatology. 1994 Feb;19(2):389-97 [8294096.001]
  • [Cites] Scand J Gastroenterol. 1985 Oct;20(8):907-11 [3001926.001]
  • [Cites] Am J Clin Pathol. 1988 Jul;90(1):120 [3291606.001]
  • [Cites] Biochemistry. 1989 Nov 14;28(23):8951-66 [2690952.001]
  • [Cites] J Clin Invest. 1989 Apr;83(4):1183-90 [2784798.001]
  • [Cites] N Engl J Med. 1986 Mar 20;314(12):736-9 [3485248.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 May;286(5):G851-62 [14684378.001]
  • [Cites] Hepatology. 2004 Apr;39(4):1048-55 [15057909.001]
  • [Cites] Gene. 2004 Mar 3;327(2):201-13 [14980717.001]
  • [Cites] Nat Rev Cancer. 2003 Nov;3(11):859-68 [14668816.001]
  • [Cites] Nucleic Acids Res. 2003 Dec 15;31(24):e154 [14654707.001]
  • [Cites] Blood. 2003 Jul 1;102(1):184-91 [12609848.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2002 Nov;283(5):G1156-65 [12381530.001]
  • [Cites] Cancer Res. 2001 Jul 15;61(14):5389-95 [11454681.001]
  • [Cites] Br J Cancer. 2001 Apr 20;84(8):1064-9 [11308255.001]
  • [Cites] J Biol Chem. 2001 Jan 12;276(2):1564-9 [11036077.001]
  • [Cites] Cancer. 2001 Jan 1;91(1):106-12 [11148566.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2000 Nov;279(5):G961-74 [11052993.001]
  • [Cites] Hepatology. 2007 Nov;46(5):1443-52 [17668872.001]
  • (PMID = 20618460.001).
  • [ISSN] 1872-034X
  • [Journal-full-title] Hepatology research : the official journal of the Japan Society of Hepatology
  • [ISO-abbreviation] Hepatol. Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK067489; United States / NIDDK NIH HHS / DK / DK067489-04; United States / NIDDK NIH HHS / DK / R01 DK067489-04; United States / NIDDK NIH HHS / DK / DK067489-05; United States / NCI NIH HHS / CA / P30 CA091842; United States / NIDDK NIH HHS / DK / R01 DK067489-05; United States / NIDDK NIH HHS / DK / P30 DK052574
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ NIHMS226769; NLM/ PMC2928671
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85. National Toxicology Program: Toxicology and carcinogenesis studies of alpha-methylstyrene (Cas No. 98-83-9) in F344/N rats and B6C3F1 mice (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2007 Nov;(543):1-210
Hazardous Substances Data Bank. ALPHA-METHYL STYRENE .

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  • [Title] Toxicology and carcinogenesis studies of alpha-methylstyrene (Cas No. 98-83-9) in F344/N rats and B6C3F1 mice (inhalation studies).
  • alpha-Methylstyrene is used in the production of acrylonitrile-butadiene-styrene resins and copolymers, which improve the impact and heat-resistant properties of polymers, specialty grades of plastics, rubber, and protective coatings. alpha-Methylstyrene also moderates polymerization rates and improves product clarity in coatings and resins.
  • Low molecular weight liquid polymers are used as plasticizers in paints, waxes, adhesives, and plastics. alpha-Methylstyrene was nominated by the U.S.
  • Male and female F344/N rats and B6C3F1 mice were exposed to alpha-methylstyrene (99.5% pure) by inhalation for 3 months or 2 years.
  • Genetic toxicology studies were conducted in Salmonella typhimurium, cultured Chinese hamster ovary cells, and mouse peripheral blood erythrocytes.
  • 3-MONTH STUDY IN RATS: Groups of 10 male and 10 female rats were exposed by whole-body inhalation to alpha-methylstyrene at concentrations of 0, 75, 150, 300, 600, or 1,000 ppm for 6 hours per day, 5 days per week for 14 weeks.
  • Consistent with the hyaline droplet accumulation, an exposure-related increase in alpha2μ-globulin was detected in the kidneys of males exposed to alpha-methylstyrene.
  • Morphologic changes were not detected in the liver.
  • 3-MONTH STUDY IN MICE: Groups of 10 male and 10 female mice were exposed by whole-body inhalation to alpha-methylstyrene at concentrations of 0, 75, 150, 300, 600, or 1,000 ppm for 6 hours per day, 5 days per week for 14 weeks.
  • Minimal to mild centrilobular hypertrophy was present in the livers of male and female mice exposed to 600 or 1,000 ppm alpha-methylstyrene.
  • 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were exposed by whole body inhalation to alpha-methylstyrene at concentrations of 0, 100, 300, or 1,000 ppm for 6 hours per day, 5 days per week, except holidays, for 105 weeks.
  • Two 1,000 ppm males and one 300 ppm male had renal tubule carcinomas, and one 300 ppm male had a renal tubule adenoma.
  • Because of the neoplasms observed in 300 and 1,000 ppm males at the end of the 2-year study and the finding of alpha2μ-globulin accumulation in the kidneys at 3 months, which is often associated with kidney neoplasms, additional step sections of kidney were prepared; additional males with focal hyperplasia or adenoma were identified.
  • The incidences of renal tubule adenoma and carcinoma (combined) in the 1,000 ppm males were significantly greater than those in the chamber controls when the single and step sections were combined.
  • The incidence of mononuclear cell leukemia in 1,000 ppm males was significantly increased compared to the chamber controls.
  • In the nose, the incidences of basal cell hyperplasia were significantly increased in all exposed groups of males and females, and the incidences of degeneration of the olfactory epithelium were increased in 1,000 ppm males and females and 300 ppm females.
  • 2-YEAR STUDY IN MICE: Groups of 50 male and 50 female mice were exposed by whole body inhalation to alpha-methylstyrene at concentrations of 0, 100, 300, or 600 ppm for 6 hours per day, 5 days per week, except holidays, for 105 weeks.
  • The incidences of hepatocellular adenoma or carcinoma (combined) were significantly increased in the 100 and 600 ppm males and in all exposed groups of females.
  • The incidences of hepatocellular adenoma were significantly increased in all exposed groups of females, and the incidences in all exposed groups of males and females exceeded the historical range for chamber controls.
  • GENETIC TOXICOLOGY: alpha-Methylstyrene was not mutagenic in four strains of Salmonella typhimurium, with or without rat or hamster liver metabolic activation enzymes (S9).
  • alpha-Methylstyrene did not induce chromosomal aberrations in cultured Chinese hamster ovary cells, with or without S9 activation, but did significantly increase the frequency of sister chromatid exchanges in cultures exposed in the presence of S9.
  • CONCLUSIONS: Under the conditions of this 2-year inhalation study, there was some evidence of carcinogenic activity of alpha-methylstyrene in male F344/N rats based on increased incidences of renal tubule adenomas and carcinomas (combined).
  • The increased incidence of mononuclear cell leukemia in 1,000 ppm male F344/N rats may have been related to alpha-methylstyrene exposure.
  • There was no evidence of carcinogenic activity of alpha-methylstyrene in female F344/N rats exposed to 100, 300, or 1,000 ppm.
  • There was equivocal evidence of carcinogenic activity of alpha-methylstyrene in male B6C3F1 mice based on marginally increased incidences of hepatocellular adenoma or carcinoma (combined).
  • There was clear evidence of carcinogenic activity of alpha-methylstyrene in female B6C3F1 mice based on increased incidences of hepatocellular adenomas and carcinomas.
  • Exposure of rats to alpha-methylstyrene resulted in kidney toxicity, which in males exhibited some features of alpha2μ-globulin nephropathy.
  • Exposure to alpha-methylstyrene resulted in nonneoplastic lesions of the nose in male and female rats and mice and of the liver and kidney in female mice.
  • [MeSH-minor] Animals. Body Weight / drug effects. CHO Cells. Cricetinae. Cricetulus. DNA Damage. Female. Inhalation Exposure. Kidney / drug effects. Kidney / pathology. Kidney Neoplasms / chemically induced. Kidney Neoplasms / pathology. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / pathology. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Male. Mice. Mice, Inbred Strains. Micronuclei, Chromosome-Defective / chemically induced. Nose Diseases / chemically induced. Rats. Rats, Inbred F344

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  • (PMID = 18685715.001).
  • [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 / Air Pollutants, Occupational; 0 / Carcinogens; 0 / Mutagens; 0 / Styrenes; 98-83-9 / alpha-methylstyrol
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86. Jain S, Singhal S, Lee P, Xu R: Molecular genetics of hepatocellular neoplasia. Am J Transl Res; 2010;2(1):105-18
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  • Recent molecular genetic, pathologic, and clinical data have led to the stratification of hepatic adenomas into three subgroups: those with mutant TCF1/HNF1 alpha gene, those with mutant beta-catenin, and those without mutations in either of these loci.
  • Hepatic adenomas with alpha-catenin mutations have a significantly greater risk for malignant transformation in comparison with the other two subgroups.
  • Telangiectatic focal nodular hyperplasia has now been reclassified as telangiectatic adenoma due to the presence of non-random methylation patterns, consistent with the monoclonal origin which is similar to hepatic adenoma and HCC.
  • HCC precursor lesions demonstrate unique molecular alterations of HSP70, CAP2, glypican 3, and glutamine synthetase that have proven useful in the histologic diagnosis of early HCC.
  • Though specific genetic alterations depend on HCC etiology, the main proteins affected include cell membrane receptors (in particular tyrosine kinase receptors) as well as proteins involved in cell signaling (specifically Wnt/beta-catenin, Ras/Raf/MEK/ERK and PI3K/Akt/mTOR pathways), cell cycle regulation (i.e. p53, p16/INK4, cyclin/cdk complex), invasiveness (EMT, TGF-beta) and DNA metabolism.
  • HCCs can now be stratified into two clinically relevant groups: Class A, the low survival subclass (overall survival time 30.3+/- 8.02 months), shows strong expression signatures of cell proliferation and antiapoptosis genes (such as PNCA and cell cycle regulators CDK4, CCNB1, CCNA2, and CKS2) as well as genes involving ubiquitination and sumoylation; Class B, the high survival subclass (overall survival time 83.7 +/-10.3 months), does not have the above expression signature.


87. Schmelz EM, Xu H, Sengupta R, Du J, Banerjee S, Sarkar FH, Rishi AK, Majumdar AP: Regression of early and intermediate stages of colon cancer by targeting multiple members of the EGFR family with EGFR-related protein. Cancer Res; 2007 Jun 1;67(11):5389-96
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  • In the present study, we evaluated the therapeutic effectiveness of ERRP on early and intermediate stages of colon cancer by examining regression of chemically induced aberrant crypt foci (ACF) in the colon of CF1 mice and intestinal adenomas in APC(Min+/-) (Min) mice.
  • After formation of ACF or adenomas, the mice were injected (i.p.) with ERRP (50 microg/mouse) for 10 consecutive days.
  • In Min mice, ERRP caused the regression of adenomas throughout the small intestine (P < 0.05) and reduced their size (P < 0.001).
  • [MeSH-minor] 1,2-Dimethylhydrazine. Adenoma / chemically induced. Adenoma / drug therapy. Adenoma / metabolism. Adenoma / pathology. Animals. Apoptosis / drug effects. Carcinogens. Cell Growth Processes / drug effects. Female. Intestinal Mucosa / drug effects. Intestinal Mucosa / metabolism. Male. Mice. Mice, Inbred C57BL. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Neoplasm Staging. Precancerous Conditions / chemically induced. Precancerous Conditions / drug therapy. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Receptors, Estrogen / genetics. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / pharmacology. Transforming Growth Factor alpha / metabolism

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  • (PMID = 17545620.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R01 AG014343
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Drosophila Proteins; 0 / ERR protein, Drosophila; 0 / NF-kappa B; 0 / Receptors, Estrogen; 0 / Recombinant Fusion Proteins; 0 / Transforming Growth Factor alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; IX068S9745 / 1,2-Dimethylhydrazine
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88. Wen Y, Giardina SF, Hamming D, Greenman J, Zachariah E, Bacolod MD, Liu H, Shia J, Amenta PS, Barany F, Paty P, Gerald W, Notterman D: GROalpha is highly expressed in adenocarcinoma of the colon and down-regulates fibulin-1. Clin Cancer Res; 2006 Oct 15;12(20 Pt 1):5951-9
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  • PURPOSE: The growth-related oncogene alpha (GROalpha) is a secreted interleukin-like molecule that interacts with the CXCR2 G-protein-coupled receptor.
  • We found that the mRNA and protein products of GROalpha are more highly expressed in neoplastic than normal colon epithelium, and we studied potential mechanisms by which GROalpha may contribute to tumor initiation or growth.
  • EXPERIMENTAL DESIGN: Cell lines that constitutively overexpress GROalpha were tested for growth rate, focus formation, and tumor formation in a xenograft model.
  • RESULTS: In cell cultures, GROalpha transfection transformed NIH 3T3 cells, whereas inhibition of GROalpha by inhibitory RNA was associated with apoptosis, decreased growth rate, and marked up-regulation of the matrix protein fibulin-1.
  • Expression of GROalpha mRNA was higher in primary adenocarcinomas (n = 132), adenomas (n = 32), and metastases (n = 52) than in normal colon epithelium (P < 0.001).
  • GROalpha overexpression abrogates contact inhibition in cell culture models, whereas inhibition of GROalpha expression is associated with apoptosis.
  • Importantly, coexpression of fibulin-1 with GROalpha abrogates key aspects of the transformed phenotype, including tumor formation in a murine xenograft model.
  • [MeSH-minor] 3T3 Cells. Animals. Cell Line, Tumor. Cell Survival. Chemokine CXCL1. DNA, Neoplasm / genetics. Gene Expression Profiling. Humans. Mice. Neoplasm Transplantation. Polymerase Chain Reaction. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Transplantation, Heterologous

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  • (PMID = 17062666.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01-CA65930; United States / NCI NIH HHS / CA / P30-CA072720
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL1 protein, human; 0 / Calcium-Binding Proteins; 0 / Chemokine CXCL1; 0 / Chemokines, CXC; 0 / DNA, Neoplasm; 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / fibulin
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89. Gentschev I, Fensterle J, Schmidt A, Potapenko T, Troppmair J, Goebel W, Rapp UR: Use of a recombinant Salmonella enterica serovar Typhimurium strain expressing C-Raf for protection against C-Raf induced lung adenoma in mice. BMC Cancer; 2005 Feb 9;5:15
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  • [Title] Use of a recombinant Salmonella enterica serovar Typhimurium strain expressing C-Raf for protection against C-Raf induced lung adenoma in mice.
  • Therefore these proteins are potential targets for immunotherapy and a possible basis for vaccine development against tumors.
  • In this study we analyzed the functionality of a new live C-Raf vaccine based on an attenuated Salmonella enterica serovar Typhimurium aroA strain in two Raf dependent lung tumor mouse models.
  • METHODS: The antigen C-Raf has been fused to the C-terminal secretion signal of Escherichia coli alpha-hemolysin and expressed in secreted form by an attenuated aroA Salmonella enterica serovar Typhimurium strain via the alpha-hemolysin secretion pathway.
  • The effect of the immunization with this recombinant C-Raf strain on wild-type C57BL/6 or lung tumor bearing transgenic BxB mice was analyzed using western blot and FACS analysis as well as specific tumor growth assays.
  • Immunization of wild-type C57BL/6 or tumor bearing mice provoked specific C-Raf antibody and T-cell responses.
  • Most importantly, the vaccine strain significantly reduced tumor growth in two transgenic mouse models of Raf oncogene-induced lung adenomas.
  • [MeSH-major] Adenoma / prevention & control. Cancer Vaccines / immunology. Escherichia coli Proteins / immunology. Hemolysin Proteins / immunology. Lung Neoplasms / prevention & control. Proto-Oncogene Proteins c-raf / immunology. Salmonella typhimurium / immunology


90. Chen HW, Chen HW, Su DH, Shun CT, Liu KL: Rare presentation of endocrine pancreatic tumor: a case of diffuse glucagonoma without metastasis and necrolytic migratory erythema. J Formos Med Assoc; 2005 May;104(5):363-6
MedlinePlus Health Information. consumer health - Pancreatic Cancer.

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  • [Title] Rare presentation of endocrine pancreatic tumor: a case of diffuse glucagonoma without metastasis and necrolytic migratory erythema.
  • Glucagonoma is a very rare endocrine pancreatic tumor.
  • At diagnosis, most glucagonomas are malignant and often metastatic.
  • Suspicion of glucagonoma is based on characteristic presentations known as "glucagonoma syndrome".
  • Glucagonoma is often found in the pancreatic body and/or tail and is usually large enough to be localized by computed tomography.
  • We report a case of diffuse glucagonoma necrolytic migratory erythema (NME) in a 45-year-old man with mild diabetes mellitus, mild anemia, and weight loss over 1.5 years.
  • Diffused enlarged pancreas was noted on abdominal ultrasonography incidentally during a routine health check-up.
  • No enlarged lymph node or extrapancreatic tumor mass was found by several imaging studies.
  • Total pancreatectomy was performed, and the pathology revealed glucagon-producing islet cells and intrapancreatic vascular emboli of tumor cells.
  • Presentation of diffuse malignant glucagonoma with tumor emboli but no metastasis or NME is unusual.

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  • (PMID = 15959605.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
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91. Lania A, Spada A: G-protein and signalling in pituitary tumours. Horm Res; 2009 Apr;71 Suppl 2:95-100

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although these neoplasias are monoclonal in origin, mutations of GNAS1, the gene encoding the alpha subunit of the stimulatory G-protein, Gs, are the only mutational changes unequivocally associated with growth hormone (GH)-secreting adenomas.
  • Consistent with a potential role of the cyclic adenosine monophosphate pathway in the proliferation of somatotrophs, germline mutations of the gene encoding the type 1alpha regulatory subunit of protein kinase A (PRKAR1A) have been found in patients with the Carney complex, a syndrome including GH-secreting adenomas, whereas alterations in the expression levels of this subunit are frequently observed in sporadic adenomas.
  • [MeSH-major] Cyclic AMP-Dependent Protein Kinase RIalpha Subunit / metabolism. GTP-Binding Protein alpha Subunits, Gs / metabolism. Growth Hormone-Secreting Pituitary Adenoma / enzymology. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Animals. Cell Proliferation. Cyclic AMP / genetics. Cyclic AMP / metabolism. Humans. Mutation. Syndrome

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19407505.001).
  • [ISSN] 1423-0046
  • [Journal-full-title] Hormone research
  • [ISO-abbreviation] Horm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / PRKAR1A protein, human; 0 / Proto-Oncogene Proteins; E0399OZS9N / Cyclic AMP; EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Number-of-references] 38
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92. Cho WS, Han BS, Nam KT, Park K, Choi M, Kim SH, Jeong J, Jang DD: Carcinogenicity study of 3-monochloropropane-1,2-diol in Sprague-Dawley rats. Food Chem Toxicol; 2008 Sep;46(9):3172-7
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  • 3-Monochloropropane-1,2-diol (alpha-chlorohydrin, 3-MCPD) is a well-known contaminant, which has been detected in a wide range of foods and ingredients, and is also a suspected cause of cancer.
  • The incidences of renal tubule adenomas or carcinomas and Leydig cell tumors occurred with dose-related positive trends in male rats.
  • The incidences of renal tubule carcinomas and Leydig cell tumors were significantly increased in male rats given 400ppm 3-MCPD.
  • The incidence of renal tubule adenomas showed a positive trend in female rats, which was significant in 400ppm 3-MCPD group.
  • In conclusion, there was clear evidence of the carcinogenic activity of 3-MCPD in male SD rats, based on the increased incidences of renal tubule carcinomas and Leydig cell tumors.
  • There was some evidence of the carcinogenic activity of 3-MCPD in female SD rats, based on the increased incidence of renal tubule adenomas.
  • [MeSH-minor] Animals. Body Weight / drug effects. Carcinogenicity Tests. Female. Male. Neoplasms / chemically induced. Neoplasms / pathology. Rats. Rats, Sprague-Dawley. Survival Analysis. alpha-Chlorohydrin

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  • (PMID = 18680782.001).
  • [ISSN] 0278-6915
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 96-24-2 / alpha-Chlorohydrin; PDC6A3C0OX / Glycerol
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93. Takashima K, Ito Y, Gonzalez FJ, Nakajima T: Different mechanisms of DEHP-induced hepatocellular adenoma tumorigenesis in wild-type and Ppar alpha-null mice. J Occup Health; 2008;50(2):169-80
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  • [Title] Different mechanisms of DEHP-induced hepatocellular adenoma tumorigenesis in wild-type and Ppar alpha-null mice.
  • Di (2-ethylhexyl) phthalate (DEHP) exposure is thought to lead to hepatocellular hypertrophy and hyperplasia in rodents mediated via peroxisome proliferator-activated receptor alpha (PPAR alpha).
  • A recent study revealed that long-term exposure to relatively low-dose DEHP (0.05%) caused liver tumors including hepatocellular carcinomas, hepatocellular adenomas, and chologiocellular carcinomas at a higher incidence in Ppar alpha-null mice (25.8%) than in wild-type mice (10.0%).
  • Using tissues with hepatocellular adenoma, microarray (Affymetrix MOE430A) as well as, in part, real-time quantitative PCR analysis was conducted to elucidate the mechanisms of the adenoma formation resulting from DEHP exposure in both genotyped mice.
  • The microarray profiles showed that the up- or down-regulated genes were quite different between hepatocellular adenoma tissues of wild-type and Ppar alpha-null mice exposed to DEHP.
  • The gene expressions of apoptotic peptidase activating factor 1 (Apaf1) and DNA-damage-inducible 45 alpha (Gadd45a) were increased in the hepatocellular adenoma tissues of wild-type mice exposed to DEHP, whereas they were unchanged in corresponding tissues of Ppar alpha-null mice.
  • On the other hand, the expressions of cyclin B2 and myeloid cell leukemia sequence 1 were increased only in the hepatocellular adenoma tissues of Ppar alpha-null mice.
  • Taken together, DEHP may induce hepatocellular adenomas, in part, via suppression of G2/M arrest regulated by Gadd45a and caspase 3-dependent apoptosis in Ppar alpha-null mice, but these genes may not be involved in tumorigenesis in the wild-type mice.
  • In contrast, the expression level of Met was notably increased in the liver adenoma tissue of wild-type mice, which may suggest the involvement of Met in DEHP-induced tumorigenesis in wild-type mice.
  • [MeSH-major] Diethylhexyl Phthalate / toxicity. Liver / drug effects. Liver Neoplasms, Experimental / chemically induced. Liver Neoplasms, Experimental / genetics. PPAR alpha / deficiency
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / physiology. Apoptotic Protease-Activating Factor 1 / antagonists & inhibitors. Apoptotic Protease-Activating Factor 1 / biosynthesis. Caspase 3 / metabolism. Cell Cycle Proteins / antagonists & inhibitors. Cell Cycle Proteins / biosynthesis. Cell Division / genetics. G2 Phase / genetics. Gene Expression Profiling. Hepatocytes / drug effects. Hyperplasia. Mice. Mice, Knockout. Microarray Analysis. Nuclear Proteins / antagonists & inhibitors. Nuclear Proteins / biosynthesis. Plasticizers / toxicity. Polymerase Chain Reaction. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 18403868.001).
  • [ISSN] 1348-9585
  • [Journal-full-title] Journal of occupational health
  • [ISO-abbreviation] J Occup Health
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Apaf1 protein, mouse; 0 / Apoptotic Protease-Activating Factor 1; 0 / Cell Cycle Proteins; 0 / Gadd45a protein, mouse; 0 / Nuclear Proteins; 0 / PPAR alpha; 0 / Plasticizers; 0 / RNA, Messenger; C42K0PH13C / Diethylhexyl Phthalate; EC 3.4.22.- / Caspase 3
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94. Liu WJ, Zhao YP, Zhang TP, Liao Q, Cong L: [Clinical experience in diagnosis and treatment of glucagonoma]. Zhonghua Wai Ke Za Zhi; 2009 Mar 1;47(5):333-6
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  • [Title] [Clinical experience in diagnosis and treatment of glucagonoma].
  • OBJECTIVE: To study the diagnosis and treatment of glucagonoma.
  • METHODS: A retrospective review of glucagonoma cases was committed between June 1993 and July 2008 in Peking Union Medical College Hospital.
  • It was measured by sex, age, misdiagnosis, clinical symptoms, laboratory data, imaging studies, diagnosis, treatment procedures and so on.
  • RESULTS: The tumors of eleven cases were found in the tail, and one case was in the head of the pancreas at the same time.
  • Nine patients had the metastasis out of pancreas and all of them had the liver metastasis.
  • One case was a member of multiple endocrine neoplasia type 1 (MEN-1) syndromes.
  • The glucagon was detected by immunohistochemistry and was positive in five patients.
  • Multimodal treatments included tumor resection, chemoembolization, treated with somatostatin analogues and (or) radionuclides and so on were applied to all patients.
  • CONCLUSIONS: Glucagonoma is a rare pancreatic endocrine tumor.
  • Radical tumor surgery is used as the first choice.
  • [MeSH-major] Glucagonoma / diagnosis. Glucagonoma / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy

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  • (PMID = 19595005.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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95. Appetecchia M, Ferretti E, Carducci M, Izzo F, Carpanese L, Marandino F, Terzoli E: Malignant glucagonoma. New options of treatment. J Exp Clin Cancer Res; 2006 Mar;25(1):135-9
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  • [Title] Malignant glucagonoma. New options of treatment.
  • Few cases of malignant glucagonomas have been described in the literature.
  • In this paper we present a case of a 77-year-old woman with necrolytic migratory erythema and high plasma glucagon and chromogranin A levels caused by a neuroendocrine tumour.
  • An abdominal CT scan suggested a pancreatic lesion and two liver metastases.
  • The patient underwent pancreatic debulking and liver metastasectomy.
  • Histological and immunohistochemical investigations revealed a well differentiated neuroendocrine tumour with vascular invasion and scattered immunopositivity for somatostatin receptors.
  • Three months after surgery symptoms of disease recurred accompanied by hyperglucagonaemia and newly diagnosed liver lesions.
  • The patient was treated with octreotide (30 mg i.m. every 28 days) and interferon-alpha (6 MU s.cc 3 times per week) plus three cycles of hepatic chemoembolisation.
  • The patient is now asymptomatic with persistent hepatic disease and normal serum glucagon levels forty months after primary treatment.
  • So far, only few immunohistochemical studies are reported on malignant glucagonoma and combined treatment schedules.
  • We demonstrated, for the first time, a scattered immunopositivity for somatostatin receptors in a malignant glucagonoma.
  • A combined antiproliferative medical treatment and the hepatic chemoembolization have been able to control tumor growth and disease symptoms for a long time after surgery.
  • [MeSH-major] Glucagonoma / therapy
  • [MeSH-minor] Aged. Chromogranin A. Chromogranins / blood. Female. Glucagon / blood. Humans. Immunohistochemistry. Interferon-alpha / metabolism. Neuroendocrine Tumors / blood. Octreotide / pharmacology. Proglucagon / metabolism. Time Factors. Tomography, X-Ray Computed

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  • (PMID = 16761630.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Chromogranin A; 0 / Chromogranins; 0 / Interferon-alpha; 55963-74-1 / Proglucagon; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide
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96. Baba Y, Iyama K, Ikeda K, Ishikawa S, Hayashi N, Miyanari N, Honda Y, Sado Y, Ninomiya Y, Baba H: Differential expression of basement membrane type IV collagen alpha chains in gastric intramucosal neoplastic lesions. J Gastroenterol; 2007 Nov;42(11):874-80
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  • [Title] Differential expression of basement membrane type IV collagen alpha chains in gastric intramucosal neoplastic lesions.
  • BACKGROUND: The histological diagnosis of gastric intramucosal neoplastic lesions (GINLs) is controversial among experienced pathologists.
  • Although the destruction of the epithelial basement membrane (BM) and the invasion of neoplastic epithelial cells into the interstitium of the lamina propria is distinct proof of "intramucosal carcinoma," histological evaluation of GINLs is difficult and ambiguous, especially intestinal-type adenocarcinoma.
  • Type IV collagen is a major component of the BM, and comprises six genetically distinct alpha(IV) chains, alpha1(IV) to alpha6(IV).
  • We examined the immunohistochemical expression of alpha(IV) chains in GINLs and investigated whether the expression pattern was a diagnostic marker of gastric intramucosal carcinoma.
  • METHODS: The expression of alpha(IV) chains and Ki-67 in 60 resected GINL specimens was immunohistochemically examined.
  • In most tubular adenomas (Japanese classification), these four chains were stained continuously in the BM, whereas in tubular adenocarcinomas (Japanese classification), the alpha5/alpha6(IV) chains had disappeared, partially or completely.
  • In addition, the loss of alpha5/alpha6(IV) chains was significantly correlated with tumor cell growth activity.
  • CONCLUSIONS: The loss of alpha5/alpha6(IV) chains might be a useful diagnostic finding for gastric intramucosal carcinoma in GINL cases.
  • [MeSH-minor] Adenoma / diagnosis. Adenoma / metabolism. Adenoma / pathology. Epithelium / metabolism. Epithelium / pathology. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism

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  • [Cites] J Biol Chem. 2000 Jul 14;275(28):21340-8 [10766752.001]
  • [Cites] Gastric Cancer. 2006;9(4):262-70 [17235627.001]
  • [Cites] Biochim Biophys Acta. 1990 Jun 1;1032(1):89-118 [1694687.001]
  • [Cites] Histochem Cell Biol. 1998 Oct;110(4):359-66 [9792414.001]
  • [Cites] Gastric Cancer. 2003;6(2):71-9 [12861397.001]
  • [Cites] J Gastroenterol Hepatol. 2002 Sep;17(9):980-6 [12167119.001]
  • [Cites] J Pathol. 2001 Aug;194(4):420-7 [11523049.001]
  • [Cites] Acta Pathol Microbiol Scand. 1965;64:31-49 [14320675.001]
  • [Cites] Lab Invest. 1999 Mar;79(3):281-92 [10092064.001]
  • [Cites] J Cell Biol. 1995 Sep;130(5):1219-29 [7657706.001]
  • [Cites] Biochem Biophys Res Commun. 2004 May 28;318(2):354-60 [15120609.001]
  • [Cites] Cancer. 1999 Oct 15;86(8):1449-54 [10526272.001]
  • [Cites] Am J Pathol. 2006 Mar;168(3):856-65 [16507901.001]
  • [Cites] Gastric Cancer. 2000 Dec;3(4):219-225 [11984739.001]
  • [Cites] J Biol Chem. 2000 Jan 14;275(2):1209-15 [10625665.001]
  • [Cites] Ann Surg. 2007 Jan;245(1):68-72 [17197967.001]
  • [Cites] Histopathology. 1998 Sep;33(3):197-202 [9777384.001]
  • [Cites] J Gastroenterol. 2006 Jun;41(6):547-53 [16868802.001]
  • [Cites] Gastric Cancer. 1998 Dec;1(1):10-24 [11957040.001]
  • [Cites] Lab Invest. 2001 Feb;81(2):167-75 [11232638.001]
  • [Cites] Gut. 1999 Jul;45 Suppl 1:I5-8 [10457028.001]
  • [Cites] Eur J Biochem. 1989 Apr 1;180(3):487-502 [2653817.001]
  • [Cites] Histochem J. 2002 Oct;34(10):479-86 [12945730.001]
  • [Cites] Exp Cell Res. 2004 Dec 10;301(2):251-65 [15530861.001]
  • [Cites] Histochem Cell Biol. 1995 Oct;104(4):267-75 [8548560.001]
  • [Cites] J Gastroenterol. 2006 Oct;41(10):929-42 [17096062.001]
  • [Cites] Pathol Int. 2002 Mar;52(3):224-33 [11972866.001]
  • [Cites] Dev Dyn. 1998 Jul;212(3):437-47 [9671947.001]
  • [Cites] J Biochem. 1998 May;123(5):767-76 [9562604.001]
  • [Cites] J Biol Chem. 1994 Sep 16;269(37):23013-7 [8083201.001]
  • [Cites] Cancer Res. 1991 Jul 1;51(13):3503-6 [2054789.001]
  • [Cites] Histochem J. 1997 Jul;29(7):563-70 [9279559.001]
  • [Cites] Virchows Arch. 2004 Jul;445(1):54-62 [15138813.001]
  • [Cites] Lab Invest. 1983 Dec;49(6):636-49 [6317982.001]
  • [Cites] Lancet. 1997 Jun 14;349(9067):1725-9 [9193382.001]
  • [Cites] Pathol Int. 2004 Jun;54(6):425-35 [15144402.001]
  • [Cites] J Biol Chem. 2000 Mar 17;275(11):8051-61 [10713126.001]
  • (PMID = 18008031.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Collagen Type IV; 0 / Ki-67 Antigen
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97. Sun K, Huan Y, Unger PD: Clear cell adenocarcinoma of urinary bladder and urethra: another urinary tract lesion immunoreactive for P504S. Arch Pathol Lab Med; 2008 Sep;132(9):1417-22
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  • [Title] Clear cell adenocarcinoma of urinary bladder and urethra: another urinary tract lesion immunoreactive for P504S.
  • CONTEXT: Clear cell carcinoma of the urinary bladder/ urethra is a rare tumor histologically resembling the neoplasms in the female genital tract.
  • Adequate characterization of this tumor has been hampered by its rarity. alpha-Methylacyl-CoA racemase (AMACR)/P504S has been reported to be positive in prostatic adenocarcinoma, papillary renal cell carcinoma, and gastrointestinal neoplasmas; however, it has never been studied in clear cell carcinoma of the lower urinary tract.
  • OBJECTIVE: To investigate the immunohistochemical staining profile in 4 primary clear cell carcinomas of the urinary tract, including P504S, which has not been previously evaluated in these tumors.
  • DESIGN: Four cases of clear cell adenocarcinoma were retrieved from our archives: 2 cases from the urinary bladder (one each from a man and a woman) and 2 cases from the urethra (both from women, 1 in a diverticulum).
  • RESULTS: We found that clear cell carcinomas had a distinct immunoreactive profile: strongly positive for P504S, K903, and CK7, and negative for p63.
  • CONCLUSION: The immunohistochemical profile of clear cell carcinomas shares some similarity to conventional urothelial carcinoma; however, it deviates from those tumors in being positive for P504S and negative for p63.
  • This staining profile may suggest a nonurothelial origin for these tumors, may serve as a useful tool in the differential diagnosis of this tumor, and may reflect its etiology.
  • Because similar expression of P504S is also seen in nephrogenic adenomas, this marker should not be used to differentiate nephrogenic adenomas from clear cell adenocarcinomas.
  • [MeSH-major] Adenocarcinoma, Clear Cell / metabolism. Biomarkers, Tumor / analysis. Racemases and Epimerases / biosynthesis. Urethral Neoplasms / metabolism. Urinary Bladder Neoplasms / metabolism

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  • (PMID = 18788852.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CA-125 Antigen; 0 / CKAP4 protein, human; 0 / Keratin-20; 0 / Keratin-7; 0 / Membrane Proteins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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98. Tsimmerman IaS: [Neuroendocrine tumours of pancreas and gastrointestinal tract]. Klin Med (Mosk); 2009;87(12):7-13
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  • [Title] [Neuroendocrine tumours of pancreas and gastrointestinal tract].
  • This paper reviews data on benign and malignant neuroendocrine tumours of pancreas and gastrointestinal tract including insulinoma, glucagonoma, somatostatinoma, gastrinoma, carcinoid syndrome, and multiple endocrine neoplasms.
  • Their origin, prevalence, clinical manifestations, laboratory and instrumental diagnosis, surgical and medicamentous treatment are discussed.
  • [MeSH-major] Gastrointestinal Neoplasms. Neuroendocrine Tumors. Pancreatic Neoplasms
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Diagnosis, Differential. Diagnostic Imaging. Digestive System Surgical Procedures / methods. Humans. Prevalence. Russia / epidemiology

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  • (PMID = 20135878.001).
  • [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)
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 39
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99. Ausch C, Kim YH, Tsuchiya KD, Dzieciatkowski S, Washington MK, Paraskeva C, Radich J, Grady WM: Comparative analysis of PCR-based biomarker assay methods for colorectal polyp detection from fecal DNA. Clin Chem; 2009 Aug;55(8):1559-63
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  • BACKGROUND: Aberrantly methylated genes are promising biomarkers for the detection of colon adenomas and colorectal cancers (CRCs).
  • The frequency of aberrant methylation of these genes in primary tumors was assessed with methylation-specific PCR (MSP).
  • RESULTS: ITGA4 [integrin, alpha 4 (antigen CD49D, alpha 4 subunit of VLA-4 receptor)] was identified as a novel gene frequently methylated in CRC.
  • Methylated ITGA4 is present in 75% of colon adenomas (n = 36) and 92% of colon adenocarcinomas (n = 75).
  • A fecal DNA qMSP assay for methylated ITGA4 can detect 69% of individuals with colon adenomas (n = 13) with a diagnostic specificity of 79% (n = 28).
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenoma / diagnosis. Colorectal Neoplasms / diagnosis. DNA / analysis. DNA Methylation. Feces / chemistry. Polymerase Chain Reaction / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Cell Line, Tumor. Early Detection of Cancer. Humans. Integrin alpha4 / genetics. Middle Aged. Molecular Diagnostic Techniques / methods. Sensitivity and Specificity

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  • (PMID = 19541867.001).
  • [ISSN] 1530-8561
  • [Journal-full-title] Clinical chemistry
  • [ISO-abbreviation] Clin. Chem.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 143198-26-9 / Integrin alpha4; 9007-49-2 / DNA
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100. Grivas PD, Tzelepi V, Sotiropoulou-Bonikou G, Kefalopoulou Z, Papavassiliou AG, Kalofonos H: Expression of ERalpha, ERbeta and co-regulator PELP1/MNAR in colorectal cancer: prognostic significance and clinicopathologic correlations. Cell Oncol; 2009;31(3):235-47
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  • METHODS: ERalpha, ERbeta and PELP1/MNAR protein expression were evaluated by immunohistochemistry in colorectal normal mucosa, adenomas and adenocarcinomas from 113 patients with colorectal cancer.
  • ERbeta and PELP1/MNAR were detected in the nucleus of epithelial, endothelial, inflammatory, smooth muscle cells and myofibroblasts.
  • When intensity of staining was taken into account, the expression of both proteins was significantly increased in epithelial cells of carcinomas compared to normal mucosa.
  • ERbeta expression in epithelial cells was correlated with decreased disease progression - free survival.
  • PELP1/MNAR overexpression in epithelial cells was found to be an independent favorable prognostic factor.
  • Additionally, the expression of both proteins was significantly increased in stromal myofibroblasts of carcinomas compared to adenomas and normal mucosa.
  • [MeSH-major] Carcinoma / metabolism. Colorectal Neoplasms / metabolism. Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Gene Expression Regulation, Neoplastic. Trans-Activators / metabolism

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  • (PMID = 19478391.001).
  • [ISSN] 1875-8606
  • [Journal-full-title] Cellular oncology : the official journal of the International Society for Cellular Oncology
  • [ISO-abbreviation] Cell. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Co-Repressor Proteins; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / PELP1 protein, human; 0 / Trans-Activators; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC4618984
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