BioMedLib Search Engine [ goto HOMEPAGE ]

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[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

Hazardous Substances Data Bank. ALPHA-METHYL STYRENE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pancreatic endocrine tumors: radiologic-clinicopathologic correlation.

Pancreatic endocrine tumors (PETs) are primarily well-differentiated tumors composed of cells that resemble normal islet cells but that arise from pancreatic ductal cells.

They are classified as functioning or nonfunctioning according to their associated clinical symptoms; insulinoma, gastrinoma, and glucagonoma are the most common functioning PETs.

Most are sporadic, but some are associated with familial syndromes such as multiple endocrine neoplasia type 1, von Hippel-Lindau syndrome, and neurofibromatosis type 1.

At imaging, PETs typically appear as well-defined hypervascular masses, a finding indicative of their rich capillary network.

Cystic change, calcification, and necrosis are common in large tumors, which are associated with a poorer prognosis and a higher prevalence of local and vascular invasion and metastases than are smaller tumors.

Poorly differentiated PETs are rare and have an infiltrative appearance; patients with such tumors have a poor prognosis.

Knowledge of the characteristic clinical, pathologic, and radiologic features of PETs is important in the evaluation and management of patients with a suspected clinical syndrome or a pancreatic mass.

[MeSH-major] Diagnostic Imaging. Pancreatic Neoplasms / diagnosis

[MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / epidemiology. Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / epidemiology. Carcinoma, Islet Cell / pathology. Diagnosis, Differential. Humans. Multiple Endocrine Neoplasia Type 1 / pathology. Neurofibromatosis 1 / pathology. Prevalence. von Hippel-Lindau Disease / pathology

MedlinePlus Health Information. consumer health - Diagnostic Imaging.

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] © RSNA, 2010.

(PMID = 21071369.001).

[ISSN] 1527-1323

[Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc

[ISO-abbreviation] Radiographics

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Hum Pathol. 1982 May;13(5):497-500 [7076228.001]

[Cites] Semin Diagn Pathol. 1987 May;4(2):117-35 [3313598.001]

[Cites] Br J Radiol. 2005 Jul;78(931):642-5 [15961849.001]

[Cites] Radiat Med. 2004 Jul-Aug;22(4):260-4 [15468947.001]

[Cites] Med Oral Patol Oral Cir Bucal. 2006 Mar;11(2):E206-9 [16505803.001]

[Cites] Ann Diagn Pathol. 2003 Oct;7(5):292-5 [14571431.001]

[Cites] J Laryngol Otol. 2000 Jan;114(1):83-5 [10789423.001]

[Cites] J Laryngol Otol. 1997 Feb;111(2):182-5 [9102452.001]

[Cites] Eur J Dent. 2008 Jul;2(3):213-6 [19212550.001]

(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

   

Advertisement

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Microvascular density and hypoxia-inducible factor pathway in pancreatic endocrine tumours: negative correlation of microvascular density and VEGF expression with tumour progression.

Tumour-associated angiogenesis is partly regulated by the hypoxia-inducible factor (HIF) pathway.

The aim of this study is to evaluate angiogenesis and expression of HIF-related molecules in a series of patients with pancreatic endocrine tumours (PETs).

The expression of vascular endothelial growth factor (VEGF), HIF-1alpha, HIF-2alpha and carbonic anhydrase 9 (CA9) was examined by immunohistochemistry in 45 patients with PETs and compared to microvascular density (MVD), endothelial proliferation, tumour stage and survival.

The regulation of HIF signalling appears to be specific in pancreatic endocrine tumours.

[MeSH-major] Adenoma, Islet Cell / blood supply. Adenoma, Islet Cell / metabolism. Neovascularization, Pathologic. Pancreatic Neoplasms / blood supply. Pancreatic Neoplasms / metabolism. Vascular Endothelial Growth Factors / metabolism

[MeSH-minor] Adult. Basic Helix-Loop-Helix Transcription Factors. Carbonic Anhydrases / metabolism. Disease Progression. Female. Humans. Hypoxia-Inducible Factor 1, alpha Subunit. Male. Microcirculation. Transcription Factors / metabolism

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Eur J Cancer. 1998 Apr;34(5):609-18 [9713263.001]

[Cites] Neuroendocrinology. 1986;43(2):159-65 [3523276.001]

[Cites] Gut. 1998 Sep;43(3):422-7 [9863490.001]

[Cites] Clin Cancer Res. 1997 Aug;3(8):1309-16 [9815813.001]

[Cites] J Pathol. 1998 Nov;186(3):313-8 [10211122.001]

[Cites] Oncogene. 1999 Sep 20;18(38):5356-62 [10498889.001]

[Cites] J Clin Invest. 1997 Jul 15;100(2):404-10 [9218518.001]

[Cites] Cancer Res. 1999 Nov 15;59(22):5830-5 [10582706.001]

[Cites] J Clin Endocrinol Metab. 2000 Mar;85(3):1159-62 [10720055.001]

[Cites] Cancer Res. 2000 Mar 1;60(5):1388-93 [10728704.001]

[Cites] Br J Cancer. 2000 Apr;82(8):1441-5 [10780524.001]

[Cites] J Endocrinol. 2000 May;165(2):475-81 [10810311.001]

[Cites] Cancer. 2000 May 15;88(10):2239-45 [10820344.001]

[Cites] Cancer. 2000 Jun 1;88(11):2606-18 [10861440.001]

[Cites] Am J Pathol. 2000 Aug;157(2):411-21 [10934146.001]

[Cites] Cancer Res. 2000 Sep 1;60(17):4693-6 [10987269.001]

[Cites] Cancer Res. 2000 Dec 15;60(24):7075-83 [11156414.001]

[Cites] Curr Opin Cell Biol. 2001 Apr;13(2):167-71 [11248550.001]

[Cites] Cancer Res. 2001 Sep 1;61(17):6394-9 [11522632.001]

[Cites] Nature. 2001 Aug 30;412(6850):877-84 [11528470.001]

[Cites] Genes Chromosomes Cancer. 2001 Oct;32(2):177-81 [11550286.001]

[Cites] Br J Cancer. 2001 Sep 14;85(6):881-90 [11556841.001]

[Cites] Novartis Found Symp. 2001;240:212-25; discussion 225-31 [11727931.001]

[Cites] Int J Cancer. 2002 Feb 20;97(6):719-25 [11857345.001]

[Cites] Nat Rev Cancer. 2002 Jan;2(1):38-47 [11902584.001]

[Cites] Br J Cancer. 2002 Apr 22;86(8):1276-82 [11953885.001]

[Cites] Semin Cell Dev Biol. 2002 Feb;13(1):29-37 [11969369.001]

[Cites] J Clin Oncol. 2002 Jun 1;20(11):2633-42 [12039924.001]

[Cites] Pancreas. 2002 Aug;25(2):122-9 [12142733.001]

[Cites] Clin Cancer Res. 2002 Aug;8(8):2595-604 [12171890.001]

[Cites] J Surg Oncol. 2002 Sep;81(1):45-53; discussion 54 [12210027.001]

[Cites] Nat Rev Cancer. 2002 Sep;2(9):673-82 [12209156.001]

[Cites] J Clin Endocrinol Metab. 2002 Nov;87(11):4961-5 [12414859.001]

[Cites] Microsc Res Tech. 2003 Feb 1;60(2):181-5 [12539172.001]

[Cites] Hum Pathol. 2003 Jan;34(1):18-27 [12605362.001]

[Cites] Histopathology. 2003 May;42(5):482-91 [12713626.001]

[Cites] Virology. 1992 Apr;187(2):620-6 [1312272.001]

[Cites] J Natl Cancer Inst. 1992 Dec 16;84(24):1875-87 [1281237.001]

[Cites] Am J Pathol. 1995 Jul;147(1):9-19 [7541613.001]

[Cites] Br J Cancer. 1995 Aug;72(2):319-23 [7543771.001]

[Cites] Hum Pathol. 1995 Nov;26(11):1196-200 [7590692.001]

[Cites] Mol Endocrinol. 1995 Dec;9(12):1760-70 [8614412.001]

[Cites] Genomics. 1996 May 1;33(3):480-7 [8661007.001]

[Cites] Histopathology. 1997 Mar;30(3):294-301 [9088964.001]

[Cites] Am J Pathol. 1997 Nov;151(5):1417-23 [9358768.001]

[Cites] Am J Clin Pathol. 1998 Mar;109(3):286-93 [9495200.001]

[Cites] Histopathology. 1998 Feb;32(2):133-8 [9543669.001]

[Cites] Mod Pathol. 1998 Apr;11(4):329-33 [9578082.001]

[Cites] J Pathol. 1998 Feb;184(2):119-22 [9602700.001]

[Cites] Nat Med. 2003 Jun;9(6):653-60 [12778163.001]

[Cites] Nat Med. 2003 Jun;9(6):677-84 [12778166.001]

[Cites] Nat Rev Cancer. 2003 Jun;3(6):401-10 [12778130.001]

[Cites] Cancer Cell. 2003 Aug;4(2):133-46 [12957288.001]

[Cites] Gastroenterology. 2003 Oct;125(4):1094-104 [14517793.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12596-601 [9770531.001]

(PMID = 15558070.001).

[ISSN] 0007-0920

[Journal-full-title] British journal of cancer

[ISO-abbreviation] Br. J. Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Transcription Factors; 0 / Vascular Endothelial Growth Factors; 0 / endothelial PAS domain-containing protein 1; EC 4.2.1.1 / Carbonic Anhydrases

[Other-IDs] NLM/ PMC2361752

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

Genetic Alliance. consumer health - Glucagonoma.

Genetic Alliance. consumer health - Glucagonoma Syndrome.

MedlinePlus Health Information. consumer health - Liver Cancer.

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Overexpression of the oxygen sensors PHD-1, PHD-2, PHD-3, and FIH Is associated with tumor aggressiveness in pancreatic endocrine tumors.

PURPOSE: Tumor hypoxia is associated with poor prognosis and resistance to treatment.

Our aim was to assess the expression of proteins that act as cellular oxygen sensors, directly regulating the hypoxia inducible factor (HIF) pathway, i.e., prolyl hydroxylase domain proteins (PHD)-1, PHD-2, PHD-3, and FIH in pancreatic endocrine tumors (PET).

The results were correlated with histoprognostic factors including Ki-67 index, presence of a fibrotic focus, and microvascular density (MVD).

FIH stromal expression was found in 23% of PETs and correlated with higher FIH nuclear expression (P = 0.0004) and poorer disease-free survival (P = 0.0018).

CONCLUSION: HIF regulatory proteins are highly expressed in PET and their expression is correlated with tumor metastases, tumor recurrence, and prognosis.

[MeSH-major] Cell Hypoxia. Dioxygenases / metabolism. Pancreatic Neoplasms / metabolism. Procollagen-Proline Dioxygenase / metabolism. Repressor Proteins / metabolism

[MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Adenoma, Islet Cell / metabolism. Adenoma, Islet Cell / pathology. Adult. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / secondary. Cell Differentiation. Cell Proliferation. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Hypoxia-Inducible Factor-Proline Dioxygenases. Immunoenzyme Techniques. Liver Neoplasms / metabolism. Liver Neoplasms / secondary. Lymphatic Metastasis. Male. Microcirculation. Mixed Function Oxygenases. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / metabolism. Neovascularization, Pathologic. Tissue Array Analysis

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18927305.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Repressor Proteins; EC 1.- / Mixed Function Oxygenases; EC 1.13.11.- / Dioxygenases; EC 1.14.11.- / HIF1AN protein, human; EC 1.14.11.2 / EGLN1 protein, human; EC 1.14.11.2 / Procollagen-Proline Dioxygenase; EC 1.14.11.29 / EGLN3 protein, human; EC 1.14.11.29 / Hypoxia-Inducible Factor-Proline Dioxygenases

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Estrogen biosynthesis in human H295 adrenocortical carcinoma cells.

The direct secretion of estradiol by adrenocortical tumors requires, in addition to the expression of aromatase (CYP19), the expression of one or more of the reductive 17beta-hydroxysteroid dehydrogenases.

The expression of CYP19 transcripts and protein were markedly induced in the H295 adrenocortical carcinoma cell line after treatment with either forskolin or vasoactive intestinal peptide (VIP).

The reductive type 5 17beta-hydroxysteroid dehydrogenase (AKR1C3) was also constitutively expressed in the H295 cells but neither its mRNA transcript nor protein levels were altered after forskolin or VIP treatment.

Western immunoblotting of an estrogen-secreting adrenal carcinoma revealed notable levels of both aromatase and AKR1C3 expression while an aldosterone-producing adrenal adenoma lacked aromatase expression and showed a reduced level of AKR1C3 expression.

Immunohistochemistry of the carcinoma-bearing adrenal revealed localization of AKR1C3 not only in the tumor but also principally in the zona reticularis of the normal adrenal tissue.

Genetic Alliance. consumer health - Adrenocortical Carcinoma.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Clin Endocrinol Metab. 2001 Feb;86(2):649-52 [11158024.001]

[Cites] J Clin Endocrinol Metab. 1996 Sep;81(9):3173-6 [8784064.001]

[Cites] J Steroid Biochem Mol Biol. 2003 Mar;84(4):485-92 [12732294.001]

[Cites] J Endocrinol. 2004 Jan;180(1):125-33 [14709151.001]

[Cites] J Mol Endocrinol. 2004 Jun;32(3):869-77 [15171718.001]

[Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]

[Cites] J Clin Invest. 1977 Aug;60(2):455-64 [874104.001]

[Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8948-52 [2848247.001]

[Cites] Lab Invest. 1990 Jul;63(1):132-6 [2374399.001]

[Cites] Cancer Res. 1990 Sep 1;50(17):5488-96 [2386954.001]

[Cites] Mol Endocrinol. 1993 Mar;7(3):423-33 [8387159.001]

[Cites] J Clin Endocrinol Metab. 1993 Sep;77(3):731-7 [8396576.001]

[Cites] Mol Cell Endocrinol. 1994 Apr;100(1-2):45-50 [8056157.001]

[Cites] J Urol. 1995 Mar;153(3 Pt 2):1039-40 [7853554.001]

[Cites] Medicine (Baltimore). 1965 Jan;44:37-79 [14264352.001]

[Cites] Mol Cell Endocrinol. 2004 Dec 30;228(1-2):23-38 [15541570.001]

[Cites] Steroids. 2004 Dec;69(13-14):795-801 [15582534.001]

[Cites] J Steroid Biochem Mol Biol. 2005 May;95(1-5):35-9 [16024247.001]

[Cites] Pharmacol Rev. 2005 Sep;57(3):359-83 [16109840.001]

[Cites] J Endocrinol. 2006 Jan;188(1):59-68 [16394175.001]

[Cites] J Clin Endocrinol Metab. 2006 Jun;91(6):2027-37 [16551738.001]

[Cites] J Steroid Biochem Mol Biol. 2006 Nov;101(4-5):254-62 [16979335.001]

[Cites] Arch Biochem Biophys. 2007 Aug 15;464(2):241-50 [17537398.001]

[Cites] J Endocrinol. 2007 Oct;195(1):39-48 [17911395.001]

[Cites] Hum Reprod. 2007 Nov;22(11):2981-91 [17848403.001]

[Cites] Eur J Endocrinol. 2003 Apr;148(4):457-61 [12656667.001]

(PMID = 19026713.001).

[ISSN] 0303-7207

[Journal-full-title] Molecular and cellular endocrinology

[ISO-abbreviation] Mol. Cell. Endocrinol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA090744-07; United States / NCI NIH HHS / CA / R01 CA090744; United States / NCI NIH HHS / CA / R01 CA090744-07; United States / NCI NIH HHS / CA / R01-CA90744

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

[Chemical-registry-number] 0 / Estrogens; 1F7A44V6OU / Colforsin; 37221-79-7 / Vasoactive Intestinal Peptide; EC 1.1.- / 17-Hydroxysteroid Dehydrogenases; EC 1.1.- / 3-Hydroxysteroid Dehydrogenases; EC 1.1.1.- / AKR1C3 protein, human; EC 1.1.1.- / Hydroxyprostaglandin Dehydrogenases; EC 1.1.1.145 / 3 beta-hydroxysteroid dehydrogenase type II; EC 1.1.1.145 / Progesterone Reductase; EC 1.14.14.1 / Aromatase; EC 1.14.15.4 / Cytochrome P-450 CYP11B2; EC 1.14.15.4 / Steroid 11-beta-Hydroxylase; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase

[Other-IDs] NLM/ NIHMS99072; NLM/ PMC2673546

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The pleomorphic adenoma gene (PLAG) family of transcription factors regulates a wide range of physiological processes, including cell proliferation, tissue-specific gene regulation, and embryonic development, although little is known regarding the mechanisms that regulate PLAG protein activity.

We show that PC2 cooperates with PLAGL2 and PU.1 to enhance the activity of a known PLAGL2 target promoter (NCF2).

The PLAGL2-binding element in the NCF2 promoter consisted of the core sequence of the bipartite PLAG1 consensus site, but lacked the G-cluster motif, and was recognized by PLAGL2 zinc fingers 5 and 6.

Co-immunoprecipitation and promoter-reporter studies reveal that the effect of PC2 on PLAGL2 target promoter activity was conferred via the C-terminus of PLAGL2, the region that is required for PC2 binding and contains the PLAGL2 activation domain.

Importantly, chromatin immunoprecipitation analysis and PC2 knockdown studies confirmed that endogenous PC2 protein associated with the NCF2 promoter in MM1 cells in the region occupied by PLAGL2, and was required for PLAGL2 target promoter activity in TNF-alpha-treated MM1 cells, respectively.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Published by Elsevier B.V.

[Cites] Cancer Res. 2000 Jan 1;60(1):106-13 [10646861.001]

[Cites] Blood. 2005 Apr 1;105(7):2900-7 [15585652.001]

[Cites] Cancer Res. 2000 Sep 1;60(17):4869-72 [10987300.001]

[Cites] J Biol Chem. 2001 Oct 19;276(42):39368-78 [11483614.001]

[Cites] J Leukoc Biol. 2002 Jan;71(1):163-72 [11781392.001]

[Cites] Cancer Res. 2002 Mar 1;62(5):1510-7 [11888928.001]

[Cites] J Biol Chem. 2002 May 3;277(18):15851-8 [11832486.001]

[Cites] J Biol Chem. 2002 May 31;277(22):19673-8 [11882654.001]

[Cites] Nucleic Acids Res. 2002 Jul 1;30(13):2930-9 [12087179.001]

[Cites] Nature. 2002 Aug 8;418(6898):641-6 [12167862.001]

[Cites] J Biol Chem. 2003 Feb 21;278(8):6041-9 [12473647.001]

[Cites] Comb Chem High Throughput Screen. 2003 Jun;6(4):381-7 [12769682.001]

[Cites] Genes Chromosomes Cancer. 2004 Feb;39(2):126-37 [14695992.001]

[Cites] Ann N Y Acad Sci. 2003 Dec;1010:264-5 [15033731.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4924-9 [15044690.001]

[Cites] Assay Drug Dev Technol. 2002 Nov;1(1 Pt 1):97-104 [15090161.001]

[Cites] J Biol Chem. 2004 Aug 20;279(34):36121-31 [15208321.001]

[Cites] Eur J Biochem. 1995 Oct 1;233(1):73-82 [7588776.001]

[Cites] Nat Genet. 1997 Feb;15(2):170-4 [9020842.001]

[Cites] Cancer Res. 1997 May 15;57(10):2029-34 [9158001.001]

[Cites] Int J Cancer. 2005 Jul 10;115(5):690-700 [15751035.001]

[Cites] Curr Opin Genet Dev. 2005 Oct;15(5):490-5 [16098738.001]

[Cites] J Biol Chem. 2005 Dec 9;280(49):40773-81 [16207715.001]

[Cites] Nature. 2006 Aug 10;442(7103):700-4 [16799563.001]

[Cites] FEBS Lett. 2006 Sep 4;580(20):4784-92 [16904669.001]

[Cites] Genomics. 2006 Nov;88(5):650-8 [16928428.001]

[Cites] J Cell Physiol. 2007 Jan;210(1):16-25 [17063461.001]

[Cites] Int J Oncol. 2007 Apr;30(4):765-74 [17332914.001]

[Cites] J Biol Chem. 2007 Jun 15;282(24):17941-52 [17462995.001]

[Cites] Biochimie. 2007 Dec;89(12):1439-46 [17870225.001]

[Cites] J Cell Biochem. 2008 Feb 15;103(3):730-9 [17551969.001]

[Cites] EMBO J. 1997 May 15;16(10):2814-25 [9184226.001]

[Cites] J Biol Chem. 1998 Sep 4;273(36):23026-32 [9722527.001]

[Cites] Dev Growth Differ. 2004 Oct;46(5):459-70 [15606491.001]

[Cites] Int J Oncol. 2000 Jun;16(6):1107-10 [10811981.001]

(PMID = 20025940.001).

[ISSN] 1879-0038

[Journal-full-title] Gene

[ISO-abbreviation] Gene

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / RR-016455; United States / NCRR NIH HHS / RR / P20 RR16455-08; United States / NCRR NIH HHS / RR / RR-020185; United States / NCRR NIH HHS / RR / P20 RR024237-026650; United States / NCRR NIH HHS / RR / RR-024237; United States / NCRR NIH HHS / RR / RR024237-026650; United States / NCRR NIH HHS / RR / P20 RR024237; United States / NCRR NIH HHS / RR / P20 RR016455; United States / NCRR NIH HHS / RR / P20 RR020185

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] Netherlands

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MED15 protein, human; 0 / Mediator Complex; 0 / Multiprotein Complexes; 0 / PLAGL2 protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA-Binding Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / proto-oncogene protein Spi-1; 67763-97-7 / Insulin-Like Growth Factor II; EC 1.6.3.1 / NADPH Oxidase; EC 1.6.3.1 / NCF2 protein, human

[Other-IDs] NLM/ NIHMS166082; NLM/ PMC2815083

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Immunohistochemical expression of stromal cell-derived factor-1 (SDF-1) and CXCR4 ligand receptor system in hepatocellular carcinoma.

The alpha-chemokine stromal cell-derived factor-1 (SDF-1) and its receptor CXCR4 have been recognized for their roles in regulating neoangiogenesis.

Formalin-fixed paraffin-embedded tissue sections of 28 HCC, 7 hepatocellular adenoma (HA), 26 cirrotic nodules (CN) and 16 normal liver tissues (NLT) were immunostained for SDF-1 and CXCR4.

SDF-1 and CXCR4 are detected in sinusoidal endothelial cells in HCC tissue, and their expressions are significantly higher than in non-HCC tissues.

Overexpressions of SDF-1 and CXCR4 in sinusoidal endothelial cells in HCC suggest that the SDF-1/CXCR4 pathway plays a possible role in HCC progression through neoangiogenesis.

[MeSH-minor] Endothelial Cells / metabolism. Humans. Immunohistochemistry. Neovascularization, Pathologic. Signal Transduction

MedlinePlus Health Information. consumer health - Liver Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18365549.001).

[ISSN] 0392-9078

[Journal-full-title] Journal of experimental & clinical cancer research : CR

[ISO-abbreviation] J. Exp. Clin. Cancer Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Chemokine CXCL12; 0 / Receptors, CXCR4

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] What is your diagnosis? Necrolytic migratory erythema associated with a glucagonoma.

[MeSH-major] Erythema / etiology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / pathology. Skin / pathology. Skin Diseases / etiology

[MeSH-minor] Female. Glucagon / blood. Humans. Middle Aged

Genetic Alliance. consumer health - Glucagonoma.

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

MedlinePlus Health Information. consumer health - Skin Conditions.

Hazardous Substances Data Bank. GLUCAGON .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18306843.001).

[ISSN] 0011-4162

[Journal-full-title] Cutis

[ISO-abbreviation] Cutis

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 9007-92-5 / Glucagon

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Here we report that infecting Rag2-deficient C57BL/6 Apc(Min/+) mice with an intestinal bacterial pathogen, Helicobacter hepaticus, significantly promotes mammary carcinoma in females and enhances intestinal adenoma multiplicity by a tumor necrosis factor alpha (TNFalpha)-dependent mechanism.

The mammary and intestinal tumor development as well as the increase in proinflammatory mediators is suppressed by adoptive transfer of interleukin 10-competent CD4+CD45RB(lo)CD25+ regulatory (T(R)) cells.

Furthermore, prior exposure of donor mice to H. hepaticus significantly enhances antitumor potency of their T(R) cells.

Interestingly, these microbially experienced T(R) cells suppress tumorigenesis more effectively in recipient mice irrespective of their tumor etiology.

These data suggest that infections with enteric pathogens enhance T(R)-cell potency and protect against epithelial cancers later in life, potentially explaining paradoxical increases in cancer risk in developed countries having more stringent hygiene practices.

MedlinePlus Health Information. consumer health - Helicobacter Pylori Infections.

COS Scholar Universe. author profiles.

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16885333.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / T32 RR 07036; United States / NIDDK NIH HHS / DK / R01 DK 52413; United States / NIAID NIH HHS / AI / R01 AI 52267-01; United States / NIEHS NIH HHS / ES / P30 ES002109; United States / NCI NIH HHS / CA / R01 CA 67529; United States / NIEHS NIH HHS / ES / P30 ES 02109; United States / NCI NIH HHS / CA / P01 CA 26731; United States / NCI NIH HHS / CA / R01 CA 108854

[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 / Immunoglobulins; 0 / Rag2 protein, mouse; 0 / Receptors, Interleukin-2; 0 / Recombinant Fusion Proteins; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

MedlinePlus Health Information. consumer health - Liver Cancer.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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. Apoptosis / physiology. Hypoxia / metabolism. 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

MedlinePlus Health Information. consumer health - Pituitary Tumors.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Oncogene. 2004 Jun 24;23(29):4975-83 [15107830.001]

[Cites] Oncogene. 2003 May 29;22(22):3431-40 [12776195.001]

[Cites] Clin Neuropathol. 2004 Jan-Feb;23(1):8-15 [14986928.001]

[Cites] Lab Invest. 2004 May;84(5):553-61 [15064771.001]

[Cites] Oncogene. 2003 Jul 24;22(30):4734-44 [12879018.001]

[Cites] Cell Cycle. 2004 Sep;3(9):1107-10 [15326390.001]

[Cites] Int J Mol Med. 2000 Mar;5(3):253-9 [10677565.001]

[Cites] J Biol Chem. 2004 Oct 1;279(40):41275-9 [15310764.001]

[Cites] FASEB J. 2002 May;16(7):745-7 [11923216.001]

[Cites] Cancer Res. 2001 Sep 1;61(17):6548-54 [11522653.001]

[Cites] Respir Physiol Neurobiol. 2004 Nov 30;144(1):71-80 [15522704.001]

[Cites] Pharmacol Ther. 2004 Nov;104(2):101-15 [15518882.001]

[Cites] J Clin Pathol. 2004 Oct;57(10):1009-14 [15452150.001]

[Cites] Drug Resist Updat. 2003 Dec;6(6):355-61 [14744499.001]

[Cites] Pathol Biol (Paris). 2004 Jun;52(5):280-4 [15217714.001]

[Cites] J Clin Pathol. 2003 Mar;56(3):209-13 [12610101.001]

[Cites] Nat Rev Cancer. 2002 Jan;2(1):38-47 [11902584.001]

[Cites] Cancer Cell. 2004 May;5(5):429-41 [15144951.001]

[Cites] Apoptosis. 2000 Apr;5(2):99-105 [11232248.001]

[Cites] Genes Cells. 2002 Feb;7(2):143-9 [11895478.001]

[Cites] Diabetes. 2004 Aug;53(8):2034-41 [15277383.001]

[Cites] Oncogene. 2000 Sep 21;19(40):4621-31 [11030151.001]

[Cites] Int J Radiat Oncol Biol Phys. 2003 Mar 15;55(4):1027-36 [12605983.001]

[Cites] Exp Cell Res. 2004 Mar 10;294(1):281-9 [14980521.001]

[Cites] EMBO J. 2004 May 5;23 (9):1949-56 [15071503.001]

[Cites] Dev Biol. 1999 May 15;209(2):254-67 [10328919.001]

[Cites] Antioxid Redox Signal. 2003 Aug;5(4):467-73 [13678535.001]

[Cites] J Biol Chem. 2002 May 3;277(18):15851-8 [11832486.001]

[Cites] Histol Histopathol. 2003 Jul;18(3):679-86 [12792878.001]

[Cites] Cancer Treat Rev. 2003 Aug;29(4):297-307 [12927570.001]

[Cites] Pharmacology. 2003 Oct;69(2):74-8 [12928580.001]

[Cites] Int J Cancer. 2004 Oct 10;111(6):849-57 [15300796.001]

[Cites] Ann N Y Acad Sci. 2003 Dec;1010:520-4 [15033783.001]

[Cites] Neurosurgery. 2003 Oct;53(4):880-5; discussion 885-6 [14519220.001]

[Cites] Front Horm Res. 2004;32:217-34 [15281349.001]

(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] United States

[Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / RNA, Small Interfering

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[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

Genetic Alliance. consumer health - Chromophobe Renal Cell Carcinoma.

Genetic Alliance. consumer health - Clear Cell Renal Cell Carcinoma.

Genetic Alliance. consumer health - Oncocytoma renal.

Genetic Alliance. consumer health - Renal cell carcinoma.

MedlinePlus Health Information. consumer health - Kidney Cancer.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17683191.001).

[ISSN] 1543-2165

[Journal-full-title] Archives of pathology & laboratory medicine

[ISO-abbreviation] Arch. Pathol. Lab. Med.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Frequent aberrant methylation of the promoter region of sterile alpha motif domain 14 in pulmonary adenocarcinoma.

Aberrant methylation of promoter CpG islands is known to be a major inactivation mechanism of tumor-suppressor and tumor-related genes.

In order to identify novel hypermethylated genes in early stage lung adenocarcinoma, we carried out methylated CpG island amplification, modified suppression subtractive hybridization, and methylation-specific polymerase chain reaction to identify aberrant methylation of CpG islands in the A/J mouse lung adenoma model, which histologically mimics the early stage of human pulmonary adenocarcinoma.

Of these two genes, we selected sterile alpha motif domain 14 (SAMD14) and further analyzed its methylation status and expression level by methylation-specific polymerase chain reaction and quantitative real-time polymerase chain reaction.

Most of the lung adenocarcinoma cell lines showed suppressed expression of SAMD14 together with hypermethylation at the promoter region, although an immortalized bronchial epithelium cell line (PL16B) did not show hypermethylation and did express SAMD14.

Hypermethylation at the CpG site of the SAMD14 promoter region was detected frequently in early invasive adenocarcinoma (8/24, 33.3%) but not in in situ adenocarcinoma (0/7, 0%) or normal lung tissue (0/31, 0%).

[MeSH-major] Adenocarcinoma / genetics. DNA Methylation. Lung Neoplasms / genetics. Promoter Regions, Genetic / genetics. Tumor Suppressor Proteins / genetics

[MeSH-minor] Animals. CpG Islands. DNA, Neoplasm / metabolism. Female. Humans. Kinesin / genetics. Kinesin / metabolism. Male. Mice. Mice, Inbred Strains. Middle Aged. Tumor Cells, Cultured

MedlinePlus Health Information. consumer health - Lung Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18823374.001).

[ISSN] 1349-7006

[Journal-full-title] Cancer science

[ISO-abbreviation] Cancer Sci.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / DNA, Neoplasm; 0 / KIF21A protein, human; 0 / Kif21a protein, mouse; 0 / Tumor Suppressor Proteins; EC 3.6.1.- / Kinesin

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pancreatic endocrine tumors.

Pancreatic endocrine tumors have been steadily growing in incidence and prevalence during the last two decades, showing an incidence of 4-5/1,000,000 population.

They represent a heterogeneous group with very varying tumor biology and prognosis.

About half of the patients present clinical symptoms and syndromes related to substances released from the tumors (Zollinger-Ellison syndrome, insulinoma, glucagonoma, etc) and the other half are so-called nonfunctioning tumors mainly presenting with symptoms such as obstruction, jaundice, bleeding, and abdominal mass.

Ten percent to 15% of the pancreatic endocrine tumors are part of an inherited syndrome such as multiple endocrine neoplasia type 1 (MEN-1), von Hippel-Lindau (VHL), neurofibromatosis, or tuberousclerosis.

The diagnosis is based on histopathology demonstrating neuroendocrine features such as positive staining for chromogranin A and specific hormones such as gastrin, proinsulin, and glucagon.

Moreover, the biochemical diagnosis includes measurement of chromogranins A and B or specific hormones such as gastrin, insulin, glucagon, and vasoactive intestinal polypeptide (VIP) in the circulation.

Surgery is still one of the cornerstones in the management of pancreatic endocrine tumors, but curative surgery is rarely obtained in most cases because of metastatic disease.

Cytotoxic drugs, biological agents, such as somatostatin analogs, alpha interferons, mammalian target of rapamycin (mTOR) inhibitors and tyrosine kinase inhibitors are routinely used.

Tumor-targeted radioactive treatment is available in many centres in Europe and is effective in patients with tumors that express high content of somatostatin receptors type 2 and 5.

In the future, treatment will be based on tumor biology and molecular genetics with the aim of so-called personalized medicine.

[MeSH-major] Pancreatic Neoplasms

[MeSH-minor] Antineoplastic Agents / therapeutic use. Biological Therapy / methods. Biomarkers, Tumor. Humans. Neoplastic Syndromes, Hereditary / diagnosis. Neoplastic Syndromes, Hereditary / therapy. Pancreatectomy. Paraneoplastic Endocrine Syndromes / diagnosis. Paraneoplastic Endocrine Syndromes / therapy

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.

(PMID = 21167379.001).

[ISSN] 1532-8708

[Journal-full-title] Seminars in oncology

[ISO-abbreviation] Semin. Oncol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clonal expansion of mutated mitochondrial DNA is associated with tumor formation and complex I deficiency in the benign renal oncocytoma.

Here we show a benign tumor type in which mtDNA mutations that lead to complex I (CI) enzyme deficiency are found in all tumors and are the only genetic alteration detected.

Actually renal oncocytomas are homogeneous tumors characterized by dense accumulation of mitochondria and we had found that they are deficient in electron transport chain complex I (CI, NADH-ubiquinone oxidoreductase).

In this work total sequencing of mtDNA showed that 9/9 tumors harbored point mutations in mtDNA, seven in CI genes, one in complex III, and one in the control region.

All tumors were somatically deficient for CI.

The clonal amplification of mutated mtDNA in 8/9 tumors demonstrates that these alterations are selected and therefore favor or trigger growth.

We hypothesize that functional deficiency of the oxidative phosphorylation CI could create a loop of amplification of mitochondria during cell division, impair substrates oxidation and increase intermediary metabolites availability.

[MeSH-major] Adenoma, Oxyphilic / genetics. DNA, Mitochondrial / genetics. Electron Transport Complex I / genetics. Kidney Neoplasms / genetics

[MeSH-minor] Cell Culture Techniques. Cell Nucleus / genetics. Cell Proliferation. Citrate (si)-Synthase / metabolism. DNA Mutational Analysis. DNA-Directed DNA Polymerase / genetics. Electron Transport Chain Complex Proteins / genetics. Electron Transport Chain Complex Proteins / metabolism. Gene Amplification. Glucose / metabolism. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. NADH Dehydrogenase / metabolism. Nucleic Acid Hybridization. Oxidative Phosphorylation. RNA, Messenger / genetics. RNA, Messenger / metabolism. Sequence Analysis, DNA

Genetic Alliance. consumer health - Oncocytoma renal.

MedlinePlus Health Information. consumer health - Kidney Cancer.

Hazardous Substances Data Bank. GLUCOSE .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18156159.001).

[ISSN] 1460-2083

[Journal-full-title] Human molecular genetics

[ISO-abbreviation] Hum. Mol. Genet.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / DNA, Mitochondrial; 0 / Electron Transport Chain Complex Proteins; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; EC 1.6.5.3 / Electron Transport Complex I; EC 1.6.99.3 / NADH Dehydrogenase; EC 2.3.3.1 / Citrate (si)-Synthase; EC 2.7.7.- / POLG protein, human; EC 2.7.7.7 / DNA-Directed DNA Polymerase; IY9XDZ35W2 / Glucose

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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.

MedlinePlus Health Information. consumer health - Pituitary Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] ER-beta expression in large bowel adenomas: implications in colon carcinogenesis.

AIM: In the present study, we evaluated oestrogen receptor-beta expression and its possible correlation with proliferative activity and apoptosis in colorectal adenomas and normal colon tissue.

RESULTS: In adenomatous tissue, a significant reduction of oestrogen receptor-beta was observed compared to normal mucosa (10.1+/-5.5% vs. 44.2+/-13.7; p<0.03), while the expression of oestrogen receptor-alpha remained unvaried.

Cell proliferative activity significantly increased in adenomatous tissue compared to normal mucosa (59.3+/-7.1 vs. 18.5+/-8.8; p<0.0001), doubling the PCNA/apoptosis ratio.

An inverse correlation was found between oestrogen receptor-beta and PCNA expression in adenomas (r=-0.81), a datum confirmed by confocal microscopy evaluation.

[MeSH-major] Adenoma / metabolism. Estrogen Receptor beta / metabolism. Intestinal Neoplasms / metabolism

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18093886.001).

[ISSN] 1590-8658

[Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver

[ISO-abbreviation] Dig Liver Dis

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Estrogen Receptor beta

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Classical proto-oncogene activation and tumor suppressor mutation are rarely responsible, and no histologic or molecular markers reliably predict behavior.

GNAS1 activation and the mutations associated with multiple endocrine neoplasia type 1 and Carney complex, aryl hydrocarbon receptor interacting protein gene mutations, and a narrowing region of chromosome 11q13 in familial isolated acromegaly together account for such a small proportion of pituitary adenomas that the pituitary adenoma pathogenic epiphany is surely yet to come.

[MeSH-major] Cell Transformation, Neoplastic / pathology. Pituitary Neoplasms / pathology

[MeSH-minor] Animals. GTP-Binding Protein alpha Subunits, Gs / genetics. GTP-Binding Protein alpha Subunits, Gs / physiology. Humans. Phenotype

MedlinePlus Health Information. consumer health - Pituitary Tumors.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18226729.001).

[ISSN] 0889-8529

[Journal-full-title] Endocrinology and metabolism clinics of North America

[ISO-abbreviation] Endocrinol. Metab. Clin. North Am.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs

[Number-of-references] 125

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

MedlinePlus Health Information. consumer health - Thyroid Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We screened ferret adrenocortical tumor specimens for expression of cytochrome b(5) (cyt b(5)), an allosteric regulator that selectively enhances the 17,20-lyase activity of P450c17.

Cyt b(5) immunoreactivity was evident in 24 of 25 (96%) adrenocortical adenomas/carcinomas from ferrets with signs of ectopic sex steroid production.

Normal adrenocortical cells lacked cyt b(5), which may account for the low production of adrenal androgens in healthy ferrets.

Other markers characteristic of gonadal somatic cells, such as luteinizing hormone receptor, aromatase, and GATA4, were coexpressed with cyt b(5) in some of the tumors.

We concluded that cyt b(5) is upregulated during gonadectomy-induced adrenocortical neoplasia and is a marker of androgen synthetic potential in these tumors.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Vet Pathol. 2003 Mar;40(2):136-42 [12637752.001]

[Cites] J Endocrinol. 1983 Dec;99(3):361-8 [6417256.001]

[Cites] J Clin Endocrinol Metab. 1993 May;76(5):1286-90 [8496319.001]

[Cites] Mol Cell Endocrinol. 2007 Feb;265-266:93-101 [17222503.001]

[Cites] J Clin Endocrinol Metab. 1994 Jan;78(1):36-40 [8288710.001]

[Cites] J Am Vet Med Assoc. 1996 Sep 15;209(6):1097-102 [8800255.001]

[Cites] Semin Reprod Med. 2004 Nov;22(4):281-8 [15635496.001]

[Cites] J Endocrinol. 2005 Nov;187(2):267-74 [16293774.001]

[Cites] Vet Pathol. 2006 Mar;43(2):97-117 [16537928.001]

[Cites] Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10619-23 [7479852.001]

(PMID = 18587089.001).

[ISSN] 0300-9858

[Journal-full-title] Veterinary pathology

[ISO-abbreviation] Vet. Pathol.

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / DK075618-02; United States / NIDDK NIH HHS / DK / P30 DK052574-09; United States / NIDDK NIH HHS / DK / R01 DK075618-02; United States / NIDDK NIH HHS / DK / DK52574; United States / NIDDK NIH HHS / DK / DK075618; United States / NIDDK NIH HHS / DK / P30 DK052574; United States / NIDDK NIH HHS / DK / R01 DK075618

[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 / GATA4 Transcription Factor; 0 / Receptors, LH; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins; 9035-39-6 / Cytochromes b5

[Other-IDs] NLM/ NIHMS45245; NLM/ PMC2497446

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

MedlinePlus Health Information. consumer health - Salivary Gland Disorders.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

It is a glycoprotein hormone secreted by the Sertoli cells of the testis and granulosa and theca cells of the ovary.

Current understanding of inhibin physiology and pathology in the human suggests that inhibin B may be of importance as a marker of Sertoli cell function in men with infertility and as a prognostic indicator in women undergoing ovulation induction therapy.

Inhibin concentrations are elevated in patients with granulosa cell tumours and in post-menopausal women with mucinous ovarian cancers.

Immunoreactivity against the inhibin alpha-subunit was identified in all cases of adrenal cortical adenoma and carcinoma, and levels are suppressed in the malignant prostate disease.

[MeSH-minor] Activins / chemistry. Activins / metabolism. Adult. Age Factors. Chromosomes, Human, Y. Exocrine Glands / metabolism. Female. Fertilization in Vitro / methods. Follistatin / chemistry. Follistatin / metabolism. Humans. Infant, Newborn. Male. Menstrual Cycle / physiology. Ovarian Neoplasms / blood. Polycystic Ovary Syndrome / physiopathology. Pregnancy. Sequence Deletion. alpha-Macroglobulins / chemistry. alpha-Macroglobulins / metabolism

MedlinePlus Health Information. consumer health - Male Infertility.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15970011.001).

[ISSN] 1472-6483

[Journal-full-title] Reproductive biomedicine online

[ISO-abbreviation] Reprod. Biomed. Online

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Follistatin; 0 / alpha-Macroglobulins; 104625-48-1 / Activins; 57285-09-3 / Inhibins

[Number-of-references] 114

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Arsenic alone induced some urogenital system tumors, including mostly benign tumors of the ovary and uterus, and adrenal adenoma.

Diethylstilbestrol alone induced some tumors (primarily cervical) but when given after in utero arsenic, it greatly enhanced urogenital tumor incidence, multiplicity, and progression.

For instance, compared with the incidence of urogenital malignancies in the control (0%), arsenic alone (9%), and diethylstilbestrol alone (21%) groups, arsenic plus diethylstilbestrol acted synergistically, inducing a 48% incidence of malignant urogenital tumors.

Of the urogenital tumors induced by arsenic plus diethylstilbestrol, 80% were malignant, and 55% were multiple site.

Arsenic plus diethylstilbestrol increased ovarian, uterine, and vaginal tumors, and urinary bladder proliferative lesions, including three transitional cell carcinomas.

Tamoxifen alone did not increase urogenital tumors or affect arsenic-induced neoplasia but did increase arsenic-induced uroepithelial proliferative lesions.

Uterine and bladder carcinoma induced by arsenic plus diethylstilbestrol greatly overexpressed estrogen receptor-alpha (ER-alpha) and pS2, an estrogen-regulated gene.

In neonatal uteri, prenatal arsenic increased ER-alpha expression and enhanced estrogen-related gene expression induced by postnatal diethylstilbestrol.

[MeSH-minor] Animals. Body Weight / drug effects. Drinking / drug effects. Drug Synergism. Estrogen Receptor alpha / biosynthesis. Estrogen Receptor alpha / genetics. Female. Gene Expression / drug effects. Maternal-Fetal Exchange. Mice. Pregnancy. Tamoxifen / toxicity. Uterus / drug effects. Uterus / metabolism. Uterus / physiology

MedlinePlus Health Information. consumer health - Arsenic.

MedlinePlus Health Information. consumer health - Bladder Cancer.

MedlinePlus Health Information. consumer health - Kidney Cancer.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. TAMOXIFEN .

Hazardous Substances Data Bank. DIETHYLSTILBESTROL .

Hazardous Substances Data Bank. ARSENIC, ELEMENTAL .

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16452187.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / NCI NIH HHS / CO / N01 CO 12400; United States / Intramural NIH HHS / /

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural

[Publication-country] United States

[Chemical-registry-number] 0 / Estrogen Receptor alpha; 094ZI81Y45 / Tamoxifen; 731DCA35BT / Diethylstilbestrol; N712M78A8G / Arsenic

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The somatostatin receptors types 1-5 expression in a series including 100 gastro-entero-pancreatic endocrine tumours were analysed.

METHODS: From a prospectively built database of patients with gastro-entero-pancreatic endocrine tumours referred from three institutions, 100 cases with clinical and pathological data were selected.

Somatostatin receptors expression by immunohistochemistry with somatostatin receptor types 1-5 antibodies in tissue paraffin sections were studied and correlated with the histological diagnosis according to the WHO classification, location and functional status.

RESULTS: Of the 100 cases, 67 were gastrointestinal tumours, 25 pancreatic and 8 liver metastasis of unknown origin.

Thirty-one of them were functioning tumours: 2 insulinomas, 5 gastrinomas, 1 glucagonoma and 23 carcinoids.

Somatostatin receptors expression was less frequent in pancreatic than in gastrointestinal tumours.

CONCLUSIONS: Immunohistochemistry revealed that somatostatin receptors were highly expressed in both primary and metastatic gastro-entero-pancreatic endocrine tumours with heterogeneous staining distribution.

It proved to be a reliable technique even in small tumour samples.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] 2009 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

[CommentIn] Dig Liver Dis. 2010 Mar;42(3):173-4 [20117969.001]

(PMID = 19819769.001).

[ISSN] 1878-3562

[Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver

[ISO-abbreviation] Dig Liver Dis

[Language] eng

[Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Receptors, Somatostatin

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We present 2 cases of hepatocyte nuclear factor 1alpha (HNF1alpha)-mutated adenomatosis, discovered for reasons unrelated to this disease, and identified using immunohistochemical methods.

These new tools may further our understanding of the link between adenomas/adenomatosis subtypes and their complications, and their association with other abnormalities.

MedlinePlus Health Information. consumer health - Liver Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Surg Pathol. 2001 Oct;25(10):1322-5 [11688469.001]

[Cites] J Hepatol. 2008 Jan;48(1):163-70 [17997499.001]

[Cites] Liver Int. 2003 Feb;23(1):35-7 [12640725.001]

[Cites] J Hepatol. 2003 Jul;39(1):77-85 [12821047.001]

[Cites] Gastroenterology. 2003 Nov;125(5):1470-5 [14598263.001]

[Cites] J Clin Endocrinol Metab. 2004 Mar;89(3):1476-80 [15001650.001]

[Cites] Gastroenterology. 2004 May;126(5):1323-9 [15131793.001]

[Cites] N Engl J Med. 1978 Aug 3;299(5):239-41 [207987.001]

[Cites] Gastroenterology. 1985 Nov;89(5):1132-8 [2412930.001]

[Cites] Mod Pathol. 1989 Sep;2(5):456-62 [2813344.001]

[Cites] Liver Transpl Surg. 1998 Sep;4(5):388-98 [9724476.001]

[Cites] Gastroenterology. 2005 May;128(5):1211-8 [15887105.001]

[Cites] Semin Liver Dis. 2005;25(2):230-6 [15918151.001]

[Cites] Hepatology. 2006 Mar;43(3):515-24 [16496320.001]

[Cites] Nat Clin Pract Gastroenterol Hepatol. 2006 Sep;3(9):526-31; quiz (following 531) [16951669.001]

[Cites] J Hepatol. 2007 Mar;46(3):521-7 [17239484.001]

[Cites] Hepatology. 2007 Jul;46(1):140-6 [17596890.001]

[Cites] Hepatology. 2007 Sep;46(3):740-8 [17663417.001]

[Cites] Nat Genet. 2002 Oct;32(2):312-5 [12355088.001]

(PMID = 18720549.001).

[ISSN] 1007-9327

[Journal-full-title] World journal of gastroenterology

[ISO-abbreviation] World J. Gastroenterol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P50 CA095817

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha

[Other-IDs] NLM/ PMC2739350

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

Genetic Alliance. consumer health - Craniopharyngioma.

MedlinePlus Health Information. consumer health - Pituitary Tumors.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

There, knowledge of skin alterations is important not only for dermatologists, but also for endocrinologists and other physicians, because a clinical diagnosis of the underlying disease is often possible.

These include acanthosis nigricans, diseases due to alterations of androgen metabolism, carcinoid syndrome, diseases due to alterations of corticosteroid metabolism, diseases in association with diabetes mellitus, diseases due to alterations of estrogen metabolism, genetic syndromes including dermatological and endocrine symptoms, the glucagonoma syndrome, diseases due to dysfunctions of growth hormone secretion, diseases in association with Merkel cells of the skin, diseases due to dysfunctions of the thyroid gland, diseases to alteration of vitamin D metabolism, and vitiligo and disorders of pigmentation.

[MeSH-minor] Androgens / deficiency. Androgens / secretion. Estrogens / deficiency. Estrogens / secretion. Glucagonoma / etiology. Malignant Carcinoid Syndrome / etiology. Thyroid Hormones / deficiency. Thyroid Hormones / secretion. Vitamin D / secretion. Vitiligo / etiology

MedlinePlus Health Information. consumer health - Skin Conditions.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16916743.001).

[ISSN] 1368-5538

[Journal-full-title] The aging male : the official journal of the International Society for the Study of the Aging Male

[ISO-abbreviation] Aging Male

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Androgens; 0 / Estrogens; 0 / Thyroid Hormones; 1406-16-2 / Vitamin D

[Number-of-references] 71

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Neuroendocrine tumors of the pancreas.

Pancreatic endocrine tumors are rare neoplasms accounting for less than 5% of pancreatic malignancies.

They are broadly classified into either functioning tumors (insulinomas, gastrinomas, glucagonomas, VIPomas, and somatostatinomas) or nonfunctioning tumors.

The diagnosis of these tumors is difficult and requires a careful history and examination combined with laboratory tests and radiologic imaging.

Signs and symptoms are usually related to hormone hypersecretion in the case of functioning tumors and to tumor size or metastases with nonfunctioning tumors.

Surgical resection remains the treatment of choice even in the face of metastatic disease.

Further development of novel diagnostic and treatment modalities offers potential to greatly improve quality of life and prolong disease-free survival for patients with pancreatic endocrine tumors.

[MeSH-major] Adenoma, Islet Cell. Carcinoma, Islet Cell. Pancreatic Neoplasms

[MeSH-minor] Algorithms. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Catheter Ablation. Chemoembolization, Therapeutic / methods. Evidence-Based Medicine. Gastrins / secretion. Glucagon / secretion. Humans. Insulin / secretion. Quality of Life. Somatostatin / secretion. Survival Analysis. Treatment Outcome

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

Hazardous Substances Data Bank. GLUCAGON .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Clin Oncol. 2002 Jun 1;20(11):2633-42 [12039924.001]

[Cites] Cancer. 1991 Sep 15;68(6):1329-34 [1678681.001]

[Cites] World J Surg. 2008 May;32(5):904-17 [18264824.001]

[Cites] World J Surg. 2002 Aug;26(8):985-90 [12016479.001]

[Cites] Ann Surg. 2007 Feb;245(2):273-81 [17245182.001]

[Cites] Ann Oncol. 1999;10 Suppl 4:182-4 [10436817.001]

[Cites] J Gastroenterol. 2007 Jun;42(6):497-500 [17671766.001]

[Cites] J Gastrointest Surg. 2006 Jan;10(1):138-45 [16368504.001]

[Cites] Gastroenterology. 1968 Dec;55(6):677-86 [4302500.001]

[Cites] Ann Surg. 2006 Sep;244(3):410-9 [16926567.001]

[Cites] Arch Surg. 1984 May;119(5):508-14 [6143548.001]

[Cites] Endocr Relat Cancer. 2008 Jun;15(2):409-27 [18508996.001]

[Cites] Eur J Surg Oncol. 2008 Mar;34(3):324-32 [17967523.001]

[Cites] Am J Med. 1999 Mar;106(3):307-10 [10190379.001]

[Cites] Ann Surg Oncol. 2008 Dec;15(12):3532-7 [18825460.001]

[Cites] AJR Am J Roentgenol. 2003 Oct;181(4):987-92 [14500214.001]

[Cites] Dig Dis Sci. 1991 Jul;36(7):933-42 [2070707.001]

[Cites] N Engl J Med. 1992 Jun 25;326(26):1721-6 [1317506.001]

[Cites] World J Surg. 1993 Jul-Aug;17 (4):427-32 [8362525.001]

[Cites] Transplantation. 1998 Nov 27;66(10):1307-12 [9846513.001]

[Cites] Medicine (Baltimore). 1996 Mar;75(2):53-63 [8606627.001]

[Cites] Curr Probl Surg. 1990 Jun;27(6):301-86 [1973365.001]

[Cites] N Engl J Med. 1977 Apr 28;296(17):963-7 [321960.001]

[Cites] Mayo Clin Proc. 1991 Jul;66(7):711-9 [1677058.001]

[Cites] Ann Surg. 2008 Jan;247(1):165-72 [18156937.001]

[Cites] Arch Surg. 2002 Feb;137(2):164-8 [11822953.001]

[Cites] Ann Surg. 1955 Oct;142(4):709-23; discussion, 724-8 [13259432.001]

[Cites] N Engl J Med. 1986 May 1;314(18):1145-51 [3007986.001]

[Cites] Ann Surg Oncol. 2001 Apr;8(3):249-53 [11314942.001]

[Cites] Am J Med. 1958 Sep;25(3):374-80 [13571250.001]

[Cites] Surg Clin North Am. 1987 Apr;67(2):379-93 [3031836.001]

[Cites] Curr Opin Oncol. 1999 Jan;11(1):32-7 [9914875.001]

[Cites] Pathol Res Pract. 1988 Apr;183(2):155-68 [2898775.001]

[Cites] J Clin Endocrinol Metab. 1997 Aug;82(8):2622-8 [9253344.001]

[Cites] J Gastrointest Surg. 1998 Sep-Oct;2(5):473-82 [18335273.001]

[Cites] Arch Surg. 2006 Aug;141(8):765-9; discussion 769-70 [16924083.001]

[Cites] J Med Res. 1902 Nov;8(2):385-95 [19971505.001]

[Cites] J Clin Oncol. 2007 Dec 10;25(35):5609-15 [18065733.001]

[Cites] Radiology. 1993 Mar;186(3):799-802 [8381551.001]

[Cites] Am J Surg. 1990 Feb;159(2):258-64 [2154144.001]

(PMID = 19281699.001).

[ISSN] 1534-312X

[Journal-full-title] Current gastroenterology reports

[ISO-abbreviation] Curr Gastroenterol Rep

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Gastrins; 0 / Insulin; 51110-01-1 / Somatostatin; 9007-92-5 / Glucagon

[Number-of-references] 44

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The short-term effect of fatty acids on glucagon secretion is influenced by their chain length, spatial configuration, and degree of unsaturation: studies in vitro.

The influence of fatty acids on beta cell function has been well established whereas little is known about the role of fatty acids on alpha cell function.

The aim of our study was to investigate the short-term effects of chain length, spatial configuration, and degree of unsaturation of fatty acids on glucagon secretion from isolated mouse islets and alpha tumor cell 1 clone 6 cells (alpha TC1-6 cells).

Glucagon release was measured with different saturated and unsaturated fatty acids as well as cis and trans isomers of fatty acids at low and high glucose.

Palmitate (0.1-0.5 mmol/L) immediately stimulated glucagon release in a dose-dependent manner from both isolated islets and alpha TC 1-6 cells.

The longer chain length of saturated fatty acids, the higher glucagon responses were obtained.

The average fold increase in glucagon to saturated fatty acids (0.3 mmol/L) compared to control was octanoate 1.5, laurate 2.0, myristate 2.9, palmitate 5.4, and stearate 6.2, respectively.

Saturated fatty acids were more effective than unsaturated fatty acids in stimulating glucagon secretion.

Fatty acids immediately stimulate glucagon secretion from isolated mouse islets pancreatic alpha cells.

[MeSH-major] Fatty Acids / pharmacology. Glucagon / secretion

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. GLUCAGON .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16154432.001).

[ISSN] 0026-0495

[Journal-full-title] Metabolism: clinical and experimental

[ISO-abbreviation] Metab. Clin. Exp.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Fatty Acids; 0 / Insulin; 9007-92-5 / Glucagon

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

MedlinePlus Health Information. consumer health - Salivary Gland Cancer.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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.

MedlinePlus Health Information. consumer health - Pituitary Tumors.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Fanconi anaemia is an autosomal recessive disease, causing secondary aplastic anaemia and congenital abnormalities, associated with an increased risk of tumours.

Liver cell adenoma and hepatocellular carcinoma have rarely been described.

Alpha-fetoprotein levels were normal in all cases.

Patient 2 had hepatic nodules diagnosed at routine examination with radiological features of adenomas.

The patient underwent resection, which showed liver cell adenoma with foci of carcinoma.

Patient 3 had three nodules, with radiological and histological diagnosis of adenoma.

In patients with Fanconi anaemia, androgen therapy and iron overload may contribute to the development of liver cell adenoma and hepatocellular carcinoma.

Hepatocellular carcinoma may occur as a transformation of liver cell adenoma.

[MeSH-major] Adenoma, Liver Cell / etiology. Carcinoma, Hepatocellular / etiology. Fanconi Anemia / complications. Liver Neoplasms / etiology

MedlinePlus Health Information. consumer health - Liver Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18787475.001).

[ISSN] 1473-5687

[Journal-full-title] European journal of gastroenterology & hepatology

[ISO-abbreviation] Eur J Gastroenterol Hepatol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Multiple endocrine neoplasia Type 1 (MEN1) is a rare hereditary tumor syndrome predisposing to tumor development in several endocrine organs.

Its major manifestations include hyperparathyroidism, tumors of endocrine pancreas and pituitary.

Beside these three, several other endocrine (adrenocortical, foregut carcinoid) and nonendocrine (lipoma, angiofibroma, collagenoma, ependymoma, meningioma) tumors have been described to be associated with this syndrome.

Both familial and sporadic forms of the disease are known.

The diagnosis of MEN1 can be established if two of the three major manifestations are found in the same patient, whereas the diagnosis of familial MEN1 requires one MEN1 patient and a first degree relative with at least one MEN1 manifestation.

Both benign (parathyroid, anterior pituitary) and malignant (gastrinoma, glucagonoma) lesions may develop in MEN1 patients.

Regular surveillance of MEN1 gene mutation carriers is necessary to reveal disease manifestations.

Several diagnostic modalities can be used to screen for and to examine MEN1-related tumors.

The therapy of MEN1-associated tumors requires specific approach in some cases, as multiple tumors and recurrence is frequently observed.

[MeSH-minor] Adult. Child. Child, Preschool. Diagnosis, Differential. Genetic Predisposition to Disease. Genetic Testing. Humans. Middle Aged. Multiple Endocrine Neoplasia Type 2a / genetics. Multiple Endocrine Neoplasia Type 2a / pathology. Multiple Endocrine Neoplasia Type 2a / physiopathology. Mutation. Young Adult

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20175448.001).

[ISSN] 0065-2598

[Journal-full-title] Advances in experimental medicine and biology

[ISO-abbreviation] Adv. Exp. Med. Biol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

CONTEXT: The unrelenting challenge encountered when differentiating limited-volume prostate carcinoma and sometimes subtle variants from its many morphologic mimics has increased the use of ancillary immunohistochemistry in routine prostate needle biopsies.

The availability of prostate cancer-associated and basal cell-associated markers has been an invaluable addition to diagnostic surgical pathology.

OBJECTIVE: To review commonly used immunohistochemical stains, including innovative combinations, for confirmation or differential diagnosis of prostate carcinoma, and to propose appropriately constructed panels using morphologic patterns in prostate needle biopsies.

CONCLUSIONS: Basal cell-associated markers p63, high-molecular-weight cytokeratin 34 beta E12, cytokeratin 5/6 or a cocktail containing p63 and high-molecular-weight cytokeratin 34 beta E12 or cytokeratin 5/6 and prostate carcinoma-specific marker alpha-methylacyl coenzyme A (coA) racemase alone or in combination are useful adjuncts in confirming prostatic carcinoma that either lacks diagnostic, qualitative or quantitative features or that has an unusual morphologic pattern (eg, atrophic, pseudohyperplastic) or is in the setting of prior treatment.

The combination of alpha-methylacyl coA racemase positivity with negative staining for basal cell-associated markers supports a malignant diagnosis in the appropriate morphologic context.

Dual chromogen basal cell- associated markers (p63 [nuclear] and high-molecular-weight cytokeratin 34 beta E12/cytokeratin 5/6 [cytoplasmic]) and alpha-methylacyl coA racemase in an antibody cocktail provide greater sensitivity for the basal cell layer, easing evaluation and minimizing loss of representation of the focal area interest because the staining is performed on one slide.

In the posttreatment setting, pancytokeratin facilitates detection of subtle-treated cancer cells.

Prostate-specific antigen and prostatic acid phosphatase markers are helpful in excluding secondary malignancies involving the prostate, such as urothelial carcinoma, and occasionally in excluding nonprostatic benign mimickers, such as nephrogenic adenoma, mesonephric gland hyperplasia, and Cowper glands.

[MeSH-major] Biomarkers, Tumor / analysis. Biopsy, Needle. Immunohistochemistry / methods. Prostatic Neoplasms / diagnosis

[MeSH-minor] Diagnosis, Differential. Humans. Male

MedlinePlus Health Information. consumer health - Prostate Cancer.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18788849.001).

[ISSN] 1543-2165

[Journal-full-title] Archives of pathology & laboratory medicine

[ISO-abbreviation] Arch. Pathol. Lab. Med.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor

[Number-of-references] 47

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Characterization of c-kit (CD117) expression in human normal pituitary cells and pituitary adenomas.

c-kit (CD117) is a tyrosine kinase receptor involved in the proliferation, differentiation, and secretory functions of various cells.

In experimental animal models, c-kit has been detected in the pars intermedia of the normal pituitary gland and in alpha-melanocyte-stimulating-hormone-positive adenomas and it has been suggested that it plays a role in regulating adrenocorticotropic hormone (ACTH) secretion.

To the best of our knowledge, the expression of c-kit in normal human pituitary cells and in pituitary adenomas has never been reported, so the possible biological role of this receptor in the control of pituitary hormone secretion remains unclear.

The aim of this study was to evaluate the immunohistochemical expression of c-kit in normal human pituitary glands and in a series of 62 well-characterized pituitary adenomas.

In normal adenohypophyses, several cells, mainly located in the central mucoid wedge, showed a c-kit immunoreactivity (IR).

Double label immunostaining procedures showed that the c-kit-IR cells corresponded to ACTH cells.

Out of 62 adenomas, 15 (24%) were c-kit-IR, including 7/16 (44%) ACTH cell, 3/7 (42%) null cell, 4/11 (36%) alpha-subunit cell, and 1/11 (10%) follicle-stimulating hormone-luteinizing hormone cell adenomas.

By contrast, all ten prolactin cell and seven growth hormone cell adenomas were c-kit negative.

[MeSH-major] Adenoma / metabolism. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis

[MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adolescent. Adult. Aged. Blotting, Western. Child. Female. Follicle Stimulating Hormone / blood. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / pathology. Humans. Immunohistochemistry. Luteinizing Hormone / blood. Male. Middle Aged. Paraffin Embedding. Prolactinoma / metabolism. Prolactinoma / pathology. Tissue Fixation

MedlinePlus Health Information. consumer health - Pituitary Tumors.

Hazardous Substances Data Bank. MENOTROPINS .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Histochem Cytochem. 1995 Jan;43(1):97-102 [7822770.001]

[Cites] Br J Dermatol. 2004 Feb;150(2):384-5 [14996126.001]

[Cites] Cancer Res. 1992 Nov 15;52(22):6139-43 [1384954.001]

[Cites] Hum Pathol. 2003 Jan;34(1):18-27 [12605362.001]

[Cites] J Histochem Cytochem. 1981 Apr;29(4):577-80 [6166661.001]

[Cites] Endocrinology. 2005 Sep;146(9):3985-98 [15932930.001]

[Cites] N Engl J Med. 2002 Aug 15;347(7):472-80 [12181401.001]

[Cites] Blood. 1999 Sep 15;94(6):1979-86 [10477727.001]

[Cites] Appl Immunohistochem Mol Morphol. 2001 Dec;9(4):319-28 [11759058.001]

[Cites] EMBO J. 1987 Nov;6(11):3341-51 [2448137.001]

[Cites] Ann Oncol. 2003 Jun;14(6):894-7 [12796027.001]

[Cites] J Histochem Cytochem. 1994 Nov;42(11):1417-25 [7523489.001]

[Cites] Endocr Pathol. 2000 Winter;11(4):315-329 [12114756.001]

[Cites] Jpn J Clin Oncol. 2006 Aug;36(8):494-8 [16844734.001]

[Cites] Virchows Arch. 2000 Sep;437(3):264-9 [11037346.001]

[Cites] Oncogene. 1997 Jun 5;14(22):2661-70 [9178764.001]

[Cites] Zentralbl Pathol. 1993 Jun;139(2):165-70 [8396420.001]

[Cites] J Clin Endocrinol Metab. 1995 Nov;80(11):3361-7 [7593452.001]

[Cites] Hum Pathol. 1998 May;29(5):498-504 [9596274.001]

[Cites] Development. 1996 Oct;122(10):3023-33 [8898216.001]

[Cites] Mod Pathol. 1998 Aug;11(8):728-34 [9720500.001]

[Cites] Biochem Biophys Res Commun. 2005 Dec 23;338(3):1307-15 [16226710.001]

[Cites] Mod Pathol. 2005 Mar;18(3):320-3 [15502806.001]

[Cites] Neuroendocrinology. 2007;85(2):110-30 [17337880.001]

[Cites] Mod Pathol. 2000 Oct;13(10):1134-42 [11048809.001]

[Cites] Pathol Int. 1994 Sep;44(9):697-703 [7804432.001]

[Cites] Appl Immunohistochem Mol Morphol. 2005 Sep;13(3):205-20 [16082245.001]

[Cites] Am J Dermatopathol. 2002 Aug;24(4):289-93 [12142606.001]

[Cites] Am J Pathol. 1993 Jan;142(1):339-46 [7678721.001]

[Cites] Clin Cancer Res. 2003 Apr;9(4):1469-73 [12684421.001]

[Cites] Am J Surg Pathol. 2003 Dec;27(12):1551-8 [14657715.001]

[Cites] J Neurosci. 1998 Feb 1;18(3):1056-71 [9437026.001]

[Cites] Virchows Arch. 1994;424(2):135-41 [7514077.001]

[Cites] J Cutan Pathol. 2004 Mar;31(3):254-61 [14984578.001]

[Cites] Stem Cells. 2005;23(1):16-43 [15625120.001]

[Cites] Endocr Relat Cancer. 2006 Jun;13(2):535-40 [16728580.001]

[Cites] J Neuroimmunol. 1996 Apr;65(2):133-41 [8964895.001]

[Cites] Am J Dermatopathol. 2004 Dec;26(6):458-62 [15618926.001]

(PMID = 18568298.001).

[ISSN] 1046-3976

[Journal-full-title] Endocrine pathology

[ISO-abbreviation] Endocr. Pathol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Glucagonoma: anaesthetic management.

[MeSH-major] Anesthesia, General / methods. Glucagonoma / surgery. Pancreatic Neoplasms / surgery

[MeSH-minor] Blood Glucose / analysis. Female. Glucagon / blood. Humans. Middle Aged

Genetic Alliance. consumer health - Glucagonoma.

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

Hazardous Substances Data Bank. GLUCAGON .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19400510.001).

[ISSN] 0310-057X

[Journal-full-title] Anaesthesia and intensive care

[ISO-abbreviation] Anaesth Intensive Care

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] Australia

[Chemical-registry-number] 0 / Blood Glucose; 9007-92-5 / Glucagon

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[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

Genetic Alliance. consumer health - Glucagonoma.

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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)

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] MicroRNA expression profiles in head and neck cancer cell lines.

In this study, the relative expression of 261 mature miRNA genes was determined in nine head and neck cancer cell lines using an oligonucleotide array platform.

Thirty-three miRNAs in the array were found to be highly expressed and 22 showed low levels of expression in all cell lines.

Potential targets of validated miRNAs included tumor suppressor genes, kinesin family member 1B isoform alpha (KIF1B), and hypermethylated in cancer 2 (HIC2), and pleomorphic adenoma gene 1 (PLAG1).

This study provides the largest genomewide survey of mature miRNA transcripts in head and neck cancer cell lines.

[MeSH-major] Biomarkers, Tumor / metabolism. Head and Neck Neoplasms / metabolism. MicroRNAs / metabolism

[MeSH-minor] Cell Line, Tumor. DNA-Binding Proteins / metabolism. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Kinesin / metabolism. Nerve Tissue Proteins / metabolism. Oligonucleotide Array Sequence Analysis

MedlinePlus Health Information. consumer health - Head and Neck Cancer.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17475218.001).

[ISSN] 0006-291X

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / KIF1B protein, human; 0 / MicroRNAs; 0 / Nerve Tissue Proteins; 0 / PLAG1 protein, human; EC 3.6.1.- / Kinesin

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Enteroendocrine tumors other than carcinoid: a review of clinically significant advances.

Only relatively recently has there been an increased clinical recognition and characterization of the heterogeneous group of rare gastroenteropancreatic neuroendocrine neoplasms.

This review summarizes the derivation of these tumors and the advances in their diagnosis and treatment over the past decade and a half.

They are varied in their biological behavior and clinical courses and, depending on their cell type, can produce different hormones causing distinct clinical endocrine syndromes (insulinoma [hypoglycemia], gastrinoma [Zollinger-Ellison syndrome (ZES)], vasoactive intestinal peptideoma [VIPoma], watery diarrhea, hypokalemia-achlorhydria [WDHA], glucagonoma [glucagonoma syndrome], and so forth).

In addition to surgery for cure or palliation (by excision and a variety of other cytoreductive techniques), they each are treated with anti-hormonal agents or drugs targeted to each tumor's specific product or its effects.

Because of their usual slow rate of growth it is recommended that, even when they are advanced and incurable, unlike in patients with common and more malignant cancers, patients with neuroendocrine tumors often can be palliated and appear to survive longer when managed with an active approach using sequential multimodality treatment.

[MeSH-major] Carcinoma, Neuroendocrine. Gastrointestinal Neoplasms

[MeSH-minor] Carcinoid Tumor. Humans

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15887158.001).

[ISSN] 0016-5085

[Journal-full-title] Gastroenterology

[ISO-abbreviation] Gastroenterology

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 222

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry.

BACKGROUND: To determine differences in biological features among different adrenal tumors, we investigated the DNA ploidy, numerical chromosomal aberration and proliferative activity in human adrenal cortical neoplasms.

METHODS: Our study included six adrenal cortical adenomas with Cushing syndrome, 12 adenomas with hyperaldosteronism, three non-functioning adenomas and three adrenal cortical carcinomas.

For FISH analysis, we used an alpha-centromeric enumeration probe for chromosome 17.

RESULTS: The mean Ki-67 labeling index (LI) of adrenal cortical carcinomas was markedly higher than that of adrenal cortical adenomas (209.4 vs 8.7).

In functional adrenal cortical adenomas, the LI was significantly lower in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004), although FCM results indicated that tetraploid patterns were more frequently observed in the former type.

Tumor size was significantly smaller in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004).

Chromosome 17 showed disomy in all adrenal cortical adenomas, whereas chromosome 17 abnormalities were found in two of three adrenal cortical carcinomas.

CONCLUSIONS: Our study characterized various biological features of benign and malignant adrenal cortical tumors.

The use of a combination of markers might provide additional information to assist our understanding of the clinical behavior of an individual adrenal cortical tumor.

[MeSH-minor] Adenoma / genetics. Adenoma / metabolism. Adenoma / pathology. Adult. Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Carcinoma / genetics. Carcinoma / metabolism. Carcinoma / pathology. Cell Proliferation. Chromosomes, Human, Pair 17. Cushing Syndrome / genetics. Cushing Syndrome / metabolism. Cushing Syndrome / pathology. DNA, Neoplasm / genetics. Female. Humans. Hyperaldosteronism / genetics. Hyperaldosteronism / metabolism. Hyperaldosteronism / pathology. Ki-67 Antigen / metabolism. Male. Middle Aged. Ploidies. Tumor Suppressor Protein p53 / metabolism

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15733104.001).

[ISSN] 0919-8172

[Journal-full-title] International journal of urology : official journal of the Japanese Urological Association

[ISO-abbreviation] Int. J. Urol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Australia

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Lymphatic vessel endothelial hyaluronan receptor 1 immunocytochemical staining for pancreatic islets and pancreatic endocrine tumors.

OBJECTIVES: Immunocytochemical staining for lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) is able to recognize lymphatic vessel endothelium and pancreatic endocrine cells (PETs).

Pancreatic endocrine tumors were studied for LYVE-1 immunocytochemical staining compared with normal pancreatic islets to detect possible presence of LYVE-1 in PETs.

METHODS: Twenty-five cases of primary and metastatic PETs were immunocytochemically stained for LYVE-1, including insulinomas, glucagonomas, somatostatinoma, pancreatic polypeptidomas, gastrinomas, and nonfunctioning tumors.

RESULTS: All normal pancreatic islet cells were positive for LYVE-1, whereas 2 cases of 25 PETs, 1 each of gastrinoma and nonfunctioning tumor, were positive for LYVE-1, retaining immunocytochemical reactivity of islet cells.

CONCLUSIONS: Normal pancreatic islets were positive for LYVE-1, whereas only 2 of 25 PETs were positive, suggesting that most PETs lost LYVE-1 or contained below detectable levels of LYVE-1.

The presence of LYVE-1 in pancreatic islets and in some PETs may suggest structure-function relationship of LYVE-1/lymphatic vessel in hormone synthesis and secretion.

[MeSH-major] Gastrinoma / chemistry. Glucagonoma / chemistry. Immunohistochemistry. Insulinoma / chemistry. Islets of Langerhans / chemistry. Pancreatic Neoplasms / chemistry. Somatostatinoma / chemistry. Vesicular Transport Proteins / analysis

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18090227.001).

[ISSN] 1536-4828

[Journal-full-title] Pancreas

[ISO-abbreviation] Pancreas

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / LYVE1 protein, human; 0 / Vesicular Transport Proteins

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Case of the season: glucagonoma syndrome.

[MeSH-major] Glucagonoma / radiography. Pancreatic Neoplasms / radiography

[MeSH-minor] Diagnosis, Differential. Female. Humans. Middle Aged. Syndrome. Tomography, X-Ray Computed

Genetic Alliance. consumer health - Glucagonoma.

Genetic Alliance. consumer health - Glucagonoma Syndrome.

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15732554.001).

[ISSN] 0037-198X

[Journal-full-title] Seminars in roentgenology

[ISO-abbreviation] Semin Roentgenol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Necrolytic migratory erythaema and glucagonoma syndrome.

[MeSH-major] Erythema / etiology. Glucagonoma / pathology. Pancreatic Neoplasms / pathology

[MeSH-minor] Female. Humans. Middle Aged. Syndrome

Genetic Alliance. consumer health - Glucagonoma.

Genetic Alliance. consumer health - Glucagonoma Syndrome.

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19317246.001).

[ISSN] 1784-3286

[Journal-full-title] Acta clinica Belgica

[ISO-abbreviation] Acta Clin Belg

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Belgium

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Comparison of immunomarkers for the identification of adrenocortical cells in cytology specimens.

We studied the immunoreactivity of three antibodies--A103, calretinin, and inhibin alpha in destained Papanicolaou (Pap) smears and cell-blocks of 40 fine-needle aspiration biopsy cases of adrenocortical lesions (35 cases of hyperplasia/adenoma and 5 cases of carcinoma).

Five cases of carcinoma (4) and melanoma (1) metastases to the adrenal gland and five cases of renal-cell carcinoma were also included for comparison.

In benign adrenocortical lesions, A103 staining was noted in 82% of the destained Pap smears and in 92% of cell-blocks.

In malignant adrenocortical lesions, A103 staining was noted in 50% of the destained Pap smears and in 80% of cell-blocks.

In comparison, calretinin staining was noted in 6% and 50% of destained smears and in 78% and 60% of the cell-blocks of benign and malignant adrenocortical lesions.

Inhibin alpha was not positive in any of the smears and showed the lowest level of positivity in the cell-block sections, namely in 11% of the benign lesions and 25% of the malignant lesions.

The sensitivity of A103 was 90% on cell-blocks and 74% on smears, that of calretinin 75% on cell-blocks and 11% on smears, and that of inhibin alpha, 13% on cell-blocks alone.

Our data show A103 to be the immunomarker with the highest sensitivity for identifying cells of adrenocortical origin in destained Pap's smears and cell-block sections with, however, a lower specificity when compared with calretinin and inhibin alpha.

Calretinin is comparable in sensitivity with A103 on cell-block sections alone and not on smears.

The results of this study suggest that if metastatic melanoma in adrenal gland is not a consideration then A103 is the marker of choice for identifying cells of adrenocortical origin in the limited material available for diagnostic purposes in cytology specimens.

[MeSH-major] Adrenal Cortex / pathology. Adrenal Cortex Neoplasms / pathology. Biomarkers, Tumor / metabolism. Inhibins / metabolism. Neoplasms / pathology. S100 Calcium Binding Protein G / metabolism

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright 2005 Wiley-Liss, Inc.

(PMID = 16007649.001).

[ISSN] 8755-1039

[Journal-full-title] Diagnostic cytopathology

[ISO-abbreviation] Diagn. Cytopathol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies; 0 / Biomarkers, Tumor; 0 / CALB2 protein, human; 0 / Calbindin 2; 0 / S100 Calcium Binding Protein G; 0 / inhibin-alpha subunit; 57285-09-3 / Inhibins

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Epigenetic repression of DNA mismatch repair by inflammation and hypoxia in inflammatory bowel disease-associated colorectal cancer.

However, tumors in germ-line MMR-deficient mouse models lack these histopathologic features.

Mice lacking the heterotrimeric G protein alpha subunit Gialpha2 develop chronic colitis and multifocal, right-sided cancers with mucinous histopathology, similar to human MMR-deficient colorectal cancer.

Chromatin immunoprecipitation identified increased binding of the transcriptional repressor DEC-1 to the proximal Mlh1 promoter in hypoxic YAMC cells and colitic Gialpha2-/- crypts.

Treating Gialpha2-/- mice with the histone deacetylase inhibitor suberoylanilide hydroxamic acid significantly decreased colitis activity and rescued MLH1 expression in crypt epithelial cells, which was associated with increased acetyl histone H3 levels and decreased DEC-1 binding at the proximal Mlh1 promoter, consistent with a histone deacetylase-dependent mechanism.

MedlinePlus Health Information. consumer health - Colorectal Cancer.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. Vorinostat .

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Cancer Cell. 2004 Aug;6(2):139-50 [15324697.001]

[Cites] J Pathol. 2004 Jul;203(3):808-13 [15221940.001]

[Cites] J Clin Invest. 2004 Oct;114(8):1098-106 [15489957.001]

[Cites] Cell. 1995 Jul 28;82(2):309-19 [7628019.001]

[Cites] Cell. 1995 Jul 28;82(2):321-30 [7628020.001]

[Cites] Nat Genet. 1995 Jun;10(2):143-50 [7663509.001]

[Cites] Cell. 1996 Jun 28;85(7):1125-34 [8674118.001]

[Cites] J Immunol. 1997 Feb 1;158(3):1068-77 [9013944.001]

[Cites] Cell. 1997 Nov 14;91(4):467-77 [9390556.001]

[Cites] Cancer Res. 1999 Mar 15;59(6):1301-7 [10096563.001]

[Cites] Cancer Res. 1999 May 1;59(9):2029-33 [10232580.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Jun 8;96(12):6850-5 [10359802.001]

[Cites] Mutat Res. 2004 Dec 21;568(2):275-82 [15542114.001]

[Cites] JAMA. 2005 Apr 27;293(16):1979-85 [15855431.001]

[Cites] Cancer Res. 2005 Oct 1;65(19):8662-70 [16204034.001]

[Cites] Inflamm Bowel Dis. 2006 Mar;12(3):153-65 [16534415.001]

[Cites] J Immunol. 2006 Apr 15;176(8):5015-22 [16585598.001]

[Cites] Hum Pathol. 2006 Jul;37(7):831-8 [16784982.001]

[Cites] Nat Genet. 2006 Jul;38(7):787-93 [16804544.001]

[Cites] N Engl J Med. 2006 Jun 29;354(26):2751-63 [16807412.001]

[Cites] Cancer Sci. 2006 Jul;97(7):582-8 [16827797.001]

[Cites] J Natl Cancer Inst. 2006 Dec 6;98(23):1731-8 [17148775.001]

[Cites] Oncogene. 2007 Feb 8;26(6):802-12 [16878149.001]

[Cites] Clin Genet. 2007 Jun;71(6):499-500 [17539898.001]

[Cites] Gastroenterology. 2007 Jul;133(1):48-56 [17631130.001]

[Cites] J Mol Med (Berl). 2007 Dec;85(12):1295-300 [18026919.001]

[Cites] Gut. 2008 May;57(5):613-22 [18194985.001]

[Cites] Inflamm Bowel Dis. 2008 Jul;14(7):898-907 [18340649.001]

[Cites] PLoS Genet. 2008 Jun;4(6):e1000092 [18551179.001]

[Cites] Oncogene. 2008 Jul 10;27(30):4200-9 [18345027.001]

[Cites] Mutat Res. 2008 Jul-Aug;659(1-2):40-8 [18407786.001]

[Cites] Stem Cells. 2008 Aug;26(8):2052-62 [18511603.001]

[Cites] Curr Opin Genet Dev. 2008 Jun;18(3):273-9 [18662779.001]

[Cites] Nat Genet. 2009 Jan;41(1):112-7 [19098912.001]

[Cites] Gastroenterology. 2009 Mar;136(3):780-98 [19263594.001]

[Cites] Cancer Res. 2000 Feb 15;60(4):803-7 [10706084.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):9082-7 [10922063.001]

[Cites] Am J Pathol. 2001 Feb;158(2):527-35 [11159189.001]

[Cites] Oncogene. 2000 Dec 14;19(54):6297-305 [11175344.001]

[Cites] Methods Enzymol. 2002;352:3-31 [12125356.001]

[Cites] Nat Genet. 2002 Aug;31(4):385-90 [12091911.001]

[Cites] Mol Cell Biol. 2003 May;23(9):3265-73 [12697826.001]

[Cites] Am J Surg Pathol. 2003 May;27(5):563-70 [12717242.001]

[Cites] EMBO J. 2003 May 1;22(9):2245-54 [12727890.001]

[Cites] N Engl J Med. 2003 Jul 17;349(3):247-57 [12867608.001]

[Cites] Mol Carcinog. 2003 Dec;38(4):155-9 [14639654.001]

[Cites] J Natl Cancer Inst. 2004 Feb 18;96(4):261-8 [14970275.001]

[Cites] Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):11-27 [15000146.001]

[Cites] Fam Cancer. 2004;3(2):93-100 [15340259.001]

(PMID = 19638594.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA98626; United States / NIEHS NIH HHS / ES / Z01 ES101643; United States / NCI NIH HHS / CA / R01 CA098626; United States / NIDDK NIH HHS / DK / K08 DK59816; United States / NIDDK NIH HHS / DK / R21 DK071591-01A2; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / CA / R56 CA098626; United States / NCI NIH HHS / CA / P30 CA062203; United States / NIDDK NIH HHS / DK / K08 DK059816; United States / NIDDK NIH HHS / DK / R21 DK071591; United States / NIDDK NIH HHS / DK / DK071591-01A2

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Mlh1 protein, mouse; 0 / Nuclear Proteins; 58IFB293JI / vorinostat; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / Pms2 protein, mouse; EC 3.6.5.1 / GTP-Binding Protein alpha Subunit, Gi2; EC 6.5.1.- / DNA Repair Enzymes

[Other-IDs] NLM/ NIHMS127354; NLM/ PMC2748849

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Protein kinase C: a target for therapy in pancreatic cancer.

OBJECTIVES: Protein kinase C (PKC) is involved in tumor growth and apoptosis and hence represents a potential target for cancer therapy.

This study investigated the expression of PKC in pancreatic tumor tissue in comparison to adjacent normal tissue and determined the modulation of PKC by bryostatin-1 (BRYO) on pancreatic cancer cell lines.

METHODS: Pancreatic tissue was obtained from 18 patients who had a resection (14 with ductal adenocarcinoma and 4 with adenoma and high-grade dysplasia).

HPAC cells were treated with gemcitabine and BRYO and in sequential and concomitant combination.

To evaluate cell viability, apoptosis, and electrophoretic mobility shift assay, 3-(4,5-dimetylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, enzyme-linked immunosorbent assay, and nuclear factor kappaB (NF-kappaB) assays were used.

RESULTS: As compared with the adjacent normal tissue, PKC-alpha, PKC-beta1, and PKC-delta were higher in the tumor; PKC-epsilon was higher in the normal tissue.

Pretreatment with gemcitabine followed by BRYO resulted in decreased cell viability, increased apoptosis, and inhibited NF-kappaB than either agent alone or BRYO followed by gemcitabine.

CONCLUSION: Protein kinase C is overexpressed and activated in pancreatic cancer as compared with normal tissue.

Inhibition of PKC could sensitize pancreatic cancer cell lines to the effects of gemcitabine.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Isoenzymes / antagonists & inhibitors. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / enzymology. Protein Kinase C / antagonists & inhibitors

[MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / enzymology. Adenocarcinoma / pathology. Adenoma / drug therapy. Adenoma / enzymology. Adenoma / pathology. Bryostatins / administration & dosage. Cell Survival / drug effects. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Humans. Protein Kinase Inhibitors / therapeutic use. Reference Values

Genetic Alliance. consumer health - Pancreatic cancer.

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18437080.001).

[ISSN] 1536-4828

[Journal-full-title] Pancreas

[ISO-abbreviation] Pancreas

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Bryostatins; 0 / Isoenzymes; 0 / Protein Kinase Inhibitors; 0W860991D6 / Deoxycytidine; 37O2X55Y9E / bryostatin 1; B76N6SBZ8R / gemcitabine; EC 2.7.11.13 / Protein Kinase C

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Neuroendocrine tumours of the pancreas: predictors of survival after surgical treatment.

AIMS: Neuroendocrine tumours of pancreatic and duodenal origin (NETP) are rare and we present a significant experience from a single centre.

RESULTS: Twenty-four patients had functioning tumours (16 insulinomas, 3 gastrinomas, 2 somatostatinomas, 1 vipoma, 1 glucagonoma and 1 carcinoid tumour).

[MeSH-major] Neuroendocrine Tumors / surgery. Pancreatic Neoplasms / surgery

MedlinePlus Health Information. consumer health - Pancreatic Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright (c) 2005 S. Karger AG, Basel.

(PMID = 16043962.001).

[ISSN] 0253-4886

[Journal-full-title] Digestive surgery

[ISO-abbreviation] Dig Surg

[Language] eng

[Publication-type] Journal Article

[Publication-country] Switzerland

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] MicroRNA profiling in hepatocellular tumors is associated with clinical features and oncogene/tumor suppressor gene mutations.

Molecular classifications defining new tumor subtypes have been recently refined with genetic and transcriptomic analyses of benign and malignant hepatocellular tumors.

Here, we performed microRNA (miRNA) profiling in two series of fully annotated liver tumors to uncover associations between oncogene/tumor suppressor mutations and clinical and pathological features.

Expression levels of 250 miRNAs in 46 benign and malignant hepatocellular tumors were compared to those of 4 normal liver samples with quantitative reverse-transcriptase polymerase chain reaction. miRNAs associated with genetic and clinical characteristics were validated in a second series of 43 liver tumor samples and 16 nontumor samples. miRNA profiling unsupervised analysis classified samples in unique clusters characterized by histological features (tumor/nontumor, P < 0.001; benign/malignant tumors, P < 0.01; inflammatory adenoma and focal nodular hyperplasia, P < 0.01), clinical characteristics [hepatitis B virus (HBV) infection, P < 0.001; alcohol consumption, P < 0.05], and oncogene/tumor suppressor gene mutations [beta-catenin, P < 0.01; hepatocyte nuclear factor 1alpha (HNF1alpha), P < 0.01].

Our study identified and validated miR-224 overexpression in all tumors and miR-200c, miR-200, miR-21, miR-224, miR-10b, and miR-222 specific deregulation in benign or malignant tumors.

Moreover, miR-96 was overexpressed in HBV tumors, and miR-126* was down-regulated in alcohol-related hepatocellular carcinoma.

Down-regulations of miR-107 and miR-375 were specifically associated with HNF1alpha and beta-catenin gene mutations, respectively. miR-375 expression was highly correlated to that of beta-catenin-targeted genes as miR-107 expression was correlated to that of HNF1alpha in a small interfering RNA cell line model.

CONCLUSION: Hepatocellular tumors may have a distinct miRNA expression fingerprint according to malignancy, risk factors, and oncogene/tumor suppressor gene alterations.

[MeSH-major] Carcinoma, Hepatocellular / genetics. Gene Expression Profiling / methods. Genes, Tumor Suppressor. Liver Neoplasms / genetics. MicroRNAs / genetics. Mutation / genetics

[MeSH-minor] Gene Expression Regulation, Neoplastic. Hepatocyte Nuclear Factor 1-alpha / genetics. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Phenotype. Risk Factors. Tumor Cells, Cultured. beta Catenin / genetics. beta Catenin / metabolism

MedlinePlus Health Information. consumer health - Liver Cancer.

HAL archives ouvertes. Full text from .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] Hepatology. 2008 Jun;47(6):1807-9 [18506877.001]

(PMID = 18433021.001).

[ISSN] 1527-3350

[Journal-full-title] Hepatology (Baltimore, Md.)

[ISO-abbreviation] Hepatology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / MicroRNAs; 0 / beta Catenin