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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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • (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. 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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  • (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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4. 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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5. de Araújo VC, Furuse C, Cury PR, Altemani A, Alves VA, de Araújo NS: Desmoplasia in different degrees of invasion of carcinoma ex-pleomorphic adenoma. Head Neck Pathol; 2007 Dec;1(2):112-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Desmoplasia in different degrees of invasion of carcinoma ex-pleomorphic adenoma.
  • Stroma desmoplasia was studied by immunohistochemistry for alpha-smooth muscle actin (alpha-SMA) in 17 instances of carcinoma ex-pleomorphic adenoma (CXPA) classified according to the presence of epithelial and myoepithelial cells and the degree of invasion: intracapsular, minimally and frankly invasive carcinoma.
  • In "resident" pleomorphic adenoma, no desmoplasia was detected.
  • In the minimally invasive type, myofibroblasts were seen in the septum between islands of malignant cells and in focal peripheral areas of the tumor interpreted as the actual front of invasion.
  • In the frankly invasive type of CXPA showing large blocks of cells, intense desmoplasia was seen, also separating the tumor cells from the neighboring normal tissue.
  • In tumors with cords and/or small nests of cells, desmoplasia was very slight.
  • In the invasive type of CXPA with a myoepithelial component, alpha-SMA expression was seen in the septum between the islands of cells.
  • In CXPA with epithelial and myoepithelial cells, myofibroblasts were rarely seen in the septum separating sheets of cells.
  • Thus, we may deduce that the presence of desmoplasia parallels the capacity of invasion of CXPA by epithelial cells, being minimum in the intracapsular and minimally invasive type of CXPA and increasing as the tumor becomes frankly invasive.
  • [MeSH-major] Adenocarcinoma / pathology. Adenoma, Pleomorphic / pathology
  • [MeSH-minor] Actins / metabolism. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasms, Multiple Primary. Stromal Cells / metabolism. Stromal Cells / pathology

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  • (PMID = 20614261.001).
  • [ISSN] 1936-0568
  • [Journal-full-title] Head and neck pathology
  • [ISO-abbreviation] Head Neck 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
  • [Other-IDs] NLM/ PMC2807519
  • [Keywords] NOTNLM ; Carcinoma ex-pleomorphic adenoma / Desmoplasia / Front of invasion / Immunohistochemistry / Intracapsular carcinoma ex-pleomorphic adenoma / Invasive carcinoma ex-pleomorphic adenoma / Malignant transformation of pleomorphic adenoma / Myofibroblast / α-Smooth muscle actin
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6. 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
MedlinePlus Health Information. consumer health - Liver Cancer.

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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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  • (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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7. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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8. 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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9. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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10. 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


11. 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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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. 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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14. Fromont G, Barcat L, Gaudin J, Irani J: Revisiting the immunophenotype of nephrogenic adenoma. Am J Surg Pathol; 2009 Nov;33(11):1654-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Revisiting the immunophenotype of nephrogenic adenoma.
  • Nephrogenic adenoma (NA) is a rare benign lesion of the urinary tract.
  • Although its histogenesis is still debated, several reports suggest that the lesion has a renal tubular cell origin or differentiation.
  • Unfortunately, it has been reported that NA cells also stained positive for the prostate cancer marker alpha-methylacyl-coenzyme A racemase (AMACR).
  • Because all the previous studies have used an avidin-biotin (AB) detection procedure, and because cells with tubular renal differentiation are likely to contain a high level of endogenous biotin, we investigated in NA the expression of several markers including AMACR, using both AB and biotin-free detection systems.
  • [MeSH-major] Adenoma / immunology. Immunophenotyping / methods. Urologic Neoplasms / immunology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / metabolism. Child. Diagnosis, Differential. Female. Fluorescent Antibody Technique, Indirect. Humans. Kidney Tubules / enzymology. Male. Middle Aged. Prostatic Neoplasms / diagnosis. Racemases and Epimerases / metabolism. Tissue Array Analysis

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  • (PMID = 19730362.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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15. 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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16. Schittenhelm J, Ebner FH, Harter P, Bornemann A: Symptomatic intraspinal oncocytic adrenocortical adenoma. Endocr Pathol; 2009;20(1):73-7
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  • [Title] Symptomatic intraspinal oncocytic adrenocortical adenoma.
  • Benign epithelial tumors are rarely found at this site.
  • We here present the case of a 44-year-old woman with a lesion in the cauda equina that fulfilled the radiologic criteria of schwannoma and caused clinical symptoms for 3 years.
  • The excised tumor was composed of nests of large polygonal cells with eosinophilic partial granular cytoplasm.
  • The tumor showed diffuse positivity for melan-A, synaptophysin, and alpha-inhibin.
  • Steroidogenic factor 1 and cytokeratins 8 and 18 were focally seen in the absence of S-100 and chromogranin.
  • Ultrastructural examination showed abundant mitochondria, suggesting an oncocytic tumor.
  • The diagnosis of an oncocytic adrenal cortical adenoma was made.
  • These extraadrenal tumors are thought to arise from heterotopic adrenocortical tissue in the spinal cavity.
  • Oncocytic tumors are rare neoplasms and they comprise non-functioning variants of adrenal cortical adenomas.
  • To date, only five such intraspinal tumors have been observed.
  • Immunohistochemistry excluded oncocytic paraganglioma, oncocytic meningioma, renal cell carcinoma, alveolar soft part sarcoma, and granular cell tumor.
  • A view of the literature of these rare but probably underdiagnosed intraspinal tumors is given.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Adrenocortical Adenoma / pathology. Spinal Cord Neoplasms / pathology

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  • (PMID = 19039533.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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17. 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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18. 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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19. Herawi M, Drew PA, Pan CC, Epstein JI: Clear cell adenocarcinoma of the bladder and urethra: cases diffusely mimicking nephrogenic adenoma. Hum Pathol; 2010 Apr;41(4):594-601
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  • [Title] Clear cell adenocarcinoma of the bladder and urethra: cases diffusely mimicking nephrogenic adenoma.
  • Although clear cell adenocarcinoma have been described focally mimicking nephrogenic adenoma, we have identified a subset of clear cell adenocarcinoma that diffusely resembles nephrogenic adenoma (nephrogenic adenoma-like clear cell adenocarcinoma).
  • Twelve classic clear cell adenocarcinomas of the bladder and urethra and 7 nephrogenic adenoma-like clear cell adenocarcinomas were compared to 10 nephrogenic adenomas.
  • Classic clear cell adenocarcinomas and nephrogenic adenoma-like clear cell adenocarcinomas comprised 4 men and 15 women.
  • The following features were seen in classic clear cell adenocarcinomas: nephrogenic adenoma-like clear cell adenocarcinomas: predominantly solid pattern (7/12:0/7), marked nuclear pleomorphism (7/12:1/7), prominent nucleoli (5/12:1/7), clear cytoplasm in 50% or greater of tumor (7/12:0/7), and necrosis (8/12:3/7), although the necrosis in nephrogenic adenoma-like clear cell adenocarcinomas was often focal and intraluminal.
  • Both patterns of clear cell adenocarcinomas showed prominent hobnail features, although more pronounced in nephrogenic adenoma-like clear cell adenocarcinomas.
  • Muscularis propria invasion was seen in 5 of 9 classic clear cell adenocarcinomas and 6 of 6 nephrogenic adenoma-like clear cell adenocarcinomas, where evaluable.
  • Classic clear cell adenocarcinoma was associated with urothelial carcinoma (n = 2) and endometriosis (n = 1).
  • The Ki-67 rate in clear cell adenocarcinomas ranged from 10% to 80% compared with 0% to 5% in nephrogenic adenoma.
  • The following antibodies were not helpful in distinguishing nephrogenic adenoma-like clear cell adenocarcinoma from nephrogenic adenoma: CD10, estrogen receptor, p63, high-molecular-weight cytokeratin, and alpha-methylacyl coenzyme-A racemase.
  • PAX2 expression was more frequent in nephrogenic adenoma (89%) compared to both patterns of clear cell adenocarcinoma (29%-32%).
  • The key features discriminating between nephrogenic adenoma-like clear cell adenocarcinoma and nephrogenic adenoma include occasional clear cells, more prominent pleomorphism especially hyperchromatic enlarged nuclei, and extensive muscular invasion.
  • Presence of mitoses and a high rate of Ki-67 expression in lesions resembling nephrogenic adenoma require clinical correlation, close follow-up, and repeat biopsy with more extensive sampling.
  • [MeSH-major] Adenocarcinoma, Clear Cell / diagnosis. Adenoma / diagnosis. Urethral Neoplasms / diagnosis. Urinary Bladder Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Urothelium / pathology

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  • [Copyright] Copyright 2010 Elsevier Inc.
  • (PMID = 20060152.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. 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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21. 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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22. Terada T: Ductal adenoma of the breast: immunohistochemistry of two cases. Pathol Int; 2008 Dec;58(12):801-5
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  • [Title] Ductal adenoma of the breast: immunohistochemistry of two cases.
  • The author reports herein two cases of ductal adenoma of the breast with an emphasis on immunohistochemistry.
  • Histologically, both cases were ductal adenomas composed of ductal epithelial cells and myoepithelial cells.
  • Immunohistochemically, myoepithelial cells were noted in both cases; cytokeratin (CK) 14 and p63 were the most reliable myoepithelial markers, followed by CD10, alpha-smooth muscle actin and S100 protein.
  • The tumor cells expressed p53 protein (case 1, positive cell percentage 5%; case 2, 7%), c-erbB2 (HER2/neu, 76%, 64%), CEA (5%, 0%), estrogen receptor (33%, 84%), but were negative for progesterone receptor.
  • [MeSH-major] Adenoma / diagnosis. Breast Neoplasms / diagnosis. Papilloma, Intraductal / diagnosis
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Diagnosis, Differential. Epithelial Cells / chemistry. Epithelial Cells / pathology. Female. Humans. Immunohistochemistry. Middle Aged


23. Olgac S, Hutchinson B, Tickoo SK, Reuter VE: Alpha-methylacyl-CoA racemase as a marker in the differential diagnosis of metanephric adenoma. Mod Pathol; 2006 Feb;19(2):218-24
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  • [Title] Alpha-methylacyl-CoA racemase as a marker in the differential diagnosis of metanephric adenoma.
  • Metanephric adenoma (MA), a well-described renal neoplasm, usually behaves in a benign fashion.
  • It may have areas that are morphologically similar to papillary renal cell carcinoma (RCC) type, or epithelial (tubular predominant) type Wilms' tumor.
  • Alpha-methylacyl-CoA racemase (AMACR), a molecular marker for prostate carcinoma, has subsequently been found to be overexpressed in breast, colorectal and ovarian cancers, among others.
  • Recent microarray analysis of renal tumors has shown an increase of AMACR mRNA levels in papillary RCC but not in other subtypes.
  • Immunohistochemical stains were performed on paraffin-embedded tissue sections from 25 papillary RCC, 10 MAs and eight Wilms' tumors.
  • AMACR was positive in one (10%) of 10 MAs and 24 (96%) of 25 papillary RCC, while it was negative in all Wilms' tumors.
  • CK7 was positive in 20 of 25 papillary RCCs, focally positive in one Wilms' tumor and was negative in all MAs.
  • CD57 was positive in all six MAs that were stained, focally positive in one of 25 papillary RCC and one of eight Wilms' tumors.
  • WT1 was positive in seven of 10 MAs, three of 25 papillary RCCs and all eight Wilms' tumors.
  • In conclusion, diffuse and strong immunoreactivity for AMACR may be useful in differentiating papillary RCC from MA but a panel which includes AMACR, CK7 and CD57 is better in this differential diagnosis.
  • AMACR is not helpful in differentiating MA from Wilms' tumor, but CD57 is helpful in this differential diagnosis.
  • WT1 may be useful in separating Wilms' tumor from MA and papillary RCC but is not helpful in differentiating MA from papillary RCC.
  • [MeSH-major] Adenoma / pathology. Biomarkers, Tumor / analysis. Kidney Neoplasms / pathology. Racemases and Epimerases / analysis
  • [MeSH-minor] Antigens, CD57 / analysis. Carcinoma, Papillary / enzymology. Carcinoma, Papillary / pathology. Carcinoma, Renal Cell / enzymology. Carcinoma, Renal Cell / pathology. Diagnosis, Differential. Humans. Immunohistochemistry. Keratin-7. Keratins / analysis. WT1 Proteins / analysis. Wilms Tumor / enzymology. Wilms Tumor / pathology

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  • (PMID = 16424894.001).
  • [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] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD57; 0 / Biomarkers, Tumor; 0 / KRT7 protein, human; 0 / Keratin-7; 0 / WT1 Proteins; 68238-35-7 / Keratins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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24. de Araújo VC, Altemani A, Furuse C, Martins MT, de Araújo NS: Immunoprofile of reactive salivary myoepithelial cells in intraductal areas of carcinoma ex-pleomorphic adenoma. Oral Oncol; 2006 Nov;42(10):1011-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoprofile of reactive salivary myoepithelial cells in intraductal areas of carcinoma ex-pleomorphic adenoma.
  • The myoepithelial cell (MC) is a component of various secretory glands, including salivary glands.
  • Besides its function, a tumor suppressor and a tumor facilitating functions have been attributed to this cell.
  • We investigated the immunoprofile of benign MC in intraductal areas of carcinoma ex-pleomorphic adenoma (CXPA), comparing them with the MC in duct-like areas of pleomorphic adenoma, origin of the malignant tumor.
  • Antibodies against myoepithelial markers-CK14, alpha-SMA, calponin, P63, CD10, and D2-40-plus laminin and maspin was applied in four selected cases of intracapsular and minimal invasive CXPA with only luminal differentiation presenting areas of intraductal carcinoma.
  • The immunohistochemical reactions of all the antibodies showed stronger staining in benign MC surrounding the malignant epithelial cells than in benign MC in duct-like areas of pleomorphic adenoma, thus revealing that in the malignization process the benign MC become differentiated and produce important proteins related to the tumor suppressor function.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenoma, Pleomorphic / metabolism. Biomarkers, Tumor / metabolism. Neoplasm Proteins / metabolism. Salivary Gland Neoplasms / metabolism
  • [MeSH-minor] Adult. Cell Differentiation. Disease Progression. Epithelial Cells / metabolism. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged

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  • (PMID = 16757205.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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25. Yu R, Nissen NN, Dhall D, Heaney AP: Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature. Pancreas; 2008 May;36(4):428-31
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  • [Title] Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature.
  • We report a rare case of nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas.
  • The patient's clinical presentation, diagnosis, treatment, pancreas pathology, and follow-up are reviewed.
  • A 60-year-old patient was incidentally found to harbor a pancreatic mass with markedly elevated glucagon levels but without glucagonoma syndrome.
  • She was initially diagnosed with glucagonoma, and the tumor was resected.
  • Pathological examination demonstrated that the tumor was a nonfunctioning islet cell tumor and revealed nesidioblastosis and hyperplasia of alpha cells and microglucagonoma in the apparently normal surgical margin.
  • No pancreatic tumors recurred 36 months after surgery.
  • This is the third case of alpha-cell nesidioblastosis reported in the English literature.
  • Nesidioblastosis and hyperplasia of alpha cells should be considered in the differential diagnosis of hyperglucagonemia.
  • Somatostatin analog may be used to suppress glucagon secretion in alpha-cell hyperplasia.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / pathology. Glucagonoma / pathology. Islets of Langerhans / pathology. Nesidioblastosis / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18437091.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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26. Gupta N, Jadhav K, Ahmed MB, Amberkar VS: Basal cell adenoma in a relatively rare site. J Oral Maxillofac Pathol; 2009 Jul;13(2):101-4

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  • [Title] Basal cell adenoma in a relatively rare site.
  • Basal cell adenoma (BCA) of the salivary glands is an uncommon type of monomorphic adenoma.
  • Histologically, it is seen as nests of isomorphic cells and interlaced trabeculae with a prominent basal membrane.
  • There is also slack, hyaline stroma with absence of a myxoid or chondroid component.
  • We describe a case of BCA of palatal minor salivary glands, a rare site for its occurrence.

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  • [Cites] Hum Pathol. 1982 May;13(5):497-500 [7076228.001]
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  • (PMID = 21887012.001).
  • [ISSN] 0973-029X
  • [Journal-full-title] Journal of oral and maxillofacial pathology : JOMFP
  • [ISO-abbreviation] J Oral Maxillofac Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Other-IDs] NLM/ PMC3162860
  • [Keywords] NOTNLM ; Basal cell adenoma / alpha smooth muscle actin / monomorphic adenoma / pancytokeratin / squamous morules
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27. Davis JR, McNeilly JR, Norris AJ, Pope C, Wilding M, McDowell G, Holland JP, McNeilly AS: Fetal gonadotrope cell origin of FSH-secreting pituitary adenoma - insight into human pituitary tumour pathogenesis. Clin Endocrinol (Oxf); 2006 Nov;65(5):648-54
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  • [Title] Fetal gonadotrope cell origin of FSH-secreting pituitary adenoma - insight into human pituitary tumour pathogenesis.
  • OBJECTIVE: The pathogenesis of human pituitary adenomas remains unclear, but we report a case of FSH-secreting pituitary adenoma whose monohormonal phenotype suggests it was of fetal origin.
  • MEASUREMENTS: Endocrine studies were performed before and after curative surgery, with assessment of tumour hormone secretion in vitro, and immunostaining of tumour tissue for a series of gonadotrope proteins.
  • RESULTS: Immunocytochemistry showed that tumour cells were monohormonal for FSH.
  • Normal components of gonadotrope signalling pathways were expressed, including oestrogen receptor-alpha, activin receptors, secretogranin-II and chromogranin-A. beta-glycan, the putative inhibin coreceptor, was absent.
  • Tumour culture in vitro confirmed secretion of FSH with minimal LH, that was unsuppressed by oestradiol or inhibin-A.
  • Human fetal pituitary tissue contained FSH-only cells at 18 weeks gestation, whereas normal adult pituitary tissue contained only bihormonal gonadotropes.
  • CONCLUSIONS: We propose that this pituitary adenoma represents an indolent tumour of monohormonal fetal gonadotrope cells that originated early in gestation.
  • Pituitary tumours may therefore arise from abnormal persistence of fetal cell types, with extremely slow growth over many years until reaching a size threshold to generate an endocrine syndrome.
  • Understanding fetal pituitary architecture and function may be more informative for new insights into pituitary tumour pathogenesis than classical theories of cancer biology that invoke unrestrained cell proliferation.
  • [MeSH-major] Adenoma / embryology. Gonadotrophs / secretion. Pituitary Neoplasms / embryology
  • [MeSH-minor] Adult. Estradiol / blood. Female. Follicle Stimulating Hormone / analysis. Follicle Stimulating Hormone / blood. Follicle Stimulating Hormone / secretion. Humans. Immunohistochemistry / methods. Immunoradiometric Assay / methods. Luteinizing Hormone / blood. Pituitary Gland, Anterior / embryology. Pituitary Gland, Anterior / secretion. Polycystic Ovary Syndrome / blood. Polycystic Ovary Syndrome / embryology. Polycystic Ovary Syndrome / etiology. Tissue Culture Techniques

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  • (PMID = 17054468.001).
  • [ISSN] 0300-0664
  • [Journal-full-title] Clinical endocrinology
  • [ISO-abbreviation] Clin. Endocrinol. (Oxf)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 4TI98Z838E / Estradiol; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone
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28. Al-Shraim M, Scheithauer BW, Horvath E, Kovacs K, Smyth H, Coire C, Lloyd RV, Jastania R, Al-Gahtany M: Plurihormonal gonadotroph cell pituitary adenoma: report of a unique case. Clin Neuropathol; 2009 May-Jun;28(3):182-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Plurihormonal gonadotroph cell pituitary adenoma: report of a unique case.
  • OBJECTIVE AND IMPORTANCE: Pituitary adenomas producing primarily FSH and to a lesser extent GH, LH, alpha-subunit, TSH and PRL without clinical or laboratory evidence of increased hormone release have not previously been reported.
  • Our aim was to obtain some insight into the possible cytogenesis of this unusual tumor.
  • The tumor was removed by the transsphenoidal approach.
  • RESULT: By light microscopy, the adenoma was chromophobic, weakly PAS-positive, and immunoreactive mainly for FSH (85%) and to a lesser extent for GH (30%), LH (15%), alpha-subunit (3%), TSH (2%), and PRL (1%).
  • Although double immunostaining showed hormone reactivities to be localized largely in separate distinct cells, the tumor was ultrastructurally monomorphous, i.e., consisted of a single-cell type, resembling gonadotrophs.
  • CONCLUSION: The cytogenesis of plurihormonal pituitary adenomas is not fully understood.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Gonadotrophs / metabolism. Gonadotrophs / pathology. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology

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  • [ErratumIn] Clin Neuropathol. 2011 May-Jun;30(3):157. Al-Sharim, M [corrected to Al-Shraim, M]
  • (PMID = 19537135.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 9002-62-4 / Prolactin; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
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29. 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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30. Katori H, Nozawa A, Tsukuda M: Expression of epidermal growth factor receptor, transforming growth factor-alpha and Ki-67 in relationship to malignant transformation of pleomorphic adenoma. Acta Otolaryngol; 2007 Nov;127(11):1207-13
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  • [Title] Expression of epidermal growth factor receptor, transforming growth factor-alpha and Ki-67 in relationship to malignant transformation of pleomorphic adenoma.
  • The data support the hypothesis that increased epidermal growth factor receptor (EGFR) and transforming growth factor (TGF)-alpha expression is associated with early events in malignant transformation of pleomorphic adenoma (PA).
  • OBJECTIVE: In the present study, we attempted to identify EGFR and TGF-alpha expression and Ki-67 index in carcinoma ex-pleomorphic adenoma (Ca ex-PA) and PA.
  • We also compared the presence of EGFR and TGF-alpha and Ki-67 index with clinical data.
  • MATERIALS AND METHODS: The tissues were stained with monoclonal antibodies to EGFR, TGF-alpha and Ki-67.
  • RESULTS: As regards the association of patients' prognosis with EGFR staining and Ki-67 index, a significant increase was observed in patients who died or had residual disease compared with patients who were alive without disease.
  • In the immunohistochemical analysis of EGFR and TGF-alpha and Ki67 index, a significant increase was observed in Ca ex-PA, especially with adenocarcinoma, compared with PA and sialadenitis.
  • [MeSH-major] Adenoma, Pleomorphic / metabolism. Biomarkers, Tumor / biosynthesis. Cell Transformation, Neoplastic. Ki-67 Antigen / genetics. Receptor, Epidermal Growth Factor / biosynthesis. Salivary Gland Neoplasms / metabolism. Transforming Growth Factor alpha / biosynthesis

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  • (PMID = 17851915.001).
  • [ISSN] 0001-6489
  • [Journal-full-title] Acta oto-laryngologica
  • [ISO-abbreviation] Acta Otolaryngol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Transforming Growth Factor alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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31. Yoshida D, Kim K, Noha M, Teramoto A: Anti-apoptotic action by hypoxia inducible factor 1-alpha in human pituitary adenoma cell line, HP-75 in hypoxic condition. J Neurooncol; 2006 Jul;78(3):217-25
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  • [Title] Anti-apoptotic action by hypoxia inducible factor 1-alpha in human pituitary adenoma cell line, HP-75 in hypoxic condition.
  • Hypoxia-inducible factor-1 (HIF-1) alpha is the major transcription factor involved in the adaptive response to hypoxia.
  • The purpose of this study was to investigate whether HIF 1-alpha protects HP75 cells, pituitary adenoma cell line from hypoxia induced apoptosis.
  • HP75 was transfected with siRNA targeting HIF 1-alpha mRNA sequences or scrambled RNA duplexes, followed by subjected to hypoxia (1% oxygen) for 24 h, compared with normoxia (21%).
  • Membrane cDNA microarray was examined to detect gene profiling among the cell in normoxia, hypoxia, or hypoxia following the RNAi.
  • A significantly greater proportion of HP75 cells transfected with specific siRNA duplexes and subsequently exposed to hypoxia demonstrated apoptosis to a large extent when compared with non-transfected cells.
  • Transfection with specific siRNA duplexes knocked down HIF 1-alpha mRNA and protein expression in hypoxia-exposed cells by approximately 80%, whereas transfection with scrambled siRNA duplexes had no noticeable effect on HIF 1-alpha expression.
  • Microarray analysis indicated that HIF1-alpha down-regulated caspase-10.
  • These findings strongly suggest that HIF 1-alpha exerts an antiapoptotic role in HP75 in hypoxia.
  • [MeSH-major] Adenoma / metabolism. Anoxia / metabolism. Apoptosis / physiology. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Pituitary Neoplasms / metabolism
  • [MeSH-minor] Adaptation, Physiological. Cell Line, Tumor. Cell Survival / genetics. Cell Survival / physiology. DNA Fingerprinting. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. RNA, Messenger / analysis. RNA, Small Interfering. Transfection

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  • (PMID = 16779673.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / RNA, Small Interfering
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32. Bioulac-Sage P, Laumonier H, Couchy G, Le Bail B, Sa Cunha A, Rullier A, Laurent C, Blanc JF, Cubel G, Trillaud H, Zucman-Rossi J, Balabaud C, Saric J: Hepatocellular adenoma management and phenotypic classification: the Bordeaux experience. Hepatology; 2009 Aug;50(2):481-9
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  • [Title] Hepatocellular adenoma management and phenotypic classification: the Bordeaux experience.
  • We took advantage of the reported genotype/phenotype classification to analyze our surgical series of hepatocellular adenoma (HCA).
  • No differences were observed in solitary or multiple tumors in terms of hemorrhagic manifestations between groups.
  • Steatosis (tumor), microadenomas (resected specimen), and additional benign nodules were more frequently observed in HNF1alpha-inactivated HCAs (P < 0.01) than in IHCAs.
  • Body mass index > 25, peliosis (tumor), and steatosis in background liver were more frequent in IHCA (P < 0.01).
  • As a consequence, we believe that management of HCA needs to be adapted to the phenotype of these tumors.
  • [MeSH-major] Adenoma, Liver Cell / classification. Liver Neoplasms / classification
  • [MeSH-minor] Adult. Aged. C-Reactive Protein / metabolism. Fatty Acid-Binding Proteins / metabolism. Female. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Male. Middle Aged. Phenotype. Serum Amyloid A Protein / metabolism. Young Adult. beta Catenin / metabolism

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  • (PMID = 19585623.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acid-Binding Proteins; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Serum Amyloid A Protein; 0 / beta Catenin; 9007-41-4 / C-Reactive Protein
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33. Borg SA, Kerry KE, Royds JA, Battersby RD, Jones TH: Correlation of VEGF production with IL1 alpha and IL6 secretion by human pituitary adenoma cells. Eur J Endocrinol; 2005 Feb;152(2):293-300
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  • [Title] Correlation of VEGF production with IL1 alpha and IL6 secretion by human pituitary adenoma cells.
  • We have examined the expression of VEGF and its relationships with IL1 and IL6 in the human pituitary tumour cell line HP75 and a series of human pituitary tumours.
  • We have also looked at the relationship of tumour volume and invasive status to VEGF secretion.
  • METHODS: Surgically resected tumours were routinely cultured in single-cell suspension at 200 K/well (standard unit for culture of dispersed primary pituitary adenoma cells).
  • We measured VEGF, IL1 alpha and IL6 levels by ELISA.
  • Tumour volume and invasion grade were assessed by preoperative magnetic resonance imaging.
  • RESULTS: VEGF was detected in conditioned medium of HP75 cells (900+/-52 pg/ml) and in 82% of tumours tested (range 26-16 464 pg/ml).
  • Tumour volume and secretion of VEGF were significantly associated with levels of IL6 (volume, P = 0.056; VEGF, P < 0.001 (P values based on Spearman's test)) and IL1 alpha produced (volume, P < 0.005; VEGF, P < 0.001).
  • Addition of exogenous IL1 alpha, but not IL6, significantly increased VEGF production.
  • CONCLUSIONS: The significant associations between VEGF and the levels of IL6 and IL1 alpha suggest an important role for these cytokines in the development of these tumours.

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  • (PMID = 15745939.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Interleukin-1; 0 / Interleukin-6; 0 / Vascular Endothelial Growth Factor A
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34. 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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  • (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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35. Miyai S, Yoshimura S, Iwasaki Y, Takekoshi S, Lloyd RV, Osamura RY: Induction of GH, PRL, and TSH beta mRNA by transfection of Pit-1 in a human pituitary adenoma-derived cell line. Cell Tissue Res; 2005 Nov;322(2):269-77
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  • [Title] Induction of GH, PRL, and TSH beta mRNA by transfection of Pit-1 in a human pituitary adenoma-derived cell line.
  • The functional development of pituitary cells depends on the expression of a combination of transcription factors and co-factors.
  • The glycoprotein hormone alpha subunit (alpha SU) is the first hormone to be expressed during pituitary development.
  • In addition to being expressed in follicle-stimulating hormone, luteinizing hormone (LH), and TSH cells, alpha SU is reported to co-localize with GH in pituitary cells.
  • These findings have led to the suggestion that the expression of Pit-1 in cells of the alpha SU-based gonadotropin cell lineage might also lead to the expression of GH.
  • In this study, we transfected HP 75 cells (derived from a human non-functioning pituitary adenoma that expressed alpha SU and LH beta) with Pit-1 by using an adenovirus FLAG-Pit-1 construct.
  • Most of the transfected cells expressed GH mRNA, with fewer cells expressing PRL and TSH beta mRNA.
  • The HP 75 cells expressed the genes for ER and GATA-2, thus allowing their expression of GH, PRL, and TSH beta mRNA in response to Pit-1.
  • These results support the hypothesis that GH can be induced in cells that possess an active alpha SU gene and shed light on the basic molecular mechanism that drives the development of GH, PRL, and TSH beta expression in the alpha SU-based gonadotroph lineage.
  • [MeSH-major] Adenoma / metabolism. Human Growth Hormone / metabolism. Pituitary Neoplasms / metabolism. Prolactin / metabolism. RNA, Messenger / metabolism. Thyrotropin, beta Subunit / metabolism. Transcription Factor Pit-1 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Lineage. GATA2 Transcription Factor / genetics. GATA2 Transcription Factor / metabolism. Glycoprotein Hormones, alpha Subunit / genetics. Glycoprotein Hormones, alpha Subunit / metabolism. Humans. Pituitary Gland / cytology. Pituitary Gland / growth & development. Pituitary Gland / metabolism. Receptors, Estrogen / genetics. Receptors, Estrogen / metabolism. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism

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  • (PMID = 16133148.001).
  • [ISSN] 0302-766X
  • [Journal-full-title] Cell and tissue research
  • [ISO-abbreviation] Cell Tissue Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / GATA2 Transcription Factor; 0 / Glycoprotein Hormones, alpha Subunit; 0 / RNA, Messenger; 0 / Receptors, Estrogen; 0 / Recombinant Fusion Proteins; 0 / Thyrotropin, beta Subunit; 0 / Transcription Factor Pit-1; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin
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36. Wang KL, Weinrach DM, Luan C, Han M, Lin F, Teh BT, Yang XJ: Renal papillary adenoma--a putative precursor of papillary renal cell carcinoma. Hum Pathol; 2007 Feb;38(2):239-46
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  • [Title] Renal papillary adenoma--a putative precursor of papillary renal cell carcinoma.
  • The precursor lesions of renal cell carcinoma (RCC) are unknown.
  • The purpose of this study is to determine the incidence, histomorphological features, and immunohistochemical features of papillary adenoma and elucidate its potential relationship to RCC.
  • Immunohistochemistry was carried out with antibodies specific for alpha-methyl-coenzyme A racemase (AMACR) and glutathione S-transferase alpha (clear-cell RCC marker).
  • Thirty-eight (7%) nephrectomy specimens showed histologic evidence of papillary adenoma.
  • Seven papillary adenomas (18%) occurred in the setting of acquired polycystic kidney disease (APKD), 6 in clear-cell RCCs, 3 in chromophobe RCCs, 2 in end-stage kidney disease, 1 in oncocytoma, 1 in angiomyolipoma, and 1 in renal schwannoma.
  • Furthermore, papillary adenomas were more commonly found in kidneys removed for PRCC (25%, 18/71) than in kidneys harboring clear-cell RCC (1.9%, 6/318).
  • Histomorphologically, papillary adenomas were characterized by varying proportions of papillae and tubules formed by cuboidal cells with scant basophilic cytoplasm similar to those in type 1 PRCC.
  • Adenomas associated with PRCC tend to be multiple in number (61% [11/18] of cases had >2 adenomas; mean, 5).
  • In contrast, 100% of papillary adenomas arising in other conditions had less than 2 adenomas.
  • Most of the adenomas (82%, 31/38) stained strongly for AMACR in a fashion similar to that of PRCC.
  • In this study of surgical specimens, the high coincidence, multifocality, and histologic and immunohistochemical similarities between papillary adenoma and PRCC suggest that the 2 are strongly associated and may represent a continuum of 1 biologic process.
  • In contrast, adenomas associated with APKD exhibit distinct morphological and immunohistochemical features and, therefore, may have an entirely different pathogenesis.
  • [MeSH-major] Carcinoma, Papillary / pathology. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Clear Cell / enzymology. Adenocarcinoma, Clear Cell / pathology. Adenoma. Adenoma, Oxyphilic / enzymology. Adenoma, Oxyphilic / pathology. Adult. Aged. Aged, 80 and over. Angiomyolipoma / enzymology. Angiomyolipoma / pathology. Disease Progression. Female. Glutathione Transferase / analysis. Humans. Immunohistochemistry. Isoenzymes / analysis. Kidney / enzymology. Kidney / pathology. Kidney Failure, Chronic / enzymology. Kidney Failure, Chronic / pathology. Male. Middle Aged. Models, Biological. Polycystic Kidney Diseases / enzymology. Polycystic Kidney Diseases / pathology. Racemases and Epimerases / analysis

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  • (PMID = 17056094.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase alpha; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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37. Antoniades D, Epivatianos A, Markopoulos A, Kolokotronis A, Zaraboukas T: Coexistence of mucous retention cyst and basal cell adenoma arising from the lining epithelium of the cyst. Report of two cases. Med Princ Pract; 2009;18(3):248-52
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  • [Title] Coexistence of mucous retention cyst and basal cell adenoma arising from the lining epithelium of the cyst. Report of two cases.
  • OBJECTIVE: To report 2 cases of coexisting mucous retention cyst and basal cell adenoma arising from the lining epithelium of the cyst.
  • CLINICAL PRESENTATION AND INTERVENTION: Two cases of painless swellings, well-demarcated, soft to palpation, and located in the submucosa of the upper lip were clinically examined with the provisional diagnosis of mucocele or salivary gland tumor.
  • Histological examination showed the presence of a large unilocular cystic cavity in many parts surrounded by single or bilayered lining epithelium composed of flattened to cuboidal cells, and in other parts surrounded by projections of cells arranged in a trabecular pattern far into the cystic cavity.
  • The trabeculae were composed of basal and low columnar cells that sometimes formed small duct-like structures.
  • Immunohistochemistry showed that the lining epithelium of the cystic cavity and the cells of the projections expressed cytokeratin 7 and high-molecular-weight cytokeratins.
  • The cells of the projections were weakly positive for S-100 protein and negative for vimentin and alpha-smooth muscle actin.
  • Based on the results, a diagnosis of coexisting mucous retention cysts and basal cell adenomas arising from the lining epithelium of cysts was made.
  • CONCLUSION: The coexistence of mucous retention cysts and basal cell adenomas arising from the lining epithelium of the cyst is reported.
  • [MeSH-major] Adenoma / complications. Adenoma / pathology. Mucocele / complications. Mucocele / pathology. Salivary Gland Diseases / complications. Salivary Gland Diseases / pathology

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19349732.001).
  • [ISSN] 1423-0151
  • [Journal-full-title] Medical principles and practice : international journal of the Kuwait University, Health Science Centre
  • [ISO-abbreviation] Med Princ Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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38. Sornmayura P, Siripornpitak S, Leela-udomlipi S, Bunyaratvej S: Hepatocellular adenoma: a case report. J Med Assoc Thai; 2010 Mar;93(3):393-7
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  • [Title] Hepatocellular adenoma: a case report.
  • A case of hepatocellular adenoma (HCA) was described in a 26-year-old woman, who was a potential kidney donor for her father and denied taking the oral contraceptive pill.
  • The normal levels of liver enzymes, negative serum markers for hepatitis viruses, and non-elevated alpha- fetoprotein level were detected.
  • Molecular biological studies disclosed three variants of HCAs, i.e., I) with mutation of HNF 1-alpha gene, II) with mutation of beta-catenin gene, and III) no mutation of the two genes.
  • [MeSH-major] Adenoma, Liver Cell / diagnosis. Liver Neoplasms / diagnosis

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  • (PMID = 20420118.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Thailand
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39. Harada O, Ota H, Katsuyama T, Hidaka E, Ishizaka K, Nakayama J: Esophageal gland duct adenoma: immunohistochemical comparison with the normal esophageal gland and ultrastractural analysis. Am J Surg Pathol; 2007 Mar;31(3):469-75
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  • [Title] Esophageal gland duct adenoma: immunohistochemical comparison with the normal esophageal gland and ultrastractural analysis.
  • Esophageal gland duct adenomas are extremely rare tumors.
  • Here, we report the case of a 75-year-old Japanese man who had undergone total gastrectomy for advanced gastric cancer.
  • Esophageal gland duct adenoma was incidentally found in the lower esophagus.
  • It appeared to be detached from the site of gastric cancer and was well demarcated without a capsule.
  • Histologic analysis revealed papillary and cystic structures mainly comprising eosinophilic cells with minimum nuclear atypia.
  • Immunohistochemical analysis revealed that the tumor were diffusely positive for the S100 protein with preserved alpha-SMA-positive myoepithelial cell layers and a characteristic cytokeratin expression pattern similar to that in normal esophageal gland ducts (CK5/6+++, CK7+++, CK17+, CK18+, CK19+++, CK20-, HMWCK+++).
  • This is the first report that refers to the ultrastructural findings of an esophageal gland duct adenoma and describes terminal duct differentiation.
  • We believe that the possibility of an esophageal gland duct adenoma should be considered when diagnosing a ductal or glandular lesion of the esophagus.
  • [MeSH-major] Adenoma / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Aged. Biomarkers, Tumor / analysis. Cardia / pathology. Cardia / surgery. Cell Nucleus / ultrastructure. Cytoplasm / ultrastructure. Humans. Immunohistochemistry. Male. Microscopy, Electron, Transmission. Mucous Membrane / chemistry. Mucous Membrane / pathology. Neoplasms, Second Primary. Stomach Neoplasms / pathology. Stomach Neoplasms / surgery

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  • (PMID = 17325490.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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40. Jurek D, Fleckl E, Marian B: Bile acid induced gene expression in LT97 colonic adenoma cells. Food Chem Toxicol; 2005 Jan;43(1):87-93
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  • [Title] Bile acid induced gene expression in LT97 colonic adenoma cells.
  • LT97 human colonic adenoma cells reflecting early premalignant genotype and growth characteristics have been posed to tumor promoting bile acids in order to identify marker genes that permit identification of tumor promoters in vitro.
  • Physiologically relevant concentrations of desoxycholate (DOC) and chenodesoxycholate (CDC) upregulated expression of c-fos and COX-2 in a concentration- and time-dependent manner.
  • Transient induction of c-fos was seen with the non-promoting taurodesoxycholate (TDOC) as well as DOC, however extended induction at 3 h was only achieved by DOC and CDC reaching 3-6-fold as compared to the control.
  • Stimulation of COX-2 expression was completely specific for the tumor promoting analogs DOC and CDC.
  • Expression of VEGF was stimulated 4-5-fold in the tumor promoter (DOC and CDC) groups and about 2-fold in the non-promoting controls TDOC and GCDC.
  • At later times the tumor promoter specific difference was lost.
  • Our results show that all three genes are modulated in a tumor promoter dependent way and that their upregulation in LT97 adenoma cells can be used for in vitro testing of colon tumor promoters and chemopreventive compounds.
  • [MeSH-major] Adenoma / metabolism. Bile Acids and Salts / pharmacology. Biomarkers, Tumor / metabolism. Colonic Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / drug effects
  • [MeSH-minor] Cell Line, Tumor. Chenodeoxycholic Acid / pharmacology. Cyclooxygenase 2. Deoxycholic Acid / pharmacology. Dose-Response Relationship, Drug. Gene Amplification. Glyceraldehyde-3-Phosphate Dehydrogenases / metabolism. Humans. Isoenzymes / genetics. Isoenzymes / metabolism. Membrane Proteins. Polymerase Chain Reaction. Prostaglandin-Endoperoxide Synthases / genetics. Prostaglandin-Endoperoxide Synthases / metabolism. Proto-Oncogene Proteins c-fos / genetics. Proto-Oncogene Proteins c-fos / metabolism. RNA / isolation & purification. Taurodeoxycholic Acid / pharmacology. Time Factors. Tumor Necrosis Factor-alpha / metabolism. Up-Regulation / drug effects. Up-Regulation / physiology. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 15582199.001).
  • [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 / Bile Acids and Salts; 0 / Biomarkers, Tumor; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins c-fos; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 005990WHZZ / Deoxycholic Acid; 0GEI24LG0J / Chenodeoxycholic Acid; 516-50-7 / Taurodeoxycholic Acid; 63231-63-0 / RNA; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases
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41. Ammons MC, Siemsen DW, Nelson-Overton LK, Quinn MT, Gauss KA: Binding of pleomorphic adenoma gene-like 2 to the tumor necrosis factor (TNF)-alpha-responsive region of the NCF2 promoter regulates p67(phox) expression and NADPH oxidase activity. J Biol Chem; 2007 Jun 15;282(24):17941-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Binding of pleomorphic adenoma gene-like 2 to the tumor necrosis factor (TNF)-alpha-responsive region of the NCF2 promoter regulates p67(phox) expression and NADPH oxidase activity.
  • NCF2, the gene encoding the NADPH oxidase cytosolic component p67(phox), is up-regulated by TNF-alpha, and we recently mapped a region in the NCF2 promoter that was required for this TNF-alpha-dependent response.
  • Because this TNF-alpha-responsive region (TRR) lacked recognizable transcription factor binding elements, we performed studies to identify factors involved in regulating NCF2 via the TRR.
  • Using the TRR sequence as bait in a yeast one-hybrid screen, we identified the zinc finger transcription factor Pleomorphic Adenoma Gene-Like 2 (PLAGL2) as a candidate regulator of NCF2 expression.
  • EMSA and DNA-binding protein affinity purification analyses demonstrated specific binding of in vitro-translated as well as endogenously expressed PLAGL2 to the TRR, and chromatin immunoprecipitation assays demonstrated enhanced binding of endogenous PLAGL2 to the TRR in vivo with TNF-alpha treatment.
  • Knockdown of PLAGL2 protein inhibited up-regulation of NCF2 transcript, p67(phox) protein expression, and subsequent superoxide production in response to TNF-alpha.
  • Furthermore, relative levels of native and SUMO1-modified endogenous PLAGL2 protein were modulated in a time-dependant manner in response to TNF-alpha treatment.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Gene Expression Regulation, Enzymologic. NADPH Oxidase / metabolism. Phosphoproteins. Promoter Regions, Genetic. RNA-Binding Proteins / metabolism. Transcription Factors / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line. Cells, Cultured. Humans. Monocytes / cytology. Monocytes / metabolism. Neutrophils / cytology. Neutrophils / metabolism. Oligonucleotides, Antisense / metabolism. SUMO-1 Protein. Small Ubiquitin-Related Modifier Proteins / metabolism. Tissue Distribution. Two-Hybrid System Techniques

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  • [ErratumIn] J Biol Chem. 2007 Jul 20;282(29):21572
  • (PMID = 17462995.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR42426; United States / NCRR NIH HHS / RR / RR020185
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oligonucleotides, Antisense; 0 / PLAGL2 protein, human; 0 / Phosphoproteins; 0 / RNA-Binding Proteins; 0 / SUMO-1 Protein; 0 / SUMO1 protein, human; 0 / Small Ubiquitin-Related Modifier Proteins; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / neutrophil cytosol factor 67K; EC 1.6.3.1 / NADPH Oxidase
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42. Harada K, Higaki S, Amano A, Hashimoto K, Hashimoto S, Gondo T, Sakaida I: A reduced COX-2 expression and a reduced number of pericryptal myofibroblasts are associated with depressed adenoma of the colon. Oncol Rep; 2007 Jun;17(6):1353-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A reduced COX-2 expression and a reduced number of pericryptal myofibroblasts are associated with depressed adenoma of the colon.
  • The histogenesis of depressed adenoma of the colon has not been sufficiently investigated.
  • Pericryptal myofibroblasts are stromal cells expressing smooth muscle actin, and are involved in the differentiation and multiplication of epithelial cells in the colonic epithelium.
  • COX-2 has been reported to be involved in the development of colon adenoma.
  • We studied the histogenesis of depressed adenoma of the colon by examining the relationship between the presence of pericryptal myofibroblasts and COX-2 expression.
  • Twenty-one depressed adenomas of the colon that had been resected endoscopically between June 1998 and May 2003 (mild-moderate atypia; mean diameter, 6.7 mm) and 23 elevated adenomas that had been resected endoscopically in 2003 (mild-moderate atypia; mean diameter, 11.7 mm), were studied.
  • We performed immunohistochemical staining using alpha-smooth muscle actin antibody to detect pericryptal myofibroblasts.
  • Eighteen (78.3%) of the 23 elevated adenomas and six (28.6%) of the 21 depressed adenomas were positive for pericryptal myofibroblasts immunohistochemically, showing a significant difference (P<0.001).
  • Seventeen elevated adenomas (73.9%) and eight depressed adenomas (38.1%) were positive for COX-2 expression (P=0.016).
  • The histogenesis of depressed adenomas differs from that of elevated adenomas.
  • Our results suggest that a low number of pericryptal myofibroblasts and a low COX-2 expression are associated with depressed adenomas.
  • [MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Cyclooxygenase 2 / metabolism. Fibroblasts / pathology. Membrane Proteins / metabolism. Myoblasts / pathology
  • [MeSH-minor] Actins / analysis. Cell Count. Down-Regulation. Humans

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  • (PMID = 17487390.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Actins; 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human
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43. Nakabayashi M, Shomori K, Kiya S, Shiomi T, Nosaka K, Ito H: Tubular-trabecular type Basal cell adenoma of the parotid gland: a patient report. Yonago Acta Med; 2010 Sep;53(3):65-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tubular-trabecular type Basal cell adenoma of the parotid gland: a patient report.
  • Basal cell adenoma (BCA) is an uncommon benign salivary gland neoplasm that includes isomorphic basaloid cells.
  • The present patient demonstrated a few tumor nests in the fibrous capsule, and her tumor was larger than usual.
  • Histopathologically, the tumor was characterized by multiple duct-like structures and tubular-trabecular masses composed of small isomorphic cells with hyperchromatic, round nuclei and an eosinophilic cytoplasm.
  • It was difficult to determine whether the ductal structures noted in the tumor capsule were invasive.
  • By immunohistochemistry, tumor cells of the tubular nests were positive for cytokeratin 7 and that the outer cells of tubular nests were positive for alpha smooth muscle actin (αSMA) and calponin.
  • Tumor cells were immuno-negative for S-100 protein and glial fibrillary acidic protein.
  • The Ki-67 labeling scores of the cells were extremely low (< 1%).
  • We could achieve an accurate diagnosis of BCA by immunohistochemistry with MIB-1 and other markers.

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  • (PMID = 24031120.001).
  • [ISSN] 0513-5710
  • [Journal-full-title] Yonago acta medica
  • [ISO-abbreviation] Yonago Acta Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Other-IDs] NLM/ PMC3763784
  • [Keywords] NOTNLM ; basal cell adenoma / immunohistochemistry / parotid gland
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44. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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45. Nibe K, Uchida K, Itoh T, Tateyama S: A case of canine apocrine sweat gland adenoma, clear cell variant. Vet Pathol; 2005 Mar;42(2):215-8

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  • [Title] A case of canine apocrine sweat gland adenoma, clear cell variant.
  • A cutaneous mass at the base of the retroauricular region of a 4-year-old, female Golden Retriever was examined pathologically.
  • Histologically, the mass formed multiple nodules consisting of a proliferation of large clear cells with abundant cytoplasm.
  • Mitotic figures among the neoplastic cells were very sparse.
  • The large clear cells were intensely positive for cytokeratins (AE1/AE4, cytokeratin 8 and 18) and moderately positive for lysozyme and contained periodic acid-Schiff-positive granules in the cytoplasm.
  • In addition, small flat cells lined the islands of neoplastic large clear cells, and these were strongly positive for alpha-smooth muscle actin and vimentin, and some were positive for cytokeratin (AE1/AE4), suggesting they were myoepithelial cells.
  • On the basis of these findings, the present tumor was diagnosed as apocrine sweat gland adenoma, clear cell variant.
  • There have been few previous reports of canine apocrine adenomas showing a clear cell morphology.
  • [MeSH-major] Adenoma, Sweat Gland / veterinary. Dog Diseases / pathology. Sweat Gland Neoplasms / veterinary

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  • (PMID = 15753476.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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46. Sakai N, Kim K, Sanno N, Yoshida D, Teramoto A, Shibasaki T: Elevation of growth hormone-releasing hormone receptor messenger ribonucleic acid expression in growth hormone-secreting pituitary adenoma with Gsalpha protein mutation. Neurol Med Chir (Tokyo); 2008;48(11):481-7; discussion 487-8
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  • [Title] Elevation of growth hormone-releasing hormone receptor messenger ribonucleic acid expression in growth hormone-secreting pituitary adenoma with Gsalpha protein mutation.
  • The expression of GHRH receptor (GHRHR) is regulated by GHRH, both of which are known to be expressed in human GH-secreting pituitary adenoma cells.
  • Somatic mutations in the subunit of Gsalpha protein (gsp), lead to the constitutive activation of adenylyl cyclase in pituitary adenomas that secrete GH.
  • It has not been examined how gsp mutations influence GHRHR expression in GH-secreting adenomas.
  • We therefore analyzed the expression levels of GHRHR messenger ribonucleic acid (mRNA) in GH-secreting pituitary adenomas focusing on a gsp mutation.
  • Furthermore, we investigated the effect of GHRH on the expression of GHRHR mRNA in primary cultures of GH-secreting pituitary adenoma cells.
  • GHRHR mRNA expression levels were significantly elevated in gsp mutation-positive GH-secreting adenomas compared with those in gsp mutation-negative ones.
  • In primary-cultured GH-secreting adenoma cells, the increase of GH secretion in response to GHRH was shown in both gsp mutation-positive and -negative adenoma cells with a significantly higher response in the latter adenoma cells.
  • GHRH increased GHRHR mRNA expression level in gsp mutation-negative adenoma cells while it was not influenced by GHRH in gsp mutation-positive adenoma cells.
  • These results suggest that gsp mutations up-regulate GHRHR mRNA expression in GH-secreting pituitary adenoma cells, and that gsp mutations desensitize the adenoma cells to GHRH in terms of their GHRHR mRNA expression probably because of their saturation of GHRH signaling.
  • [MeSH-major] Adenoma / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Growth Hormone-Releasing Hormone / secretion. Mutation, Missense. Neoplasm Proteins / genetics. Nerve Tissue Proteins / genetics. Pituitary Neoplasms / genetics. Point Mutation. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Receptors, Neuropeptide / genetics. Receptors, Pituitary Hormone-Regulating Hormone / genetics
  • [MeSH-minor] Acromegaly / etiology. Acromegaly / surgery. Adult. Amino Acid Substitution. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cell Line, Tumor / secretion. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged

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  • (PMID = 19029774.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / somatotropin releasing hormone receptor; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
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47. Hague A, Hicks DJ, Hasan F, Smartt H, Cohen GM, Paraskeva C, MacFarlane M: Increased sensitivity to TRAIL-induced apoptosis occurs during the adenoma to carcinoma transition of colorectal carcinogenesis. Br J Cancer; 2005 Feb 28;92(4):736-42
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  • [Title] Increased sensitivity to TRAIL-induced apoptosis occurs during the adenoma to carcinoma transition of colorectal carcinogenesis.
  • The death ligand TRAIL (Apo2L) has potential for cancer therapy, since tumour cells are thought to be more sensitive than normal cells.
  • We investigated whether sensitivity to TRAIL increases during the adenoma to carcinoma transition of colorectal carcinogenesis.
  • Under the same culture conditions, we compared the extent of TRAIL-induced apoptosis in four premalignant adenoma and three carcinoma cell lines.
  • Although TRAIL induced some apoptosis in adenoma cultures, the carcinoma cell lines were significantly more sensitive (P<0.001).
  • This finding was recapitulated in an in vitro model of tumour progression in which conversion of the adenoma cell line AA/C1 to a tumorigenic phenotype was associated with increased TRAIL sensitivity (P<0.001).
  • To address this, cell surface receptor expression was measured by flow cytometry.
  • In summary, during colorectal carcinogenesis, there is a marked increase in sensitivity to TRAIL-induced apoptosis associated with progression from benign to malignant tumour that could be exploited for colon cancer therapy, but alterations in cell surface TRAIL receptor expression may not be the primary reason for this change.
  • [MeSH-major] Adenoma / pathology. Apoptosis. Carcinoma / pathology. Cell Transformation, Neoplastic. Colorectal Neoplasms / pathology. Membrane Glycoproteins / metabolism. Receptors, Tumor Necrosis Factor / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / metabolism. Apoptosis Regulatory Proteins. Blotting, Western. Cell Line, Tumor. Electrophoresis, Polyacrylamide Gel. Flow Cytometry. GPI-Linked Proteins. Humans. Mice. Mice, Nude. Receptors, TNF-Related Apoptosis-Inducing Ligand. TNF-Related Apoptosis-Inducing Ligand. Tumor Necrosis Factor Decoy Receptors

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  • (PMID = 15685228.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFRSF10C protein, human; 0 / TNFSF10 protein, human; 0 / Tnfrsf10b protein, mouse; 0 / Tnfsf10 protein, mouse; 0 / Tumor Necrosis Factor Decoy Receptors; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2361885
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48. Holten-Andersen MN, Hansen U, Brünner N, Nielsen HJ, Illemann M, Nielsen BS: Localization of tissue inhibitor of metalloproteinases 1 (TIMP-1) in human colorectal adenoma and adenocarcinoma. Int J Cancer; 2005 Jan 10;113(2):198-206
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Localization of tissue inhibitor of metalloproteinases 1 (TIMP-1) in human colorectal adenoma and adenocarcinoma.
  • However, TIMP-1 also possesses other functions such as inhibition of apoptosis, induction of malignant transformation and stimulation of cell-growth.
  • To clarify the role of TIMP-1 in colorectal tumorigenesis, the expression pattern of TIMP-1 in benign and malignant colorectal tumors was studied.
  • In all cases TIMP-1 expression was found in fibroblast-like cells located at the invasive front but was seen only sporadically in normal mucosa.
  • No TIMP-1 mRNA was seen in any of the cases in benign or malignant epithelial cells, in vascular cells or smooth muscle cells.
  • Combining TIMP-1 in situ hybridization with immunohistochemical staining for alpha-smooth muscle actin or CD68 showed TIMP-1 mRNA in myofibroblasts but not in macrophages.
  • TIMP-1 mRNA was detected in 2 of 7 adenomatous polyps in the adenoma area: in both cases associated with focal stromal inflammation at the epithelial-stromal interface.
  • In conclusion, TIMP-1 expression is a rare event in benign human colon tissue but is highly expressed by myofibroblasts in association with invading colon cancer cells.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adenoma / genetics. Adenoma / pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Tissue Inhibitor of Metalloproteinase-1 / biosynthesis. Tissue Inhibitor of Metalloproteinase-1 / pharmacology
  • [MeSH-minor] Case-Control Studies. Cell Transformation, Neoplastic. Diagnosis, Differential. Fibroblasts / physiology. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Neoplasm Invasiveness. RNA, Messenger / analysis. RNA, Messenger / biosynthesis

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  • (PMID = 15386409.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Tissue Inhibitor of Metalloproteinase-1
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49. Horvath E, Kovacs K, Smyth HS, Cusimano M, Singer W: Silent adenoma subtype 3 of the pituitary--immunohistochemical and ultrastructural classification: a review of 29 cases. Ultrastruct Pathol; 2005 Nov-Dec;29(6):511-24
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  • [Title] Silent adenoma subtype 3 of the pituitary--immunohistochemical and ultrastructural classification: a review of 29 cases.
  • The silent adenoma subtype 3 (SAS-3) of undetermined cellular derivation is a seemingly nonfunctioning aggressive pituitary tumor with a high recurrence rate.
  • At the time of diagnosis SAS-3s are macro- or giant adenomas particularly aggressive in young individuals, especially women.
  • Immunohistochemistry, demonstrating scattered immunoreactivity mostly for GH, PRL, TSH, and alpha-subunit, is not diagnostic.
  • Presently, only TEM permits conclusive diagnosis.
  • Ultrastructurally, the large polar adenoma cells contain abundant RER, masses of SER, extensive multipolar Golgi apparatus, and unevenly clustered mitochondria, displaced by RER and SER, which may show close spatial relationship to RER.
  • Cell membranes often form plexiform interdigitations.
  • The 100- to 200-nm secretory granules accumulate heavily in cell processes, which is a hallmark of glycoprotein hormone cell differentiation.
  • The endothelial cells may contain tubuloreticular inclusions.
  • Complete surgical removal of the large often invasive tumors is difficult necessitating postoperative treatment.
  • Some tumors express somatostatin receptors and respond well to somatostatin analogues, offering long-term control in patients with residual tumor.
  • Possible derivation of SAS-3 from rostral thyrotrophs, a cell type presently known in rodents is contemplated.
  • [MeSH-major] Adenoma / metabolism. Adenoma / ultrastructure. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / ultrastructure

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  • (PMID = 16316952.001).
  • [ISSN] 0191-3123
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 15
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50. 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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51. Jeannot E, Mellottee L, Bioulac-Sage P, Balabaud C, Scoazec JY, Tran Van Nhieu J, Bacq Y, Michalak S, Buob D, Groupe d'étude Génétique des Tumeurs Hépatiques (INSERM Network), Laurent-Puig P, Rusyn I, Zucman-Rossi J: Spectrum of HNF1A somatic mutations in hepatocellular adenoma differs from that in patients with MODY3 and suggests genotoxic damage. Diabetes; 2010 Jul;59(7):1836-44
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  • [Title] Spectrum of HNF1A somatic mutations in hepatocellular adenoma differs from that in patients with MODY3 and suggests genotoxic damage.
  • A subtype of hepatocellular adenoma (HCA) is also caused by biallelic somatic HNF1A mutations (H-HCA), and rare HCA may be related to MODY3.

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  • (PMID = 20393147.001).
  • [ISSN] 1939-327X
  • [Journal-full-title] Diabetes
  • [ISO-abbreviation] Diabetes
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NIEHS NIH HHS / ES / R01-ES-15241; United States / NIEHS NIH HHS / ES / R01 ES015241; United States / NIAAA NIH HHS / AA / R01-AA-16258; United States / NIAAA NIH HHS / AA / R01 AA016258
  • [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 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha
  • [Other-IDs] NLM/ PMC2889786
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52. Drake WM, Berney DM, Kovacs K, Monson JP: Markers of cell proliferation in a GH-producing adenoma of a patient treated with pegvisomant. Eur J Endocrinol; 2005 Aug;153(2):203-5
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  • [Title] Markers of cell proliferation in a GH-producing adenoma of a patient treated with pegvisomant.
  • We report our findings on markers of cell proliferation (Ki-67 labelling index and topoisomerase-alpha expression) in a somatotroph pituitary tumour before and after exposure to pegvisomant, a GH receptor antagonist developed for the treatment of acromegaly.
  • Ki-67 labelling index and topoisomerase-alpha expression were both markedly greater (1-3% compared with 0-0.5% and 15-80% compared with 2-10% respectively) in the pegvisomant-exposed tumour compared with the earlier specimen.
  • However, our data reinforce the requirement for careful radiological surveillance of the pituitary in the context of a drug that does not target the tumour responsible and where serum GH cannot serve as a marker of disease activity or tumour size.

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  • (PMID = 16061824.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / Receptors, Somatotropin; 0 / pegvisomant; 12629-01-5 / Human Growth Hormone; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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53. Yoshida A, Sen C, Asa SL, Rosenblum MK: Composite pituitary adenoma and craniopharyngioma?: an unusual sellar neoplasm with divergent differentiation. Am J Surg Pathol; 2008 Nov;32(11):1736-41
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  • [Title] Composite pituitary adenoma and craniopharyngioma?: an unusual sellar neoplasm with divergent differentiation.
  • The patient was treated with thyroid radioablation and hormone replacement and followed for 7 years, during which time the tumor grew to 4.6 cm.
  • At transsphenoidal surgery, a tumor consisting of a pituitary adenoma and adamantinomatous craniopharyngiomalike components was resected.
  • Both components were closely intermingled, but there was no evidence of an intermediate morphologic phenotype.
  • Immunohistochemically, the adenoma was not only positive for beta-thyroid stimulating hormone, alpha subunit, and pituitary transcription factor 1, but also stained for beta-follicle stimulating hormone, steroidogenic factor-1, adrenocorticotropic hormone, and pituitary-restricted transcription factor (Tpit), exhibiting an unusual plurihormonal profile.
  • This lesion may represent an unusual composite tumor attributable to divergent differentiation of a common precursor.
  • Alternatively, it may be viewed as a pituitary adenoma showing metaplastic change analogous to the development of squamous cell nests of the pars tuberalis from adenohypophyseal endocrine cells.
  • [MeSH-major] Adenoma / pathology. Craniopharyngioma / pathology. Neoplasms, Multiple Primary / pathology. Pituitary Neoplasms / pathology

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  • (PMID = 18769335.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-71-5 / Thyrotropin
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54. Jeannot E, Poussin K, Chiche L, Bacq Y, Sturm N, Scoazec JY, Buffet C, Van Nhieu JT, Bellanné-Chantelot C, de Toma C, Laurent-Puig P, Bioulac-Sage P, Zucman-Rossi J: Association of CYP1B1 germ line mutations with hepatocyte nuclear factor 1alpha-mutated hepatocellular adenoma. Cancer Res; 2007 Mar 15;67(6):2611-6
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  • [Title] Association of CYP1B1 germ line mutations with hepatocyte nuclear factor 1alpha-mutated hepatocellular adenoma.
  • Biallelic somatic mutations of TCF1 coding for hepatocyte nuclear factor 1alpha (HNF1alpha) are found in 50% of the hepatocellular adenoma (HCA) cases usually associated with oral contraception.
  • For 10 genes (CYP1A1, CYP1A2, CYP3A4, CYP3A5, COMT, UGT2B7, NQO1, GSTM1, GSTP1, and GSTT1), we did not find mutations nor differences in the allele distribution among 32 women presenting HNF1alpha-mutated adenomas compared with 58 controls.
  • In contrast, we identified a CYP1B1 germ line heterozygous mutation in 4 of 32 women presenting HNF1alpha-mutated adenomas compared with none in 58 controls.
  • [MeSH-major] Adenoma, Liver Cell / genetics. Cytochrome P-450 Enzyme System / genetics. Germ-Line Mutation. Hepatocyte Nuclear Factor 1-alpha / genetics. Liver Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Alleles. Aryl Hydrocarbon Hydroxylases. Child. Cytochrome P-450 CYP1B1. Female. Genetic Predisposition to Disease. Genotype. Humans. Middle Aged. Mutagenesis, Site-Directed. Pedigree

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  • (PMID = 17363580.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP1B1 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP1B1
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55. Mărgăritescu C, Raica M, Simionescu C, Mogoantă L, Surpăţeanu M, Jaubert F, Bogdan F: Tumoral stroma of salivary pleomorphic adenoma -- histopathological, histochemical and immunohistochemical study. Rom J Morphol Embryol; 2005;46(3):211-23
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  • [Title] Tumoral stroma of salivary pleomorphic adenoma -- histopathological, histochemical and immunohistochemical study.
  • The aims of our paper were to establish the main histopathological, histochemical and immunohistochemical aspects of tumoral stroma from salivary pleomorphic adenomas.
  • Immunohistochemically, they were investigated for AE1-AE3, MNF116, CK8, EMA, vimentin, alpha-actin calponin, S-100, GFAP, collagen IV, and PCNA.
  • The results of our study suggest the key role of neoplastic myoepithelial cell in the achievement of diverse morphological aspects of stroma in such neoplasms.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Salivary Gland Neoplasms / pathology. Stromal Cells / pathology

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  • (PMID = 16444308.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Romania
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56. 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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  • (PMID = 17549440.001).
  • [ISSN] 1432-1173
  • [Journal-full-title] Der Hautarzt; Zeitschrift für 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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57. 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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58. Zucman-Rossi J, Jeannot E, Nhieu JT, Scoazec JY, Guettier C, Rebouissou S, Bacq Y, Leteurtre E, Paradis V, Michalak S, Wendum D, Chiche L, Fabre M, Mellottee L, Laurent C, Partensky C, Castaing D, Zafrani ES, Laurent-Puig P, Balabaud C, Bioulac-Sage P: Genotype-phenotype correlation in hepatocellular adenoma: new classification and relationship with HCC. Hepatology; 2006 Mar;43(3):515-24
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  • [Title] Genotype-phenotype correlation in hepatocellular adenoma: new classification and relationship with HCC.
  • Hepatocellular adenomas are benign tumors that can be difficult to diagnose.
  • A multicentric series of 96 liver tumors with a firm or possible diagnosis of hepatocellular adenoma was reviewed by liver pathologists.
  • No tumors were mutated in both HNF1alpha and beta-catenin enabling tumors to be classified into 3 groups, according to genotype.
  • Tumors with HNF1alpha mutations formed the most important group of adenomas (44 cases).
  • In contrast, the group of tumors defined by beta-catenin activation included 13 lesions with frequent cytological abnormalities and pseudo-glandular formation (P < 10(-5)).
  • The third group of tumors without mutation was divided into two subgroups based on the presence of inflammatory infiltrates.
  • The subgroup of tumors consisting of 17 inflammatory lesions, resembled telangiectatic focal nodular hyperplasias, with frequent cytological abnormalities (P = 10(-3)), ductular reaction (P < 10(-2)), and dystrophic vessels (P = .02).
  • In this classification, hepatocellular carcinoma associated with adenoma or borderline lesions between carcinoma and adenoma is found in 46% of the beta-catenin-mutated tumors whereas they are never observed in inflammatory lesions and are rarely found in HNF1alpha mutated tumors (P = .004).
  • In conclusion, the molecular and pathological classification of hepatocellular adenomas permits the identification of strong genotype-phenotype correlations and suggests that adenomas with beta-catenin activation have a higher risk of malignant transformation.
  • [MeSH-major] Adenoma, Liver Cell / genetics. Carcinoma, Hepatocellular / genetics. Hepatocyte Nuclear Factor 1-alpha / genetics. Liver Neoplasms / genetics. beta Catenin / genetics

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  • [CommentIn] Hepatology. 2006 Mar;43(3):401-4 [16496344.001]
  • [CommentIn] Histopathology. 2007 Dec;51(6):855-6 [17903198.001]
  • (PMID = 16496320.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / beta Catenin
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59. Daniel CR, Bostick RM, Flanders WD, Long Q, Fedirko V, Sidelnikov E, Seabrook ME: TGF-alpha expression as a potential biomarker of risk within the normal-appearing colorectal mucosa of patients with and without incident sporadic adenoma. Cancer Epidemiol Biomarkers Prev; 2009 Jan;18(1):65-73
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  • [Title] TGF-alpha expression as a potential biomarker of risk within the normal-appearing colorectal mucosa of patients with and without incident sporadic adenoma.
  • BACKGROUND: Transforming growth factor-alpha (TGF-alpha), a stimulatory growth factor and member of the epidermal growth factor family, is a mediator of oncogenesis and malignant progression in colorectal carcinogenesis.
  • METHODS: We measured expression of TGF-alpha in biopsies of normal-appearing colorectal mucosa using automated immunohistochemistry and quantitative image analysis in a subsample of 29 cases and 31 controls from a colonoscopy-based case-control study (n = 203) of biomarkers of risk for incident sporadic colorectal adenoma.
  • RESULTS: TGF-alpha expression in the rectum was 51% higher in cases compared with controls (P = 0.05) and statistically significantly associated with accepted risk factors for colorectal neoplasms (36% lower among nonsteroidal anti-inflammatory drug users, 49% lower among women using hormone replacement therapy, 79% higher among persons with a family history of colorectal cancer).
  • CONCLUSIONS: TGF-alpha expression in the normal-appearing rectal mucosa shows promise as an early, potentially modifiable biomarker of risk for colorectal cancer.

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  • (PMID = 19124482.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA115230-02; United States / NCI NIH HHS / CA / R03 CA115230; United States / NCI NIH HHS / CA / R03 CA115230-02
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Transforming Growth Factor alpha
  • [Other-IDs] NLM/ NIHMS253319; NLM/ PMC2995992
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60. Galamb O, Sipos F, Spisák S, Galamb B, Krenács T, Valcz G, Tulassay Z, Molnár B: Potential biomarkers of colorectal adenoma-dysplasia-carcinoma progression: mRNA expression profiling and in situ protein detection on TMAs reveal 15 sequentially upregulated and 2 downregulated genes. Cell Oncol; 2009;31(1):19-29
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  • [Title] Potential biomarkers of colorectal adenoma-dysplasia-carcinoma progression: mRNA expression profiling and in situ protein detection on TMAs reveal 15 sequentially upregulated and 2 downregulated genes.
  • BACKGROUND: As most colorectal cancers (CRC) develop from villous adenomas, studying alterations in gene expression profiles across the colorectal adenoma-dysplasia-carcinoma sequence may yield potential biomarkers of disease progression.
  • METHODS: Total RNA was extracted, amplified, and biotinylated from colonic biopsies of 15 patients with CRC, 15 with villous adenoma and 8 normal controls.
  • Gene expression profiles were evaluated using HGU133Plus2.0 microarrays and disease progression associated data were validated with RT-PCR.
  • RESULTS: 17 genes were validated to show sequentially altered expression at mRNA level through the normal-adenoma-dysplasia-carcinoma progression.
  • Prostaglandin-D2 receptor (PTGDR) and amnionless homolog (AMN) genes revealed gradually decreasing expression while the rest of 15 genes including osteonectin, osteopontin, collagen IV-alpha 1, biglycan, matrix GLAprotein, and von Willebrand factor demonstrated progressively increasing expression.
  • CONCLUSIONS: Downregulated AMN and PTGDR and upregulated osteopontin and osteonectin were found as potential biomarkers of colorectal carcinogenesis and disease progression to be utilized for prospective biopsy screening both at mRNA and protein levels.
  • [MeSH-major] Adenoma / genetics. Biomarkers, Tumor / genetics. Colorectal Neoplasms / genetics. Disease Progression. Gene Expression Profiling. Gene Expression Regulation

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  • (PMID = 19096147.001).
  • [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
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC4618585
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61. Brown RL, Muzzafar T, Wollman R, Weiss RE: A pituitary carcinoma secreting TSH and prolactin: a non-secreting adenoma gone awry. Eur J Endocrinol; 2006 May;154(5):639-43
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  • [Title] A pituitary carcinoma secreting TSH and prolactin: a non-secreting adenoma gone awry.
  • To our knowledge, only one case of a TSH-secreting carcinoma has previously been reported.
  • We describe here a second patient with a pituitary carcinoma producing TSH and prolactin (PRL).
  • Except for mildly increased PRL and elevated alpha-subunit, hormone evaluation was normal.
  • Pathologic examination revealed a chromophobe adenoma with increased mitotic forms.
  • Nine months later, the patient underwent further debulking of metastatic disease.
  • Although development of a carcinoma from a pituitary adenoma is very rare (<0.5%), macroadenomas that become hormonally active should be suspect for transformation into pituitary cancer.

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  • (PMID = 16645009.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK07011; United States / NCRR NIH HHS / RR / RR00055; United States / NCRR NIH HHS / RR / RR18372
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin
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62. Matsuda K, Kousaka Y, Nagamine N, Tsunoda N, Taniyama H: Papillary renal adenoma of distal nephron differentiation in a horse. J Vet Med Sci; 2007 Jul;69(7):763-5
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  • [Title] Papillary renal adenoma of distal nephron differentiation in a horse.
  • The mass was encapsulated with fibrous capsule and composed of variably-sized papillary projections lined by a single layer of flattened to cuboidal neoplastic epithelial cells with no cytological and nuclear atypia.
  • Immunohistochemically, the neoplastic cells were broadly positive for cytokeratin AE1/AE3 and granular staining for alpha-1-antitrypsin was focally detected; this immunohistochemical property was similar to that of the normal distal nephron.
  • From these results, this case was diagnosed as papillary renal adenoma of distal nephron differentiation.

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  • (PMID = 17675811.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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63. Demasi AP, Furuse C, Soares AB, Altemani A, Araújo VC: Peroxiredoxin I, platelet-derived growth factor A, and platelet-derived growth factor receptor alpha are overexpressed in carcinoma ex pleomorphic adenoma: association with malignant transformation. Hum Pathol; 2009 Mar;40(3):390-7
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  • [Title] Peroxiredoxin I, platelet-derived growth factor A, and platelet-derived growth factor receptor alpha are overexpressed in carcinoma ex pleomorphic adenoma: association with malignant transformation.
  • Carcinoma ex pleomorphic adenoma is a rare salivary gland malignancy.
  • It constitutes an important model for the study of carcinogenesis, as it can display the tumor in different stages of progression, from benign pleomorphic adenoma to frankly invasive carcinoma.
  • Growth signaling pathways undergo continuous activation in human tumors, commonly as a consequence of the overexpression of ligands and receptors such as platelet-derived growth factor and platelet-derived growth factor receptor.
  • Hydrogen peroxide is produced after platelet-derived growth factor receptor activation, and it is essential for the sequential phosphorylation cascade that drives cell proliferation and migration.
  • To verify the potential association of peroxiredoxin I, platelet-derived growth factor-A, and platelet-derived growth factor receptor-alpha with carcinoma ex pleomorphic adenoma progression, we investigated the expression of these molecules in carcinoma ex pleomorphic adenoma showing different degrees of invasion.
  • The peroxiredoxin I, platelet-derived growth factor-A, and platelet-derived growth factor receptor-alpha proteins were present in remnant pleomorphic adenoma to only a small extent, but, collectively, they were highly expressed as soon as the malignant phenotype was achieved and remained at elevated concentrations during progression to the advanced stages of carcinoma ex pleomorphic adenoma.
  • Our results indicate that carcinoma ex pleomorphic adenoma cells acquire at least 2 significant advantages relative to their normal counterparts: resistance to oxidative stress-induced apoptosis, conferred by high peroxiredoxin I concentrations, and sustained growth, reflecting platelet-derived growth factor-A and platelet-derived growth factor receptor-alpha overexpression.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenoma, Pleomorphic / metabolism. Cell Transformation, Neoplastic / metabolism. Neoplasms, Second Primary / metabolism. Peroxiredoxins / metabolism. Receptor, Platelet-Derived Growth Factor alpha / metabolism. Salivary Gland Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / metabolism. Humans. Male. Middle Aged. Salivary Glands / metabolism. Salivary Glands / pathology. Signal Transduction

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  • (PMID = 18992915.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 1.11.1.15 / PRDX1 protein, human; EC 1.11.1.15 / Peroxiredoxins; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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64. Halsey MA, Calder KB, Mathew R, Schlauder S, Morgan MB: Expression of alpha-methylacyl-CoA racemase (P504S) in sebaceous neoplasms. J Cutan Pathol; 2010 Apr;37(4):446-51

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  • [Title] Expression of alpha-methylacyl-CoA racemase (P504S) in sebaceous neoplasms.
  • BACKGROUND: Alpha-methylacyl-CoA racemase (AMACR), also known as P504S, is a protein that plays an important role in mitochondrial and peroxisomal beta-oxidation of branched-chain fatty acid and bile acid intermediates.
  • AMACR has been established as a valuable diagnostic marker for prostate cancer and has recently been shown to be useful in the diagnosis of colorectal carcinoma.
  • METHODS: Five samples of normal sebaceous glands as well as five cases each of sebaceous hyperplasia (SH), sebaceous adenoma (SA), basal cell carcinoma (BCC) with sebaceous differentiation and extraocular sebaceous carcinoma (SC) were evaluated for immunohistochemical (IHC) expression of AMACR.
  • CONCLUSIONS: The expression of AMACR is increased in benign sebaceous glands and SH; with decreasing AMACR expression in tumors with less sebaceous differentiation (i.e.
  • [MeSH-major] Adenoma / enzymology. Carcinoma / enzymology. Racemases and Epimerases / metabolism. Sebaceous Gland Neoplasms / enzymology. Sebaceous Glands / enzymology

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  • (PMID = 19638170.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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65. Cossu-Rocca P, Contini M, Brunelli M, Festa A, Pili F, Gobbo S, Eccher A, Mura A, Massarelli G, Martignoni G: S-100A1 is a reliable marker in distinguishing nephrogenic adenoma from prostatic adenocarcinoma. Am J Surg Pathol; 2009 Jul;33(7):1031-6
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  • [Title] S-100A1 is a reliable marker in distinguishing nephrogenic adenoma from prostatic adenocarcinoma.
  • Nephrogenic adenoma is a benign lesion that may occur at any site of the genitourinary tract, usually in association with previous urothelial injuries.
  • In addition to its uncertain origin, there can be diagnostic difficulty in distinguishing nephrogenic adenoma from prostatic adenocarcinoma, particularly with lesions arising in the prostatic urethra.
  • S100A1 is a calcium binding protein that has been recently reported to be expressed in renal tubular cells and in a subset of renal cell neoplasms.
  • Alpha-methylacyl-CoA racemase (AMACR), a recently identified prostate cancer marker, has also been found to be expressed in renal tubules and in some renal epithelial neoplasms.
  • In this study, we investigated the expression of S100A1 and AMACR in 18 nephrogenic adenomas and in 100 prostatic adenocarcinomas.
  • A strong and distinct cytoplasmic or nucleocytoplasmic staining of S100A1 was found in 17 out of 18 cases of nephrogenic adenoma (94%), but never in prostatic adenocarcinoma.
  • In contrast, AMACR expression was detected in 14 of 18 nephrogenic adenomas (78%) and in 96 of 100 prostatic adenocarcinomas (96%).
  • We conclude that (1) S100A1 is a specific and sensitive immunohistochemical marker to differentiate nephrogenic adenoma from prostatic adenocarcinoma;.
  • (3) given that both S100A1 and AMACR have been reported to be expressed in renal tubular cells and in a subset of renal cell neoplasms, our findings confirm the histogenetic relationship between nephrogenic adenoma and renal tubular epithelium.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenoma / diagnosis. Prostatic Neoplasms / diagnosis. S100 Proteins / biosynthesis. Urogenital Neoplasms / diagnosis
  • [MeSH-minor] Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Racemases and Epimerases / biosynthesis. Sensitivity and Specificity

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  • (PMID = 19384190.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / S100 Proteins; 0 / S100A1 protein; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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66. Molinié V, Balaton A, Rotman S, Mansouri D, De Pinieux I, Homsi T, Guillou L: Alpha-methyl CoA racemase expression in renal cell carcinomas. Hum Pathol; 2006 Jun;37(6):698-703
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  • [Title] Alpha-methyl CoA racemase expression in renal cell carcinomas.
  • Alpha-methyl CoA racemase (AMACR), a new molecular marker for prostate cancer, has been recently reported to be one of the most highly expressed genes in papillary renal cell carcinomas (RCCs).
  • We tested the diagnostic usefulness of AMACR antibody in a series of 110 renal tumors: 53 papillary RCCs (33 type 1, 20 type 2); 25 conventional RCCs; 6 chromophobe RCCs; 9 oncocytomas; 5 mucinous tubular and spindle tumors; 2 urothelial carcinomas; 7 angiomyolipomas; and 2 Bellini carcinomas.
  • Both type 1 and type 2 papillary RCCs exhibited cytoplasmic immunoreactivity for AMACR, with diffuse strong granular staining in 96.4% (53/55) of tumors, without correlation with type or nuclear grade.
  • The 5 mucinous, tubular, and spindle cell carcinomas strongly expressed AMACR, and only 5 of 25 clear cell RCCs and 1 of 9 oncocytomas were focally reactive.
  • Because high expression of AMACR is found in papillary RCCs (type 1 and 2) and in mucinous, tubular, and spindle cell carcinomas of the kidney, immunostaining for AMACR should be used in conjunction with other markers when histological typing of a renal tumor is difficult.
  • [MeSH-major] Carcinoma, Renal Cell / enzymology. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / enzymology. Kidney Neoplasms / pathology. Racemases and Epimerases / metabolism
  • [MeSH-minor] Adenocarcinoma, Mucinous / enzymology. Adenocarcinoma, Mucinous / pathology. Adenoma, Oxyphilic / enzymology. Adenoma, Oxyphilic / pathology. Carcinoma, Papillary / enzymology. Carcinoma, Papillary / pathology. Humans. Immunohistochemistry

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  • (PMID = 16733210.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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67. 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


68. Iino K, Oki Y, Yamashita M, Matsushita F, Hayashi C, Yogo K, Nishizawa S, Yamada S, Maekawa M, Sasano H, Nakamura H: Possible relevance between prohormone convertase 2 expression and tumor growth in human adrenocorticotropin-producing pituitary adenoma. J Clin Endocrinol Metab; 2010 Aug;95(8):4003-11
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  • [Title] Possible relevance between prohormone convertase 2 expression and tumor growth in human adrenocorticotropin-producing pituitary adenoma.
  • CONTEXT: Methods for preoperative diagnosis of prohormone convertase 2 (PC2)-positive ACTH-producing pituitary adenomas (APPAs) have not been established.
  • OBJECTIVE: This study was designed to understand the meaning of plasma alphaMSH levels and the role of cell proliferation-signaling molecules in PC2-positive APPAs.
  • RESULTS: Nine adenomas (47.4%) were immunopositive for PC2 and were large and invasive in nature.
  • Eight adenomas (42.1%) were immunopositive for both PC2 and p-Akt, and seven others (36.8%) were immunonegative for both, suggesting significant coexpression of PC2 and p-Akt in tumors.
  • CONCLUSIONS: Our study suggests that PC2 expression and Akt phosphorylation are related at the molecular level, resulting in a change in cell cycle and an increase in pituitary adenoma size.
  • An elevation of plasma alphaMSH could conjecture the activation of the phosphatidylinositol 3/Akt cascade in PC2-positive APPAs and may become a valuable clinical marker of tumor growth in Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Proprotein Convertase 2 / metabolism. alpha-MSH / blood

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  • (PMID = 20501680.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 581-05-5 / alpha-MSH; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.21.94 / Proprotein Convertase 2
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69. Jeannot E, Wendum D, Paye F, Mourra N, de Toma C, Fléjou JF, Zucman-Rossi J: Hepatocellular adenoma displaying a HNF1alpha inactivation in a patient with familial adenomatous polyposis coli. J Hepatol; 2006 Dec;45(6):883-6
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  • [Title] Hepatocellular adenoma displaying a HNF1alpha inactivation in a patient with familial adenomatous polyposis coli.
  • Patients with familial adenomatous polyposis coli (FAP) may rarely develop hepatocellular adenoma.
  • Here we report the case of a 37-year-old FAP woman presenting a hepatocellular adenoma after oestroprogestative oral contraception use.
  • In this steatotic adenoma, we identified an inactivating biallelic mutation of HNF1alpha.
  • Our findings contrast with two hepatocellular adenoma cases related to FAP, for which a biallelic inactivation of the APC gene was previously described.
  • [MeSH-major] Adenomatous Polyposis Coli / complications. Carcinoma, Hepatocellular / genetics. Gene Silencing. Germ-Line Mutation. Hepatocyte Nuclear Factor 1-alpha / genetics. Liver Neoplasms / genetics
  • [MeSH-minor] Adult. Alleles. Diagnosis, Differential. Female. Genes, APC. Genetic Predisposition to Disease. Humans. Immunohistochemistry. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17049664.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha
  • [Other-IDs] NLM/ HALMS130312; NLM/ PMC2121664
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70. Abbud RA, Takumi I, Barker EM, Ren SG, Chen DY, Wawrowsky K, Melmed S: Early multipotential pituitary focal hyperplasia in the alpha-subunit of glycoprotein hormone-driven pituitary tumor-transforming gene transgenic mice. Mol Endocrinol; 2005 May;19(5):1383-91
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  • [Title] Early multipotential pituitary focal hyperplasia in the alpha-subunit of glycoprotein hormone-driven pituitary tumor-transforming gene transgenic mice.
  • Pituitary tumor-transforming gene (PTTG), a securin protein isolated from pituitary tumor cell lines, is highly expressed in invasive tumors and exhibits characteristics of a transforming gene.
  • To determine the role of PTTG in pituitary tumorigenesis, transgenic human PTTG1 was targeted to the mouse pituitary using the alpha-subunit of glycoprotein hormone.
  • Males showed plurihormonal focal pituitary transgene expression with LH-, TSH-, and, unexpectedly, also GH-cell focal hyperplasia and adenoma, associated with increased serum LH, GH, testosterone, and/or IGF-I levels.
  • These results provide evidence for early pituitary plasticity, whereby PTTG overexpression results in a phenotype switch in early pituitary stem cells and promotes differentiated polyhormonal cell focal expansion.

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  • (PMID = 15677710.001).
  • [ISSN] 0888-8809
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA 075979; United States / NICHD NIH HHS / HD / U54 HD 28934
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glycoprotein Hormones, alpha Subunit; 0 / Neoplasm Proteins; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human; 9002-68-0 / Follicle Stimulating Hormone
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71. 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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72. 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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73. Hsu HH, Cheng SF, Chen LM, Liu JY, Chu CH, Weng YJ, Li ZY, Lin CS, Lee SD, Kuo WW, Huang CY: Over-expressed estrogen receptor-alpha up-regulates hTNF-alpha gene expression and down-regulates beta-catenin signaling activity to induce the apoptosis and inhibit proliferation of LoVo colon cancer cells. Mol Cell Biochem; 2006 Sep;289(1-2):101-9
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  • [Title] Over-expressed estrogen receptor-alpha up-regulates hTNF-alpha gene expression and down-regulates beta-catenin signaling activity to induce the apoptosis and inhibit proliferation of LoVo colon cancer cells.
  • Patients that received E(2) replacement therapy were found to have a reduction in the incidence of colon adenoma and carcinoma.
  • However, the mechanisms of ERalpha effects on colorectal cancer cells remained un-clear.
  • LoVo cells were transient transfected to overexpress ERalpha, DNA fragmentation and the activated caspases measurements were performed to evaluate apoptotic effects.
  • The results clearly demonstrated that overexpressed ERalpha with or without E(2) (10(-8) M) treatment could activate caspase -8, -9, and 3 and induce DNA fragmentation in LoVo cell.
  • At the same time, overexpressed ERalpha plus E(2) significantly increases the expression and promoter activity of hTNF-alpha, and the DNA fragmentation effect induced by E(2) plus ERalpha were reduced by the addition of hTNF antibody (0.1 ng(ml).
  • In addition, E(2) plus ERalpha significantly upregulated p21 and p27 levels and downregulated the beta-catenin and its target genes, cyclin D1 and Rb, which regulate the cell cycle and cell proliferation.
  • The results indicate that E(2) plus overexpressed ERalpha induce LoVo cell apoptosis might mediate through the increase of hTNF-alpha gene expression, which in turn activate caspase-8, -9 and caspase-3 and lead to the DNA fragmentation and apoptosis.
  • E(2) plus ERalpha also showed the downregulation of beta-catenin signalings implicating the suppression of proliferation and metastasis of colorectal cells.
  • [MeSH-major] Apoptosis. Colonic Neoplasms / pathology. Estrogen Receptor alpha / metabolism. Gene Expression Regulation. Signal Transduction. Tumor Necrosis Factor-alpha / genetics. beta Catenin / metabolism
  • [MeSH-minor] Adenomatous Polyposis Coli Protein / metabolism. Caspases / metabolism. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Proliferation. DNA Fragmentation. Down-Regulation / genetics. Estrogens / pharmacology. Female. Humans. Male. Middle Aged. Promoter Regions, Genetic / drug effects. Transfection. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / metabolism. Up-Regulation / genetics. Wnt Proteins / metabolism

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  • (PMID = 16628468.001).
  • [ISSN] 0300-8177
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Cell Cycle Proteins; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / TNF protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 0 / Wnt Proteins; 0 / beta Catenin; EC 3.4.22.- / Caspases
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74. Bioulac-Sage P, Rebouissou S, Thomas C, Blanc JF, Saric J, Sa Cunha A, Rullier A, Cubel G, Couchy G, Imbeaud S, Balabaud C, Zucman-Rossi J: Hepatocellular adenoma subtype classification using molecular markers and immunohistochemistry. Hepatology; 2007 Sep;46(3):740-8
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  • [Title] Hepatocellular adenoma subtype classification using molecular markers and immunohistochemistry.
  • Hepatocellular adenomas (HCA) with activated beta-catenin present a high risk of malignant transformation.
  • To permit robust routine diagnosis to allow for HCA subtype classification, we searched new useful markers.
  • We analyzed the expression of candidate genes by quantitative reverse transcription polymerase chain reaction QRT-PCR followed by immunohistochemistry to validate their specificity and sensitivity according to hepatocyte nuclear factor 1 alpha (HNF1alpha) and beta-catenin mutations as well as inflammatory phenotype.
  • Previously described associations were confirmed and in particular the significant association between beta-catenin-activated HCA and hepatocellular carcinomas (HCC) at diagnosis or during follow-up (P < 10(-5)).
  • CONCLUSION: We refined HCA classification and its phenotypic correlations, providing a routine test to classify hepatocellular adenomas using simple and robust immunohistochemistry.
  • [MeSH-major] Adenoma, Liver Cell / classification. Adenoma, Liver Cell / pathology. Biomarkers, Tumor / analysis. Liver Neoplasms / classification. Liver Neoplasms / pathology
  • [MeSH-minor] Adult. Fatty Acid-Binding Proteins / analysis. Fatty Acid-Binding Proteins / genetics. Fatty Acid-Binding Proteins / metabolism. Female. Glucuronosyltransferase / analysis. Glucuronosyltransferase / genetics. Glucuronosyltransferase / metabolism. Glutamate-Ammonia Ligase / analysis. Glutamate-Ammonia Ligase / genetics. Glutamate-Ammonia Ligase / metabolism. Hepatocyte Nuclear Factor 1-alpha / analysis. Hepatocyte Nuclear Factor 1-alpha / genetics. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Immunohistochemistry / methods. Male. beta Catenin / metabolism


75. 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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76. Wang Y, Hua Q: [Clinical significance of HIF-1 alpha,VEGF and VEGF-C expression in papillary thyroid carcinoma]. Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi; 2007 Mar;21(5):204-6, 208
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  • [Title] [Clinical significance of HIF-1 alpha,VEGF and VEGF-C expression in papillary thyroid carcinoma].
  • OBJECTIVE: To evaluate clinical significance of HIF-1 alpha,VEGF and VEGF-C expression in papillary thyroid carcinoma.
  • METHOD: HIF-1a,VEGF and VEGF-C expression were detected by immunohistochemical method in 73 patients of papillary thyroid carcinoma(group I ), 32 patients of thyroid adenoma(group II) and 35 patients of nodular goiter(group II ) respectively.
  • RESULT: The expression of HIF-1 alpha in group I (75.
  • VEGF and VEGF-C expression had a positive correlation with HIF-1 alpha ( P <0. 05).
  • CONCLUSION: In papillary thyroid carcinoma, HIF-1 alpha, VEGF and VEGF-C expression are significantly increased.
  • Furthermore,VEGF and VEGF-C expression may be regulated by HIF-1 alpha, involving in the process of cancer cell spreading to lymph nodes.
  • [MeSH-major] Carcinoma, Papillary / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Thyroid Neoplasms / metabolism. Vascular Endothelial Growth Factor A / metabolism. Vascular Endothelial Growth Factor C / metabolism

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  • (PMID = 17536453.001).
  • [ISSN] 1001-1781
  • [Journal-full-title] Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology, head, and neck surgery
  • [ISO-abbreviation] Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] Controlled Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / VEGFA protein, human; 0 / VEGFC protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C
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77. Dourakis SP, Alexopoulou A, Georgousi KK, Delladetsima JK, Tolis G, Archimandritis AJ: Glucagonoma syndrome: survival 21 years with concurrent liver metastases. Am J Med Sci; 2007 Sep;334(3):225-7
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  • [Title] Glucagonoma syndrome: survival 21 years with concurrent liver metastases.
  • A patient who survived for 21 years since initial discovery of glucagonoma with concurrent liver metastases is described.
  • Psychiatric symptoms, weight loss, necrolytic migratory erythema, diarrhea, and diabetes mellitus developed gradually after diagnosis of the tumor.
  • The longevity of this patient may be related to the slow tumor growth expressed histologically by ischemic necrosis of the malignant cells and in imaging by extensive tumor calcifications, a very rare finding in this type of the tumor.
  • [MeSH-major] Glucagonoma / pathology. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology

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  • (PMID = 17873541.001).
  • [ISSN] 0002-9629
  • [Journal-full-title] The American journal of the medical sciences
  • [ISO-abbreviation] Am. J. Med. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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78. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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79. 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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80. 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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81. 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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82. 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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83. 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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84. 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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85. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


86. Sugai M, Umezu H, Yamamoto T, Jiang S, Iwanari H, Tanaka T, Hamakubo T, Kodama T, Naito M: Expression of hepatocyte nuclear factor 4 alpha in primary ovarian mucinous tumors. Pathol Int; 2008 Nov;58(11):681-6
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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 hepatocyte nuclear factor 4 alpha in primary ovarian mucinous tumors.
  • Hepatocyte nuclear factor 4 alpha (HNF4 alpha) is a member of the nuclear receptor superfamily and is expressed in several endodermal tissues.
  • The aim of the present study was to examine the expression of HNF4 alpha on ovarian epithelial tumors with immunocytochemistry and immunohistochemistry using mAbs recognizing P1 and P2 promoter-driven HNF4 alpha.
  • Ovarian mucinous adenoma, mucinous tumors of borderline malignancy, and mucinous adenocarcinoma had positive nuclear staining for HNF4 alpha (41/45, 91%).
  • One-third (34%) of mucinous tumors had P1-positive staining and most had P1/P2-positive staining (93%).
  • MUC2- and MUC5AC-positive staining was observed in 34% and 95% of mucinous tumors, respectively.
  • The histological subtype of these mucinous tumors was not correlated with HNF4 alpha expression.
  • On cytology it was found that cancer cells in the ascites from ovarian mucinous adenocarcinomas were HNF4 alpha positive, but tumor cells in ascites from other types of ovarian carcinomas were negative for HNF4 alpha.
  • Thus, HNF4 alpha is demonstrated to be a useful marker for histological and cytological diagnosis of ovarian mucinous tumors.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Cystadenocarcinoma, Mucinous / metabolism. Cystadenoma, Mucinous / metabolism. Hepatocyte Nuclear Factor 4 / metabolism. Ovarian Neoplasms / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Ascitic Fluid / metabolism. Ascitic Fluid / pathology. Cell Nucleus / metabolism. Cell Nucleus / pathology. Female. Humans. Immunohistochemistry. Middle Aged. Mucin 5AC. Mucin-2. Mucins / metabolism

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  • (PMID = 18844932.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HNF4A protein, human; 0 / Hepatocyte Nuclear Factor 4; 0 / MUC2 protein, human; 0 / MUC5AC protein, human; 0 / Mucin 5AC; 0 / Mucin-2; 0 / Mucins
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87. Rebouissou S, Imbeaud S, Balabaud C, Boulanger V, Bertrand-Michel J, Tercé F, Auffray C, Bioulac-Sage P, Zucman-Rossi J: HNF1alpha inactivation promotes lipogenesis in human hepatocellular adenoma independently of SREBP-1 and carbohydrate-response element-binding protein (ChREBP) activation. J Biol Chem; 2007 May 11;282(19):14437-46
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HNF1alpha inactivation promotes lipogenesis in human hepatocellular adenoma independently of SREBP-1 and carbohydrate-response element-binding protein (ChREBP) activation.
  • Biallelic inactivating mutations of the transcription factor 1 gene (TCF1), encoding hepatocyte nuclear factor 1alpha (HNF1alpha) were identified in 50% of hepatocellular adenomas (HCA) phenotypically characterized by a striking steatosis.
  • In addition, transcriptional profile analysis of the observed deregulated genes in non-HNF1alpha-mutated HCA as well as in non-tumor livers allowed us to define a specific signature of the HNF1alpha-mutated HCA.
  • In these tumors, lipid composition was dramatically modified according to the transcriptional deregulations identified in the fatty acid synthetic pathway.
  • [MeSH-major] Adenoma, Liver Cell / metabolism. Hepatocyte Nuclear Factor 1-alpha / antagonists & inhibitors. Lipogenesis. Liver / metabolism. Response Elements / physiology. Sterol Regulatory Element Binding Protein 1 / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Citric Acid. Fatty Acids / pharmacokinetics. Fatty Liver / genetics. Fatty Liver / metabolism. Fatty Liver / pathology. Female. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Gluconeogenesis. Glycolysis. Humans. Liver Neoplasms / genetics. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. Signal Transduction

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  • (PMID = 17379603.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Fatty Acids; 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Sterol Regulatory Element Binding Protein 1; 0 / Transcription Factors; 2968PHW8QP / Citric Acid
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88. 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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89. Okada A, Sasaki S, Fujiyoshi Y, Niimi K, Kurokawa S, Umemoto Y, Kohri K: A case of oncocytic papillary renal cell carcinoma. Int J Urol; 2009 Sep;16(9):765-7
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  • [Title] A case of oncocytic papillary renal cell carcinoma.
  • Papillary renal cell carcinomas (RCC) are the second most frequently identified pathological subtypes of RCC.
  • Occasionally, papillary RCC demonstrate pathological characteristics of renal oncocytomas (RO), benign renal tumors.
  • Morphological examination showed oncocytic tumor region and partially scattered regions with papillary structure.
  • Immunohistochemical examinations demonstrated strongly positive staining of alpha-methylacyl-CoA racemase in the papillary region and negative staining of progesterone receptor and CD117 in both regions.
  • No evidence of disease recurrence was found at 12 months' follow up.
  • [MeSH-major] Adenoma, Oxyphilic / pathology. Carcinoma, Papillary / pathology. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology
  • [MeSH-minor] Aged, 80 and over. Biomarkers, Tumor / analysis. Chromosomes, Human, Pair 7. Diagnosis, Differential. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Karyotyping. Racemases and Epimerases. Treatment Outcome

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  • (PMID = 19769658.001).
  • [ISSN] 1442-2042
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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90. Al-Ghnaniem R, Peters J, Foresti R, Heaton N, Pufulete M: Methylation of estrogen receptor alpha and mutL homolog 1 in normal colonic mucosa: association with folate and vitamin B-12 status in subjects with and without colorectal neoplasia. Am J Clin Nutr; 2007 Oct;86(4):1064-72
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  • [Title] Methylation of estrogen receptor alpha and mutL homolog 1 in normal colonic mucosa: association with folate and vitamin B-12 status in subjects with and without colorectal neoplasia.
  • BACKGROUND: Greater promoter methylation in some tumor-suppressor genes underlies most sporadic colorectal cancers and increases with age in the colon.
  • OBJECTIVE: We tested the hypothesis that biomarkers of folate and vitamin B-12 status are associated with estrogen receptor alpha (ERalpha) and mutL homolog 1 (MLH1) promoter methylation in subjects with and without neoplasia.
  • DESIGN: Biopsies of normal-appearing colorectal mucosa from 156 subjects with and without colorectal neoplasia (disease free, n = 76; cancer, n = 28; adenoma, n = 35; hyperplastic polyps, n = 17) were obtained at colonoscopy and used to evaluate methylation in 7 CpG sites in the ERalpha promoter and 13 CpG sites in the MLH1 promoter.
  • Blood samples were obtained for the measurement of serum and red cell folate, serum vitamin B-12, and plasma homocysteine concentrations.
  • RESULTS: The methylation indexes for ERalpha and MLH1 generally were significantly (P < 0.05) higher in subjects with neoplasia than in disease-free subjects.
  • Disease status (P < 0.005), age (P < 0.001), and serum vitamin B-12 concentrations (P = 0.006) were independent determinants of ERalpha promoter methylation.
  • Serum and red cell folate concentrations had no influence on ERalpha promoter methylation.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Colorectal Neoplasms / genetics. DNA Methylation. Estrogen Receptor alpha / metabolism. Folic Acid / blood. Nuclear Proteins / metabolism. Vitamin B 12 / blood
  • [MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Aged. Base Sequence. Biomarkers / blood. Case-Control Studies. Colon / metabolism. Colonic Polyps / genetics. Colonic Polyps / metabolism. Erythrocytes / chemistry. Female. Homocysteine / blood. Humans. Intestinal Mucosa / metabolism. Male. Middle Aged. Nutritional Status

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  • (PMID = 17921385.001).
  • [ISSN] 0002-9165
  • [Journal-full-title] The American journal of clinical nutrition
  • [ISO-abbreviation] Am. J. Clin. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Biomarkers; 0 / Estrogen Receptor alpha; 0 / MLH1 protein, human; 0 / Nuclear Proteins; 0LVT1QZ0BA / Homocysteine; 935E97BOY8 / Folic Acid; P6YC3EG204 / Vitamin B 12
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91. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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92. Chierigo P, Puccetti O, Visonà A, Bassan F, Rahmati M, Lazzarotto M, Franzolin N: [High alpha-fetoprotein persistence after orchiectomy. On a case of uncommon etiology]. Urologia; 2010 Oct-Dec;77 Suppl 17:27-31

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [High alpha-fetoprotein persistence after orchiectomy. On a case of uncommon etiology].
  • [Transliterated title] Persistenza di alfa-fetoproteina elevata dopo orchiectomia. Su di un caso ad etiologia inusuale.
  • BACKGROUND: The following report describes a case of inherited elevation of alpha-fetoprotein (AFP) in a young male suspected for testicular cancer.
  • From this age on, serum AFP can rise above normal in some diseases, e.g. liver disorders, and in some kind of tumors.
  • Careful evaluation for occult cancer showed no abnormality.
  • Histology showed necrotic tissue and could not make a reliable diagnosis.
  • A literature search was done using PubMed by key word "alpha-fetoprotein" and "elevation".
  • Thinking of a hereditary trait, we decided to screen patient's blood-related family members.
  • RESULTS: AFP was found to be elevated in another four out of six relatives within three generations, unrelated to any disease.
  • The existence of this clinically benign condition needs to be considered in both children and adults with unexplained and persistent elevation of AFP, e.g. those diagnosed or suspected for germ cell tumor.
  • [MeSH-major] Metabolism, Inborn Errors / diagnosis. Orchiectomy. alpha-Fetoproteins / analysis
  • [MeSH-minor] Adenoma / complications. Adrenal Gland Neoplasms / complications. Adult. Diagnosis, Differential. Genes, Dominant. Humans. Ischemia / surgery. Male. Neoplasms, Germ Cell and Embryonal / diagnosis. Postoperative Period. Testicular Neoplasms / diagnosis. Testis / blood supply. Testis / pathology. Unnecessary Procedures

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  • (PMID = 21308671.001).
  • [ISSN] 0391-5603
  • [Journal-full-title] Urologia
  • [ISO-abbreviation] Urologia
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AFP protein, human; 0 / alpha-Fetoproteins
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93. Miguita L, Martinez EF, de Araújo NS, de Araújo VC: FGF-2, TGFbeta-1, PDGF-A and respective receptors expression in pleomorphic adenoma myoepithelial cells: an in vivo and in vitro study. J Appl Oral Sci; 2010 Jan-Feb;18(1):83-91
MedlinePlus Health Information. consumer health - Salivary Gland Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FGF-2, TGFbeta-1, PDGF-A and respective receptors expression in pleomorphic adenoma myoepithelial cells: an in vivo and in vitro study.
  • Myoepithelial cells have an important role in salivary gland tumor development, contributing to a low grade of aggressiveness of these tumors.
  • Normal myoepithelial cells are known by their suppressor function presenting increased expression of extracellular matrix genes and protease inhibitors.
  • The importance of stromal cells and growth factors during tumor initiation and progression has been highlighted by recent literature.
  • Many tumors result from the alteration of paracrine growth factors pathways.
  • Growth factors mediate a wide variety of biological processes such as development, tissue repair and tumorigenesis, and also contribute to cellular proliferation and transformation in neoplastic cells.
  • OBJECTIVES: This study evaluated the expression of fibroblast growth factor-2 (FGF-2), transforming growth factor beta-1 (TGFbeta-1), platelet-derived growth factor-A (PDGF-A) and their respective receptors (FGFR-1, FGFR-2, TGFbetaR-II and PDGFR-alpha) in myoepithelial cells from pleomorphic adenomas (PA) by in vivo and in vitro experiments.
  • Myoepithelial cells were obtained from explants of PA tumors provided by surgery from different donors.
  • Immunohistochemistry, cell culture and immunofluorescence assays were used to evaluate growth factor expression.
  • RESULTS: The present findings demonstrated that myoepithelial cells from PA were mainly positive to FGF-2 and FGFR-1 by immunohistochemistry and immunofluorescence.
  • PDGF-A and PDGFR-alpha had moderate expression by immunohistochemistry and presented punctated deposits throughout cytoplasm of myoepithelial cells.
  • CONCLUSIONS: These data suggested that FGF-2 compared to the other studied growth factors has an important role in PA benign myoepithelial cells, probably contributing to proliferation of these cells through the FGFR-1.
  • [MeSH-major] Adenoma, Pleomorphic / pathology. Fibroblast Growth Factor 2 / analysis. Platelet-Derived Growth Factor / analysis. Protein-Serine-Threonine Kinases / analysis. Receptor, Fibroblast Growth Factor, Type 1 / analysis. Receptor, Fibroblast Growth Factor, Type 2 / analysis. Receptor, Platelet-Derived Growth Factor alpha / analysis. Receptors, Transforming Growth Factor beta / analysis. Salivary Gland Neoplasms / pathology. Transforming Growth Factor beta1 / analysis
  • [MeSH-minor] Actins / analysis. Adult. Calcium-Binding Proteins / analysis. Cell Nucleus / ultrastructure. Cells, Cultured. Cytoplasm / ultrastructure. Epithelial Cells / pathology. Female. Fluorescent Antibody Technique. Humans. Immunohistochemistry. Keratin-7 / analysis. Lip Neoplasms / pathology. Male. Microfilament Proteins / analysis. Muscle Cells / pathology. Muscle Proteins / analysis. Muscle, Smooth / pathology. Palatal Neoplasms / pathology. Vimentin / analysis. Young Adult

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  • [Cites] J Mammary Gland Biol Neoplasia. 2005 Jul;10(3):249-60 [16807804.001]
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  • (PMID = 20379686.001).
  • [ISSN] 1678-7765
  • [Journal-full-title] Journal of applied oral science : revista FOB
  • [ISO-abbreviation] J Appl Oral Sci
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Actins; 0 / Calcium-Binding Proteins; 0 / Keratin-7; 0 / Microfilament Proteins; 0 / Muscle Proteins; 0 / Platelet-Derived Growth Factor; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Vimentin; 0 / calponin; 0 / platelet-derived growth factor A; 103107-01-3 / Fibroblast Growth Factor 2; EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / FGFR2 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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94. 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 .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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95. Nishiuchi T, Imachi H, Murao K, Fujiwara M, Muraoka T, Kikuchi F, Nishiuchi Y, Kushida Y, Haba R, Ishida T: Co-existence of glucagonoma with recurrent insulinoma in a patient with multiple endocrine neoplasia-type 1 (MEN-1). Endocrine; 2009 Aug;36(1):20-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Co-existence of glucagonoma with recurrent insulinoma in a patient with multiple endocrine neoplasia-type 1 (MEN-1).
  • Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by tumors of the parathyroid glands, the anterior pituitary, and the endocrine pancreas.
  • He was admitted to our hospital because of recurrent hypoglycemia and a growth of pancreatic tumors.
  • He subsequently underwent surgery for the pancreatic tumors.
  • The majority of these tumor cells were immunohistochemically positive for insulin and negative for glucagon.
  • A few nodules showed immunohistochemical staining positivity for glucagon but they were negative for insulin.
  • Although it is uncommon for patients with MEN1 to exhibit insulinoma and glucagonoma, this case suggests the need for careful analysis of pancreatic tumors in patients with MEN1.
  • [MeSH-major] Glucagonoma / pathology. Insulinoma / pathology. Multiple Endocrine Neoplasia Type 1 / pathology. Pancreatic Neoplasms / pathology


96. Egan JB, Thompson PA, Ashbeck EL, Conti DV, Duggan D, Hibler E, Jurutka PW, Leroy EC, Martínez ME, Mount D, Jacobs ET: Genetic polymorphisms in vitamin D receptor VDR/RXRA influence the likelihood of colon adenoma recurrence. Cancer Res; 2010 Feb 15;70(4):1496-504
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic polymorphisms in vitamin D receptor VDR/RXRA influence the likelihood of colon adenoma recurrence.
  • No gene-level associations were observed for VDR, nor was any single SNP in VDR related to any metachronous adenoma after correction for multiple comparisons.
  • Haplotypes within linkage blocks of RXRA support an approximately 30% reduction in odds of metachronous neoplasia arising in the proximal colon among carriers of specific haplotypes, which was strongest (OR(proximal), 0.67; 95% CI, 0.52-0.86) for carriers of a CGGGCA haplotype (rs1805352, rs3132297, rs3132296, rs3118529, rs3118536, and rs7861779).

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  • (PMID = 20145122.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K07 CA106269; United States / NCI NIH HHS / CA / CA023074-22S1; United States / NCI NIH HHS / CA / P50 CA095060-01; United States / NCI NIH HHS / CA / P30 CA023074; United States / NCI NIH HHS / CA / K07CA106269; United States / NCI NIH HHS / CA / CA95060; United States / NCI NIH HHS / CA / CA77145; United States / NCI NIH HHS / CA / P01 CA041108; United States / NCI NIH HHS / CA / CA23074; United States / NCI NIH HHS / CA / CA095060-01; United States / NCI NIH HHS / CA / P50 CA095060; United States / NCI NIH HHS / CA / R01 CA123065; United States / NCI NIH HHS / CA / K07 CA106269-01A1; United States / NCI NIH HHS / CA / P30 CA023074-22S1; United States / NCI NIH HHS / CA / P01 CA041108-13; United States / NCI NIH HHS / CA / P01CA41108; United States / NCI NIH HHS / CA / CA041108-13; United States / NCI NIH HHS / CA / CA106269-01A1
  • [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 / Receptors, Calcitriol; 0 / Retinoid X Receptor alpha
  • [Other-IDs] NLM/ NIHMS262521; NLM/ PMC3019606
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97. Horvath E, Kovacs K: Pathology of acromegaly. Neuroendocrinology; 2006;83(3-4):161-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The histologic, immunohistochemical and electron microscopic study provided conclusive evidence that a marked diversity exists between the tumors which secrete growth hormone (GH) in excess, such as densely and sparsely granulated GH cell adenoma, the mixed GH prolactin cell adenoma and the mammosomatotrope adenoma.
  • The latter two tumors produce GH and prolactin simultaneously.
  • Densely granulated GH cell tumors may produce thyrotropin and alpha subunit as well.
  • GH cell hyperplasia can also be associated with acromegaly in patients with extrapituitary GH-releasing hormone secreting tumors.
  • [MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Adenoma / therapy. Adenoma / ultrastructure. Carcinoma / metabolism. Carcinoma / pathology. Carcinoma / therapy. Carcinoma / ultrastructure. Humans. Immunohistochemistry

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  • (PMID = 17047379.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
  • [Number-of-references] 22
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98. Kaidi A, Qualtrough D, Williams AC, Paraskeva C: Direct transcriptional up-regulation of cyclooxygenase-2 by hypoxia-inducible factor (HIF)-1 promotes colorectal tumor cell survival and enhances HIF-1 transcriptional activity during hypoxia. Cancer Res; 2006 Jul 1;66(13):6683-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Direct transcriptional up-regulation of cyclooxygenase-2 by hypoxia-inducible factor (HIF)-1 promotes colorectal tumor cell survival and enhances HIF-1 transcriptional activity during hypoxia.
  • Cyclooxygenase (COX)-2, the inducible key enzyme for prostanoid biosynthesis, is overexpressed in most colorectal carcinomas and a subset of colorectal adenomas.
  • For the first time, we report that under hypoxic conditions COX-2 protein levels increase in colorectal adenoma and carcinoma cells.
  • COX-2 up-regulation during hypoxia is accompanied by increased levels of prostaglandin E(2) (PGE(2)), which promote tumor cell survival under hypoxic conditions.
  • In addition, elevated levels of PGE(2) in hypoxic colorectal tumor cells enhance vascular endothelial growth factor expression and HIF-1 transcriptional activity by activating the mitogen-activated protein kinase pathway, showing a potential positive feedback loop that contributes to COX-2 up-regulation during hypoxia.
  • This study identifies COX-2 as a direct target for HIF-1 in colorectal tumor cells.
  • In addition, COX-2 up-regulation represents a pivotal cellular adaptive response to hypoxia with implication for colorectal tumor cell survival and angiogenesis.
  • [MeSH-major] Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Cyclooxygenase 2 / biosynthesis. Hypoxia-Inducible Factor 1, alpha Subunit / physiology
  • [MeSH-minor] Base Sequence. Cell Growth Processes / physiology. Cell Hypoxia / physiology. Cell Survival / physiology. Dinoprostone / metabolism. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. HCT116 Cells. HT29 Cells. Humans. MAP Kinase Signaling System. Molecular Sequence Data. Promoter Regions, Genetic. Transcription, Genetic. Up-Regulation

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  • (PMID = 16818642.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone
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99. de Pinho LK, Neto LV, Cardão Chimelli LM, Gasparetto EL, Warszawski L, do Souto AA, Gadelha MR: Germ cell tumor presenting as sellar mass with suprasellar extension and long history of hypopituitarism. Neuro Endocrinol Lett; 2010;31(3):306-9
MedlinePlus Health Information. consumer health - Pituitary Tumors.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Germ cell tumor presenting as sellar mass with suprasellar extension and long history of hypopituitarism.
  • OBJECTIVE: Primary central nervous system germ cell tumors are rare neoplasms usually located in the pineal and/or suprasellar region.
  • Pure germinomas do not usually secrete beta-human chorionic gonadotropin hormone (beta-HCG) or alpha-fetoprotein (AFP) and diagnosis is made a few weeks or months after beginning of symptoms.
  • CASE: Here we report a case of a pure germinoma in a 20 year-old woman presenting as a sellar mass with suprasellar extension, abnormal serum beta-HCG and a long history of polyuria and polydipsia (4 years), that was initially diagnosed as a pituitary macroadenoma.
  • CONCLUSION: This presentation highlights the importance of thinking in alternative diagnosis to pituitary adenoma when diabetes insipidus is the initial symptom.
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Young Adult

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  • (PMID = 20588244.001).
  • [ISSN] 0172-780X
  • [Journal-full-title] Neuro endocrinology letters
  • [ISO-abbreviation] Neuro Endocrinol. Lett.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
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100. Liu L, Qian J, Singh H, Meiers I, Zhou X, Bostwick DG: Immunohistochemical analysis of chromophobe renal cell carcinoma, renal oncocytoma, and clear cell carcinoma: an optimal and practical panel for differential diagnosis. Arch Pathol Lab Med; 2007 Aug;131(8):1290-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunohistochemical analysis of chromophobe renal cell carcinoma, renal oncocytoma, and clear cell carcinoma: an optimal and practical panel for differential diagnosis.
  • CONTEXT: The separation of chromophobe renal cell carcinoma, oncocytoma, and clear cell renal cell carcinoma using light microscopy remains problematic in some cases.
  • OBJECTIVE: To determine a practical immunohistochemical panel for the differential diagnosis of chromophobe carcinoma.
  • DESIGN: Vimentin, glutathione S-transferase alpha (GST-alpha), CD10, CD117, cytokeratin (CK) 7, and epithelial cell adhesion molecule (EpCAM) were investigated in 22 cases of chromophobe carcinoma, 17 cases of oncocytoma, and 45 cases of clear cell carcinoma.
  • RESULTS: Vimentin and GST-alpha expression were exclusively observed in clear cell carcinoma.
  • CD10 staining was more frequently detected in clear cell carcinoma (91%) than in chromophobe carcinoma (45%) and oncocytoma (29%).
  • CD117 was strongly expressed in chromophobe carcinoma (82%) and oncocytoma (100%), whereas none of the cases of clear cell carcinomas were immunoreactive.
  • EpCAM protein was expressed in all 22 cases of chromophobe carcinoma in more than 90% of cells, whereas all EpCAM-positive oncocytomas (5/17; 29%) displayed positivity in single cells or small cell clusters.
  • CONCLUSIONS: Using the combination of 3 markers (vimentin, GST-alpha, and EpCAM), we achieved 100% sensitivity and 100% specificity for the differential diagnosis of chromophobe carcinoma, oncocytoma, and clear cell carcinoma.
  • The pattern of "vimentin(-)/GST-alpha(-)" effectively excluded clear cell carcinoma, and homogeneous EpCAM expression confirmed the diagnosis of chromophobe carcinoma rather than oncocytoma.
  • CD117 and CK7 were also useful markers and could be used as second-line markers for the differential diagnosis, with high specificity (100%) and high sensitivity (90% and 86%, respectively).
  • [MeSH-major] Adenocarcinoma, Clear Cell / diagnosis. Adenoma, Oxyphilic / diagnosis. Biomarkers, Tumor / analysis. Carcinoma, Renal Cell / diagnosis. Immunoenzyme Techniques / methods. Kidney Neoplasms / diagnosis. Neoplasm Proteins / analysis
  • [MeSH-minor] Diagnosis, Differential. Fluorescent Antibody Technique, Indirect. Humans. Predictive Value of Tests






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