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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] Alpha-catenin is essential in intestinal adenoma formation.

Although the molecular mechanism of tumor initiation is complex, several modifier genes have been identified using mouse models, including the ApcMin mouse.

Among the familial adenomatous polyposis mouse lines carrying a truncation mutation at codon 580 in Apc (Apc580D), one line (line19-Apc(580D/+)) showed a remarkably reduced incidence of intestinal adenomas (<5% compared with other lines).

Extensive genetic analysis identified a deletion in the alpha-catenin (Ctnna1) gene as the cause of this suppression.

In all adenomas generated in line19-Apc(580D/+), somatic recombination between the Apc and Ctnna1 loci retained the wild-type Ctnna1 allele.

These data strongly indicate that simultaneous inactivation of alpha-catenin and Apc during tumor initiation suppresses adenoma formation in line19-Apc(580D/+), suggesting that alpha-catenin plays an essential role in the initiation of intestinal adenomas.

Although accumulating evidence obtained from human colon tumors with invasive or metastatic potential has established a tumor-suppressive role for alpha-catenin in late-stage tumorigenesis, the role of alpha-catenin in the initiation of intestinal tumorigenesis is not well documented, especially compared with that of beta-catenin.

A mouse model used in this study focused on the early stage of tumor initiation and clearly indicated an essential role for alpha-catenin.

Thus, alpha-catenin has dual roles in intestinal tumorigenesis, a supporting role in tumor initiation, and a suppressive role in tumor progression.

[MeSH-major] Adenoma / pathology. Intestinal Neoplasms / pathology. alpha Catenin / physiology

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(PMID = 17989230.001).

[ISSN] 1091-6490

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA Primers; 0 / alpha Catenin

[Other-IDs] NLM/ PMC2084320

   

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

[Title] Different mechanisms of DEHP-induced hepatocellular adenoma tumorigenesis in wild-type and Ppar alpha-null mice.

Di (2-ethylhexyl) phthalate (DEHP) exposure is thought to lead to hepatocellular hypertrophy and hyperplasia in rodents mediated via peroxisome proliferator-activated receptor alpha (PPAR alpha).

A recent study revealed that long-term exposure to relatively low-dose DEHP (0.05%) caused liver tumors including hepatocellular carcinomas, hepatocellular adenomas, and chologiocellular carcinomas at a higher incidence in Ppar alpha-null mice (25.8%) than in wild-type mice (10.0%).

Using tissues with hepatocellular adenoma, microarray (Affymetrix MOE430A) as well as, in part, real-time quantitative PCR analysis was conducted to elucidate the mechanisms of the adenoma formation resulting from DEHP exposure in both genotyped mice.

The microarray profiles showed that the up- or down-regulated genes were quite different between hepatocellular adenoma tissues of wild-type and Ppar alpha-null mice exposed to DEHP.

The gene expressions of apoptotic peptidase activating factor 1 (Apaf1) and DNA-damage-inducible 45 alpha (Gadd45a) were increased in the hepatocellular adenoma tissues of wild-type mice exposed to DEHP, whereas they were unchanged in corresponding tissues of Ppar alpha-null mice.

On the other hand, the expressions of cyclin B2 and myeloid cell leukemia sequence 1 were increased only in the hepatocellular adenoma tissues of Ppar alpha-null mice.

Taken together, DEHP may induce hepatocellular adenomas, in part, via suppression of G2/M arrest regulated by Gadd45a and caspase 3-dependent apoptosis in Ppar alpha-null mice, but these genes may not be involved in tumorigenesis in the wild-type mice.

In contrast, the expression level of Met was notably increased in the liver adenoma tissue of wild-type mice, which may suggest the involvement of Met in DEHP-induced tumorigenesis in wild-type mice.

[MeSH-major] Diethylhexyl Phthalate / toxicity. Liver / drug effects. Liver Neoplasms, Experimental / chemically induced. Liver Neoplasms, Experimental / genetics. PPAR alpha / deficiency

[MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / physiology. Apoptotic Protease-Activating Factor 1 / antagonists & inhibitors. Apoptotic Protease-Activating Factor 1 / biosynthesis. Caspase 3 / metabolism. Cell Cycle Proteins / antagonists & inhibitors. Cell Cycle Proteins / biosynthesis. Cell Division / genetics. G2 Phase / genetics. Gene Expression Profiling. Hepatocytes / drug effects. Hyperplasia. Mice. Mice, Knockout. Microarray Analysis. Nuclear Proteins / antagonists & inhibitors. Nuclear Proteins / biosynthesis. Plasticizers / toxicity. Polymerase Chain Reaction. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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(PMID = 18403868.001).

[ISSN] 1348-9585

[Journal-full-title] Journal of occupational health

[ISO-abbreviation] J Occup Health

[Language] eng

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

[Publication-country] Japan

[Chemical-registry-number] 0 / Apaf1 protein, mouse; 0 / Apoptotic Protease-Activating Factor 1; 0 / Cell Cycle Proteins; 0 / Gadd45a protein, mouse; 0 / Nuclear Proteins; 0 / PPAR alpha; 0 / Plasticizers; 0 / RNA, Messenger; C42K0PH13C / Diethylhexyl Phthalate; EC 3.4.22.- / Caspase 3

   

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

[Title] Desmoplasia in different degrees of invasion of carcinoma ex-pleomorphic adenoma.

Stroma desmoplasia was studied by immunohistochemistry for alpha-smooth muscle actin (alpha-SMA) in 17 instances of carcinoma ex-pleomorphic adenoma (CXPA) classified according to the presence of epithelial and myoepithelial cells and the degree of invasion: intracapsular, minimally and frankly invasive carcinoma.

In "resident" pleomorphic adenoma, no desmoplasia was detected.

In the minimally invasive type, myofibroblasts were seen in the septum between islands of malignant cells and in focal peripheral areas of the tumor interpreted as the actual front of invasion.

In the frankly invasive type of CXPA showing large blocks of cells, intense desmoplasia was seen, also separating the tumor cells from the neighboring normal tissue.

In tumors with cords and/or small nests of cells, desmoplasia was very slight.

In the invasive type of CXPA with a myoepithelial component, alpha-SMA expression was seen in the septum between the islands of cells.

In CXPA with epithelial and myoepithelial cells, myofibroblasts were rarely seen in the septum separating sheets of cells.

Thus, we may deduce that the presence of desmoplasia parallels the capacity of invasion of CXPA by epithelial cells, being minimum in the intracapsular and minimally invasive type of CXPA and increasing as the tumor becomes frankly invasive.

[MeSH-major] Adenocarcinoma / pathology. Adenoma, Pleomorphic / pathology

[MeSH-minor] Actins / metabolism. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Neoplasms, Multiple Primary. Stromal Cells / metabolism. Stromal Cells / pathology

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(PMID = 20614261.001).

[ISSN] 1936-0568

[Journal-full-title] Head and neck pathology

[ISO-abbreviation] Head Neck Pathol

[Language] eng

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

[Publication-country] United States

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

[Other-IDs] NLM/ PMC2807519

[Keywords] NOTNLM ; Carcinoma ex-pleomorphic adenoma / Desmoplasia / Front of invasion / Immunohistochemistry / Intracapsular carcinoma ex-pleomorphic adenoma / Invasive carcinoma ex-pleomorphic adenoma / Malignant transformation of pleomorphic adenoma / Myofibroblast / α-Smooth muscle actin

   

[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] 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] 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.

[Title] Revisiting the immunophenotype of nephrogenic adenoma.

Nephrogenic adenoma (NA) is a rare benign lesion of the urinary tract.

Although its histogenesis is still debated, several reports suggest that the lesion has a renal tubular cell origin or differentiation.

Unfortunately, it has been reported that NA cells also stained positive for the prostate cancer marker alpha-methylacyl-coenzyme A racemase (AMACR).

Because all the previous studies have used an avidin-biotin (AB) detection procedure, and because cells with tubular renal differentiation are likely to contain a high level of endogenous biotin, we investigated in NA the expression of several markers including AMACR, using both AB and biotin-free detection systems.

[MeSH-major] Adenoma / immunology. Immunophenotyping / methods. Urologic Neoplasms / immunology

[MeSH-minor] Adult. Aged. Biomarkers, Tumor / metabolism. Child. Diagnosis, Differential. Female. Fluorescent Antibody Technique, Indirect. Humans. Kidney Tubules / enzymology. Male. Middle Aged. Prostatic Neoplasms / diagnosis. Racemases and Epimerases / metabolism. Tissue Array Analysis

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(PMID = 19730362.001).

[ISSN] 1532-0979

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

[ISO-abbreviation] Am. J. Surg. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase

   

[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] Symptomatic intraspinal oncocytic adrenocortical adenoma.

Benign epithelial tumors are rarely found at this site.

We here present the case of a 44-year-old woman with a lesion in the cauda equina that fulfilled the radiologic criteria of schwannoma and caused clinical symptoms for 3 years.

The excised tumor was composed of nests of large polygonal cells with eosinophilic partial granular cytoplasm.

The tumor showed diffuse positivity for melan-A, synaptophysin, and alpha-inhibin.

Steroidogenic factor 1 and cytokeratins 8 and 18 were focally seen in the absence of S-100 and chromogranin.

Ultrastructural examination showed abundant mitochondria, suggesting an oncocytic tumor.

The diagnosis of an oncocytic adrenal cortical adenoma was made.

These extraadrenal tumors are thought to arise from heterotopic adrenocortical tissue in the spinal cavity.

Oncocytic tumors are rare neoplasms and they comprise non-functioning variants of adrenal cortical adenomas.

To date, only five such intraspinal tumors have been observed.

Immunohistochemistry excluded oncocytic paraganglioma, oncocytic meningioma, renal cell carcinoma, alveolar soft part sarcoma, and granular cell tumor.

A view of the literature of these rare but probably underdiagnosed intraspinal tumors is given.

[MeSH-major] Adenoma, Oxyphilic / pathology. Adrenocortical Adenoma / pathology. Spinal Cord Neoplasms / pathology

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(PMID = 19039533.001).

[ISSN] 1046-3976

[Journal-full-title] Endocrine pathology

[ISO-abbreviation] Endocr. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[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] 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] Clear cell adenocarcinoma of the bladder and urethra: cases diffusely mimicking nephrogenic adenoma.

Although clear cell adenocarcinoma have been described focally mimicking nephrogenic adenoma, we have identified a subset of clear cell adenocarcinoma that diffusely resembles nephrogenic adenoma (nephrogenic adenoma-like clear cell adenocarcinoma).

Twelve classic clear cell adenocarcinomas of the bladder and urethra and 7 nephrogenic adenoma-like clear cell adenocarcinomas were compared to 10 nephrogenic adenomas.

Classic clear cell adenocarcinomas and nephrogenic adenoma-like clear cell adenocarcinomas comprised 4 men and 15 women.

The following features were seen in classic clear cell adenocarcinomas: nephrogenic adenoma-like clear cell adenocarcinomas: predominantly solid pattern (7/12:0/7), marked nuclear pleomorphism (7/12:1/7), prominent nucleoli (5/12:1/7), clear cytoplasm in 50% or greater of tumor (7/12:0/7), and necrosis (8/12:3/7), although the necrosis in nephrogenic adenoma-like clear cell adenocarcinomas was often focal and intraluminal.

Both patterns of clear cell adenocarcinomas showed prominent hobnail features, although more pronounced in nephrogenic adenoma-like clear cell adenocarcinomas.

Muscularis propria invasion was seen in 5 of 9 classic clear cell adenocarcinomas and 6 of 6 nephrogenic adenoma-like clear cell adenocarcinomas, where evaluable.

Classic clear cell adenocarcinoma was associated with urothelial carcinoma (n = 2) and endometriosis (n = 1).

The Ki-67 rate in clear cell adenocarcinomas ranged from 10% to 80% compared with 0% to 5% in nephrogenic adenoma.

The following antibodies were not helpful in distinguishing nephrogenic adenoma-like clear cell adenocarcinoma from nephrogenic adenoma: CD10, estrogen receptor, p63, high-molecular-weight cytokeratin, and alpha-methylacyl coenzyme-A racemase.

PAX2 expression was more frequent in nephrogenic adenoma (89%) compared to both patterns of clear cell adenocarcinoma (29%-32%).

The key features discriminating between nephrogenic adenoma-like clear cell adenocarcinoma and nephrogenic adenoma include occasional clear cells, more prominent pleomorphism especially hyperchromatic enlarged nuclei, and extensive muscular invasion.

Presence of mitoses and a high rate of Ki-67 expression in lesions resembling nephrogenic adenoma require clinical correlation, close follow-up, and repeat biopsy with more extensive sampling.

[MeSH-major] Adenocarcinoma, Clear Cell / diagnosis. Adenoma / diagnosis. Urethral Neoplasms / diagnosis. Urinary Bladder Neoplasms / diagnosis

[MeSH-minor] Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Urothelium / pathology

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[Copyright] Copyright 2010 Elsevier Inc.

(PMID = 20060152.001).

[ISSN] 1532-8392

[Journal-full-title] Human pathology

[ISO-abbreviation] Hum. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[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] Genotype phenotype classification of hepatocellular adenoma.

Studies that compare tumor genotype with phenotype have provided the basis of a new histological/molecular classification of hepatocellular adenomas.

Based on two molecular criteria (presence of a TCF1/HNF1 alpha or beta-catenin mutation), and an additional histological criterion (presence or absence of an inflammatory infiltrate), subgroups of hepatocellular adenoma can be defined and distinguished from focal nodular hyperplasia.

Analysis of 96 hepatocellular adenomas performed by a French collaborative network showed that they can be divided into four broad subgroups: the first one is defined by the presence of mutations in TCF1 gene inactivating the hepatocyte nuclear factor 1 (HNF1 alpha); the second by the presence of beta-catenin activating mutations; the category without mutations of HNF1 alpha or beta-catenin is further divided into 2 subgroups depending on the presence or absence of inflammation.

Therefore, the approach to the diagnosis of problematic benign hepatocytic nodules may be entering a new era directed by new molecular information.

It is hoped that immunohistological tools will improve significantly diagnosis of liver biopsy in our ability to distinguish hepatocellular adenoma from focal nodular hyperplasia (FNH), and to delineate clinically meaningful entities within each group to define the best clinical management.

[MeSH-major] Adenoma, Liver Cell / classification. Genotype. Liver Neoplasms / classification. Phenotype

[MeSH-minor] Biopsy. Diagnosis, Differential. Focal Nodular Hyperplasia / diagnosis. Hepatocyte Nuclear Factor 1-alpha / genetics. Humans. Liver / pathology. Mutation / genetics. beta Catenin / genetics

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(PMID = 17569132.001).

[ISSN] 1007-9327

[Journal-full-title] World journal of gastroenterology

[ISO-abbreviation] World J. Gastroenterol.

[Language] eng

[Publication-type] Editorial; Review

[Publication-country] China

[Chemical-registry-number] 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / beta Catenin

[Number-of-references] 23

[Other-IDs] NLM/ PMC4147112

   

[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.

[Title] Ductal adenoma of the breast: immunohistochemistry of two cases.

The author reports herein two cases of ductal adenoma of the breast with an emphasis on immunohistochemistry.

Histologically, both cases were ductal adenomas composed of ductal epithelial cells and myoepithelial cells.

Immunohistochemically, myoepithelial cells were noted in both cases; cytokeratin (CK) 14 and p63 were the most reliable myoepithelial markers, followed by CD10, alpha-smooth muscle actin and S100 protein.

The tumor cells expressed p53 protein (case 1, positive cell percentage 5%; case 2, 7%), c-erbB2 (HER2/neu, 76%, 64%), CEA (5%, 0%), estrogen receptor (33%, 84%), but were negative for progesterone receptor.

[MeSH-major] Adenoma / diagnosis. Breast Neoplasms / diagnosis. Papilloma, Intraductal / diagnosis

[MeSH-minor] Aged. Biomarkers, Tumor / analysis. Diagnosis, Differential. Epithelial Cells / chemistry. Epithelial Cells / pathology. Female. Humans. Immunohistochemistry. Middle Aged

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(PMID = 19067857.001).

[ISSN] 1440-1827

[Journal-full-title] Pathology international

[ISO-abbreviation] Pathol. Int.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Australia

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

   

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

[Title] Alpha-methylacyl-CoA racemase as a marker in the differential diagnosis of metanephric adenoma.

Metanephric adenoma (MA), a well-described renal neoplasm, usually behaves in a benign fashion.

It may have areas that are morphologically similar to papillary renal cell carcinoma (RCC) type, or epithelial (tubular predominant) type Wilms' tumor.

Alpha-methylacyl-CoA racemase (AMACR), a molecular marker for prostate carcinoma, has subsequently been found to be overexpressed in breast, colorectal and ovarian cancers, among others.

Recent microarray analysis of renal tumors has shown an increase of AMACR mRNA levels in papillary RCC but not in other subtypes.

Immunohistochemical stains were performed on paraffin-embedded tissue sections from 25 papillary RCC, 10 MAs and eight Wilms' tumors.

AMACR was positive in one (10%) of 10 MAs and 24 (96%) of 25 papillary RCC, while it was negative in all Wilms' tumors.

CK7 was positive in 20 of 25 papillary RCCs, focally positive in one Wilms' tumor and was negative in all MAs.

CD57 was positive in all six MAs that were stained, focally positive in one of 25 papillary RCC and one of eight Wilms' tumors.

WT1 was positive in seven of 10 MAs, three of 25 papillary RCCs and all eight Wilms' tumors.

In conclusion, diffuse and strong immunoreactivity for AMACR may be useful in differentiating papillary RCC from MA but a panel which includes AMACR, CK7 and CD57 is better in this differential diagnosis.

AMACR is not helpful in differentiating MA from Wilms' tumor, but CD57 is helpful in this differential diagnosis.

WT1 may be useful in separating Wilms' tumor from MA and papillary RCC but is not helpful in differentiating MA from papillary RCC.

[MeSH-major] Adenoma / pathology. Biomarkers, Tumor / analysis. Kidney Neoplasms / pathology. Racemases and Epimerases / analysis

[MeSH-minor] Antigens, CD57 / analysis. Carcinoma, Papillary / enzymology. Carcinoma, Papillary / pathology. Carcinoma, Renal Cell / enzymology. Carcinoma, Renal Cell / pathology. Diagnosis, Differential. Humans. Immunohistochemistry. Keratin-7. Keratins / analysis. WT1 Proteins / analysis. Wilms Tumor / enzymology. Wilms Tumor / pathology

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(PMID = 16424894.001).

[ISSN] 0893-3952

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

[ISO-abbreviation] Mod. Pathol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD57; 0 / Biomarkers, Tumor; 0 / KRT7 protein, human; 0 / Keratin-7; 0 / WT1 Proteins; 68238-35-7 / Keratins; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase

   

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

[Title] Immunoprofile of reactive salivary myoepithelial cells in intraductal areas of carcinoma ex-pleomorphic adenoma.

The myoepithelial cell (MC) is a component of various secretory glands, including salivary glands.

Besides its function, a tumor suppressor and a tumor facilitating functions have been attributed to this cell.

We investigated the immunoprofile of benign MC in intraductal areas of carcinoma ex-pleomorphic adenoma (CXPA), comparing them with the MC in duct-like areas of pleomorphic adenoma, origin of the malignant tumor.

Antibodies against myoepithelial markers-CK14, alpha-SMA, calponin, P63, CD10, and D2-40-plus laminin and maspin was applied in four selected cases of intracapsular and minimal invasive CXPA with only luminal differentiation presenting areas of intraductal carcinoma.

The immunohistochemical reactions of all the antibodies showed stronger staining in benign MC surrounding the malignant epithelial cells than in benign MC in duct-like areas of pleomorphic adenoma, thus revealing that in the malignization process the benign MC become differentiated and produce important proteins related to the tumor suppressor function.

[MeSH-major] Adenocarcinoma / metabolism. Adenoma, Pleomorphic / metabolism. Biomarkers, Tumor / metabolism. Neoplasm Proteins / metabolism. Salivary Gland Neoplasms / metabolism

[MeSH-minor] Adult. Cell Differentiation. Disease Progression. Epithelial Cells / metabolism. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged

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(PMID = 16757205.001).

[ISSN] 1368-8375

[Journal-full-title] Oral oncology

[ISO-abbreviation] Oral Oncol.

[Language] eng

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

[Publication-country] England

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

   

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

[Title] Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature.

We report a rare case of nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas.

The patient's clinical presentation, diagnosis, treatment, pancreas pathology, and follow-up are reviewed.

A 60-year-old patient was incidentally found to harbor a pancreatic mass with markedly elevated glucagon levels but without glucagonoma syndrome.

She was initially diagnosed with glucagonoma, and the tumor was resected.

Pathological examination demonstrated that the tumor was a nonfunctioning islet cell tumor and revealed nesidioblastosis and hyperplasia of alpha cells and microglucagonoma in the apparently normal surgical margin.

No pancreatic tumors recurred 36 months after surgery.

This is the third case of alpha-cell nesidioblastosis reported in the English literature.

Nesidioblastosis and hyperplasia of alpha cells should be considered in the differential diagnosis of hyperglucagonemia.

Somatostatin analog may be used to suppress glucagon secretion in alpha-cell hyperplasia.

[MeSH-major] Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / pathology. Glucagonoma / pathology. Islets of Langerhans / pathology. Nesidioblastosis / pathology. Pancreatic Neoplasms / pathology

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(PMID = 18437091.001).

[ISSN] 1536-4828

[Journal-full-title] Pancreas

[ISO-abbreviation] Pancreas

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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

[Title] Basal cell adenoma in a relatively rare site.

Basal cell adenoma (BCA) of the salivary glands is an uncommon type of monomorphic adenoma.

Histologically, it is seen as nests of isomorphic cells and interlaced trabeculae with a prominent basal membrane.

There is also slack, hyaline stroma with absence of a myxoid or chondroid component.

We describe a case of BCA of palatal minor salivary glands, a rare site for its occurrence.

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

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

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

(PMID = 21887012.001).

[ISSN] 0973-029X

[Journal-full-title] Journal of oral and maxillofacial pathology : JOMFP

[ISO-abbreviation] J Oral Maxillofac Pathol

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

[Other-IDs] NLM/ PMC3162860

[Keywords] NOTNLM ; Basal cell adenoma / alpha smooth muscle actin / monomorphic adenoma / pancytokeratin / squamous morules

   

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

[Title] Fetal gonadotrope cell origin of FSH-secreting pituitary adenoma - insight into human pituitary tumour pathogenesis.

OBJECTIVE: The pathogenesis of human pituitary adenomas remains unclear, but we report a case of FSH-secreting pituitary adenoma whose monohormonal phenotype suggests it was of fetal origin.

MEASUREMENTS: Endocrine studies were performed before and after curative surgery, with assessment of tumour hormone secretion in vitro, and immunostaining of tumour tissue for a series of gonadotrope proteins.

RESULTS: Immunocytochemistry showed that tumour cells were monohormonal for FSH.

Normal components of gonadotrope signalling pathways were expressed, including oestrogen receptor-alpha, activin receptors, secretogranin-II and chromogranin-A. beta-glycan, the putative inhibin coreceptor, was absent.

Tumour culture in vitro confirmed secretion of FSH with minimal LH, that was unsuppressed by oestradiol or inhibin-A.

Human fetal pituitary tissue contained FSH-only cells at 18 weeks gestation, whereas normal adult pituitary tissue contained only bihormonal gonadotropes.

CONCLUSIONS: We propose that this pituitary adenoma represents an indolent tumour of monohormonal fetal gonadotrope cells that originated early in gestation.

Pituitary tumours may therefore arise from abnormal persistence of fetal cell types, with extremely slow growth over many years until reaching a size threshold to generate an endocrine syndrome.

Understanding fetal pituitary architecture and function may be more informative for new insights into pituitary tumour pathogenesis than classical theories of cancer biology that invoke unrestrained cell proliferation.

[MeSH-major] Adenoma / embryology. Gonadotrophs / secretion. Pituitary Neoplasms / embryology

[MeSH-minor] Adult. Estradiol / blood. Female. Follicle Stimulating Hormone / analysis. Follicle Stimulating Hormone / blood. Follicle Stimulating Hormone / secretion. Humans. Immunohistochemistry / methods. Immunoradiometric Assay / methods. Luteinizing Hormone / blood. Pituitary Gland, Anterior / embryology. Pituitary Gland, Anterior / secretion. Polycystic Ovary Syndrome / blood. Polycystic Ovary Syndrome / embryology. Polycystic Ovary Syndrome / etiology. Tissue Culture Techniques

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(PMID = 17054468.001).

[ISSN] 0300-0664

[Journal-full-title] Clinical endocrinology

[ISO-abbreviation] Clin. Endocrinol. (Oxf)

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 4TI98Z838E / Estradiol; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone

   

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

[Title] Plurihormonal gonadotroph cell pituitary adenoma: report of a unique case.

OBJECTIVE AND IMPORTANCE: Pituitary adenomas producing primarily FSH and to a lesser extent GH, LH, alpha-subunit, TSH and PRL without clinical or laboratory evidence of increased hormone release have not previously been reported.

Our aim was to obtain some insight into the possible cytogenesis of this unusual tumor.

The tumor was removed by the transsphenoidal approach.

RESULT: By light microscopy, the adenoma was chromophobic, weakly PAS-positive, and immunoreactive mainly for FSH (85%) and to a lesser extent for GH (30%), LH (15%), alpha-subunit (3%), TSH (2%), and PRL (1%).

Although double immunostaining showed hormone reactivities to be localized largely in separate distinct cells, the tumor was ultrastructurally monomorphous, i.e., consisted of a single-cell type, resembling gonadotrophs.

CONCLUSION: The cytogenesis of plurihormonal pituitary adenomas is not fully understood.

[MeSH-major] Adenoma / metabolism. Adenoma / pathology. Gonadotrophs / metabolism. Gonadotrophs / pathology. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology

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[ErratumIn] Clin Neuropathol. 2011 May-Jun;30(3):157. Al-Sharim, M [corrected to Al-Shraim, M]

(PMID = 19537135.001).

[ISSN] 0722-5091

[Journal-full-title] Clinical neuropathology

[ISO-abbreviation] Clin. Neuropathol.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] 9002-62-4 / Prolactin; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone

   

[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] Expression of epidermal growth factor receptor, transforming growth factor-alpha and Ki-67 in relationship to malignant transformation of pleomorphic adenoma.

The data support the hypothesis that increased epidermal growth factor receptor (EGFR) and transforming growth factor (TGF)-alpha expression is associated with early events in malignant transformation of pleomorphic adenoma (PA).

OBJECTIVE: In the present study, we attempted to identify EGFR and TGF-alpha expression and Ki-67 index in carcinoma ex-pleomorphic adenoma (Ca ex-PA) and PA.

We also compared the presence of EGFR and TGF-alpha and Ki-67 index with clinical data.

MATERIALS AND METHODS: The tissues were stained with monoclonal antibodies to EGFR, TGF-alpha and Ki-67.

RESULTS: As regards the association of patients' prognosis with EGFR staining and Ki-67 index, a significant increase was observed in patients who died or had residual disease compared with patients who were alive without disease.

In the immunohistochemical analysis of EGFR and TGF-alpha and Ki67 index, a significant increase was observed in Ca ex-PA, especially with adenocarcinoma, compared with PA and sialadenitis.

[MeSH-major] Adenoma, Pleomorphic / metabolism. Biomarkers, Tumor / biosynthesis. Cell Transformation, Neoplastic. Ki-67 Antigen / genetics. Receptor, Epidermal Growth Factor / biosynthesis. Salivary Gland Neoplasms / metabolism. Transforming Growth Factor alpha / biosynthesis

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(PMID = 17851915.001).

[ISSN] 0001-6489

[Journal-full-title] Acta oto-laryngologica

[ISO-abbreviation] Acta Otolaryngol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Norway

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Transforming Growth Factor alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor

   

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

[Title] Anti-apoptotic action by hypoxia inducible factor 1-alpha in human pituitary adenoma cell line, HP-75 in hypoxic condition.

Hypoxia-inducible factor-1 (HIF-1) alpha is the major transcription factor involved in the adaptive response to hypoxia.

The purpose of this study was to investigate whether HIF 1-alpha protects HP75 cells, pituitary adenoma cell line from hypoxia induced apoptosis.

HP75 was transfected with siRNA targeting HIF 1-alpha mRNA sequences or scrambled RNA duplexes, followed by subjected to hypoxia (1% oxygen) for 24 h, compared with normoxia (21%).

Membrane cDNA microarray was examined to detect gene profiling among the cell in normoxia, hypoxia, or hypoxia following the RNAi.

A significantly greater proportion of HP75 cells transfected with specific siRNA duplexes and subsequently exposed to hypoxia demonstrated apoptosis to a large extent when compared with non-transfected cells.

Transfection with specific siRNA duplexes knocked down HIF 1-alpha mRNA and protein expression in hypoxia-exposed cells by approximately 80%, whereas transfection with scrambled siRNA duplexes had no noticeable effect on HIF 1-alpha expression.

Microarray analysis indicated that HIF1-alpha down-regulated caspase-10.

These findings strongly suggest that HIF 1-alpha exerts an antiapoptotic role in HP75 in hypoxia.

[MeSH-major] Adenoma / metabolism. Anoxia / metabolism. Apoptosis / physiology. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Pituitary Neoplasms / metabolism

[MeSH-minor] Adaptation, Physiological. Cell Line, Tumor. Cell Survival / genetics. Cell Survival / physiology. DNA Fingerprinting. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. RNA, Messenger / analysis. RNA, Small Interfering. Transfection

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(PMID = 16779673.001).

[ISSN] 0167-594X

[Journal-full-title] Journal of neuro-oncology

[ISO-abbreviation] J. Neurooncol.

[Language] eng

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

[Publication-country] Netherlands

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

   

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

[Title] Hepatocellular adenoma management and phenotypic classification: the Bordeaux experience.

We took advantage of the reported genotype/phenotype classification to analyze our surgical series of hepatocellular adenoma (HCA).

No differences were observed in solitary or multiple tumors in terms of hemorrhagic manifestations between groups.

Steatosis (tumor), microadenomas (resected specimen), and additional benign nodules were more frequently observed in HNF1alpha-inactivated HCAs (P < 0.01) than in IHCAs.

Body mass index > 25, peliosis (tumor), and steatosis in background liver were more frequent in IHCA (P < 0.01).

As a consequence, we believe that management of HCA needs to be adapted to the phenotype of these tumors.

[MeSH-major] Adenoma, Liver Cell / classification. Liver Neoplasms / classification

[MeSH-minor] Adult. Aged. C-Reactive Protein / metabolism. Fatty Acid-Binding Proteins / metabolism. Female. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Male. Middle Aged. Phenotype. Serum Amyloid A Protein / metabolism. Young Adult. beta Catenin / metabolism

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(PMID = 19585623.001).

[ISSN] 1527-3350

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

[ISO-abbreviation] Hepatology

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Fatty Acid-Binding Proteins; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Serum Amyloid A Protein; 0 / beta Catenin; 9007-41-4 / C-Reactive Protein

   

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

[Title] Correlation of VEGF production with IL1 alpha and IL6 secretion by human pituitary adenoma cells.

We have examined the expression of VEGF and its relationships with IL1 and IL6 in the human pituitary tumour cell line HP75 and a series of human pituitary tumours.

We have also looked at the relationship of tumour volume and invasive status to VEGF secretion.

METHODS: Surgically resected tumours were routinely cultured in single-cell suspension at 200 K/well (standard unit for culture of dispersed primary pituitary adenoma cells).

We measured VEGF, IL1 alpha and IL6 levels by ELISA.

Tumour volume and invasion grade were assessed by preoperative magnetic resonance imaging.

RESULTS: VEGF was detected in conditioned medium of HP75 cells (900+/-52 pg/ml) and in 82% of tumours tested (range 26-16 464 pg/ml).

Tumour volume and secretion of VEGF were significantly associated with levels of IL6 (volume, P = 0.056; VEGF, P < 0.001 (P values based on Spearman's test)) and IL1 alpha produced (volume, P < 0.005; VEGF, P < 0.001).

Addition of exogenous IL1 alpha, but not IL6, significantly increased VEGF production.

CONCLUSIONS: The significant associations between VEGF and the levels of IL6 and IL1 alpha suggest an important role for these cytokines in the development of these tumours.

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(PMID = 15745939.001).

[ISSN] 0804-4643

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] ENG

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

[Publication-country] England

[Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Interleukin-1; 0 / Interleukin-6; 0 / Vascular Endothelial Growth Factor A

   

[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] Induction of GH, PRL, and TSH beta mRNA by transfection of Pit-1 in a human pituitary adenoma-derived cell line.

The functional development of pituitary cells depends on the expression of a combination of transcription factors and co-factors.

The glycoprotein hormone alpha subunit (alpha SU) is the first hormone to be expressed during pituitary development.

In addition to being expressed in follicle-stimulating hormone, luteinizing hormone (LH), and TSH cells, alpha SU is reported to co-localize with GH in pituitary cells.

These findings have led to the suggestion that the expression of Pit-1 in cells of the alpha SU-based gonadotropin cell lineage might also lead to the expression of GH.

In this study, we transfected HP 75 cells (derived from a human non-functioning pituitary adenoma that expressed alpha SU and LH beta) with Pit-1 by using an adenovirus FLAG-Pit-1 construct.

Most of the transfected cells expressed GH mRNA, with fewer cells expressing PRL and TSH beta mRNA.

The HP 75 cells expressed the genes for ER and GATA-2, thus allowing their expression of GH, PRL, and TSH beta mRNA in response to Pit-1.

These results support the hypothesis that GH can be induced in cells that possess an active alpha SU gene and shed light on the basic molecular mechanism that drives the development of GH, PRL, and TSH beta expression in the alpha SU-based gonadotroph lineage.

[MeSH-major] Adenoma / metabolism. Human Growth Hormone / metabolism. Pituitary Neoplasms / metabolism. Prolactin / metabolism. RNA, Messenger / metabolism. Thyrotropin, beta Subunit / metabolism. Transcription Factor Pit-1 / metabolism

[MeSH-minor] Animals. Cell Line, Tumor. Cell Lineage. GATA2 Transcription Factor / genetics. GATA2 Transcription Factor / metabolism. Glycoprotein Hormones, alpha Subunit / genetics. Glycoprotein Hormones, alpha Subunit / metabolism. Humans. Pituitary Gland / cytology. Pituitary Gland / growth & development. Pituitary Gland / metabolism. Receptors, Estrogen / genetics. Receptors, Estrogen / metabolism. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism

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(PMID = 16133148.001).

[ISSN] 0302-766X

[Journal-full-title] Cell and tissue research

[ISO-abbreviation] Cell Tissue Res.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] 0 / GATA2 Transcription Factor; 0 / Glycoprotein Hormones, alpha Subunit; 0 / RNA, Messenger; 0 / Receptors, Estrogen; 0 / Recombinant Fusion Proteins; 0 / Thyrotropin, beta Subunit; 0 / Transcription Factor Pit-1; 12629-01-5 / Human Growth Hormone; 9002-62-4 / Prolactin

   

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

[Title] Renal papillary adenoma--a putative precursor of papillary renal cell carcinoma.

The precursor lesions of renal cell carcinoma (RCC) are unknown.

The purpose of this study is to determine the incidence, histomorphological features, and immunohistochemical features of papillary adenoma and elucidate its potential relationship to RCC.

Immunohistochemistry was carried out with antibodies specific for alpha-methyl-coenzyme A racemase (AMACR) and glutathione S-transferase alpha (clear-cell RCC marker).

Thirty-eight (7%) nephrectomy specimens showed histologic evidence of papillary adenoma.

Seven papillary adenomas (18%) occurred in the setting of acquired polycystic kidney disease (APKD), 6 in clear-cell RCCs, 3 in chromophobe RCCs, 2 in end-stage kidney disease, 1 in oncocytoma, 1 in angiomyolipoma, and 1 in renal schwannoma.

Furthermore, papillary adenomas were more commonly found in kidneys removed for PRCC (25%, 18/71) than in kidneys harboring clear-cell RCC (1.9%, 6/318).

Histomorphologically, papillary adenomas were characterized by varying proportions of papillae and tubules formed by cuboidal cells with scant basophilic cytoplasm similar to those in type 1 PRCC.

Adenomas associated with PRCC tend to be multiple in number (61% [11/18] of cases had >2 adenomas; mean, 5).

In contrast, 100% of papillary adenomas arising in other conditions had less than 2 adenomas.

Most of the adenomas (82%, 31/38) stained strongly for AMACR in a fashion similar to that of PRCC.

In this study of surgical specimens, the high coincidence, multifocality, and histologic and immunohistochemical similarities between papillary adenoma and PRCC suggest that the 2 are strongly associated and may represent a continuum of 1 biologic process.

In contrast, adenomas associated with APKD exhibit distinct morphological and immunohistochemical features and, therefore, may have an entirely different pathogenesis.

[MeSH-major] Carcinoma, Papillary / pathology. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology

[MeSH-minor] Adenocarcinoma, Clear Cell / enzymology. Adenocarcinoma, Clear Cell / pathology. Adenoma. Adenoma, Oxyphilic / enzymology. Adenoma, Oxyphilic / pathology. Adult. Aged. Aged, 80 and over. Angiomyolipoma / enzymology. Angiomyolipoma / pathology. Disease Progression. Female. Glutathione Transferase / analysis. Humans. Immunohistochemistry. Isoenzymes / analysis. Kidney / enzymology. Kidney / pathology. Kidney Failure, Chronic / enzymology. Kidney Failure, Chronic / pathology. Male. Middle Aged. Models, Biological. Polycystic Kidney Diseases / enzymology. Polycystic Kidney Diseases / pathology. Racemases and Epimerases / analysis

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(PMID = 17056094.001).

[ISSN] 0046-8177

[Journal-full-title] Human pathology

[ISO-abbreviation] Hum. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Isoenzymes; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase alpha; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase

   

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

[Title] Coexistence of mucous retention cyst and basal cell adenoma arising from the lining epithelium of the cyst. Report of two cases.

OBJECTIVE: To report 2 cases of coexisting mucous retention cyst and basal cell adenoma arising from the lining epithelium of the cyst.

CLINICAL PRESENTATION AND INTERVENTION: Two cases of painless swellings, well-demarcated, soft to palpation, and located in the submucosa of the upper lip were clinically examined with the provisional diagnosis of mucocele or salivary gland tumor.

Histological examination showed the presence of a large unilocular cystic cavity in many parts surrounded by single or bilayered lining epithelium composed of flattened to cuboidal cells, and in other parts surrounded by projections of cells arranged in a trabecular pattern far into the cystic cavity.

The trabeculae were composed of basal and low columnar cells that sometimes formed small duct-like structures.

Immunohistochemistry showed that the lining epithelium of the cystic cavity and the cells of the projections expressed cytokeratin 7 and high-molecular-weight cytokeratins.

The cells of the projections were weakly positive for S-100 protein and negative for vimentin and alpha-smooth muscle actin.

Based on the results, a diagnosis of coexisting mucous retention cysts and basal cell adenomas arising from the lining epithelium of cysts was made.

CONCLUSION: The coexistence of mucous retention cysts and basal cell adenomas arising from the lining epithelium of the cyst is reported.

[MeSH-major] Adenoma / complications. Adenoma / pathology. Mucocele / complications. Mucocele / pathology. Salivary Gland Diseases / complications. Salivary Gland Diseases / pathology

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[Copyright] Copyright 2009 S. Karger AG, Basel.

(PMID = 19349732.001).

[ISSN] 1423-0151

[Journal-full-title] Medical principles and practice : international journal of the Kuwait University, Health Science Centre

[ISO-abbreviation] Med Princ Pract

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

   

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

[Title] Hepatocellular adenoma: a case report.

A case of hepatocellular adenoma (HCA) was described in a 26-year-old woman, who was a potential kidney donor for her father and denied taking the oral contraceptive pill.

The normal levels of liver enzymes, negative serum markers for hepatitis viruses, and non-elevated alpha- fetoprotein level were detected.

Molecular biological studies disclosed three variants of HCAs, i.e., I) with mutation of HNF 1-alpha gene, II) with mutation of beta-catenin gene, and III) no mutation of the two genes.

[MeSH-major] Adenoma, Liver Cell / diagnosis. Liver Neoplasms / diagnosis

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(PMID = 20420118.001).

[ISSN] 0125-2208

[Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet

[ISO-abbreviation] J Med Assoc Thai

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Thailand

   

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

[Title] Esophageal gland duct adenoma: immunohistochemical comparison with the normal esophageal gland and ultrastractural analysis.

Esophageal gland duct adenomas are extremely rare tumors.

Here, we report the case of a 75-year-old Japanese man who had undergone total gastrectomy for advanced gastric cancer.

Esophageal gland duct adenoma was incidentally found in the lower esophagus.

It appeared to be detached from the site of gastric cancer and was well demarcated without a capsule.

Histologic analysis revealed papillary and cystic structures mainly comprising eosinophilic cells with minimum nuclear atypia.

Immunohistochemical analysis revealed that the tumor were diffusely positive for the S100 protein with preserved alpha-SMA-positive myoepithelial cell layers and a characteristic cytokeratin expression pattern similar to that in normal esophageal gland ducts (CK5/6+++, CK7+++, CK17+, CK18+, CK19+++, CK20-, HMWCK+++).

This is the first report that refers to the ultrastructural findings of an esophageal gland duct adenoma and describes terminal duct differentiation.

We believe that the possibility of an esophageal gland duct adenoma should be considered when diagnosing a ductal or glandular lesion of the esophagus.

[MeSH-major] Adenoma / pathology. Esophageal Neoplasms / pathology. Esophagus / pathology

[MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Aged. Biomarkers, Tumor / analysis. Cardia / pathology. Cardia / surgery. Cell Nucleus / ultrastructure. Cytoplasm / ultrastructure. Humans. Immunohistochemistry. Male. Microscopy, Electron, Transmission. Mucous Membrane / chemistry. Mucous Membrane / pathology. Neoplasms, Second Primary. Stomach Neoplasms / pathology. Stomach Neoplasms / surgery

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(PMID = 17325490.001).

[ISSN] 0147-5185

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

[ISO-abbreviation] Am. J. Surg. Pathol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

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

   

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

[Title] Bile acid induced gene expression in LT97 colonic adenoma cells.

LT97 human colonic adenoma cells reflecting early premalignant genotype and growth characteristics have been posed to tumor promoting bile acids in order to identify marker genes that permit identification of tumor promoters in vitro.

Physiologically relevant concentrations of desoxycholate (DOC) and chenodesoxycholate (CDC) upregulated expression of c-fos and COX-2 in a concentration- and time-dependent manner.

Transient induction of c-fos was seen with the non-promoting taurodesoxycholate (TDOC) as well as DOC, however extended induction at 3 h was only achieved by DOC and CDC reaching 3-6-fold as compared to the control.

Stimulation of COX-2 expression was completely specific for the tumor promoting analogs DOC and CDC.

Expression of VEGF was stimulated 4-5-fold in the tumor promoter (DOC and CDC) groups and about 2-fold in the non-promoting controls TDOC and GCDC.

At later times the tumor promoter specific difference was lost.

Our results show that all three genes are modulated in a tumor promoter dependent way and that their upregulation in LT97 adenoma cells can be used for in vitro testing of colon tumor promoters and chemopreventive compounds.

[MeSH-major] Adenoma / metabolism. Bile Acids and Salts / pharmacology. Biomarkers, Tumor / metabolism. Colonic Neoplasms / metabolism. Gene Expression Regulation, Neoplastic / drug effects

[MeSH-minor] Cell Line, Tumor. Chenodeoxycholic Acid / pharmacology. Cyclooxygenase 2. Deoxycholic Acid / pharmacology. Dose-Response Relationship, Drug. Gene Amplification. Glyceraldehyde-3-Phosphate Dehydrogenases / metabolism. Humans. Isoenzymes / genetics. Isoenzymes / metabolism. Membrane Proteins. Polymerase Chain Reaction. Prostaglandin-Endoperoxide Synthases / genetics. Prostaglandin-Endoperoxide Synthases / metabolism. Proto-Oncogene Proteins c-fos / genetics. Proto-Oncogene Proteins c-fos / metabolism. RNA / isolation & purification. Taurodeoxycholic Acid / pharmacology. Time Factors. Tumor Necrosis Factor-alpha / metabolism. Up-Regulation / drug effects. Up-Regulation / physiology. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor A / metabolism

Hazardous Substances Data Bank. DEOXYCHOLIC ACID .

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(PMID = 15582199.001).

[ISSN] 0278-6915

[Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

[ISO-abbreviation] Food Chem. Toxicol.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Biomarkers, Tumor; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins c-fos; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A; 005990WHZZ / Deoxycholic Acid; 0GEI24LG0J / Chenodeoxycholic Acid; 516-50-7 / Taurodeoxycholic Acid; 63231-63-0 / RNA; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases

   

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

[Title] Binding of pleomorphic adenoma gene-like 2 to the tumor necrosis factor (TNF)-alpha-responsive region of the NCF2 promoter regulates p67(phox) expression and NADPH oxidase activity.

NCF2, the gene encoding the NADPH oxidase cytosolic component p67(phox), is up-regulated by TNF-alpha, and we recently mapped a region in the NCF2 promoter that was required for this TNF-alpha-dependent response.

Because this TNF-alpha-responsive region (TRR) lacked recognizable transcription factor binding elements, we performed studies to identify factors involved in regulating NCF2 via the TRR.

Using the TRR sequence as bait in a yeast one-hybrid screen, we identified the zinc finger transcription factor Pleomorphic Adenoma Gene-Like 2 (PLAGL2) as a candidate regulator of NCF2 expression.

EMSA and DNA-binding protein affinity purification analyses demonstrated specific binding of in vitro-translated as well as endogenously expressed PLAGL2 to the TRR, and chromatin immunoprecipitation assays demonstrated enhanced binding of endogenous PLAGL2 to the TRR in vivo with TNF-alpha treatment.

Knockdown of PLAGL2 protein inhibited up-regulation of NCF2 transcript, p67(phox) protein expression, and subsequent superoxide production in response to TNF-alpha.

Furthermore, relative levels of native and SUMO1-modified endogenous PLAGL2 protein were modulated in a time-dependant manner in response to TNF-alpha treatment.

[MeSH-major] DNA-Binding Proteins / metabolism. Gene Expression Regulation, Enzymologic. NADPH Oxidase / metabolism. Phosphoproteins. Promoter Regions, Genetic. RNA-Binding Proteins / metabolism. Transcription Factors / metabolism. Tumor Necrosis Factor-alpha / metabolism

[MeSH-minor] Animals. Cell Line. Cells, Cultured. Humans. Monocytes / cytology. Monocytes / metabolism. Neutrophils / cytology. Neutrophils / metabolism. Oligonucleotides, Antisense / metabolism. SUMO-1 Protein. Small Ubiquitin-Related Modifier Proteins / metabolism. Tissue Distribution. Two-Hybrid System Techniques

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[ErratumIn] J Biol Chem. 2007 Jul 20;282(29):21572

(PMID = 17462995.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

[Grant] United States / NIAMS NIH HHS / AR / AR42426; United States / NCRR NIH HHS / RR / RR020185

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

[Publication-country] United States

[Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Oligonucleotides, Antisense; 0 / PLAGL2 protein, human; 0 / Phosphoproteins; 0 / RNA-Binding Proteins; 0 / SUMO-1 Protein; 0 / SUMO1 protein, human; 0 / Small Ubiquitin-Related Modifier Proteins; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / neutrophil cytosol factor 67K; EC 1.6.3.1 / NADPH Oxidase

   

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

[Title] A reduced COX-2 expression and a reduced number of pericryptal myofibroblasts are associated with depressed adenoma of the colon.

The histogenesis of depressed adenoma of the colon has not been sufficiently investigated.

Pericryptal myofibroblasts are stromal cells expressing smooth muscle actin, and are involved in the differentiation and multiplication of epithelial cells in the colonic epithelium.

COX-2 has been reported to be involved in the development of colon adenoma.

We studied the histogenesis of depressed adenoma of the colon by examining the relationship between the presence of pericryptal myofibroblasts and COX-2 expression.

Twenty-one depressed adenomas of the colon that had been resected endoscopically between June 1998 and May 2003 (mild-moderate atypia; mean diameter, 6.7 mm) and 23 elevated adenomas that had been resected endoscopically in 2003 (mild-moderate atypia; mean diameter, 11.7 mm), were studied.

We performed immunohistochemical staining using alpha-smooth muscle actin antibody to detect pericryptal myofibroblasts.

Eighteen (78.3%) of the 23 elevated adenomas and six (28.6%) of the 21 depressed adenomas were positive for pericryptal myofibroblasts immunohistochemically, showing a significant difference (P<0.001).

Seventeen elevated adenomas (73.9%) and eight depressed adenomas (38.1%) were positive for COX-2 expression (P=0.016).

The histogenesis of depressed adenomas differs from that of elevated adenomas.

Our results suggest that a low number of pericryptal myofibroblasts and a low COX-2 expression are associated with depressed adenomas.

[MeSH-major] Adenoma / pathology. Colonic Neoplasms / pathology. Cyclooxygenase 2 / metabolism. Fibroblasts / pathology. Membrane Proteins / metabolism. Myoblasts / pathology

[MeSH-minor] Actins / analysis. Cell Count. Down-Regulation. Humans

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(PMID = 17487390.001).

[ISSN] 1021-335X

[Journal-full-title] Oncology reports

[ISO-abbreviation] Oncol. Rep.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

[Chemical-registry-number] 0 / Actins; 0 / Membrane Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human

   

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

[Title] Tubular-trabecular type Basal cell adenoma of the parotid gland: a patient report.

Basal cell adenoma (BCA) is an uncommon benign salivary gland neoplasm that includes isomorphic basaloid cells.

The present patient demonstrated a few tumor nests in the fibrous capsule, and her tumor was larger than usual.

Histopathologically, the tumor was characterized by multiple duct-like structures and tubular-trabecular masses composed of small isomorphic cells with hyperchromatic, round nuclei and an eosinophilic cytoplasm.

It was difficult to determine whether the ductal structures noted in the tumor capsule were invasive.

By immunohistochemistry, tumor cells of the tubular nests were positive for cytokeratin 7 and that the outer cells of tubular nests were positive for alpha smooth muscle actin (αSMA) and calponin.

Tumor cells were immuno-negative for S-100 protein and glial fibrillary acidic protein.

The Ki-67 labeling scores of the cells were extremely low (< 1%).

We could achieve an accurate diagnosis of BCA by immunohistochemistry with MIB-1 and other markers.

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(PMID = 24031120.001).

[ISSN] 0513-5710

[Journal-full-title] Yonago acta medica

[ISO-abbreviation] Yonago Acta Med

[Language] eng

[Publication-type] Journal Article

[Publication-country] Japan

[Other-IDs] NLM/ PMC3763784

[Keywords] NOTNLM ; basal cell adenoma / immunohistochemistry / parotid gland

   

[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] A case of canine apocrine sweat gland adenoma, clear cell variant.

A cutaneous mass at the base of the retroauricular region of a 4-year-old, female Golden Retriever was examined pathologically.

Histologically, the mass formed multiple nodules consisting of a proliferation of large clear cells with abundant cytoplasm.

Mitotic figures among the neoplastic cells were very sparse.

The large clear cells were intensely positive for cytokeratins (AE1/AE4, cytokeratin 8 and 18) and moderately positive for lysozyme and contained periodic acid-Schiff-positive granules in the cytoplasm.

In addition, small flat cells lined the islands of neoplastic large clear cells, and these were strongly positive for alpha-smooth muscle actin and vimentin, and some were positive for cytokeratin (AE1/AE4), suggesting they were myoepithelial cells.

On the basis of these findings, the present tumor was diagnosed as apocrine sweat gland adenoma, clear cell variant.

There have been few previous reports of canine apocrine adenomas showing a clear cell morphology.

[MeSH-major] Adenoma, Sweat Gland / veterinary. Dog Diseases / pathology. Sweat Gland Neoplasms / veterinary

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(PMID = 15753476.001).

[ISSN] 0300-9858

[Journal-full-title] Veterinary pathology

[ISO-abbreviation] Vet. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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

[Title] Elevation of growth hormone-releasing hormone receptor messenger ribonucleic acid expression in growth hormone-secreting pituitary adenoma with Gsalpha protein mutation.

The expression of GHRH receptor (GHRHR) is regulated by GHRH, both of which are known to be expressed in human GH-secreting pituitary adenoma cells.

Somatic mutations in the subunit of Gsalpha protein (gsp), lead to the constitutive activation of adenylyl cyclase in pituitary adenomas that secrete GH.

It has not been examined how gsp mutations influence GHRHR expression in GH-secreting adenomas.

We therefore analyzed the expression levels of GHRHR messenger ribonucleic acid (mRNA) in GH-secreting pituitary adenomas focusing on a gsp mutation.

Furthermore, we investigated the effect of GHRH on the expression of GHRHR mRNA in primary cultures of GH-secreting pituitary adenoma cells.

GHRHR mRNA expression levels were significantly elevated in gsp mutation-positive GH-secreting adenomas compared with those in gsp mutation-negative ones.

In primary-cultured GH-secreting adenoma cells, the increase of GH secretion in response to GHRH was shown in both gsp mutation-positive and -negative adenoma cells with a significantly higher response in the latter adenoma cells.

GHRH increased GHRHR mRNA expression level in gsp mutation-negative adenoma cells while it was not influenced by GHRH in gsp mutation-positive adenoma cells.

These results suggest that gsp mutations up-regulate GHRHR mRNA expression in GH-secreting pituitary adenoma cells, and that gsp mutations desensitize the adenoma cells to GHRH in terms of their GHRHR mRNA expression probably because of their saturation of GHRH signaling.

[MeSH-major] Adenoma / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Growth Hormone-Releasing Hormone / secretion. Mutation, Missense. Neoplasm Proteins / genetics. Nerve Tissue Proteins / genetics. Pituitary Neoplasms / genetics. Point Mutation. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Receptors, Neuropeptide / genetics. Receptors, Pituitary Hormone-Regulating Hormone / genetics

[MeSH-minor] Acromegaly / etiology. Acromegaly / surgery. Adult. Amino Acid Substitution. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cell Line, Tumor / secretion. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged

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(PMID = 19029774.001).

[ISSN] 1349-8029

[Journal-full-title] Neurologia medico-chirurgica

[ISO-abbreviation] Neurol. Med. Chir. (Tokyo)

[Language] eng

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

[Publication-country] Japan

[Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / somatotropin releasing hormone receptor; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs

   

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

[Title] Increased sensitivity to TRAIL-induced apoptosis occurs during the adenoma to carcinoma transition of colorectal carcinogenesis.

The death ligand TRAIL (Apo2L) has potential for cancer therapy, since tumour cells are thought to be more sensitive than normal cells.

We investigated whether sensitivity to TRAIL increases during the adenoma to carcinoma transition of colorectal carcinogenesis.

Under the same culture conditions, we compared the extent of TRAIL-induced apoptosis in four premalignant adenoma and three carcinoma cell lines.

Although TRAIL induced some apoptosis in adenoma cultures, the carcinoma cell lines were significantly more sensitive (P<0.001).

This finding was recapitulated in an in vitro model of tumour progression in which conversion of the adenoma cell line AA/C1 to a tumorigenic phenotype was associated with increased TRAIL sensitivity (P<0.001).

To address this, cell surface receptor expression was measured by flow cytometry.

In summary, during colorectal carcinogenesis, there is a marked increase in sensitivity to TRAIL-induced apoptosis associated with progression from benign to malignant tumour that could be exploited for colon cancer therapy, but alterations in cell surface TRAIL receptor expression may not be the primary reason for this change.

[MeSH-major] Adenoma / pathology. Apoptosis. Carcinoma / pathology. Cell Transformation, Neoplastic. Colorectal Neoplasms / pathology. Membrane Glycoproteins / metabolism. Receptors, Tumor Necrosis Factor / metabolism. Tumor Necrosis Factor-alpha / metabolism

[MeSH-minor] Animals. Antineoplastic Agents / metabolism. Apoptosis Regulatory Proteins. Blotting, Western. Cell Line, Tumor. Electrophoresis, Polyacrylamide Gel. Flow Cytometry. GPI-Linked Proteins. Humans. Mice. Mice, Nude. Receptors, TNF-Related Apoptosis-Inducing Ligand. TNF-Related Apoptosis-Inducing Ligand. Tumor Necrosis Factor Decoy Receptors

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[Cites] Cancer Res. 1999 Dec 15;59(24):6153-8 [10626806.001]

[Cites] Clin Cancer Res. 2000 Feb;6(2):335-46 [10690508.001]

[Cites] J Cell Biol. 2000 Mar 20;148(6):1239-54 [10725337.001]

[Cites] J Immunol. 2000 Apr 15;164(8):3961-70 [10754286.001]

[Cites] Biochem J. 2000 May 15;348 Pt 1:93-101 [10794718.001]

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(PMID = 15685228.001).

[ISSN] 0007-0920

[Journal-full-title] British journal of cancer

[ISO-abbreviation] Br. J. Cancer

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFRSF10C protein, human; 0 / TNFSF10 protein, human; 0 / Tnfrsf10b protein, mouse; 0 / Tnfsf10 protein, mouse; 0 / Tumor Necrosis Factor Decoy Receptors; 0 / Tumor Necrosis Factor-alpha

[Other-IDs] NLM/ PMC2361885

   

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

[Title] Localization of tissue inhibitor of metalloproteinases 1 (TIMP-1) in human colorectal adenoma and adenocarcinoma.

However, TIMP-1 also possesses other functions such as inhibition of apoptosis, induction of malignant transformation and stimulation of cell-growth.

To clarify the role of TIMP-1 in colorectal tumorigenesis, the expression pattern of TIMP-1 in benign and malignant colorectal tumors was studied.

In all cases TIMP-1 expression was found in fibroblast-like cells located at the invasive front but was seen only sporadically in normal mucosa.

No TIMP-1 mRNA was seen in any of the cases in benign or malignant epithelial cells, in vascular cells or smooth muscle cells.

Combining TIMP-1 in situ hybridization with immunohistochemical staining for alpha-smooth muscle actin or CD68 showed TIMP-1 mRNA in myofibroblasts but not in macrophages.

TIMP-1 mRNA was detected in 2 of 7 adenomatous polyps in the adenoma area: in both cases associated with focal stromal inflammation at the epithelial-stromal interface.

In conclusion, TIMP-1 expression is a rare event in benign human colon tissue but is highly expressed by myofibroblasts in association with invading colon cancer cells.

[MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adenoma / genetics. Adenoma / pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. Tissue Inhibitor of Metalloproteinase-1 / biosynthesis. Tissue Inhibitor of Metalloproteinase-1 / pharmacology

[MeSH-minor] Case-Control Studies. Cell Transformation, Neoplastic. Diagnosis, Differential. Fibroblasts / physiology. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Neoplasm Invasiveness. RNA, Messenger / analysis. RNA, Messenger / biosynthesis

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(PMID = 15386409.001).

[ISSN] 0020-7136

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / RNA, Messenger; 0 / Tissue Inhibitor of Metalloproteinase-1

   

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

[Title] Silent adenoma subtype 3 of the pituitary--immunohistochemical and ultrastructural classification: a review of 29 cases.

The silent adenoma subtype 3 (SAS-3) of undetermined cellular derivation is a seemingly nonfunctioning aggressive pituitary tumor with a high recurrence rate.

At the time of diagnosis SAS-3s are macro- or giant adenomas particularly aggressive in young individuals, especially women.

Immunohistochemistry, demonstrating scattered immunoreactivity mostly for GH, PRL, TSH, and alpha-subunit, is not diagnostic.

Presently, only TEM permits conclusive diagnosis.

Ultrastructurally, the large polar adenoma cells contain abundant RER, masses of SER, extensive multipolar Golgi apparatus, and unevenly clustered mitochondria, displaced by RER and SER, which may show close spatial relationship to RER.

Cell membranes often form plexiform interdigitations.

The 100- to 200-nm secretory granules accumulate heavily in cell processes, which is a hallmark of glycoprotein hormone cell differentiation.

The endothelial cells may contain tubuloreticular inclusions.

Complete surgical removal of the large often invasive tumors is difficult necessitating postoperative treatment.

Some tumors express somatostatin receptors and respond well to somatostatin analogues, offering long-term control in patients with residual tumor.

Possible derivation of SAS-3 from rostral thyrotrophs, a cell type presently known in rodents is contemplated.

[MeSH-major] Adenoma / metabolism. Adenoma / ultrastructure. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / ultrastructure

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(PMID = 16316952.001).

[ISSN] 0191-3123

[Journal-full-title] Ultrastructural pathology

[ISO-abbreviation] Ultrastruct Pathol

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] United States

[Number-of-references] 15

   

[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] Spectrum of HNF1A somatic mutations in hepatocellular adenoma differs from that in patients with MODY3 and suggests genotoxic damage.

A subtype of hepatocellular adenoma (HCA) is also caused by biallelic somatic HNF1A mutations (H-HCA), and rare HCA may be related to MODY3.

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[Cites] J Bacteriol. 1996 Jul;178(13):3885-92 [8682794.001]

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(PMID = 20393147.001).

[ISSN] 1939-327X

[Journal-full-title] Diabetes

[ISO-abbreviation] Diabetes

[Language] ENG

[Grant] United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NIEHS NIH HHS / ES / R01-ES-15241; United States / NIEHS NIH HHS / ES / R01 ES015241; United States / NIAAA NIH HHS / AA / R01-AA-16258; United States / NIAAA NIH HHS / AA / R01 AA016258

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

[Publication-country] United States

[Chemical-registry-number] 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha

[Other-IDs] NLM/ PMC2889786

   

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

[Title] Markers of cell proliferation in a GH-producing adenoma of a patient treated with pegvisomant.

We report our findings on markers of cell proliferation (Ki-67 labelling index and topoisomerase-alpha expression) in a somatotroph pituitary tumour before and after exposure to pegvisomant, a GH receptor antagonist developed for the treatment of acromegaly.

Ki-67 labelling index and topoisomerase-alpha expression were both markedly greater (1-3% compared with 0-0.5% and 15-80% compared with 2-10% respectively) in the pegvisomant-exposed tumour compared with the earlier specimen.

However, our data reinforce the requirement for careful radiological surveillance of the pituitary in the context of a drug that does not target the tumour responsible and where serum GH cannot serve as a marker of disease activity or tumour size.

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(PMID = 16061824.001).

[ISSN] 0804-4643

[Journal-full-title] European journal of endocrinology

[ISO-abbreviation] Eur. J. Endocrinol.

[Language] ENG

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / Receptors, Somatotropin; 0 / pegvisomant; 12629-01-5 / Human Growth Hormone; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha

   

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

[Title] Composite pituitary adenoma and craniopharyngioma?: an unusual sellar neoplasm with divergent differentiation.

The patient was treated with thyroid radioablation and hormone replacement and followed for 7 years, during which time the tumor grew to 4.6 cm.

At transsphenoidal surgery, a tumor consisting of a pituitary adenoma and adamantinomatous craniopharyngiomalike components was resected.

Both components were closely intermingled, but there was no evidence of an intermediate morphologic phenotype.

Immunohistochemically, the adenoma was not only positive for beta-thyroid stimulating hormone, alpha subunit, and pituitary transcription factor 1, but also stained for beta-follicle stimulating hormone, steroidogenic factor-1, adrenocorticotropic hormone, and pituitary-restricted transcription factor (Tpit), exhibiting an unusual plurihormonal profile.

This lesion may represent an unusual composite tumor attributable to divergent differentiation of a common precursor.

Alternatively, it may be viewed as a pituitary adenoma showing metaplastic change analogous to the development of squamous cell nests of the pars tuberalis from adenohypophyseal endocrine cells.

[MeSH-major] Adenoma / pathology. Craniopharyngioma / pathology. Neoplasms, Multiple Primary / pathology. Pituitary Neoplasms / pathology

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(PMID = 18769335.001).

[ISSN] 1532-0979

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

[ISO-abbreviation] Am. J. Surg. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 9002-71-5 / Thyrotropin

   

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

[Title] Association of CYP1B1 germ line mutations with hepatocyte nuclear factor 1alpha-mutated hepatocellular adenoma.

Biallelic somatic mutations of TCF1 coding for hepatocyte nuclear factor 1alpha (HNF1alpha) are found in 50% of the hepatocellular adenoma (HCA) cases usually associated with oral contraception.

For 10 genes (CYP1A1, CYP1A2, CYP3A4, CYP3A5, COMT, UGT2B7, NQO1, GSTM1, GSTP1, and GSTT1), we did not find mutations nor differences in the allele distribution among 32 women presenting HNF1alpha-mutated adenomas compared with 58 controls.

In contrast, we identified a CYP1B1 germ line heterozygous mutation in 4 of 32 women presenting HNF1alpha-mutated adenomas compared with none in 58 controls.

[MeSH-major] Adenoma, Liver Cell / genetics. Cytochrome P-450 Enzyme System / genetics. Germ-Line Mutation. Hepatocyte Nuclear Factor 1-alpha / genetics. Liver Neoplasms / genetics

[MeSH-minor] Adolescent. Adult. Alleles. Aryl Hydrocarbon Hydroxylases. Child. Cytochrome P-450 CYP1B1. Female. Genetic Predisposition to Disease. Genotype. Humans. Middle Aged. Mutagenesis, Site-Directed. Pedigree

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(PMID = 17363580.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP1B1 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP1B1

   

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

[Title] Tumoral stroma of salivary pleomorphic adenoma -- histopathological, histochemical and immunohistochemical study.

The aims of our paper were to establish the main histopathological, histochemical and immunohistochemical aspects of tumoral stroma from salivary pleomorphic adenomas.

Immunohistochemically, they were investigated for AE1-AE3, MNF116, CK8, EMA, vimentin, alpha-actin calponin, S-100, GFAP, collagen IV, and PCNA.

The results of our study suggest the key role of neoplastic myoepithelial cell in the achievement of diverse morphological aspects of stroma in such neoplasms.

[MeSH-major] Adenoma, Pleomorphic / pathology. Salivary Gland Neoplasms / pathology. Stromal Cells / pathology

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(PMID = 16444308.001).

[ISSN] 1220-0522

[Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie

[ISO-abbreviation] Rom J Morphol Embryol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Romania

   

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

[Title] [Necrolytic migratory erythema in glucagonoma syndrome].

The glucagonoma syndrome is a rare disease in which a typical skin lesion, necrolytic migratory erythema, is often one of the presenting symptoms.

Skin biopsies, laboratory studies and imaging confirmed the diagnosis of necrolytic migratory erythema as part of a glucagonoma syndrome.

[MeSH-major] Ciprofloxacin / administration & dosage. Erythema / diagnosis. Erythema / drug therapy. Glucagonoma / diagnosis. Glucagonoma / drug therapy

[MeSH-minor] Administration, Oral. Aged. Anti-Infective Agents / administration & dosage. Female. Humans. Necrosis / diagnosis. Necrosis / drug therapy. Syndrome. Treatment Outcome

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[Cites] J Clin Oncol. 2003 Jul 15;21(14 ):2689-96 [12860945.001]

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(PMID = 17549440.001).

[ISSN] 1432-1173

[Journal-full-title] Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete

[ISO-abbreviation] Hautarzt

[Language] ger

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

[Publication-country] Germany

[Chemical-registry-number] 0 / Anti-Infective Agents; 5E8K9I0O4U / Ciprofloxacin

   

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

[Title] [Glucagonoma syndrome without diabetes mellitus].

Computerised tomography and endoscopic ultrasound showed a solid tumour of the pancreas.

A blood sample showed an increased level of glucagon without diabetes.

Glucagonoma syndrome is characterized by glucagon overproduction, diabetes, depression, deep venous thrombosis and necrolytic migrating erythema.

Glucagonoma is frequently diagnosed late which increases the risk of metastases.

It is important not to rule out glucagonoma in patients with a relevant clinical picture but without diabetes.

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

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[CommentIn] Ugeskr Laeger. 2008 Dec 15;170(51):4241; author reply 4241 [19160469.001]

(PMID = 19014744.001).

[ISSN] 1603-6824

[Journal-full-title] Ugeskrift for laeger

[ISO-abbreviation] Ugeskr. Laeg.

[Language] dan

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

[Publication-country] Denmark

   

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

[Title] Genotype-phenotype correlation in hepatocellular adenoma: new classification and relationship with HCC.

Hepatocellular adenomas are benign tumors that can be difficult to diagnose.

A multicentric series of 96 liver tumors with a firm or possible diagnosis of hepatocellular adenoma was reviewed by liver pathologists.

No tumors were mutated in both HNF1alpha and beta-catenin enabling tumors to be classified into 3 groups, according to genotype.

Tumors with HNF1alpha mutations formed the most important group of adenomas (44 cases).

In contrast, the group of tumors defined by beta-catenin activation included 13 lesions with frequent cytological abnormalities and pseudo-glandular formation (P < 10(-5)).

The third group of tumors without mutation was divided into two subgroups based on the presence of inflammatory infiltrates.

The subgroup of tumors consisting of 17 inflammatory lesions, resembled telangiectatic focal nodular hyperplasias, with frequent cytological abnormalities (P = 10(-3)), ductular reaction (P < 10(-2)), and dystrophic vessels (P = .02).

In this classification, hepatocellular carcinoma associated with adenoma or borderline lesions between carcinoma and adenoma is found in 46% of the beta-catenin-mutated tumors whereas they are never observed in inflammatory lesions and are rarely found in HNF1alpha mutated tumors (P = .004).

In conclusion, the molecular and pathological classification of hepatocellular adenomas permits the identification of strong genotype-phenotype correlations and suggests that adenomas with beta-catenin activation have a higher risk of malignant transformation.

[MeSH-major] Adenoma, Liver Cell / genetics. Carcinoma, Hepatocellular / genetics. Hepatocyte Nuclear Factor 1-alpha / genetics. Liver Neoplasms / genetics. beta Catenin / genetics

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[CommentIn] Hepatology. 2006 Mar;43(3):401-4 [16496344.001]

[CommentIn] Histopathology. 2007 Dec;51(6):855-6 [17903198.001]

(PMID = 16496320.001).

[ISSN] 0270-9139

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

[ISO-abbreviation] Hepatology

[Language] eng

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

[Publication-country] United States

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

   

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

[Title] TGF-alpha expression as a potential biomarker of risk within the normal-appearing colorectal mucosa of patients with and without incident sporadic adenoma.

BACKGROUND: Transforming growth factor-alpha (TGF-alpha), a stimulatory growth factor and member of the epidermal growth factor family, is a mediator of oncogenesis and malignant progression in colorectal carcinogenesis.

METHODS: We measured expression of TGF-alpha in biopsies of normal-appearing colorectal mucosa using automated immunohistochemistry and quantitative image analysis in a subsample of 29 cases and 31 controls from a colonoscopy-based case-control study (n = 203) of biomarkers of risk for incident sporadic colorectal adenoma.

RESULTS: TGF-alpha expression in the rectum was 51% higher in cases compared with controls (P = 0.05) and statistically significantly associated with accepted risk factors for colorectal neoplasms (36% lower among nonsteroidal anti-inflammatory drug users, 49% lower among women using hormone replacement therapy, 79% higher among persons with a family history of colorectal cancer).

CONCLUSIONS: TGF-alpha expression in the normal-appearing rectal mucosa shows promise as an early, potentially modifiable biomarker of risk for colorectal cancer.

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(PMID = 19124482.001).

[ISSN] 1055-9965

[Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

[ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA115230-02; United States / NCI NIH HHS / CA / R03 CA115230; United States / NCI NIH HHS / CA / R03 CA115230-02

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

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Transforming Growth Factor alpha

[Other-IDs] NLM/ NIHMS253319; NLM/ PMC2995992