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[Title] Multimodality treatment of unresectable hepatic metastases from pancreatic glucagonoma.

Glucagonomas are pancreatic islet cell tumors arising from the alpha cells which belong to neuroendocrine tumors.

We report the case of a 52- year old man with a pancreatic glucagonoma with synchronous multiple liver metastases treated by surgery, transarterial chemoembolization, percutaneous radiofrequency thermal ablation and long-acting octreotide.

Our report confirms that a multimodal approach is very effective in patients with unresectable liver metastases from pancreatic endocrine tumors providing long-lasting palliation and probably prolonging survival.

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(PMID = 21139900.001).

[ISSN] 2036-3613

[Journal-full-title] Rare tumors

[ISO-abbreviation] Rare Tumors

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Other-IDs] NLM/ PMC2994425

   

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

[Title] Glucagonoma diagnosed by arterial stimulation and venous sampling (ASVS).

To identify the location of pancreatic endocrine tumors, arterial stimulation and venous sampling (ASVS) is known to be useful for insulinoma and gastrinoma, but its usefulness for glucagonoma has not been verified to date.

Here we report a case of glucagonoma that was diagnosed by ASVS with calcium loading, in which an approximately 6-fold increase of glucagon was observed in the splenic artery territory.

MEN1 gene analysis verified the presence of a mutation and the glucagonoma was confirmed after operation.

In conclusion, ASVS could be useful for the diagnosis of glucagonoma.

[MeSH-major] Glucagon / blood. Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis

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(PMID = 19525592.001).

[ISSN] 1349-7235

[Journal-full-title] Internal medicine (Tokyo, Japan)

[ISO-abbreviation] Intern. Med.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 9007-92-5 / Glucagon; SY7Q814VUP / Calcium

   

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

[Title] Malignant transformation of hepatic adenomas.

Hepatic adenomas are benign neoplasms of the liver that occur in several well-defined clinical settings, but principally that of excess hormone exposure.

The clinical presentation and pathological findings were reviewed for all hepatic adenomas resected between January 1, 2003 and July 1, 2006.

Immunohistochemistry for p53, beta-catenin and alpha-fetoprotein (AFP) were performed on those cases with malignant transformation and exon 3 of beta-catenin was amplified and sequenced.

A total of 17 hepatic adenomas were resected and 3 showed malignant transformation.

Histologically, the malignant transformation occurred within otherwise typical hepatic adenomas.

Two of three cases showed patchy atypia throughout the hepatic adenoma.

The hepatocellular carcinoma arose as distinct nodules directly within the adenomas, effectively ruling out synchronous lesions.

Immunostains for AFP and beta-catenin were negative in both the hepatic adenomas and areas of hepatocellular carcinoma. p53 immunostaining was positive within the areas of malignant transformation in one case.

No mutations or deletions were seen in exon 3 of the beta-catenin gene for either the adenomas or the carcinoma.

In conclusion, two of the cases that developed hepatocellular carcinomas showed cytological atypia in the background adenoma.

The hepatocellular carcinomas arose as distinct nodules within the adenomas.

[MeSH-major] Adenoma, Liver Cell / pathology. Carcinoma, Hepatocellular / pathology. Cell Transformation, Neoplastic / pathology. Liver Neoplasms / pathology

[MeSH-minor] Adult. Contraceptives, Oral, Hormonal / adverse effects. Female. Humans. Immunohistochemistry. Tumor Suppressor Protein p53 / biosynthesis. alpha-Fetoproteins / biosynthesis. beta Catenin / genetics

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(PMID = 18246041.001).

[ISSN] 0893-3952

[Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

[ISO-abbreviation] Mod. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Contraceptives, Oral, Hormonal; 0 / Tumor Suppressor Protein p53; 0 / alpha-Fetoproteins; 0 / beta Catenin

   

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

[Title] Circulating levels of inflammatory cytokines and risk of colorectal adenomas.

Circulating levels of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) are elevated in the obese.

We examined circulating levels of CRP, IL-6, and TNF-alpha in relation to risk factors and the prevalence of colorectal adenomas.

Plasma levels of CRP, IL-6, and TNF-alpha were quantified in 873 participants (242 colorectal adenoma cases and 631 controls) in a colonoscopy-based cross-sectional study conducted between 1998 and 2002.

Multivariable logistic regression was used to estimate associations between known risk factors for colorectal neoplasia and circulating levels of inflammatory cytokines and associations between inflammatory cytokines and colorectal adenomas.

The prevalence of colorectal adenomas was associated with higher concentrations of IL-6 and TNF-alpha and, to a lesser degree, with CRP.

For IL-6, adjusted odds ratios (OR) for colorectal adenomas were 1.79 [95% confidence interval (CI), 1.19-2.69] for the second highest plasma level and 1.85 (95% CI, 1.24-2.75) for the highest level compared with the reference level.

A similar association was found with TNF-alpha, with adjusted ORs of 1.56 (95% CI, 1.03-2.36) and 1.66 (95% CI, 1.10-2.52), respectively.

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(PMID = 18172326.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA044684; United States / NCI NIH HHS / CA / R01 CA044684-17; United States / NCI NIH HHS / CA / R01 CA 44684; United States / NIDDK NIH HHS / DK / P30 DK034987; United States / NCI NIH HHS / CA / CA044684-17; United States / NIDDK NIH HHS / DK / P30 DK034987-23; United States / NIDDK NIH HHS / DK / P30 DK34987

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

[Publication-country] United States

[Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha

[Other-IDs] NLM/ NIHMS92897; NLM/ PMC2675825

   

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

[Title] [Glucagonoma without glucagonoma syndrome].

INTRODUCTION: Glucagonomas are rare, frequently malignant tumours, arising from the Langerhans' islets of the pancreas.

They usually secrete large amounts of glucagon that can cause a characteristic "glucagonoma syndrome", which includes necrolytic migratory erythema, glucose intolerance or diabetes, weight loss and sometimes, normochromic normocytic anaemia, stomatitis or cheilitis, diarrhoea or other digestive symptoms, thoromboembolism, hepatosplenomegaly, depression or other psychiatric and paraneoplastic symptoms.

In certain cases, some or all glucagonoma symptoms may appear late, or even may be completely absent.

CASE OUTLINE: The authors present a 43-year-old woman in whom an investigation for abdominal pain revealed a tumour of the body of the pancreas.

During operation, the tumour of the body of the pancreas extending to the mesentery measuring 85 x 55 x 55 mm was excised.

Histology and immunohistochemistry showed malignant glucagonoma, with co-expression of somatostatin in about 5% and pancreatic polypeptide in a few tumour cells.

CONCLUSION: Glucagonoma syndrome may be absent in glucagonoma tumour patients so that in unclear pancreatic tumours the clinician should frequently request the serum hormone level (including glucagon) measurement by radioimmunoassay and the pathologist should perform immunohistochemistry investigation.

Those two would probably result in discovery of more glucagonomas and other neuroendocrine tumours without characteristic clinical syndromes.

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

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(PMID = 20499510.001).

[ISSN] 0370-8179

[Journal-full-title] Srpski arhiv za celokupno lekarstvo

[ISO-abbreviation] Srp Arh Celok Lek

[Language] srp

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Serbia

   

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

[Title] Glucagonoma syndrome and necrolytic migratory erythema.

The glucagonoma syndrome is a rare disorder, characterized by necrolytic migratory erythema, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia in association with a glucagon-secreting alpha-cell tumor of the pancreas.

The clinical investigation revealed a pancreatic glucagonoma with resolution of the cutaneous and systemic features after surgical removal.

The dermatologic and endocrine approach to this syndrome is discussed here.

Early recognition and treatment may prevent metastatic disease and ensure its cure with resolution of the cutaneous and catabolic manifestations.

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

[MeSH-minor] Aged. Biopsy. Glucagon / blood. Humans. Male. Necrosis. Pancreatectomy. Tomography, X-Ray Computed

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(PMID = 20465606.001).

[ISSN] 1365-4632

[Journal-full-title] International journal of dermatology

[ISO-abbreviation] Int. J. Dermatol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

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

   

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

[Title] A case of pancreatic glucagonoma with erythema.

Full-body computed tomography (CT) scanning revealed a tumor mass in the tail of the pancreas; CT and magnetic resonance imaging (MRI) scans confirmed the presence of a spherical mass.

In contrast CT scans, although the contrast was gradually increased, no strong contrast differences were observed between the tumor and the surrounding tissue.

Blood test results revealed that the patient had a high glucagon level.

We diagnosed glucagonoma syndrome on the basis of the above results and resected the tail of the pancreas.

Pathological analysis revealed that the tumor cells had proliferated in ribbon-like, cord-like structures.

Immunostaining results were positive for glucagon, which confirmed our diagnosis.

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

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(PMID = 20530930.001).

[ISSN] 0446-6586

[Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology

[ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

   

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

[Title] [A case of pancreatic glucagonoma].

Neuroendocrine tumor consisting of pancreatic alpha-cells -- glucagonoma -- is a very rare finding (one case per two million people a year).

This functionally active, usually malignant tumor has typical clinical manifestations.

Glucagonoma syndrome is a disease that has an original clinical picture that includes necrolytic migrating erythema with secondary bullous dermatitis, glucose tolerance disorder or diabetes mellitus, weight loss, anemia, hypoaminoacidemia, venous thrombosis, and alimentary and mental disturbances.

By the time diagnosis is made, 60 to 70% of glucagonomas already give metastases, and even small glucagonomas should be considered tumors with unknown malignant potential or malignant tumors.

Glucagonomas grow slowly, and patients live long (the survival median is approximately 15 years).

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

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(PMID = 17926496.001).

[ISSN] 0023-2149

[Journal-full-title] Klinicheskaia meditsina

[ISO-abbreviation] Klin Med (Mosk)

[Language] rus

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Russia (Federation)

   

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

[Title] Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma.

Necrolytic migratory erythema is a cutaneous paraneoplastic manifestation, which is usually associated with a glucagon-secreting pancreatic tumor.

However, it also may occur in other circumstances in which serum glucagon is elevated, as in hepatic cirrhosis.

Rarely, necrolytic migratory erythema is reported in association with a jejunal and rectal adenocarcinoma or villous atrophy of the small intestine without any evidence for increased serum glucagon levels.

In this context we report the case of an 85-year-old male with myelodysplastic syndrome who developed typical necrolytic migratory erythema without glucagonoma syndrome or evidence for other pancreatic or liver disease.

We suggest that, in addition to the diseases listed, myelodysplastic syndrome might be able to cause necrolytic migratory erythema.

[MeSH-major] Erythema / complications. Glucagonoma / complications. Myelodysplastic Syndromes / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / complications

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(PMID = 15757825.001).

[ISSN] 1167-1122

[Journal-full-title] European journal of dermatology : EJD

[ISO-abbreviation] Eur J Dermatol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] France

   

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

[Title] Diagnostic challenge of glucagonoma: case report and literature review.

OBJECTIVE: To report the diagnostic difficulties encountered in a case of glucagonoma.

METHODS: We provide a literature review and present the clinical findings, pertinent laboratory data, and results of related studies in a patient with a glucagonoma.

The patient was hospitalized, and because of the dermatologic findings suggestive of necrolytic migratory erythema, the presence of a glucagonoma was suspected.

Glucagon levels were found to be elevated, and imaging studies confirmed the presence of an enlarged mass in the pancreatic tail, without evidence of extension to surrounding structures.

After surgical removal of the tumor, the skin and oral mucosal lesions disappeared spontaneously.

The histologic appearance and immunohistochemical staining results confirmed the diagnosis of a glucagonoma.

Subsequently, all related symptoms resolved, and the glucagon levels normalized.

CONCLUSION: The diagnosis of glucagonoma is often delayed.

Clinicians should be aware of the unusual initial manifestations of this tumor and the potential for less than a full spectrum of the characteristic features of the glucagonoma syndrome.

[MeSH-major] Glucagonoma / diagnosis

[MeSH-minor] Erythema / etiology. Humans. Hyperpigmentation / etiology. Male. Middle Aged. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / ultrasonography. Pancreatic Neoplasms / ultrastructure. Regional Blood Flow. Tomography, X-Ray Computed. Wound Healing

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(PMID = 16901799.001).

[ISSN] 1530-891X

[Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists

[ISO-abbreviation] Endocr Pract

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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

[Title] [Clinically non functioning pituitary adenomas and gonadotroph-cell adenomas].

Clinically non-functioning pituitary adenomas and gonadotroph-cell adenomas are relatively common: microadenomas (< 1cm) are usually pituitary incidentalomas while most macroadenomas are revealed by mass effect and/or hypopituitarism.

They are rarely associated with high gonadotropin (Luteinizing hormone, LH; Follicle-stimulating hormone FSH) levels while increased alpha-subunit levels are more frequent.

Immunocytochemistry of pituitary tumor confirms the diagnosis of clinically non-functioning or gonadotroph-cell adenoma.

Treatment of macroadenoma with visual field defect or hypopituitarism is transphenoidal surgery, but cure is rarely obtained and tumor recurrence is significant during follow-up.

[MeSH-major] Adenoma / diagnosis. Pituitary Neoplasms / diagnosis

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(PMID = 18990542.001).

[ISSN] 2213-0276

[Journal-full-title] Presse medicale (Paris, France : 1983)

[ISO-abbreviation] Presse Med

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] France

[Chemical-registry-number] 0 / Follicle Stimulating Hormone, Human; 9002-67-9 / Luteinizing Hormone

   

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

[Title] Successful treatment of canine necrolytic migratory erythema (superficial necrolytic dermatitis) due to metastatic glucagonoma with octreotide.

Necrolytic migratory erythema (NME; also known as superficial necrolytic dermatitis) is a syndrome most often associated with certain chronic liver diseases or pancreatic glucagonomas.

In humans with glucagonoma-associated NME, skin lesions usually respond to octreotide, a somatostatin analogue that inhibits glucagon release.

In this report an 11-year-old golden retriever dog with pancreatic glucagonoma and metastasis to the regional lymph nodes, spleen and liver was diagnosed with NME.

The dog was later euthanized because of progressive metastatic disease.

In conclusion, subcutaneous octreotide injections were beneficial in this dog with glucagonoma-associated NME.

This somatostatin analogue could be a valuable option to treat canine patients with non-resectable or relapsing pancreatic glucagonoma-associated NME.

[MeSH-major] Dog Diseases / drug therapy. Glucagonoma / veterinary. Necrolytic Migratory Erythema / veterinary. Octreotide / therapeutic use. Pancreatic Neoplasms / veterinary

[MeSH-minor] Animals. Anorexia / chemically induced. Anorexia / veterinary. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Hormonal / adverse effects. Antineoplastic Agents, Hormonal / therapeutic use. Dogs. Dose-Response Relationship, Drug. Lymph Nodes / pathology. Male. Paraneoplastic Syndromes / pathology. Paraneoplastic Syndromes / veterinary

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[Copyright] © 2010 The Authors. Journal compilation © 2010 ESVD and ACVD.

(PMID = 20500495.001).

[ISSN] 1365-3164

[Journal-full-title] Veterinary dermatology

[ISO-abbreviation] Vet. Dermatol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide

   

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

[Title] Non-functioning pituitary adenomas.

The vast majority (>80%) of clinically non-functioning pituitary adenomas (NFPAs) are gonadotroph-cell adenomas, as demonstrated by immunocytochemistry.

Increased levels of uncombined subunits (free alpha-subunit mainly, LH-beta subunit more rarely) are more frequently encountered, but are generally modest.

The main problems raised by NFPA are mass effects problems, responsible for optic chiasm compression or deficient hormone secretion resulting from compression of normal anterior pituitary cells.

The strategy of observation only for patients with incidentally discovered pituitary adenomas may be appropriate, provided that the tumor is well-delimited, small, has no extension with risk of neurological or visual chiasm compression, and that a meticulous hormonal work-up has ruled out the possibility of a minimal hormonal hypersecretion.

Transsphenoidal surgery allows improvement in visual disturbances due to chiasmal syndrome in most patients, and sometimes, in pituitary function.

Dopamine agonist bromocriptine decreases gonadotropin and alpha-subunit in vitro and in vivo, but, in clinical studies, was poorly effective in reducing supranormal gonadotropins and free subunits levels, and rarely produced a minimal tumoral shrinkage.

Prolonged administration of GnRH antagonist in a small number of patients with a secreting gonadotroph cell adenoma has been reported to reduce supranormal gonadotropins levels but not to produce any change in tumoral size.

[MeSH-major] Adenoma. Pituitary Neoplasms

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(PMID = 16625856.001).

[ISSN] 0391-4097

[Journal-full-title] Journal of endocrinological investigation

[ISO-abbreviation] J. Endocrinol. Invest.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Italy

[Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone

[Number-of-references] 66

   

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

[Title] ACTH and alpha-subunit are co-expressed in rare human pituitary corticotroph cell adenomas proposed to originate from ACTH-committed early pituitary progenitor cells.

The functional differentiation of pituitary cells and adenomas follows the combination of transcription factors and co-factors in three cell lineages [growth hormone-prolactin-thyroid-stimulating hormone lineage, adrenocorticotrophic hormone (ACTH)/pro-opiomelanocortin (POMC) lineage, and follicular stimulating hormone (FSH)/luteinizing hormone (LH) lineage], which include Pit-1, GATA-2, SF-1, NeuroD1/beta2, Tpit, ERalpha, and others.

Only rarely are hormones from different lineages co-expressed in the same adenoma cells.

Most corticotroph cell adenomas belonging to the ACTH/POMC lineage are mono-hormonal.

In our study of 89 corticotroph cell adenomas, 5 cases expressed both ACTH and alpha-subunit; these adenomas did not express any other anterior pituitary hormones or subunits.

To clarify the mechanism involved, we studied the transcription factors that regulate pituitary cell differentiation.

NeuroD1 and T-pit, markers of the ACTH/POMC lineage, and SF-1 and DAX-1, related to the LH/FSH cell lineage were expressed in all cases.

GATA2, a synergistic factor in the gonadotroph cell lineage with SF-1, was also expressed in three of five cases.

As ACTH and alpha-subunit are the earliest hormones to appear during development, we speculate that these particular adenomas are derived from committed ACTH progenitor cells.

The molecular process governing functional differentiation of these adenomas requires further investigation.

[MeSH-major] Adenoma / genetics. Adrenocorticotropic Hormone / genetics. Gene Expression Regulation, Neoplastic. Glycoprotein Hormones, alpha Subunit / genetics. Pituitary Neoplasms / genetics. Pituitary Neoplasms / pathology

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(PMID = 18228160.001).

[ISSN] 1559-0097

[Journal-full-title] Endocrine pathology

[ISO-abbreviation] Endocr. Pathol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Glycoprotein Hormones, alpha Subunit; 0 / NEUROD1 protein, human; 0 / Transcription Factor Pit-1; 0 / Transcription Factors; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone

   

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

[Title] Endocrine pancreatic tumors with glucagon hypersecretion: a retrospective study of 23 cases during 20 years.

BACKGROUND: Glucagon-secreting endocrine pancreatic tumor is a rare disease, hence controlled studies on clinical management are lacking.

In an attempt to assess the efficacy of diagnostic and therapeutic measures in patients with glucagonoma, a retrospective study was performed using the archives of a tertiary care center.

PATIENTS AND METHODS: Records from 340 patients with endocrine pancreatic tumors were reassessed and 23 patients with malignant endocrine pancreatic tumor and elevated plasma glucagon levels were identified.

RESULTS: About 7% of patients with histologically verified tumors fullfilled our criteria for glucagonoma.

Only 22% of these patients had developed diabetes prior to the diagnosis of glucagonoma.

Seventy eight percent had metastatic disease to the liver at diagnosis.

During the study period, 11 patients died at a median of 80 months from diagnosis whereas 11 patients are still alive after a median follow up of 52 months.

CONCLUSIONS: Glucagonomas represent 7% of our comprehensive referral material of endocrine pancreatic tumors.

Necrolytic migratory erythema was a common finding (52%) and diabetes less frequent at presentation than previously reported.

Tumors were positive on somatostatin receptor scintigraphy and objective responses were seen to chemotherapy.

[MeSH-major] Antineoplastic Agents / therapeutic use. Erythema / complications. Glucagonoma / therapy. Pancreatic Neoplasms / therapy

[MeSH-minor] Adult. Aged. Combined Modality Therapy. Female. Glucagon / blood. Humans. Interferons. Liver Neoplasms / secondary. Male. Middle Aged. Receptors, Somatostatin / metabolism. Retrospective Studies. Sex Factors. Survival Analysis. Treatment Outcome

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(PMID = 17873310.001).

[ISSN] 1357-0560

[Journal-full-title] Medical oncology (Northwood, London, England)

[ISO-abbreviation] Med. Oncol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Somatostatin; 9007-92-5 / Glucagon; 9008-11-1 / Interferons

   

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

[Title] Duodeno-pancreatic neuroendocrine tumours.

Duodeno-pancreatic neuroendocrine tumours (DP-ETs) are increasingly diagnosed today due to the widespread use of modern imaging methods.

Duodeno-pancreatic endocrine tumours should be treated by radical surgical resection, which offers a high chance for cure when the disease is localized.

A high index of suspicion is required in these patients for the presence of a multiple endocrine neoplasia type syndrome.

Histological/immunohistochemical diagnosis was somatostatin-producing tumour in the first patient, oncocytic endocrine tumour positive for neurone-specific enolase and focally for chromogranin in the second patient, glucagonoma and pancreatic polypeptide-producing endocrine pancreatic tumour in the third patient, and gastrin, somatostatin, calcitonin, insulin and adrenocorticotropic hormone (ACTH)-producing tumour in the fourth.

The second patient died 6.5 years following surgery due to disseminated disease.

[MeSH-major] Duodenal Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Pancreatic Neoplasms / diagnosis

[MeSH-minor] Adult. Aged. Biomarkers, Tumor / analysis. Biopsy. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Proteins / metabolism. Treatment Outcome

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(PMID = 19708940.001).

[ISSN] 1365-2354

[Journal-full-title] European journal of cancer care

[ISO-abbreviation] Eur J Cancer Care (Engl)

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

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

   

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

The classical symptoms are associated with alpha-cell pancreatic islet cell tumor or 'glucagonoma'.

Generally, extracutaneous hallmarks of this disease include weight loss, diabetes, anaemia and diarrhoea.

OBSERVATION: We report a case of a 39-year-old woman with a 3-year history of recalcitrant psoriasiform eruption, who had no other associated symptoms on routine examination.

Abdominal computer tomography was performed, which revealed a tumor in the tail of the pancreas.

After distal resection of the pancreas her skin symptoms resolved in a few days time.

Histology was consistent with glucagonoma.

CONCLUSIONS: It is infrequent to have only necrolytic migratory erythema, hyperglucagonaemia and islet-cell tumor but no other extracutaneous symptoms in glucagonoma syndrome.

Skin symptoms are important, often they are the clue to the diagnosis of glucagonoma syndrome.

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

[MeSH-minor] Adult. Female. Humans. Necrosis. Paraneoplastic Syndromes. Treatment Outcome

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(PMID = 16466513.001).

[ISSN] 0303-6987

[Journal-full-title] Journal of cutaneous pathology

[ISO-abbreviation] J. Cutan. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Denmark

   

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

[Title] Estrogen receptors alpha and beta immunohistochemical expression: clinicopathological correlations in pituitary adenomas.

AIM: We investigated the immunohistochemical expression of estrogen receptors alpha (ERalpha) and beta (ERbeta) in pituitary adenoma subtypes combined with clinicopathological factors.

MATERIALS AND METHODS: Pituitary adenomas (n=75) were immunostained for ERalpha and ERbeta using the streptavidin-biotin-peroxidase complex method with a monoclonal ERalpha antibody and polyclonal ERbeta antibody.

RESULTS: Nuclear immunoreactivity for both receptors was highest among PRL, FSH/LH, null cell, and GH adenomas.

ACTH, silent subtypes I and II corticotrophs, and subtype III adenomas were the least immunoreactive for both receptors.

ACTH adenomas expressed significantly less ERalpha than FSH-LH, GH, and null cell adenomas.

A significantly elevated ERalpha expression was observed in macroadenomas compared to microadenomas and non-invasive compared to invasive tumors.

CONCLUSION: ERalpha and ERbeta are differentially expressed in the various pituitary adenoma subtypes suggesting a cell-specific function for these receptors.

To elucidate the role of ERalpha in tumor size and invasiveness, additional studies are required.

[MeSH-major] Adenoma / metabolism. Adenoma / pathology. Estrogen Receptor alpha / biosynthesis. Estrogen Receptor beta / biosynthesis. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology

[MeSH-minor] Cell Nucleus / metabolism. Cytoplasm / metabolism. Female. Humans. Immunohistochemistry. Male. Neoplasm Invasiveness

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(PMID = 20683030.001).

[ISSN] 1791-7530

[Journal-full-title] Anticancer research

[ISO-abbreviation] Anticancer Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

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

   

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

[Title] Expression of Ki-67, PCNA, and p27kip1 in canine pituitary corticotroph adenomas.

Pituitary-dependent hypercortisolism (PDH), which is caused by adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas, is a common endocrinopathy in dogs.

The aim of this study was to investigate the expression of the proliferation markers Ki-67 and proliferating cell nuclear antigen (PCNA) and the cell-cycle inhibitor p27kip1 in corticotroph adenomas in enlarged and non-enlarged pituitaries.

The expression of Ki-67, PCNA, and p27kip1 was analyzed by immunohistochemical staining of 17 pituitary adenoma samples harvested during pituitary surgery in dogs with PDH.

The labeling index was calculated by counting the number of immunopositive cells per 1,000 cells.

It is concluded that Ki-67 and PCNA are not useful as proliferative markers for studying the pathobiology of pituitary corticotroph adenomas in dogs.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Cyclin-Dependent Kinase Inhibitor p27 / analysis. Dog Diseases / metabolism. Ki-67 Antigen / analysis. Pituitary Neoplasms / veterinary. Proliferating Cell Nuclear Antigen / analysis

[MeSH-minor] Adrenocorticotropic Hormone / analysis. Animals. Dogs. Female. Immunohistochemistry. Male. alpha-MSH / analysis

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[Copyright] Copyright (c) 2009 Elsevier Inc. All rights reserved.

(PMID = 20022446.001).

[ISSN] 1879-0054

[Journal-full-title] Domestic animal endocrinology

[ISO-abbreviation] Domest. Anim. Endocrinol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Proliferating Cell Nuclear Antigen; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone

   

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

[Title] [Necrolytic migratory erythema associated with glucagonoma].

[Transliterated title] Eritema necrolítico migratorio asociado a glucagonoma.

Glucagonoma is a rare pancreatic tumor that is usually associated with a syndrome that includes diabetes, anemia, weight loss and skin lesions in the form of necrolytic migratory erythema.

We present the case of a patient with malignant glucagonoma treated with surgery and octreotide, which manifested with skin lesions.

The discussion will review the physiopathology, other causes of necrolytic erythema, diagnosis and differential diagnosis and treatment.

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

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(PMID = 16476361.001).

[ISSN] 0001-7310

[Journal-full-title] Actas dermo-sifiliográficas

[ISO-abbreviation] Actas Dermosifiliogr

[Language] spa

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Spain

   

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

[Title] Hormonal signaling and pituitary adenomas.

In recent years the demonstration that human pituitary adenomas are monoclonal in origin provides further evidence that pituitary neoplasia arise from the replication of a single mutated cell in which growth advantage results from either activation of proto-oncogenes or inactivation of tumor suppressor genes.

Mutations in common oncogenes and tumor suppressor genes are only exceptionally involved in pituitary tumors.

Since pituicytes may proliferate in response to hypothalamic neurohormones, locally produced growth factors and peripheral hormones, it has been speculated that dysregulation of the signaling molecules that constitute these pathways may confer growth advantage to the target cell, finally resulting in tumor formation.

The only mutational change so far recognized to be unequivocally associated with pituitary tumors occur in the Gs alpha gene (GNAS1) and cause constitutive activation of the cAMP-dependent pathway.

[MeSH-major] Adenoma / etiology. Hormones / physiology. Pituitary Neoplasms / etiology. Signal Transduction / physiology

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(PMID = 17337884.001).

[ISSN] 0028-3835

[Journal-full-title] Neuroendocrinology

[ISO-abbreviation] Neuroendocrinology

[Language] eng

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

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Hormones; 0 / Hypothalamic Hormones; 0 / Intercellular Signaling Peptides and Proteins; 0 / Receptors, G-Protein-Coupled

[Number-of-references] 66

   

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

[Title] Diagnosis and treatment of cutaneous paraneoplastic disorders.

Cutaneous signs of these disorders afford clinicians opportunities for early diagnosis and treatment.

We aim to succinctly review the recognition, diagnosis, and treatment of selected cutaneous paraneoplastic diseases.

Skin disorders that may be associated with paraneoplastic syndromes include: cutaneous metastases, tripe palms, Sweet's syndrome, glucagonoma, Paget's disease and extramammary Paget's disease, acanthosis nigricans, Birt-Hogg-Dube syndrome, basal cell nevus syndrome, Bazex syndrome (acrokeratosis paraneoplastica), carcinoid syndrome, Cowden's disease(multiple hamartoma syndrome), dermatomyositis, erythema gyratum repens, ichthyosis aquisita, von Recklinghausen's disease, pityriasis rotunda, pyoderma gangrenosum, Quincke's edema (angioedema and paraneoplastic uricaria), paraneoplastic pemphigus, Degos' disease, superior vena cava syndrome, Werner's syndrome, diffuse normolipemic plane xanthomas, and yellow nail syndrome.

[MeSH-major] Paraneoplastic Syndromes / diagnosis. Paraneoplastic Syndromes / therapy. Skin Diseases / diagnosis. Skin Diseases / therapy

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[Copyright] © 2010 Wiley Periodicals, Inc.

(PMID = 21054710.001).

[ISSN] 1529-8019

[Journal-full-title] Dermatologic therapy

[ISO-abbreviation] Dermatol Ther

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Denmark

   

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

[Title] Immunohistochemical expression of SNAP-25 protein in adenomas of the human pituitary.

SNAP-25, a synaptosome-associated exocytosis protein of 25 kd mw, plays an important role in the secretory activity of several endocrine cells.

In the present study, we investigated surgically removed pituitary adenomas including 40 prolactin (PRL), 31 growth hormone, 5 adrenocorticotropic hormone, 5 thyroid-stimulating hormone, 14 follicle-stimulating hormone/luteinizing hormone/alpha-subunit-producing tumors, and 5 null cell adenomas.

Among the 40 patients with PRL-producing pituitary adenoma, 16 had been preoperatively treated with the dopamine agonist bromocriptine.

Similarly, of the 31 patients with GH-producing pituitary adenomas, 15 had been treated with the long-acting somatostatin analog, octreotide.

All tumors were subjected to transsphenoidal surgery, formalin-fixed, routinely processed, and paraffin-embedded.

Immunostaining for SNAP-25 (streptavidin-biotin peroxidase complex method) showed that 10 PRL-producing adenomas were strongly immunoreactive.

Immunopositivity was mainly cell membrane in distribution but several cells showed mild cytoplasmic staining.

Among GH-producing adenomas, SNAP-25 was seen in 5 cases; reactivity being mild-to-moderate, membrane-bound, and cytoplasmic.

Other adenoma types were virtually immunonegative.

It is conceivable that SNAP-25 plays an important role in PRL release and is involved in the bromocriptine-induced suppression of PRL secretion from PRL-producing adenoma cells.

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(PMID = 18633321.001).

[ISSN] 1533-4058

[Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM

[ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / SNAP25 protein, human; 0 / Synaptosomal-Associated Protein 25; 12629-01-5 / Human Growth Hormone; 3A64E3G5ZO / Bromocriptine; 9002-62-4 / Prolactin; RWM8CCW8GP / Octreotide

   

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

[Title] MAP-2 expression in the human adenohypophysis and in pituitary adenomas. An immunohistochemical study.

MAP-2, a well characterized member of the microtubule associated protein (MAP) family, binds to and stabilizes microtubules and is involved in cell proliferation as well as neuronal differentiation.

The aim of the present work was to study MAP-2 expression in human adenohypophyses and pituitary adenomas.

Nine non-tumorous adenohypophyses and 77 adenomas (GH-, PRL-, ACTH-, TSH-, FSH/LH- and/or alpha subunit- producing or immunonegative tumors) were investigated.

The results show that MAP-2 is expressed in the cytoplasm of non-tumorous adenohypophysial cells as well as of various pituitary adenoma types.

Thus MAP-2 expression cannot be used to estimate cell proliferation rate, growth potential, endocrine activity or biologic behaviour of an adenoma.

Immunopositivity appeared to be stronger in the cytoplasm of adenoma cells than in that of non-tumorous adenohypophysial cells, implying that the adenoma cells contain larger quantities of MAP-2.

It can be concluded that the functional activity of MAP-2 is not associated with the manufacture of any specific adenohypophysial hormone(s) and is not limited to one specific cell type.

[MeSH-major] Adenoma / metabolism. Microtubule-Associated Proteins / biosynthesis. Pituitary Gland, Anterior / metabolism. Pituitary Neoplasms / metabolism

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(PMID = 16195780.001).

[ISSN] 1386-341X

[Journal-full-title] Pituitary

[ISO-abbreviation] Pituitary

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / MAP2 protein, human; 0 / Microtubule-Associated Proteins

   

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

[Title] Silent corticogonadotroph adenomas: clinical and cellular characteristics and long-term outcomes.

Silent corticotrophins adenomas (SCAs) are clinically silent and non-secreting but immunostain positively for ACTH.

We compared preoperative and postoperative clinical results and tumor cytogenesis in 25 SCAs and 84 nonfunctioning adenomas in 109 consecutive patients diagnosed pre-operatively with nonfunctioning pituitary adenomas.

Preoperative SCA presentation was similar to that observed for nonfunctioning adenomas.

However, SCAs recurred postoperatively at a median of 3 years vs. 8 years for nonfunctioning adenomas (p<0.0001).

Fifty-four percent of patients with SCAs had new onset postoperative hypopituitarism vs. 17% of nonfunctioning adenomas (p<0.025).

SCAs (n=18) were immunopositive for ACTH, cytoplasmic and nuclear SF-1, NeuroD1, DAX-1, and alpha-gonadotropin subunit, but Tpit negative, and co-expression of tumor ACTH with either SF-1 or LH was detected.

In contrast, functional corticotroph adenomas (n=11) were immunopositive for ACTH, nuclear SF-1, NeuroD1, and Tpit, but negative for DAX-1, a gonadotroph cell transcription factor.

Gonadotroph adenomas (n=23) were immunonegative for ACTH and Tpit but positive for nuclear SF-1, NeuroD1, and DAX-1.

SCA electron microscopy demonstrated ultrastructural features consistent with corticotroph and gonadotroph cells.

As SCAs exhibit features consistent with both corticotroph and gonadotroph cytologic origin, we propose a pathologic and clinically distinct classification of SCAs as silent corticogonadotroph adenomas.

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(PMID = 20717480.001).

[ISSN] 1868-8500

[Journal-full-title] Hormones & cancer

[ISO-abbreviation] Horm Cancer

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / T32 DK007770-08; United States / NCI NIH HHS / CA / R01 CA075979-08; United States / NIDDK NIH HHS / DK / T32 DK007770; United States / NIDDK NIH HHS / DK / T32 DK07770; United States / NIDDK NIH HHS / DK / DK007770-08; United States / NCI NIH HHS / CA / CA 075979; United States / NCI NIH HHS / CA / R01 CA075979; United States / NCI NIH HHS / CA / CA075979-08

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

[Publication-country] United States

[Chemical-registry-number] 0 / Gonadotropins

[Keywords] NOTNLM ; Corticotroph adenoma / Gonadotroph adenoma / Nonfunctioning adenoma / Pituitary adenoma

   

[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.

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(PMID = 20430720.001).

[ISSN] 1897-5631

[Journal-full-title] Folia histochemica et cytobiologica

[ISO-abbreviation] Folia Histochem. Cytobiol.

[Language] ENG

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

[Publication-country] Poland

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Protein Precursors; 0 / prothymosin alpha; 61512-21-8 / Thymosin

   

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

[Title] Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors.

The computed tomographic scan of the abdomen revealed multiple hepatic tumors.

Histopathological examination of ultrasound-guided needle biopsy from a hepatic lesion demonstrated a neuroendocrine tumor.

Somatostatin-receptor scintigraphy with radio-labelled octreotide confirmed the likelihood of the neuroendocrine nature of the hepatic tumors and excluded the presence of other such lesions throughout the rest of the body, including the pancreas.

The serum glucagon level was markedly increased.

The diagnosis of necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors was made and therapy with the long-acting somatostatin analogue octreotide was started.

Having reached the final stage of the disease, which was further complicated by congestive heart failure, the patient died one year later.

As no autopsy was performed, we were unable to establish whether the hepatic tumors represented a metastatic process of previously undetected pancreatic glucagonoma or if they were extra-pancreatic glucagon-secreting tumors.

The correct diagnosis of necrolytic migratory erythema is important, since it might be the clue for early detection of glucagonoma or of extra-pancreatic glucagon-secreting tumors.

[MeSH-major] Dermatitis / etiology. Erythema / etiology. Liver Neoplasms / diagnosis. Neuroendocrine Tumors / diagnosis. Paraneoplastic Syndromes / diagnosis

[MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Glucagon / blood. Humans. Male. Middle Aged. Octreotide / therapeutic use

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(PMID = 16435046.001).

[ISSN] 1318-4458

[Journal-full-title] Acta dermatovenerologica Alpina, Pannonica, et Adriatica

[ISO-abbreviation] Acta Dermatovenerol Alp Pannonica Adriat

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Slovenia

[Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 9007-92-5 / Glucagon; RWM8CCW8GP / Octreotide

   

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

Of these, the homoeodomain protein PDX-1 (pancreatic duodenal homeobox factor-1), the basic leucine zipper protein MafA and the basic helix-loop-helix heterodimer E47/BETA2 (beta-cell E box transactivator 2; referred to here as beta2) bind to important regulatory sites.

Mutagenesis of the PDX-1, MafA and E47/beta2 binding sites reduced promoter activity by 60, 74 and 94% respectively, in INS-1 beta-cells.

In the islet glucagonoma cell line alphaTC1.6, overexpression of PDX-1 and MafA separately increased promoter activity approx.

In HeLa cells, PDX-1 stimulated the basal promoter by approx.

PDX-1 was shown further to activate the endogenous insulin 1 gene in alphaTC1.6 cells, whereas MafA activated the insulin 2 gene.

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(PMID = 15862113.001).

[ISSN] 1470-8728

[Journal-full-title] The Biochemical journal

[ISO-abbreviation] Biochem. J.

[Language] ENG

[Grant] United Kingdom / Wellcome Trust / /

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

[Publication-country] England

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / HMGB Proteins; 0 / Homeodomain Proteins; 0 / Insulin; 0 / MAFA protein, human; 0 / Maf Transcription Factors, Large; 0 / NEUROD1 protein, human; 0 / TCF Transcription Factors; 0 / TCF7L1 protein, human; 0 / Tcf7l1 protein, rat; 0 / Trans-Activators; 0 / Transcription Factor 7-Like 1 Protein; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein

[Other-IDs] NLM/ PMC1180732

   

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

[Title] Subclinical adenomas in postmortem pituitaries: classification and correlations to clinical data.

OBJECTIVE: The aim of this study was to examine pituitary adenomas in a series of postmortem pituitaries by use of modern technologies of immunostaining, to classify the adenomas according to the current WHO classification and to analyse the possible associations to the available clinical data.

RESULTS: A total of 334 pituitary adenomas were found in 316 pituitaries.

One hundred and thirty-two sparsely granulated prolactin cell adenomas (39.5%), 75 null cell adenomas (22.5%) and 31 oncocytomas were diagnosed.

Forty-six ACTH cell adenomas (13.8%, 27 densely granulated, 19 sparsely granulated) and one adenoma composed of Crooke's cells were detected.

Twenty-two gonadotroph cell adenomas (6.6%), seven GH cell adenomas (four sparsely granulated, three densely granulated), one mixed GH cell-PRL cell adenoma, two TSH cell adenomas, five plurihormonal adenoma type I, four plurihormonal adenoma type II and two alpha-subunit-only adenomas were seen.

Six adenomas remained unclassified because the tissue was not contained in all sections for immunohistochemistry.

The overall tumour size ranged from 0.1 to 20 mm in diameter.

Among 76 adenomas (22.7%), which had a tumour size of > or = 3 mm, only three tumours were macroadenomas corresponding to a tumour size of more than 10 mm.

CONCLUSIONS: Adenomas in postmortem pituitaries differ from those in surgical series in proportion of adenoma types and biological behaviour.

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(PMID = 16645024.001).

[ISSN] 0804-4643

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Glycoprotein Hormones, alpha Subunit; 0 / Gonadotropins; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin

   

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

[Title] The expression of AIP-related molecules in elucidation of cellular pathways in pituitary adenomas.

Germline mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene predispose to the development of pituitary adenomas.

Here, we characterized AIP mutation positive (AIPmut+) and AIP mutation negative (AIPmut-) pituitary adenomas by immunohistochemistry.

The expressions of the AIP-related proteins aryl hydrocarbon receptor (AHR), AHR nuclear translocator (ARNT), cyclin-dependent kinase inhibitor 1B encoding p27(Kip1), and hypoxia-inducible factor 1-alpha were examined in 14 AIPmut+ and 53 AIPmut- pituitary adenomas to detect possible expression differences.

In addition, the expression of CD34, an endothelial and hematopoietic stem cell marker, was analyzed.

We found ARNT to be less frequently expressed in AIPmut+ pituitary adenomas (P = 0.001), suggesting that AIP regulates the ARNT levels.

AIP small interfering RNA-treated HeLa, HEK293, or Aip-null mouse embryonic fibroblast cells did not show lowered expression of ARNT.

Instead, in the pituitary adenoma cell line GH3, Aip silencing caused a partial reduction of Arnt and a clear increase in cell proliferation.

The expressions of p27(Kip1), hypoxia-inducible factor 1-alpha, or CD34 did not differ between tumor types.

The present study shows that the expression of ARNT protein is significantly reduced in AIPmut+ tumors.

[MeSH-minor] Animals. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Blotting, Western. Cyclin-Dependent Kinase Inhibitor p27. Down-Regulation. Gene Expression. Gene Expression Profiling. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Immunohistochemistry. Mice. Mutation. RNA, Small Interfering. Receptors, Aryl Hydrocarbon / biosynthesis. Receptors, Aryl Hydrocarbon / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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(PMID = 19850893.001).

[ISSN] 1525-2191

[Journal-full-title] The American journal of pathology

[ISO-abbreviation] Am. J. Pathol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / ARNT protein, human; 0 / Antigens, CD34; 0 / CDKN1B protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; 0 / Receptors, Aryl Hydrocarbon; 0 / aryl hydrocarbon receptor-interacting protein; 138391-32-9 / Aryl Hydrocarbon Receptor Nuclear Translocator; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27

[Other-IDs] NLM/ PMC2789606

   

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

[Title] Presence of HIF-1 and related genes in normal mucosa, adenomas and carcinomas of the colorectum.

Expression of the transcription factor hypoxia-inducible factor 1 (HIF-1), which plays a key role in cellular adaptation to hypoxia, was investigated in normal colorectal mucosa (ten), adenomas (61), and carcinomas (23).

Tissue samples were analyzed for HIF-1 alpha, its upstream regulators, von Hippel-Lindau factor, AKT, and mammalian target of rapamycin (mTOR) and its downstream targets glucose transporter 1 (GLUT1), carbonic anhydrase IX, stromal-cell-derived factor 1 (SDF-1) by immunohistochemistry.

In normal colorectal mucosa, HIF-1 alpha was observed in almost all nuclei of surface epithelial cells, probably secondary to a gradient of oxygenation, as indicated by pimonidazole staining.

The same staining pattern was present in 87% of adenomas.

In carcinomas, HIF-1 alpha was present predominantly around areas of necrosis (78%).

Active AKT and mTOR, were present in all adenomas, carcinomas, and in normal colorectal mucosa.

GLUT1 and SDF-1 were present in the normal surface epithelium of all adenoma cases, whereas in the carcinoma GLUT1 was located around necrotic regions and SDF-1 was present in all epithelial cells.

In conclusion, HIF-1 alpha appears to be physiologically expressed in the upper part of the colorectal mucosa.

The present observations support that upregulation of HIF-1 alpha and its downstream targets GLUT1 and SDF-1 in colorectal adenomas and carcinomas may be due to hypoxia, in close interaction with an active phosphatidylinositol 3-kinases-AKT-mTOR pathway.

[MeSH-major] Adenoma / metabolism. Chemokine CXCL12 / metabolism. Colorectal Neoplasms / metabolism. Glucose Transporter Type 1 / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Intestinal Mucosa / metabolism

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(PMID = 18351386.001).

[ISSN] 0945-6317

[Journal-full-title] Virchows Archiv : an international journal of pathology

[ISO-abbreviation] Virchows Arch.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Chemokine CXCL12; 0 / Glucose Transporter Type 1; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / SLC2A1 protein, human; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Oncogene Protein v-akt; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases

[Other-IDs] NLM/ PMC2329727

   

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

[Title] Synaptophysin immunoreactivity in adrenocortical adenomas: a correlation between synaptophysin and CYP17A1 expression.

DESIGN AND METHODS: The adrenal cortex is not considered to be an intrinsic part of the diffuse neuroendocrine system, but adrenocortical neoplasms possess neuroendocrine properties.

In this study, we examined synaptophysin (SYP) and neural cell adhesion molecule (NCAM) expression in adrenocortical adenomas in relation to adrenal function.

RESULTS: Immunohistochemical analysis showed that 50.7 and 98.6% of the cortical adenomas showed SYP and NCAM immunoreactivities respectively.

There was no apparent difference in NCAM immunoreactivity among the adenomas.

However, the immunostaining for SYP was significantly stronger in cortisol-producing adenomas (CPA) than in aldosterone-producing adenomas (APA), nonfunctioning adenomas (NFA), showing no clinical or endocrinological abnormality, or adenomas associated with preclinical Cushing's syndrome (preCS).

It was unexpected that the ratio of positive cells for SYP in preCS was less than that in APA and NFA.

CONCLUSIONS: We propose that SYP expression in adrenocortical cells may be involved in some aspect of adrenal function such as transport or secretion of glucocorticoids.

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(PMID = 19755404.001).

[ISSN] 1479-683X

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Neural Cell Adhesion Molecules; 0 / RNA, Messenger; 0 / Synaptophysin; EC 1.14.99.9 / CYP17A1 protein, human; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase

   

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

[Title] Signalling pathway alterations in pituitary adenomas: involvement of Gsalpha, cAMP and mitogen-activated protein kinases.

Despite extensive research on sporadic pituitary adenomas, it is not yet possible to assign one protein alteration to one specific type of pituitary adenomas.

Nevertheless, alterations of the cAMP pathway appear to be molecular hallmarks of most growth hormone (GH)-secreting adenomas.

In this review, we summarise the literature regarding signalling alterations observed in GH-secreting adenomas.

In the light of results obtained on human somatotroph adenoma cells in primary culture and on models of murine somatotroph cell lines, we postulate a crucial role for ERK1/2 in GH-secreting adenomas downstream of cAMP pathway alterations that might impact the tumoural phenotype.

[MeSH-major] Adenoma / metabolism. Cyclic AMP / metabolism. GTP-Binding Protein alpha Subunits, Gs / metabolism. Mitogen-Activated Protein Kinases / metabolism. Pituitary Neoplasms / metabolism. Signal Transduction

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(PMID = 19732293.001).

[ISSN] 1365-2826

[Journal-full-title] Journal of neuroendocrinology

[ISO-abbreviation] J. Neuroendocrinol.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 9002-72-6 / Growth Hormone; E0399OZS9N / Cyclic AMP; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs

[Number-of-references] 95

   

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

[Title] The zinc finger-containing transcription factor Gata-4 is expressed in the developing endocrine pancreas and activates glucagon gene expression.

We show here that Gata-4 and/or Gata-6 are not only expressed in the adult exocrine pancreas but also in glucagonoma and insulinoma cell lines, whereas Gata-5 is restricted to the exocrine pancreas.

During pancreas development, Gata-4 is expressed already at embryonic d 10.5 and colocalizes with early glucagon+ cells at embryonic d 12.5.

Gata-4 was able to transactivate the glucagon gene both in heterologous BHK-21 (nonislet Syrian baby hamster kidney) and in glucagon-producing InR1G9 cells.

Using gel-mobility shift assays, we identified a complex formed with nuclear extracts from InR1G9 cells on the G5 control element (-140 to -169) of the glucagon gene promoter as Gata-4.

Mutation of the GATA binding site on G5 abrogated the transcriptional activation mediated by Gata-4 and reduced basal glucagon gene promoter activity in glucagon-producing cells by 55%.

Furthermore, Gata-4 acted more than additively with Forkhead box A (hepatic nuclear factor-3) to trans-activate the glucagon gene promoter.

We conclude that, besides its role in endoderm differentiation, Gata-4 might be implicated in the regulation of glucagon gene expression in the fetal pancreas and that Gata activity itself may be modulated by interactions with different cofactors.

[MeSH-major] DNA-Binding Proteins / chemistry. Gene Expression Regulation. Glucagon / metabolism. Islets of Langerhans / metabolism. Transcription Factors / chemistry. Zinc Fingers

[MeSH-minor] Animals. Base Sequence. Binding Sites. Cell Differentiation. Cell Line. Cell Nucleus / metabolism. Chloramphenicol O-Acetyltransferase / metabolism. Cricetinae. Dose-Response Relationship, Drug. GATA4 Transcription Factor. GATA6 Transcription Factor. Humans. Mice. Microscopy, Fluorescence. Molecular Sequence Data. Mutation. Pancreas / embryology. Promoter Regions, Genetic. Protein Binding. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tissue Distribution. Transcriptional Activation. Transfection

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(PMID = 15539431.001).

[ISSN] 0888-8809

[Journal-full-title] Molecular endocrinology (Baltimore, Md.)

[ISO-abbreviation] Mol. Endocrinol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / GATA4 Transcription Factor; 0 / GATA6 Transcription Factor; 0 / GATA6 protein, human; 0 / Gata6 protein, mouse; 0 / Transcription Factors; 9007-92-5 / Glucagon; EC 2.3.1.28 / Chloramphenicol O-Acetyltransferase

   

[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

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(PMID = 18568298.001).

[ISSN] 1046-3976

[Journal-full-title] Endocrine pathology

[ISO-abbreviation] Endocr. Pathol.

[Language] eng

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

[Publication-country] United States

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

   

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

[Title] Metastatic glucagonoma.

We report a case of a very rare endocrine tumor of the pancreas.

Because the CA 19-9 and glucagon levels were high, and abdominal dynamic CT showed a mass in the pancreas body and metastatic lesions in the liver, the decision was made to operate.

The histopathology of the tumor was reported as a neuroendocrine tumor, which was concordant with glucagonoma.

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(PMID = 25610069.001).

[ISSN] 1308-8734

[Journal-full-title] The Eurasian journal of medicine

[ISO-abbreviation] Eurasian J Med

[Language] eng

[Publication-type] Journal Article

[Publication-country] Turkey

[Other-IDs] NLM/ PMC4261651

[Keywords] NOTNLM ; Glucagonoma / Liver / Metastases

   

[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

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(PMID = 18093886.001).

[ISSN] 1590-8658

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

[ISO-abbreviation] Dig Liver Dis

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

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

   

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

[Title] Expression of MSX1 in human normal pituitaries and pituitary adenomas.

Transcription factors play specific roles in the development and differentiation of normal pituitary tissues and pituitary adenoma.

The transcription factor, muscle segment homeobox 1 (MSX1), which belongs to the homeobox gene family, binds the promoter region of the glycoprotein hormone alpha-subunit (SU) in TSH-producing cells in the mouse pituitary and regulates alpha-SU expression.

In addition, 50 pituitary adenomas were examined using immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) to clarify the role of MSX1 in the development and functional differentiation of pituitary adenoma cells.

In the normal pituitary, MSX1 was predominantly expressed in the cytoplasm of GH-producing cells.

Furthermore, MSX1 immunoreactivity was observed in the cytoplasm of some alpha-SU-producing cells.

It is interesting to note that, in the pituitary adenoma, MSX1 was expressed in the nucleus of GH- and TSH-producing adenomas.

RT-PCR using RNA extracted and purified from formalin-fixed paraffin-embedded pituitary adenoma specimens revealed MSX1 mRNA expressed in GH- and TSH-producing adenomas.

These results suggest that MSX1 plays a specific role in human pituitary adenoma.

[MeSH-major] Adenoma / genetics. MSX1 Transcription Factor / genetics. Pituitary Gland / physiology. Pituitary Neoplasms / genetics

[MeSH-minor] Animals. Autopsy. Blotting, Western. Cell Differentiation. DNA Primers. Humans. Immunohistochemistry. Mice. Microscopy, Immunoelectron. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 18379900.001).

[ISSN] 1559-0097

[Journal-full-title] Endocrine pathology

[ISO-abbreviation] Endocr. Pathol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA Primers; 0 / MSX1 Transcription Factor; 0 / MSX1 protein, human; 0 / Msx1 protein, mouse; 0 / RNA, Messenger; 0 / RNA, Neoplasm

   

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

[Title] Folate receptor expression in pituitary adenomas cellular and molecular analysis.

Clinically nonfunctional pituitary adenomas cause hypopituitarism or compression of regional structures.

Unlike functional tumors, there is no available medical treatment or specific imaging technique for these tumors.

We have recently discovered that both folate receptor (FR)alpha mRNA and protein are uniquely overexpressed in nonfunctional pituitary tumors, but not in functional adenomas.

Here, we used murine pituitary tumor cell line alphaT3-1 as a model to investigate the biological significance of FRalpha and its mutant FR67.

We demonstrate that overexpression of FR facilitated tumor cell growth and anchorage-independent growth in soft agar.

More colonies were observed in FR overexpressing cells than in mutant FR67 clones in soft agar.

Cell proliferation rate was increased, the percentage of cells in S-phase was increased, and high PCNA staining was detected in cells overexpressing the receptor.

In alphaT3-1 cells transfected with mutant FR67, cell proliferation rate was reduced, the percentage of cells residing in S-phase was slightly decreased, and low PCNA staining was observed.

By real-time quantitative PCR, the genes involved in NOTCH3 pathway including NOTCH3, HES-1, and TLE2 were altered; the mRNA expression of FGFR1 was upregulated, and ERbeta mRNA was downregulated in FR overexpressing cells.

Our findings suggest that FRalpha plays a role in pituitary tumor formation, and this effect may in part be due to its regulation of the NOTCH3 pathway.

[MeSH-major] Adenoma / metabolism. Pituitary Neoplasms / metabolism. Receptors, Cell Surface / metabolism

[MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Cell Line. Cell Proliferation. Female. Folate Receptor 1. Folic Acid / metabolism. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Male. Mice. Middle Aged. Mutation. Protein Binding. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Notch / metabolism

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(PMID = 18804697.001).

[ISSN] 0083-6729

[Journal-full-title] Vitamins and hormones

[ISO-abbreviation] Vitam. Horm.

[Language] eng

[Grant] United States / NINDS NIH HHS / NS / R01-NS5143901

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

[Publication-country] United States

[Chemical-registry-number] 0 / Folate Receptor 1; 0 / Folr1 protein, mouse; 0 / Notch3 protein, mouse; 0 / RNA, Messenger; 0 / Receptors, Cell Surface; 0 / Receptors, Notch; 935E97BOY8 / Folic Acid

   

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[Title] Proopiomelanocortin heterozygous and homozygous null mutant mice develop pituitary adenomas.

Mice lacking all pro-opiomelanocortin (POMC)-derived peptides have been created by gene targeting of the POMC locus in embryonic stem cells.

Here, we report that both POMC null homozygous and heterozygous mutants also develop pituitary gland tumors, which result in their premature death.

The tumors occur with 100% penetrance in both POMC heterozygous and homozygous genotypes.

Histological examinations reveal that tumors start from hyperplastic focal points of melanotrophic cells within the intermediate lobe.

Based on the morphological and immunohistological features, we have classified the tumors as non-invasive, non-secreting, intermediate lobe adenomas.

These findings uncover potential novel roles of melanocortins in the regulation of cell proliferation.

[MeSH-major] Adenoma / genetics. Pituitary Neoplasms / genetics. Pro-Opiomelanocortin / genetics

[MeSH-minor] Adrenocorticotropic Hormone / analysis. Animals. Disease Progression. Heterozygote. Homozygote. Immunohistochemistry. In Situ Hybridization. Mice. Mice, Knockout. Survival Analysis. Survival Rate. alpha-MSH / analysis

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(PMID = 16914086.001).

[ISSN] 1165-158X

[Journal-full-title] Cellular and molecular biology (Noisy-le-Grand, France)

[ISO-abbreviation] Cell. Mol. Biol. (Noisy-le-grand)

[Language] eng

[Publication-type] Journal Article

[Publication-country] France

[Chemical-registry-number] 581-05-5 / alpha-MSH; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone

   

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[Title] Transanal endoscopic microsurgery versus endoscopic mucosal resection for large rectal adenomas (TREND-study).

BACKGROUND: Recent non-randomized studies suggest that extended endoscopic mucosal resection (EMR) is equally effective in removing large rectal adenomas as transanal endoscopic microsurgery (TEM).

Furthermore, EMR appears to be associated with fewer complications.The aim of this study is to compare the cost-effectiveness and cost-utility of TEM and EMR for the resection of large rectal adenomas.

Patients with a rectal adenoma > or = 3 cm, located between 1-15 cm ab ano, will be randomized to a TEM- or EMR-treatment strategy.

For TEM, patients will be treated under general anesthesia, adenomas will be dissected en-bloc by a full-thickness excision, and patients will be admitted to the hospital.

Residual adenoma that is visible during the first surveillance endoscopy at 3 months will be removed endoscopically in both treatment strategies and is considered as part of the primary treatment.

4) disease specific and general quality of life;.

A cost-effectiveness and cost-utility analysis of EMR against TEM for large rectal adenomas will be performed from a societal perspective with respectively the costs per recurrence free patient and the cost per quality adjusted life year as outcome measures.

Based on comparable recurrence rates for TEM and EMR of 3.3% and considering an upper-limit of 10% for EMR to be non-inferior (beta-error 0.2 and one-sided alpha-error 0.05), 89 patients are needed per group.

DISCUSSION: The TREND study is the first randomized trial evaluating whether TEM or EMR is more cost-effective for the treatment of large rectal adenomas.

[MeSH-major] Adenoma / surgery. Endoscopy / economics. Rectal Neoplasms / surgery

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(PMID = 19284647.001).

[ISSN] 1471-2482

[Journal-full-title] BMC surgery

[ISO-abbreviation] BMC Surg

[Language] eng

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

[Publication-country] England

[Other-IDs] NLM/ PMC2664790

   

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

[Title] Clinicopathological features of growth hormone-producing pituitary adenomas: difference among various types defined by cytokeratin distribution pattern including a transitional form.

Pituitary adenomas producing almost exclusively growth hormones (GH) have been ultrastructurally classified into two distinct types: densely granulated somatotroph (DG) adenomas and sparsely granulated (SG) adenomas.

Fibrous body (FB), an intracytoplasmic globular aggregation of cytokeratin (CK) filaments, is a hallmark of SG adenomas.

Under light microscope, FB could be identified by CK immunohistochemistry as a dot-pattern immunoreaction versus a perinuclear pattern for cells without FB.

However, it has been noted that numerous adenomas contain mixed populations of the two patterns.

To clarify clinicopathological characteristics of the adenomas with mixed populations ("intermediate type" adenomas) and to confirm clinicopathological differences between strictly defined DG-type and SG-type adenomas, we performed this study on 104 GH cell adenomas.

Having segregated "intermediate-type" adenomas (26 cases), we found significant differences between typical DG-type (47 cases) and SG-type adenomas (31 cases); SG-type adenomas had younger ages (44 vs. 50), higher frequency of macroadenomas (86% vs. 58%), invasiveness (65% vs. 38%), advanced grades (3 or 4) in Knosp's classification (50% vs. 24%), and weaker immunoreaction for GH, beta-TSH, alpha-subunit, E-cadherin, and beta-catenin.

Clinicopathological characteristics of "intermediate-type" adenomas were identical to those of DG-type adenomas.

These findings confirm that SG-type adenoma is a distinct section of GH cell adenomas with special properties and biological behavior, and suggest that intermediate-phenotype adenomas are enrolled in DG-type adenomas.

Special properties and biological behavior of SG-type adenomas may appear after the majority of tumor cells possess a fully developed fibrous body.

[MeSH-major] Adenoma / metabolism. Adenoma / pathology. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / pathology. Keratins / metabolism. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology

[MeSH-minor] Acromegaly / pathology. Adolescent. Adult. Aged. Aging / pathology. Cadherins / metabolism. Cell Count. Cytoplasm / metabolism. Female. Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Thyrotropin / metabolism. Tissue Fixation. beta Catenin / metabolism

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(PMID = 18629656.001).

[ISSN] 1046-3976

[Journal-full-title] Endocrine pathology

[ISO-abbreviation] Endocr. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Cadherins; 0 / beta Catenin; 12629-01-5 / Human Growth Hormone; 68238-35-7 / Keratins; 9002-71-5 / Thyrotropin

   

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

[Title] Effects of rosiglitazone--peroxisome proliferators-activated receptor gamma (PPARgamma) agonist on cell viability of human pituitary adenomas in vitro.

It was shown that tumoral tissue, including the pituitary adenomas, posses PPARgamma receptors.

The activation of PPARgamma receptors inhibits tumour growth in rodents and induces the oncostatic effect on human cancer cell lines.

The aim of the present study was to examine the anti-tumour effect of RGZ on human pituitary adenomas in vitro.

MATERIALS AND METHODS: Cells of eight pituitary adenomas removed neurosurgically were used to our experiment.

Before the operation, the hormonal secretion of the tumour was estimated.

After the surgery, the histological diagnosis and immunohistochemical detection of pituitary hormones and PPARgamma receptors were performed.

The cells of pituitary tumours were exposed in the primary culture to RGZ at the concentrations of 10(-9)-10(-4) M for 24 hours.

To measure the cell growth the modified colorimetric Mossman method detecting the cells viability was applied.

RESULTS: On the basis of the pre-operative diagnosis the 6 clinically non-functioning adenomas (CNFPA), one case of acromegaly and one case of Cushing's disease were recognized.

In 5 out of 6 CNFPA the immunopositive reaction for different pituitary hormones such as: LH, HGH, PRL, FSH and alpha-subunit was detected.

Rosiglitazone decreased the cell viability of all CNFPA and corticotropinoma for 20% or more.

In somatotropinoma inhibition of the cell growth was about 13%.

THE MAIN FINDING: The obtained results indicate that RZG exerts a suppressive effect on the cell viability in non-functioning pituitary adenomas.

CONCLUSION: Our data suggest that rosiglitazone may be useful in the treatment of non-functioning pituitary adenomas, but its efficacy in Cushing's disease and acromegaly requires further study.

[MeSH-major] Adenoma / pathology. PPAR gamma / agonists. Pituitary Neoplasms / pathology. Thiazolidinediones / pharmacology

[MeSH-minor] Acromegaly / etiology. Acromegaly / pathology. Adrenocorticotropic Hormone / secretion. Adult. Aged. Cell Proliferation / drug effects. Cell Survival / drug effects. Drug Evaluation, Preclinical. Female. Human Growth Hormone / secretion. Humans. Hypoglycemic Agents / pharmacology. Male. Middle Aged. Pituitary ACTH Hypersecretion / etiology. Pituitary ACTH Hypersecretion / pathology. Tumor Cells, Cultured

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(PMID = 19300395.001).

[ISSN] 0172-780X

[Journal-full-title] Neuro endocrinology letters

[ISO-abbreviation] Neuro Endocrinol. Lett.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Sweden

[Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / PPAR gamma; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone

   

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

[Title] Chromosomal and genetic alterations in human hepatocellular adenomas associated with type Ia glycogen storage disease.

Hepatocellular adenoma (HCA) is a frequent long-term complication of glycogen storage disease type I (GSD I) and malignant transformation to hepatocellular carcinoma (HCC) is known to occur in some cases.

However, the molecular pathogenesis of tumor development in GSD I is unclear.

The sizes of GSD Ia adenomas with chromosome 6 aberrations were larger than the sizes of adenomas without the changes (P = 0.012).

Expression of IGF2R and LATS1 candidate tumor suppressor genes at 6q was reduced in more than 50% of GSD Ia HCA that were examined (n = 7).

[MeSH-major] Adenoma, Liver Cell / genetics. Chromosome Aberrations. Chromosomes, Human, Pair 6 / genetics. Glycogen Storage Disease Type I / genetics. Liver Neoplasms / genetics

[MeSH-minor] Adolescent. Adult. Child. Female. Gene Dosage. Gene Expression. Hepatocyte Nuclear Factor 1-alpha / genetics. Humans. Male. Polymorphism, Single Nucleotide. Protein-Serine-Threonine Kinases / genetics. Receptor, IGF Type 2 / genetics. Young Adult. beta Catenin / genetics

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(PMID = 19762333.001).

[ISSN] 1460-2083

[Journal-full-title] Human molecular genetics

[ISO-abbreviation] Hum. Mol. Genet.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Receptor, IGF Type 2; 0 / beta Catenin; EC 2.7.1.- / LATS1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases

   

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

[Title] Expression of Wnt4 in human pituitary adenomas regulates activation of the beta-catenin-independent pathway.

A member of the Wnt family of genes, Wnt4, has been known to regulate proliferation of anterior pituitary cell types in the mouse during embryonic development.

In order to elucidate the roles of Wnt signaling in human pituitary adenomas, we examined the expression of Wnt4 and its putative receptor Frizzled6 (Fzd6) by immunohistochemistry in pituitary adenomas and normal pituitaries.

Expression of Wnt4 was higher in growth hormone-producing adenomas (GHomas), prolactin-producing adenomas (PRLomas), and thyroid-stimulating hormone-producing adenomas (TSHomas) than in the normal pituitary.

Fzd6 was widely expressed in GHomas, PRLomas, TSHomas, and gonadotropin subunit (GnSU)-positive adenomas.

In normal pituitary glands, Wnt4 and Fzd6 were colocalized predominantly in follicle-stimulating hormone-, luteinizing hormone-, and alpha-subunits of glycoprotein hormone-positive cells.

The canonical Wnt/beta-catenin signaling pathway was analyzed by beta-catenin immunohistochemistry. beta-Catenin was localized at the cell membrane in all pituitary adenomas, but not in the nuclei.

These results suggested that activation of Wnt4/Fzd6 signaling through a "beta-catenin-independent" pathway played a role in proliferation and survival of the pituitary adenoma cells.

[MeSH-major] Adenoma / metabolism. Biomarkers, Tumor / metabolism. Pituitary Neoplasms / metabolism. Wnt Proteins / metabolism. beta Catenin / metabolism

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(PMID = 19034702.001).

[ISSN] 1046-3976

[Journal-full-title] Endocrine pathology

[ISO-abbreviation] Endocr. Pathol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CTNNB1 protein, human; 0 / FZD6 protein, human; 0 / Frizzled Receptors; 0 / Receptors, G-Protein-Coupled; 0 / WNT4 protein, human; 0 / Wnt Proteins; 0 / Wnt4 Protein; 0 / Wnt4 protein, mouse; 0 / beta Catenin

   

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

[Title] Expression of hypoxia-inducible factor 1alpha and cathepsin D in pituitary adenomas.

Hypoxia-inducible factor (HIF)-1alpha is a crucial transcription factor involved in the adaptive response to hypoxia, whereas cathepsin D, which regulates angiostatin in several cancer cell lines, has been reported to be upregulated by HIF-1alpha.

In order to determine the involvement of angiogenesis in pituitary adenomas, we studied the expression of both HIF-1alpha and cathepsin D in tissues from 58 patients (39 women, 19 men, ranging in age from 20 to 78 yr), sorted by histological group, and assayed by double immunohistochemistry.

HIF-1alpha immunoreactivity, confined to the nucleoplasm, was present in both tumor and vascular endothelial cells.

ACTH-producing adenomas showed the lowest level of HIF-1alpha, whereas prolactin (PRL)-producing adenomas and HIF-1alpha-positive microvessels showed the highest (p < 0.001).

In contrast, the lowest expression of cathepsin D was observed in PRL-producing adenomas, whereas the highest expression was detected in ACTH-producing adenomas (p < 0.0001).

Imaging analysis with fluorescence double immunohistochemistry showed that HIF-1alpha-negative tumor cells did not express significantly higher levels of cathepsin D.

In these poorly vascularized tumors, the hypoxic marker HIF-1alpha may not downregulate cathepsin D.

The mechanisms of tumor angiogenesis and cell invasion in pituitary adenomas may differ from those in other tumor cells.

[MeSH-major] Adenoma / metabolism. Cathepsin D / biosynthesis. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Pituitary Neoplasms / metabolism

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(PMID = 16199897.001).

[ISSN] 1046-3976

[Journal-full-title] Endocrine pathology

[ISO-abbreviation] Endocr. Pathol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 3.4.23.5 / Cathepsin D

   

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

[Title] Antagonistic effects of aspirin and folic acid on inflammation markers and subsequent risk of recurrent colorectal adenomas.

The Aspirin/Folate Polyp Prevention Trial found that aspirin, but not folic acid, reduced recurrence of colorectal adenomas.

There were 884 subjects who had colonoscopic evaluation for adenomas at year 3 and plasma levels of C-reactive protein (CRP), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), soluble TNF receptor type II (sTNF-R2), and IL-1 receptor antagonist (IL-1Ra) measured at baseline and year 3.

Changes in inflammation markers were not associated with adenoma recurrence.

Nevertheless, inflammation markers do not mediate the chemopreventive effect of aspirin on colorectal adenomas.

[MeSH-major] Adenoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Aspirin / pharmacology. C-Reactive Protein / metabolism. Colorectal Neoplasms / blood. Folic Acid / pharmacology. Inflammation / blood

[MeSH-minor] Aged. Biomarkers / blood. Drug Administration Schedule. Drug Antagonism. Female. Humans. Interleukin-6 / blood. Male. Middle Aged. Risk Assessment. Risk Factors. Tumor Necrosis Factor-alpha / blood

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(PMID = 19822838.001).

[ISSN] 1460-2105

[Journal-full-title] Journal of the National Cancer Institute

[ISO-abbreviation] J. Natl. Cancer Inst.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA108841; United States / NCI NIH HHS / CA / U54 CA100971; United States / NCI NIH HHS / CA / U54-CA100971; United States / NCI NIH HHS / CA / R01 CA059005; United States / PHS HHS / / R01-108841; United States / NCI NIH HHS / CA / R01-CA059005

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

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Biomarkers; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 9007-41-4 / C-Reactive Protein; 935E97BOY8 / Folic Acid; R16CO5Y76E / Aspirin

[Other-IDs] NLM/ PMC2786916

   

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

[Title] Expression of leukemia inhibitory factor and leukemia inhibitory factor receptor in the canine pituitary gland and corticotrope adenomas.

Leukemia inhibitory factor (LIF) is a pleiotropic cytokine of the IL-6 family that activates the hypothalamic-pituitary-adrenal axis and promotes corticotrope cell differentiation during development.

The aim of this study was to investigate the expression of LIF and its receptor (LIFR) in the canine pituitary gland and in corticotrope adenomas, and to perform a mutation analysis of LIFR.

Using immunohistochemistry, immunofluorescence, and quantitative expression analysis, LIF and LIFR expression were studied in pituitary glands of control dogs and in specimens of corticotrope adenoma tissue collected through hypophysectomy in dogs with pituitary-dependent hypercortisolism (PDH, Cushing's disease).

In the control pituitary tissues and corticotrope adenomas, there was a low magnitude of LIF expression.

Cytoplasmatic immunoreactivity of LIFR was preserved in corticotrope adenomas and adjacent nontumorous cells of pars intermedia.

Surprisingly, nuclear to perinuclear immunoreactivity for LIFR was present in nontumorous pituitary cells of the pars distalis in 10 of 12 tissue specimens from PDH dogs.

These data show that LIFR is highly co-expressed with adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) in the canine pituitary gland and in corticotrope adenomas.

Nuclear immunoreactivity for LIFR in nontumorous cells of the pars distalis may indicate the presence of a corticotrope adenoma.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / veterinary. Dog Diseases / metabolism. Leukemia Inhibitory Factor / analysis. Pituitary Gland / chemistry. Pituitary Neoplasms / veterinary. Receptors, OSM-LIF / analysis

[MeSH-minor] Animals. Cell Nucleus / chemistry. Cosyntropin / analysis. Cytoplasm / chemistry. DNA, Complementary / analysis. Dogs. Female. Fluorescent Antibody Technique. Immunohistochemistry. Male. Mutation. Polymerase Chain Reaction. Sequence Analysis, DNA. alpha-MSH / analysis

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[Copyright] Copyright (c) 2009 Elsevier Inc. All rights reserved.

(PMID = 20036483.001).

[ISSN] 1879-0054

[Journal-full-title] Domestic animal endocrinology

[ISO-abbreviation] Domest. Anim. Endocrinol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA, Complementary; 0 / Leukemia Inhibitory Factor; 0 / Receptors, OSM-LIF; 16960-16-0 / Cosyntropin; 581-05-5 / alpha-MSH

   

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

[Title] [Dramatic efficacy of chemotherapy with 5-fluorouracil and dacarbazine in a patient with metastatic glucagonoma and cardiac insufficiency].

[Transliterated title] Efficacité spectaculaire d'une chimiothérapie par 5-fluoro-uracile et dacarbazine chez un malade atteint de glucagonome métastatique avec insuffisance cardiaque.

Malignant glucagonoma is an exceptional pancreatic endocrine tumour, with frequent dermatologic symptoms, diabetes and degradation of the general health status.

We report here an observation of a patient who was treated for a glucagonoma with multiple liver metastases, migratory necrolytic erythema, dilated cardiomypathy and diabetes that dramatically improved after a dacarbazin-based chemotherapy, allowing subsequent surgical resection of the primary.

The patient was still alive and asymptomatic without progressive disease nearly two years after surgery.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cardiomyopathy, Dilated / complications. Glucagonoma / drug therapy. Liver Neoplasms / drug therapy

[MeSH-minor] Adult. Dacarbazine / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery

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[Copyright] Copyright 2009. Published by Elsevier Masson SAS.

(PMID = 19875259.001).

[ISSN] 0399-8320

[Journal-full-title] Gastroentérologie clinique et biologique

[ISO-abbreviation] Gastroenterol. Clin. Biol.

[Language] fre

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] France

[Chemical-registry-number] 7GR28W0FJI / Dacarbazine; U3P01618RT / Fluorouracil

   

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

[Title] Folate receptor alpha regulates cell proliferation in mouse gonadotroph alphaT3-1 cells.

We have previously found that the mRNA and protein levels of the folate receptor alpha (FRalpha) are uniquely over-expressed in clinically human nonfunctional (NF) pituitary adenomas, but the mechanistic role of FRalpha has not fully been determined.

We investigated the effect of FRalpha over-expression in the mouse gonadotroph alphaT3-1 cell line as a model for NF pituitary adenomas.

Furthermore, we found a higher cell growth rate, an enhanced percentage of cells in S-phase by BrdU assay, and a higher PCNA staining.

These observations indicate that over-expression of FRalpha promotes cell proliferation.

These effects were abrogated in the same alphaT3-1 cells when transfected with a mutant FRalpha cDNA that confers a dominant-negative phenotype by inhibiting folic acid binding.

Finally, by real-time quantitative PCR, we found that mRNA expression of NOTCH3 was up-regulated in FRalpha over-expressing cells.

In summary, our data suggests that FRalpha regulates pituitary tumor cell proliferation and mechanistically may involve the NOTCH pathway.

Potentially, this finding could be exploited to develop new, innovative molecular targeted treatment for human NF pituitary adenomas.

[MeSH-major] Carrier Proteins / metabolism. Folic Acid / metabolism. Gonadotrophs / metabolism. Receptors, Cell Surface / metabolism. Receptors, Notch / metabolism

[MeSH-minor] Adenoma / metabolism. Adenoma / pathology. Animals. Cell Line. Cell Proliferation. Disease Models, Animal. Folate Receptors, GPI-Anchored. Humans. Mice. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology. Proliferating Cell Nuclear Antigen / metabolism. Transfection. Up-Regulation / genetics. Up-Regulation / physiology

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(PMID = 19446551.001).

[ISSN] 1090-2422

[Journal-full-title] Experimental cell research

[ISO-abbreviation] Exp. Cell Res.

[Language] eng

[Grant] United States / NINDS NIH HHS / NS / R01-NS5143901

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

[Publication-country] United States

[Chemical-registry-number] 0 / Carrier Proteins; 0 / Folate Receptors, GPI-Anchored; 0 / Notch3 protein, mouse; 0 / Proliferating Cell Nuclear Antigen; 0 / Receptors, Cell Surface; 0 / Receptors, Notch; 935E97BOY8 / Folic Acid

   

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

[Title] Superficial necrolytic dermatitis associated with extrapancreatic glucagonoma in a dog.

Based on histopathological findings, blood examinations and necropsy findings, the condition was diagnosed as superficial necrolytic dermatitis associated with a glucagon-secreting extrapancreatic neuroendocrine tumour.

Gross necropsy revealed tumour invasion into the spleen, liver, adrenal glands and mesenteric lymph nodes.

Immunohistochemical analysis of the neoplastic cells revealed that the tumour was a glucagonoma, consistent with earlier findings of persistent glucagonaemia and hypoaminoacidaemia.

[MeSH-major] Dermatitis / veterinary. Dog Diseases / pathology. Glucagonoma / veterinary

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(PMID = 19152590.001).

[ISSN] 1365-3164

[Journal-full-title] Veterinary dermatology

[ISO-abbreviation] Vet. Dermatol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

   

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

[Title] Pasireotide, a multiple somatostatin receptor subtypes ligand, reduces cell viability in non-functioning pituitary adenomas by inhibiting vascular endothelial growth factor secretion.

Somatostatin (SRIF) analogs have been employed in medical therapy of non-functioning pituitary adenomas (NFA), with contrasting results.

Previous evidence showed that SRIF can exert its antiproliferative effects by reducing vascular endothelial growth factor (VEGF) secretion and action, and that VEGF expression may be related to pituitary tumor growth.

The aim of our study was to clarify the possible effects of a multireceptor SRIF ligand on VEGF secretion and cell proliferation in human NFA primary cultures.

We assessed the expression of SRIF receptors (SSTR1-5), the in vitro effects on VEGF secretion, and on cell viability of SRIF and of the stable SRIF analog pasireotide (SOM230), which activates SSTR1, 2, 3, and 5.

Twenty-five NFA were examined by RT-PCR for expression of alpha-subunit, SSTR, VEGF, and VEGF receptors 1 (VEGF-R1) and 2 (VEGF-R2).

All NFA samples expressed alpha-sub, VEGF and VEGFR-1 and 2, while SSTR expression pattern was highly variable.

VEGF secretion and cell viability were reduced by SRIF and pasireotide in the 'responder' group, but not in the 'non-responder' group, including NFA expressing SSTR5.

In addition, SRIF and pasireotide completely abrogated the promoting effects of VEGF on NFA cell viability.

Our data demonstrate that pasireotide can inhibit NFA cell viability by inhibiting VEGF secretion, and suggest that the multireceptor-SSTR agonist pasireotide might be useful in medical therapy of selected NFA.

[MeSH-major] Adenoma / secretion. Oligopeptides / pharmacology. Pituitary Neoplasms / secretion. Somatostatin / pharmacology. Vascular Endothelial Growth Factor A / secretion

[MeSH-minor] Adult. Aged. Cell Survival / drug effects. Female. Hormones / pharmacology. Humans. Ligands. Male. RNA, Messenger / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism

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(PMID = 17395978.001).

[ISSN] 1351-0088

[Journal-full-title] Endocrine-related cancer

[ISO-abbreviation] Endocr. Relat. Cancer

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Hormones; 0 / Ligands; 0 / Oligopeptides; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / Vascular Endothelial Growth Factor A; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide

   

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

[Title] Alpha1-adrenergic receptor antagonists: novel therapy for pituitary adenomas.

Pituitary tumors are common and cause considerable morbidity due to local invasion and altered hormone secretion.

Doxazosin (dox), a selective alpha(1)-adrenergic receptor antagonist, used to treat hypertension, also inhibits prostate cancer cell proliferation.

We examined the effects of dox on murine and human pituitary tumor cell proliferation in vitro and in vivo. dox treatment inhibited proliferation of murine pituitary tumor cells, induced G(0)-G(1) cell cycle arrest, and reduced phosphorylated retinoblastoma levels.

In addition, increased annexin-fluorescein isothiocyanate immunoreactivity and cleaved caspase-3 levels, in keeping with dox-mediated apoptosis, were observed in the human and murine pituitary tumor cells, and dox administration to mice, harboring corticotroph tumors, decreased tumor growth and reduced plasma ACTH levels. dox-mediated antiproliferative and proapoptotic actions were not confined to alpha-adrenergic receptor-expressing pituitary tumor cells and were unaffected by cotreatment with the alpha-adrenergic receptor blocker, phenoxybenzamine. dox treatment led to reduced phosphorylated inhibitory kappaB (IkappaB)-alpha expression, and nuclear factor-kappaB transcription and decreased basal and TNFalpha-induced proopiomelanocortin transcriptional activation.

These results demonstrate that the selective alpha(1)-adrenergic receptor antagonist dox inhibits pituitary tumor cell growth in vitro and in vivo by mechanisms that are in part independent of its alpha-adrenergic receptor-blocking actions and involve down-regulation of nuclear factor-kappaB signaling. dox is proposed as a possible novel medical therapy for pituitary tumors.

[MeSH-major] ACTH-Secreting Pituitary Adenoma / drug therapy. Adenoma / drug therapy. Adrenergic alpha-1 Receptor Antagonists. Adrenergic alpha-Antagonists / therapeutic use. Antineoplastic Agents / therapeutic use. Doxazosin / therapeutic use

[MeSH-minor] Adrenocorticotropic Hormone / blood. Animals. Apoptosis. Caspase 3. Caspases / metabolism. Cell Cycle / drug effects. Cell Proliferation / drug effects. Humans. I-kappa B Proteins / metabolism. Mice. Mice, Nude. NF-kappa B / metabolism. Neoplasm Transplantation. Pro-Opiomelanocortin / genetics. Receptors, Adrenergic, alpha-1 / genetics. Receptors, Adrenergic, alpha-1 / metabolism. Transcriptional Activation. Tumor Cells, Cultured. Tumor Necrosis Factor-alpha / metabolism

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(PMID = 16020484.001).

[ISSN] 0888-8809

[Journal-full-title] Molecular endocrinology (Baltimore, Md.)

[ISO-abbreviation] Mol. Endocrinol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Antineoplastic Agents; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Receptors, Adrenergic, alpha-1; 0 / Tumor Necrosis Factor-alpha; 139874-52-5 / NF-kappaB inhibitor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; NW1291F1W8 / Doxazosin

   

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

[Title] Peroxisome proliferator-activated receptor expression and activation in normal human colonic epithelial cells and tubular adenomas.

OBJECTIVE: Peroxisome proliferator-activated receptor (PPAR) ligands, widely used in type 2 diabetes treatment, have variably been shown to promote or prevent colon tumor formation in animal models and cell lines, but their role in normal human colon is unknown.

The aim of this study was to determine PPAR expression and function in normal human colonic epithelial cells and tubular adenomas.

MATERIAL AND METHODS: Short-term cultures of normal human colonic epithelial cells were established from biopsies obtained in 42 patients with normal colonoscopy.

PPARs were activated by ligands for PPAR alpha (Wy-14643), PPAR delta (GW-501516) and PPAR gamma (rosiglitazone or troglitazone).

Cell viability was measured using the methyltetrazoleum assay, proliferation by thymidine incorporation, and DNA profiles by flow cytometry.

PPAR mRNA levels in tubular adenomas or metaplastic polyps (n=12) were compared with those in controls.

RESULTS: PPAR alpha and gamma were consistently expressed in normal colonocytes while no PPAR delta expression could be detected.

PPAR gamma activation had no effect on viability or DNA profiles, but led to a 25% significant decrease in cell proliferation.

Finally, a selective and significant 2.5-fold decrease in PPAR alpha expression was observed in tubular adenomas, but not in metaplastic polyps, compared to controls.

Moreover, they raise interest in investigation of PPAR alpha as a therapeutic target to prevent adenoma formation.

[MeSH-major] Adenoma / metabolism. Colonic Neoplasms / metabolism. Epithelial Cells / metabolism. Peroxisome Proliferator-Activated Receptors / biosynthesis

[MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Proliferation. Cell Survival / physiology. Colon. Female. Humans. Male. Middle Aged

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

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(PMID = 15764152.001).

[ISSN] 0036-5521

[Journal-full-title] Scandinavian journal of gastroenterology

[ISO-abbreviation] Scand. J. Gastroenterol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Norway

[Chemical-registry-number] 0 / Peroxisome Proliferator-Activated Receptors

   

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

[Title] Matrix metalloproteinase-9 is differentially expressed in nonfunctioning invasive and noninvasive pituitary adenomas and increases invasion in human pituitary adenoma cell line.

The complete resection of pituitary adenomas (PAs) is unlikely when there is an extensive local dural invasion and given that the molecular mechanisms remain primarily unknown.

Gene clustering revealed a robust eightfold increase in matrix metalloproteinase (MMP)-9 expression in surgically resected human invasive PAs and in the (nonfunctioning) HP75 human pituitary tumor-derived cell line treated with phorbol-12-myristate-13-acetate; these results were confirmed by real-time polymerase chain reaction, gelatin zymography, reverse transcriptase-polymerase chain reaction, Western blot, immunohistochemistry, and Northern blot analyses.

The activation of protein kinase C (PKC) increased both MMP-9 activity and expression, which were blocked by some PKC inhibitors (Gö6976, bisindolylmaleimide, and Rottlerin), PKC-alpha, and PKC-delta small interfering (si)RNAs but not by hispidin (PKC-beta inhibitor).

In a transmembrane invasion assay, phorbol-12-myristate-13-acetate (100 nmol/L) increased the number of invaded HP75 cells, a process that was attenuated by PKC inhibitors, MMP-9 antibody, PKC-alpha siRNA, or PKC-delta siRNA.

These results demonstrate that MMP-9 and PKC-alpha or PKC-delta may provide putative therapeutic targets for the control of PA dural invasion.

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(PMID = 17200207.001).

[ISSN] 0002-9440

[Journal-full-title] The American journal of pathology

[ISO-abbreviation] Am. J. Pathol.

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / R01 NS035122; United States / NCI NIH HHS / CA / R01 CA090851; United States / NINDS NIH HHS / NS / R29 NS035122; United States / NINDS NIH HHS / NS / NS35122; United States / NCI NIH HHS / CA / CA90851

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

[Publication-country] United States

[Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Pyrones; 0 / RNA, Small Interfering; 56937-68-9 / phorbolol myristate acetate; EC 2.7.11.13 / Protein Kinase C; EC 3.4.24.35 / Matrix Metalloproteinase 9; NI40JAQ945 / Tetradecanoylphorbol Acetate; SSJ18CG55E / hispidin

[Other-IDs] NLM/ PMC1762693