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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] Homozygous P86S mutation of the human glucagon receptor is associated with hyperglucagonemia, alpha cell hyperplasia, and islet cell tumor.

OBJECTIVE: The goal of the study was to investigate the genetic and molecular basis of a novel syndrome of marked hyperglucagonemia and pancreatic alpha cell hyperplasia without glucagonoma syndrome.

METHODS: The glucagon receptor (GCGR) gene and the glucagon gene were sequenced in a patient with hyperglucagonemia and pancreatic alpha cell hyperplasia without glucagonoma syndrome.

RESULTS: The glucagon gene sequence was normal, but the GCGR sequencing uncovered a homozygous missense mutation, c.256C>T, p.P86S in the extracellular domain of GCGR.

When expressed in human embryonic kidney 293 cells, GCGR P86S localized to the plasma membrane but bound 96% less radiolabeled glucagon than WT GCGR.

The median effective concentration of glucagon-induced cyclic adenosine monophosphate production was 24 nmol/L for GCGR P86S but 2.4 nmol/L for WT GCGR.

The patient's alpha cells also express glucagonlike peptide 1 and pancreatic polypeptide.

CONCLUSIONS: We hereby report the first homozygous missense mutation in the human GCGR, which is associated with alpha cell hyperplasia and hyperglucagonemia.

This mutation lowers the receptor's affinity to glucagon and decreases cyclic adenosine monophosphate production with physiological concentrations of glucagon.

Thus, the P86S mutation in GCGR likely causes alpha cell hyperplasia and hyperglucagonemia.

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(PMID = 19657311.001).

[ISSN] 1536-4828

[Journal-full-title] Pancreas

[ISO-abbreviation] Pancreas

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / DK071870-04; United States / NIDDK NIH HHS / DK / K08 DK071870; United States / NIDDK NIH HHS / DK / DK071870; United States / NIDDK NIH HHS / DK / K08 DK071870-04

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

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, Glucagon; 147336-22-9 / Green Fluorescent Proteins; 9007-92-5 / Glucagon

[Other-IDs] NLM/ NIHMS139678; NLM/ PMC2767399

   

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

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

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

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

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

The serum glucagon level was markedly increased.

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

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

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

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

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

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

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(PMID = 16435046.001).

[ISSN] 1318-4458

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

[ISO-abbreviation] Acta Dermatovenerol Alp Pannonica Adriat

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Slovenia

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

   

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

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

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

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

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

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

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(PMID = 15862113.001).

[ISSN] 1470-8728

[Journal-full-title] The Biochemical journal

[ISO-abbreviation] Biochem. J.

[Language] ENG

[Grant] United Kingdom / Wellcome Trust / /

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

[Publication-country] England

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

[Other-IDs] NLM/ PMC1180732

   

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

[Title] [Glucagonoma without glucagonoma syndrome].

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

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

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

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

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

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

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

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

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

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(PMID = 20499510.001).

[ISSN] 0370-8179

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

[ISO-abbreviation] Srp Arh Celok Lek

[Language] srp

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

[Publication-country] Serbia

   

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

[Title] Glucagonoma syndrome and necrolytic migratory erythema.

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

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

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

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

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

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

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(PMID = 20465606.001).

[ISSN] 1365-4632

[Journal-full-title] International journal of dermatology

[ISO-abbreviation] Int. J. Dermatol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

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

   

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

[Title] A case of pancreatic glucagonoma with erythema.

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

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

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

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

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

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

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

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(PMID = 20530930.001).

[ISSN] 0446-6586

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

[ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

   

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

[Title] [A case of pancreatic glucagonoma].

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

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

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

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

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

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

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(PMID = 17926496.001).

[ISSN] 0023-2149

[Journal-full-title] Klinicheskaia meditsina

[ISO-abbreviation] Klin Med (Mosk)

[Language] rus

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

[Publication-country] Russia (Federation)

   

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

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

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

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

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

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

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

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

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(PMID = 15757825.001).

[ISSN] 1167-1122

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

[ISO-abbreviation] Eur J Dermatol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] France

   

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

[Title] 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] 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.

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.

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] 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] [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] Histogenesis of solid pseudopapillary tumor of the pancreas: the case for the centroacinar cell of origin.

Solid pseudopapillary tumor (SPT) is an unusual pancreatic neoplasm of low malignant potential that most frequently occurs in young women.

The tumor is indolent, with long patient survival, even in the presence of extension into adjacent organs and metastases.

Histologically, it is a solid and cystic tumor with a prominent vascular network and degenerative pseudopapillae formation.

Herein, we report a case of solid pseudopapillary tumor in a 41-year-old female in which the tumor cells immunohistochemically and ultrastructurally suggest a centroacinar cell origin.

The tumor cells and the normal centroacinar cells stained positive for alpha-antitrypsin (alpha-AT), CD10, cyclin D1 and NSE.

Ultrastructural examination shows similarities in nuclear shape, nucleoli location and cytoplasmic contents between neoplastic cells and normal centroacinar cells of the pancreas.

Based on both immunohistochemical and ultrastructural features, we propose that the centroacinar cell is the origin of SPT.

[MeSH-major] Carcinoma, Papillary / pathology. Islets of Langerhans / pathology. Pancreatic Neoplasms / pathology

[MeSH-minor] Adult. Cyclin D1 / analysis. Female. Humans. Neprilysin / analysis. Phosphopyruvate Hydratase / analysis. alpha 1-Antitrypsin / analysis

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(PMID = 16916512.001).

[ISSN] 0014-4800

[Journal-full-title] Experimental and molecular pathology

[ISO-abbreviation] Exp. Mol. Pathol.

[Language] eng

[Grant] United States / PHS HHS / / P50-019991

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

[Publication-country] United States

[Chemical-registry-number] 0 / alpha 1-Antitrypsin; 136601-57-5 / Cyclin D1; EC 3.4.24.11 / Neprilysin; EC 4.2.1.11 / Phosphopyruvate Hydratase

   

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

[Title] [Solid pseudopapillary tumor of the pancreas].

The paper reviews the data available in the literature and describes the authors' observation of solid pseudopapillary tumor of the pancreas in a 33-year-old woman.

Microscopically, the tumor, 2.5 x 2.5 x 2 cm in size, appeared predominantly as solid areas and solitary pseudopapillae comprising monomorphic round and oval cells with a light cytoplasm and round nuclei.

Immunohistochemical study revealed diffuse cytoplasmic tumor cell staining in response to vimentin, alpha-antitrypsin, neuronspecific enolase, and cytokeratin 18; focal expression of synaptophysin and CD117; a negative reaction with antibodies to epithelial membrane antigen, S-100 protein, cytokeratins 7, 8, and 19, and CD57.

Progesterone receptors were detectable in the nuclei of solitary tumor cells and the reaction with estrogen receptor was negative.

[MeSH-major] Carcinoma, Papillary / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology

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(PMID = 18368811.001).

[ISSN] 0004-1955

[Journal-full-title] Arkhiv patologii

[ISO-abbreviation] Arkh. Patol.

[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] 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] 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] Ischemia-reperfusion of the pancreas induced hyperresponsiveness of the airways in rats.

OBJECTIVES: Ischemia-reperfusion (I/R) of the rat pancreas induced acute pancreatitis with systemic inflammatory response syndrome.

Activated inflammatory cells sequestered in the lung and the proteases released from the inflammatory pancreas both could induce lung inflammation and lung injury.

METHODS: Ischemia of the pancreas was induced by clamping the gastroduodenal and the splenic artery for 2 hours followed by reperfusion for 6 hours.

The pulmonary function test of Penh was used to reflect the airway responses. mRNA expression of iNOS and tumor necrosis factor-alpha (TNFalpha) in the lung tissue were measured by real time polymerase chain reactions.

RESULTS: This protocol resulted in significant elevations of the blood concentrations of nitric oxide, hydroxyl radical, amylase, TNFalpha, and white cells among the I/R group.

Pulmonary function data showed that I/R of the pancreas induced significant increases in the responses to methacholine challenge: Penh was significantly increased in the I/R group compared with the sham group.

Lavage white cells were significantly increased in the I/R group.

CONCLUSIONS: I/R of the pancreas induced systemic inflammatory responses and increased white cell sequestration in the lung.

Hyperresponsive responses in the airways of the reperfusion group may be due to airways inflammation, which increased white cell sequesteration in the lung and the expressions iNOS and TNFalpha inflammatory mediators in lung tissues.

[MeSH-major] Pancreas / physiopathology. Reperfusion Injury / physiopathology

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(PMID = 19249477.001).

[ISSN] 0041-1345

[Journal-full-title] Transplantation proceedings

[ISO-abbreviation] Transplant. Proc.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Nitrates; 0 / Nitrites; 0W5ETF9M2K / Methacholine Chloride; 31C4KY9ESH / Nitric Oxide; EC 3.2.1.- / Amylases

   

[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] Interleukin-32 expression in the pancreas.

We studied IL-32 expression in human pancreatic tissue and pancreatic cancer cell lines.

IL-32 was weakly immunoexpressed by pancreatic duct cells.

In the inflamed lesions of chronic pancreas, the ductal expression of IL-32 was markedly increased.

A strong expression of IL-32alpha was detected in the pancreatic cancer cells.

In pancreatic cancer cell lines (PANC-1, MIA PaCa-2, and BxPC-3 cells), the expression of IL-32 mRNA and protein was enhanced by IL-1beta, interferon (IFN)-gamma, and tumor necrosis factor (TNF)-alpha.

An inhibitor of phosphatidylinositol 3-kinase (LY294002) significantly suppressed the IL-1beta-, IFN-gamma- and TNF-alpha-induced IL-32 mRNA expression.

The blockade of NF-kappaB and activated protein-1 activation markedly suppressed the IL-1beta-, IFN-gamma-, and/or TNF-alpha-induced IL-32 mRNA expression.

Furthermore, IL-32-specific small interfering RNA significantly decreased the uptake of [3H]thymidine and increased the annexin V-positive population (apoptotic cells) in PANC-1 cells.

Pancreatic duct cells are the local source of IL-32, and IL-32 may play an important role in inflammatory responses and pancreatic cancer growth.

[MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Gene Expression Regulation, Neoplastic. Interleukins / metabolism. Pancreas / metabolism. Pancreatic Neoplasms / metabolism

[MeSH-minor] Apoptosis. Blotting, Northern. Blotting, Western. Cell Proliferation. Cells, Cultured. Electrophoretic Mobility Shift Assay. Enzyme-Linked Immunosorbent Assay. Humans. Immunoenzyme Techniques. Interferon-gamma / genetics. Interferon-gamma / metabolism. Interleukin-1beta / genetics. Interleukin-1beta / metabolism. NF-kappa B / antagonists & inhibitors. NF-kappa B / genetics. NF-kappa B / metabolism. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Transcription Factor AP-1 / genetics. Transcription Factor AP-1 / metabolism. Transfection. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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(PMID = 19386602.001).

[ISSN] 0021-9258

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

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / IL32 protein, human; 0 / Interleukin-1beta; 0 / Interleukins; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Transcription Factor AP-1; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 2.7.1.- / Phosphatidylinositol 3-Kinases

[Other-IDs] NLM/ PMC2719425

   

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

[Title] Necrolytic migratory erythema without glucagonoma associated with hepatitis B.

We report a case of necrolytic migratory erythema (NME) without glucagonoma associated with hepatitis B.

Although the most common cause of NME is a glucagon-secreting alpha-islet cell tumor of the pancreas, a dermatitis clinically and histologicaly identical to NME has been described in patients without glucagonoma.

We added some discussion on the terminology of this disease.

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(PMID = 15701595.001).

[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] High levels of endogenous tumor necrosis factor-related apoptosis-inducing ligand expression correlate with increased cell death in human pancreas.

OBJECTIVES: Type 1 diabetes (T1D) has been characterized by the T cell-mediated destruction of pancreatic beta cells.

Although various members of the tumor necrosis factor (TNF) family, such as Fas ligand or TNF, have recently been implicated in the development of T1D, the lack of TNF-related apoptosis-inducing ligand (TRAIL) expression or function facilitates the onset of T1D.

Thus, the goal of the present study was to investigate the expression profiles of TRAIL and its receptors in human pancreas.

RESULTS: Acinar cells displayed high levels of TRAIL and death receptor 4, but only low levels of death receptor 5.

In contrast, only TRAIL and TRAIL decoy receptors (DcR1, DcR2) were detected in ductal cells.

High levels of TRAIL expression in pancreas correlated with increased number of apoptotic cells.

CONCLUSIONS: Although the expression of TRAIL decoy receptors might be necessary for defense from TRAIL-induced apoptosis, high levels of TRAIL may provide protection for Langerhans islets from the immunological attack of cytotoxic T cells.

[MeSH-major] Apoptosis / physiology. Cell Death / physiology. Pancreas / cytology. Pancreas / physiology. Tumor Necrosis Factor-alpha / physiology

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(PMID = 18437085.001).

[ISSN] 1536-4828

[Journal-full-title] Pancreas

[ISO-abbreviation] Pancreas

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Tumor Necrosis Factor-alpha

   

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

[Title] Protective effect of alpha-melanocyte-stimulating hormone on pancreas islet cell against peripheral blood mononuclear cell-mediated cytotoxicity in vitro.

The alpha-melanocyte-stimulating hormone (alpha-MSH) has been shown to interact with various cells of the immune and inflammatory systems and down-regulate either the production or the action of proinflammatory cytokines.

In this study, we investigated the potential of alpha-MSH to prevent pancreatic islet cells from cytotoxic injury by inflammatory cytokines released from peripheral blood mononuclear cells (PBMCs) in rats.

Pancreatic islets were cocultured with PBMCs in a transwell system during stimulation by phorbol myristic acid and ionomycin. alpha-MSH (50 nmol/L) was added to PBMCs for 2 hours before coculture.

Insulin release from islets cocultured with mononuclear cells was checked as the metric of islet function.

In comparison to the control group, the viability of islets with alpha-MSH-treated mononuclear cells was increased and apoptosis reduced significantly.

Inflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-1beta, were significantly reduced among the alpha-MSH-treated group.

NO production in the alpha-MSH-treated group was decreased significantly.

Insulin secretory function of the islets recovered in conditions of alpha-MSH treatment.

This study demonstrated that alpha-MSH protected pancreatic islet cells from PBMC-mediated cytotoxicity and preserved insulin secretory function.

This treatment may have the potential to improve graft survival in clinical islet transplantation.

[MeSH-major] Antibody-Dependent Cell Cytotoxicity. Islets of Langerhans / immunology. Leukocytes, Mononuclear / immunology. alpha-MSH / therapeutic use

[MeSH-minor] Animals. Apoptosis. Cell Survival. Coculture Techniques. Cytokines / biosynthesis. Cytokines / secretion. Nitric Oxide / biosynthesis. Rats. Rats, Inbred Lew

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(PMID = 17580198.001).

[ISSN] 0041-1345

[Journal-full-title] Transplantation proceedings

[ISO-abbreviation] Transplant. Proc.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Cytokines; 31C4KY9ESH / Nitric Oxide; 581-05-5 / alpha-MSH

   

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

[Title] Mechanism for Src activation by the CCK2 receptor: Patho-physiological functions of this receptor in pancreas.

AIM: To investigate in vivo, whether CCK2 receptors (CCK2R) regulate proteins known to play a crucial role in cell proliferation and cancer development and analyse in vitro the molecular mechanisms that lead to Src activation; in particular, to identify the domains within the CCK2R sequence that are implicated in this activation.

We used pancreatic tissues derived from wild type or Elas-CCK2 mice that expressed the CCK2R in pancreatic acini, displayed an increased pancreatic growth and developed preneoplastic lesions.

The pancreatic tumor cell line AR4-2J expressing the endogenous CCK2R or COS-7 cells transiently transfected with wild type or mutant CCK2R were used as in vitro models to study the mechanism of Src activation.

Src activation was measured by in vitro kinase assays, ERK activation by western blot using anti-phospho-ERK antibodies and the involvement of Src in gastrin-induced cell proliferation by MTT test.

RESULTS: We showed in vivo that the targeted CCK2R expression in the pancreas of Elas-CCK2 mice, led to the activation of Src and the ERK pathway.

Src was activated upstream of the ERK pathway by the CCK2R in pancreatic tumoral cells and contributed to the proliferative effects mediated by this receptor.

CONCLUSION: Deregulation of the Src/ERK pathway by the CCK2R might represent an early step that contributes to cell proliferation, formation of preneoplastic lesions and pancreatic tumor development.

[MeSH-major] Pancreas / metabolism. Pancreatic Neoplasms / physiopathology. Precancerous Conditions / physiopathology. Receptor, Cholecystokinin B / physiology. src-Family Kinases / metabolism

[MeSH-minor] Amino Acid Motifs / physiology. Animals. Cell Line. Cell Proliferation. Cell Transformation, Neoplastic. Enzyme Activation / physiology. Extracellular Signal-Regulated MAP Kinases / metabolism. GTP-Binding Protein alpha Subunits, Gq-G11 / physiology. Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Mice. Mice, Transgenic. Protein Structure, Tertiary / physiology. Signal Transduction / physiology

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[Cites] J Biol Chem. 2000 Jun 9;275(23):17321-7 [10748160.001]

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(PMID = 16874861.001).

[ISSN] 1007-9327

[Journal-full-title] World journal of gastroenterology

[ISO-abbreviation] World J. Gastroenterol.

[Language] eng

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

[Publication-country] China

[Chemical-registry-number] 0 / Receptor, Cholecystokinin B; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11

[Other-IDs] NLM/ PMC4125636

   

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

[Title] RP101 improves the efficacy of chemotherapy in pancreas carcinoma cell lines and pancreatic cancer patients.

RP101 [(E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU)], which supports apoptosis and prevents the acquisition of chemoresistance, was tested in cultured human pancreatic tumor cells.

Furthermore, RP101 activated antitumor immunity as demonstrated by enhanced cytolytic activity of NK-92 natural killer cells.

This was concomitant with an enhanced expression of lymphotoxins alpha and beta, natural killer cell transcript 4, tumor necrosis factor LIGHT/TNFSF-14, and intercellular adhesion molecule-1 in pancreas carcinoma cells.

These results encouraged us to investigate the effect of RP101 in pancreas cancer patients.

In a first pilot study, 13 patients in stage III and VI of the disease were treated with gemcitabine +cisplatin+RP101.

A second study with 21 patients in similar stages of disease, treated with RP101+gemcitabine alone, confirmed the results of the pilot study.

Considering both studies, the tumor control was 94%.

[MeSH-major] Bromodeoxyuridine / analogs & derivatives. Pancreatic Neoplasms / drug therapy

[MeSH-minor] Adult. Aged. Cell Line, Tumor. Cisplatin / pharmacology. DNA-(Apurinic or Apyrimidinic Site) Lyase / genetics. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacokinetics. Deoxycytidine / pharmacology. Humans. Killer Cells, Natural / immunology. Middle Aged

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(PMID = 17001178.001).

[ISSN] 0959-4973

[Journal-full-title] Anti-cancer drugs

[ISO-abbreviation] Anticancer Drugs

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0W860991D6 / Deoxycytidine; 2M3055079H / brivudine; B76N6SBZ8R / gemcitabine; EC 4.2.99.18 / APEX1 protein, human; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase; G34N38R2N1 / Bromodeoxyuridine; Q20Q21Q62J / Cisplatin

   

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

[Title] First case of primary phyllodes tumor of the pancreas: case report and findings of immunohistochemical and ultrastructural studies.

A 37-year-old Japanese man with a solid and cystic pancreatic mass was referred to our hospital.

Computed tomography revealed a well-demarcated solid and cystic mass measuring approximately 3.0 cm in diameter in the pancreatic body.

The patient underwent middle segment pancreatectomy, and the retrieved tumor specimen was found to be a well-demarcated solid and cystic lesion measuring 3.0 x 3.0 cm.

On histological examination, the cyst walls were found to be lined with a monolayer of non-atypical tall columnar epithelial cells.

The solid areas surrounded the cystic ones and showed storiform proliferation of spindle cells that contained round, oval, or elongated nuclei and were present among abundant collagen fibers.

The solid areas sent phylloid projections into the cystic spaces and the main pancreatic duct.

The spindle cells were found to be diffusely positive for alpha-smooth muscle actin, desmin, and h-caldesmon on immunohistochemical analysis.

Electron microscopy revealed that these cells possessed well-developed myofilaments with dense bodies, pinocytic vesicles, and basal lumina.

After the operation (4 years), tumor recurrence has not occurred.

The main differential diagnoses of spindle cell tumors are leiomyomas, leiomyosarcomas, inflammatory myofibroblastic tumors, solitary fibrous tumors, extra-gastrointestinal stromal tumors, and schwannomas.

However, the histological findings in the present case differed from those of these tumors.

The present lesion is the first reported case of a primary pancreatic phyllodes tumor.

[MeSH-major] Pancreatic Neoplasms / pathology. Phyllodes Tumor / pathology

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[Cites] Virchows Arch. 2006 May;448(5):552-60 [16538442.001]

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(PMID = 20182743.001).

[ISSN] 1432-2307

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

[ISO-abbreviation] Virchows Arch.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Actins; 0 / Calmodulin-Binding Proteins; 0 / Desmin

   

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

[Title] Biliary pancreatitis-associated ascitic fluid activates the production of tumor necrosis factor-alpha in acinar cells.

OBJECTIVE: Acute pancreatitis is associated with increased cytokine release from different cell sources.

We have investigated the ability of acinar cells, in comparison with inflammatory peripheral blood cells, to produce tumor necrosis factor (TNF)-alpha in response to pancreatitis-associated ascitic fluid (PAAF).

INTERVENTIONS: Flow cytometry using phycoerythrin-labeled monoclonal anti-TNF-alpha antiserum.

MEASUREMENTS AND MAIN RESULTS: PAAF (20%, v:v) obtained from rats with acute pancreatitis induced by bile-pancreatic duct obstruction significantly increased TNF-alpha production in acinar cells, as measured by flow cytometry using phycoerythrin-labeled monoclonal anti-TNF-alpha antiserum.

Neither heating of PAAF nor the addition of soybean trypsin inhibitor or neutralizing amounts of anti-TNF-alpha monoclonal antiserum reduced the acinar cell TNF-alpha production.

Monocytes and lymphocytes did not produce TNF-alpha in response to PAAF.

Likewise, the typical monocyte and lymphocyte stimulating factors-lipopolysaccharide (10 microg/microL) and phorbol 12-myristate 13-acetate (250 ng/mL) plus ionomycin (1 microg/mL), respectively-were not able to produce TNF-alpha in acinar cells.

By comparison of the two acinar cell populations differentiated by flow cytometry, R2 cells (with higher forward scatter values) showed a greater ability to produce TNF-alpha in response to PAAF than R1 cells.

Acinar cell nuclear factor-kappaB was activated, but TNF-alpha production was not totally inhibited in presence of N-acetyl cysteine (30, 100 mM).

CONCLUSIONS: The production of TNF-alpha from different cell sources is selectively activated.

PAAF may be involved in the pathophysiology of acute pancreatitis by TNF-alpha production in acinar cells through mechanisms partially mediated by nuclear factor-kappaB activation.

PAAF components, such as TNF-alpha or trypsin, are not responsible for acinar cell activation.

TNF-alpha was induced by heat-resistant PAAF factors, displaying acinar cells with higher forward scatter (R2) a greater ability to increase the TNF-alpha production than R1 cells.

[MeSH-major] Ascitic Fluid / immunology. Cholestasis, Extrahepatic / immunology. Pancreas, Exocrine / immunology. Tumor Necrosis Factor-alpha / metabolism

[MeSH-minor] Acute Disease. Animals. Cytokines / metabolism. Disease Models, Animal. Endothelial Cells / immunology. Flow Cytometry. Lymphocytes / immunology. Male. Monocytes / immunology. NF-kappa B / metabolism. Rats. Rats, Wistar. Systemic Inflammatory Response Syndrome / immunology

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[CommentIn] Crit Care Med. 2005 Jan;33(1):248 [15644687.001]

(PMID = 15644661.001).

[ISSN] 0090-3493

[Journal-full-title] Critical care medicine

[ISO-abbreviation] Crit. Care Med.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Cytokines; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha

   

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

[Title] Is serous cystadenoma of the pancreas a model of clear-cell-associated angiogenesis and tumorigenesis?

BACKGROUND: Similar to the other von Hippel-Lindau (VHL)-related tumors such as renal cell carcinomas and capillary hemangioblastomas, serous cystadenomas (SCAs) of the pancreas are also characterized by clear cells.

Over the years, we have also noticed that the tumor epithelium shows a prominent capillary network.

METHODS: Eighteen cases of SCA were reviewed histologically, and immunohistochemical analysis was performed for CD31 and vascular endothelial growth factor (VEGF) as well as the molecules implicated in clear-cell tumorigenesis: GLUT-1, hypoxia-inducible factor-1 (HIF-1alpha), and carbonic anhydrase IX (CA IX).

RESULTS: There was an extensively rich capillary network that appears almost intraepithelially in all cases of SCA, which was confirmed by CD31 stain that showed, on average, 26 capillaries per every 100 epithelial cells.

Among the clear-cell tumorigenesis markers, CA IX was detected in all cases, GLUT-1 and HIF-1alpha in most cases.

CONCLUSION: As in other VHL-related clear-cell tumors, there is a prominent capillary network immediately adjacent to the epithelium of SCA, confirming that the clear-cell- angiogenesis association is also valid for this tumor type.

Molecules implicated in clear-cell tumorigenesis are also consistently expressed in SCA.

More importantly, SCA may also serve as a model of clear-cell-associated angiogenesis and tumorigenesis, and the information gained from this tumor type may also be applicable to other clear-cell tumors.

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[Copyright] Copyright 2008 S. Karger AG, Basel and IAP.

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(PMID = 19077470.001).

[ISSN] 1424-3911

[Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]

[ISO-abbreviation] Pancreatology

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P20 CA101936; United States / NCI NIH HHS / CA / CA101936

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

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Antigens, CD31; 0 / Glucose Transporter Type 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A

[Other-IDs] NLM/ PMC2835376

   

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

[Title] Overexpression of interleukin-1beta in the murine pancreas results in chronic pancreatitis.

BACKGROUND & AIMS: Chronic pancreatitis is a significant cause of morbidity and a known risk factor for pancreatic adenocarcinoma.

Interleukin-1beta is a proinflammatory cytokine involved in pancreatic inflammation.

We sought to determine whether targeted overexpression of interleukin-1beta in the pancreas could elicit localized inflammatory responses and chronic pancreatitis.

RESULTS: Three transgenic lines were generated, and in each line the pancreas was atrophic and occasionally showed dilation of pancreatic and biliary ducts secondary to proximal fibrotic stenosis.

Pancreatic histology showed typical features of chronic pancreatitis.

There was evidence for increased acinar proliferation and apoptosis, along with prominent expression of tumor necrosis factor-alpha; chemokine (C-X-C motif) ligand 1; stromal cell-derived factor 1; transforming growth factor-beta1; matrix metallopeptidase 2, 7, and 9; inhibitor of metalloproteinase 1; and cyclooxygenase 2.

Older mice displayed acinar-ductal metaplasia but did not develop mouse pancreatic intraepithelial neoplasia or tumors.

CONCLUSIONS: Overexpression of interleukin-1beta in the murine pancreas induces chronic pancreatitis.

Elastase sshIL-1beta mice consistently develop severe chronic pancreatitis and constitute a promising model for studying chronic pancreatitis and its relationship with pancreatic adenocarcinoma.

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(PMID = 18789941.001).

[ISSN] 1528-0012

[Journal-full-title] Gastroenterology

[ISO-abbreviation] Gastroenterology

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA093405; United States / NCI NIH HHS / CA / R01 CA120979-03; United States / NCI NIH HHS / CA / U54 CA126513; United States / NCI NIH HHS / CA / R01 CA093405-07A1; United States / NCI NIH HHS / CA / CA093405-07A1; United States / NCI NIH HHS / CA / CA120979-03; United States / NCI NIH HHS / CA / U54 CA126513-03; United States / NCI NIH HHS / CA / CA126513-03; United States / NCI NIH HHS / CA / R01 CA120979

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

[Publication-country] United States

[Chemical-registry-number] 0 / Interleukin-1beta; EC 3.4.21.36 / Pancreatic Elastase

[Other-IDs] NLM/ NIHMS73579; NLM/ PMC2707078

   

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

[Title] Immunohistochemical similarities between pancreatic mucinous cystic tumor and ovarian mucinous cystic tumor.

OBJECTIVE: Pancreatic mucinous cystic tumor (MCT(P)) and ovarian mucinous cystic tumor (MCT(O)) show common features.

However, there are few studies showing a comparison of both types of tumor.

We immunohistochemically studied both types of tumor to clarify their characteristics.

The tumors were immunohistochemically examined using antibodies against female sex hormone receptors (estrogen receptor, progesterone receptor, and alpha-inhibin), pancreatobiliary tissue markers (carbohydrate antigen 19-9 and DUPAN2) and cell cycle regulators (p27kip1 and phosphorylated retinoblastoma).

Samples from 7 female patients with invasive pancreatic ductal carcinoma (DC), 8 female patients with normal pancreatic tissue, and 10 patients with normal ovarian tissue were also examined.

RESULTS: In the tumor epithelial cells, the expressions of DUPAN2 and p27/kip1 were similar between MCT(P) (38% and 88%, respectively) and MCT(O) (14% and 76%, respectively), but significantly different between both tumors and DC (100% and 0%).

In the stromal cells, the expressions of estrogen receptor, progesterone receptor, alpha-inhibin, and p27/kip1 were similar between MCT(P) (63%, 75%, 50%, and 63%, respectively) and MCT(O) (57%, 71%, 81%, and 57%, respectively), but significantly different between both tumors and DC (0%, 0%, 0%, and 0%, respectively).

A frequent p27/kip1 expression level was associated with nonaggressive progression of both tumors.

[MeSH-major] Carcinoma, Pancreatic Ductal / chemistry. Cystadenocarcinoma, Mucinous / chemistry. Cystadenoma, Mucinous / chemistry. Immunohistochemistry. Ovarian Neoplasms / chemistry. Pancreatic Neoplasms / chemistry

[MeSH-minor] Adult. Aged. Cyclin-Dependent Kinase Inhibitor p27 / analysis. Epithelial Cells / chemistry. Female. Humans. Inhibins / analysis. Middle Aged. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis

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(PMID = 18192871.001).

[ISSN] 1536-4828

[Journal-full-title] Pancreas

[ISO-abbreviation] Pancreas

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / inhibin-alpha subunit; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 57285-09-3 / Inhibins

   

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

[Title] Solid pseudopapillary tumor of the pancreas in children: report of a case and review of the literature.

Solid pseudopapillary tumor (SPT) of the pancreas is an infrequent neoplasm of low malignant potential, first described by Frantz in 1933 and representing less than 3% of all exocrine tumors.

A 15-year-old girl with a 12 × 14 × 10 cm solid mass growing from the tail and the body of the pancreas, involving spleen, left adrenal gland and kidney, stomach and some bowel loops, was referred for surgical treatment.

Histopathological examination revealed that the tumor was a 14-cm well-circumscribed solid mass, with pseudopapillary cell architecture, showing strong cellular immunoreactivity for alpha-1 antitrypsin, vimentin, neurone-specific enolase, progesterone receptors and in part to CD10 and CAM 5.2, but not to sinaptofisin and chromogranin.

A 24-month post-surgical follow-up after successful surgical resection showed no evidence of recurrent disease.

High survival rates can be achieved in most cases, warranting aggressive treatments even in metastatic disease.

[MeSH-major] Pancreatic Neoplasms

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(PMID = 20845104.001).

[ISSN] 2038-131X

[Journal-full-title] Updates in surgery

[ISO-abbreviation] Updates Surg

[Language] eng

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

[Publication-country] Italy

   

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

[Title] Effect of portal vein occlusion on the pancreas: an experimental model.

BACKGROUND: The effects of portal vein occlusion on the pancreas are not clearly understood.

Therefore, we studied histomorphological changes induced in the rat pancreas by various periods of portal vein occlusion.

The pancreas was removed immediately after sham laparotomy in Group I and immediately after clamp release in Groups II-IV.

Pancreatic tissue specimens were subjected to histochemical analysis for cell typing and diagnosis, immunohistochemical analysis for identification of the inflammatory markers tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), endothelial nitric oxide synthase (eNOS), and inducible NOS (iNOS), and TUNEL analysis was carried out for identification of apoptotic cells.

RESULTS: Histochemistry revealed signs of inflammation in pancreatic tissue from rats subjected to portal vein occlusion.

Immunohistochemistry revealed that the expression of proinflammatory cytokines TNF-alpha and IL-1beta and the oxidative damage indicator iNOS in rat pancreatic tissue increased progressively with the duration of portal vein occlusion.

CONCLUSION: We conclude that portal vein occlusion triggers an inflammatory response in the pancreas that worsens the longer the occlusion lasts.

[MeSH-major] Pancreas / pathology. Pancreatitis / physiopathology. Portal Vein / pathology

[MeSH-minor] Animals. Apoptosis. Constriction, Pathologic / physiopathology. Female. Immunohistochemistry. In Situ Nick-End Labeling. Interleukin-1beta / analysis. Nitric Oxide Synthase Type II / analysis. Nitric Oxide Synthase Type III / analysis. Rats. Rats, Wistar. Tumor Necrosis Factor-alpha / analysis

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(PMID = 16736328.001).

[ISSN] 0364-2313

[Journal-full-title] World journal of surgery

[ISO-abbreviation] World J Surg

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nitric Oxide Synthase Type III

   

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

[Title] Roles of tumor necrosis factor alpha (TNF-alpha) and the p55 TNF receptor in CD1d induction and coxsackievirus B3-induced myocarditis.

Giving C57BL/6 mice 10(4) PFU of coxsackievirus B3 (H3 variant) fails to induce myocarditis, but increasing the initial virus inoculum to 10(5) or 10(6) PFU causes significant cardiac disease.

Tumor necrosis factor alpha (TNF-alpha) concentrations in the heart were increased in all infected mice, but cytokine levels were highest in mice given the larger virus inocula.

TNF-alpha(-/-) and p55 TNF receptor-negative (TNFR(-/-)) mice developed minimal myocarditis compared to B6;129 or C57BL/6 control mice. p75 TNFR(-/-) mice were as disease susceptible as C57BL/6 animals.

No significant differences in virus titers in heart or pancreas were observed between the groups, but C57BL/6 and p75 TNFR(-/-) animals showed 10-fold more inflammatory cells in the heart than p55 TNFR(-/-) mice, and the cell population was comprised of high concentrations of CD4(+) gamma interferon-positive and Vgamma4(+) cells.

Cardiac endothelial cells isolated from C57BL/6 and p75 TNFR(-/-) mice upregulate CD1d, the molecule recognized by Vgamma4(+) cells, but infection of TNF(-/-) or p55 TNFR(-/-) endothelial cells failed to upregulate CD1d.

Infection of C57BL/6 endothelial cells with a nonmyocarditic coxsackievirus B3 variant, H310A1, which is a poor inducer of TNF-alpha, failed to elicit CD1d expression, but TNF-alpha treatment of H310A1-infected endothelial cells increased CD1d levels to those seen in H3-infected cells.

TNF-alpha treatment of uninfected endothelial cells had only a modest effect on CD1d expression, suggesting that optimal CD1d upregulation requires both infection and TNF-alpha signaling.

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(PMID = 15708985.001).

[ISSN] 0022-538X

[Journal-full-title] Journal of virology

[ISO-abbreviation] J. Virol.

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / P01 AI045666; United States / NHLBI NIH HHS / HL / R01 HL058583; United States / NHLBI NIH HHS / HL / HL58583; United States / NIAID NIH HHS / AI / P01 AI45666

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD1; 0 / Antigens, CD1d; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Tumor Necrosis Factor-alpha

[Other-IDs] NLM/ PMC548425

   

[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] Pancreatic acinar cell carcinoma with excessive alpha-fetoprotein expression.

We report a case of acinar cell carcinoma of the pancreas associated with excessively elevated levels of serum alpha-fetoprotein (>32,000 ng/ml).

Abdominal computed tomography scan revealed a large pancreatic mass with infiltration of the splenic artery.

This regimen was associated with clinical improvement and dramatic decreases in both tumor size and serum alpha-fetoprotein.

[MeSH-major] Carcinoma, Acinar Cell / metabolism. Pancreatic Neoplasms / metabolism. alpha-Fetoproteins / metabolism

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[Copyright] 2007 S. Karger AG, Basel and IAP

(PMID = 17703084.001).

[ISSN] 1424-3911

[Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]

[ISO-abbreviation] Pancreatology

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / alpha-Fetoproteins; 0W860991D6 / Deoxycytidine; 50SG953SK6 / Mitomycin; B76N6SBZ8R / gemcitabine

   

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

[Title] Acinar cell carcinoma of the pancreas metastatic to the ovary: a report of 4 cases.

We report 4 cases of acinar cell carcinoma of the pancreas, 3 presenting as metastases in the ovary, the first report of this circumstance, which may pose a broad differential diagnosis and caused significant diagnostic difficulty in all the cases.

In 3 cases, the ovarian tumors were detected before the pancreatic tumor; in 1 case, a large abdominal mass and ovarian tumors were discovered synchronously.

The ovarian tumors were large, solid, white-tan on gross examination, and bilateral in 3 cases; the single case involving only 1 ovary had 2 discrete masses of tumor.

Two cases had a predominant acinar growth pattern of cells with brightly eosinophilic, granular cytoplasm.

In 2 cases, the pattern was predominantly solid-cribriform with areas of comedolike necrosis, and the cells had pale eosinophilic, finely granular cytoplasm.

The main differential diagnostic consideration was well-differentiated neuroendocrine neoplasm (carcinoid tumor); positive immunostaining with antibodies against chymotrypsin and trypsin and negative immunostaining with antibodies against synaptophysin and chromogranin helped exclude this diagnosis.

We observed focal alpha-inhibin immunostaining in 2 cases, which may represent a potential diagnostic pitfall, as a Sertoli cell tumor or unusual granulosa cell tumor may also enter the differential diagnosis.

Inclusion of antibodies against the pancreatic enzymes chymotrypsin and trypsin in the immunohistochemical panel is critical in establishing the correct diagnosis and should be considered when evaluating ovarian tumors with architectural (mainly acinar) and cytologic (granular eosinophilic cytoplasm) characteristics that should bring a metastatic acinar cell carcinoma into consideration.

[MeSH-major] Carcinoma, Acinar Cell / secondary. Ovarian Neoplasms / secondary. Pancreatic Neoplasms / pathology

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

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(PMID = 18724247.001).

[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

   

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

[Title] [Effects of Chaiqin Chengqi Decoction on activation of nuclear factor-kappaB in pancreas of rats with acute necrotizing pancreatitis].

Blood sample was collected from abdominal vein for examination and the pancreatic tissue samples were taken for making pathology section 6 hours later.

The pancreatic tissue (HE staining) was observed by light microscope.

The content of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) was detected with the method of enzyme-linked immunosorbent assay, and the activation of nuclear factor-kappaB (NF-kappaB) in pancreas was detected by immunohistochemical method.

RESULTS: Compared with the SO group, there was dramatic increase in the white blood cell (WBC) counts and AMY level in the ANP group (P<0.05, P<0.01).

The integral optical density of NF-kappaB p65 positive cells of pancreas in CQCQD-treated group was lower than that in the ANP group (P<0.05).

CONCLUSION: CQCQD can reduce the content of serum TNF-alpha and IL-6, depress the activation of NF-kappaB, and lessen the pancreatic lesions.

[MeSH-major] Drugs, Chinese Herbal / therapeutic use. NF-kappa B / metabolism. Pancreas / metabolism. Pancreatitis, Acute Necrotizing / drug therapy. Phytotherapy

[MeSH-minor] Animals. Female. Interleukin-6 / blood. Male. Random Allocation. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / blood

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(PMID = 18241655.001).

[ISSN] 1672-1977

[Journal-full-title] Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine

[ISO-abbreviation] Zhong Xi Yi Jie He Xue Bao

[Language] chi

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

[Publication-country] China

[Chemical-registry-number] 0 / Chai Qin Cheng Qi decoction; 0 / Drugs, Chinese Herbal; 0 / Interleukin-6; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha

   

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

[Title] Pdx-1 modulates histone H4 acetylation and insulin gene expression in terminally differentiated alpha-TC-1 cells.

OBJECTIVES: Islet-associated transcription factors play a critical role in regulating pancreatic endocrine cell differentiation and islet hormone gene expression.

Both alpha- and beta-cells differentiate from a common endocrine precursor cell.

Therefore, it is important to reveal the differential gene expression profiles between alpha- and beta-cells that can direct their terminal cell fates. alpha-TC-1 and beta-TC-1 are 2 terminally differentiated islet tumor cell lines derived from islets transformed by promoter-specific driven SV40 T antigen overexpression.

In this study, we demonstrated that Pdx-1 is a potent transcriptional regulator of endogenous insulin gene expression in alpha-TC-1 cells.

RESULTS: Differential transcription factor expression profiles of alpha-TC-1 and beta-TC-1 cells revealed that INSM-1 and Pdx-1 transcription factors were expressed exclusively in beta-TC-1 cells.

Overexpression of Ad-Pdx-1 in alpha-TC-1 cells induced insulin gene expression.

Chromatin immunoprecipitation assays in Ad-Pdx-1 alpha-TC-1 cells demonstrated Pdx-1 occupancy and the hyperacetylation of histone H4 in the insulin promoter region.

CONCLUSIONS: Collectively, these experiments revealed that Pdx-1 is a potent transcriptional regulator that is capable of modulating histone H4 acetylation and activates the insulin gene in a terminally differentiated glucagonoma cell line.

[MeSH-major] Glucagon-Secreting Cells / physiology. Histones / metabolism. Homeodomain Proteins / metabolism. Insulin / genetics. Insulin-Secreting Cells / physiology. Trans-Activators / metabolism

[MeSH-minor] Acetylation. Animals. Cell Differentiation. Cell Line, Tumor. Gene Expression / physiology. Mice. Mice, Transgenic. Pancreatic Neoplasms. Polymerase Chain Reaction. Promoter Regions, Genetic / physiology. Transcription Factors / genetics. Transcription, Genetic / physiology

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(PMID = 17312465.001).

[ISSN] 1536-4828

[Journal-full-title] Pancreas

[ISO-abbreviation] Pancreas

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / DK061436

[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 / Histones; 0 / Homeodomain Proteins; 0 / Insulin; 0 / Trans-Activators; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein

   

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

[Title] Successful en bloc resection of primary hepatocellular carcinoma directly invading the stomach and pancreas.

Multivisceral surgical resection for cure was successfully performed in a 70-year-old man suffering from a primary hepatocellular carcinoma (HCC) associated with direct invasion to the stomach and pancreas.

The patient presented with gastric outlet obstruction, upper abdominal pain and a history of chronic liver disease due to hepatitis B virus (HBV) infection.

Upper gastrointestinal (GI) endoscopy revealed an infiltrating tumor protruding through the gastric wall and obliterating the lumen.

Computer tomograghy (CT) and magnetic resonance imaging (MRI) scan demonstrated a 15-cm tumor in the left lateral segment of the liver with invasion to the stomach and pancreas.

Alpha-foetoprotein (AFP) levels and liver function tests were normal.

Pathology revealed a poorly differentiated, giant cell HCC involving the stomach and pancreas.

Disease-free margins of resection were achieved.

[MeSH-major] Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology. Liver Neoplasms / surgery. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery. Stomach Neoplasms / surgery

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(PMID = 19266609.001).

[ISSN] 2219-2840

[Journal-full-title] World journal of gastroenterology

[ISO-abbreviation] World J. Gastroenterol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] China

[Other-IDs] NLM/ PMC2655177

   

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

[Title] Solid-papillary tumors of the pancreas: histopathology.

A solid-pseudopapillary tumor is an uncommon and "enigmatic" pancreatic neoplasm, and the term encompasses the two most conspicuous histological features: solid and pseudopapillary areas.

Histologically, solid-pseudopapillary tumors are generally characterized by solid areas alternating with a pseudopapillary pattern, and cystic spaces which are the results of degenerative changes occurring in the solid neoplasm.

Its immunohistochemical pattern is very distinctive and neoplastic cells are consistently vimentin-, CD10- and CD56-positive.

Some cases express focal positivity for alpha-1-antitrypsin, alpha-1-antichymotrypsin, neuron-specific enolase and synaptophysin.

Endocrine and pancreatic enzyme markers are absent; the origin of solid-pseudopapillary tumors has not yet been clarified.

Many investigators favor the theory that solid-pseudopapillary tumors originate from multipotent primordial cells while others suggest an extra-pancreatic origin from genital ridge angle-related cells.

Solid-pseudopapillary tumors appear as a low malignancy tumor and only a small number of cases recur or develop metastases after resection.

[MeSH-major] Carcinoma, Papillary / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology

[MeSH-minor] Antigens, CD56 / analysis. Cell Proliferation. Humans. Immunohistochemistry. Neoplasm Invasiveness. Neprilysin / analysis. Receptors, Progesterone / analysis. Vimentin / analysis

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(PMID = 16407635.001).

[ISSN] 1590-8577

[Journal-full-title] JOP : Journal of the pancreas

[ISO-abbreviation] JOP

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Antigens, CD56; 0 / Receptors, Progesterone; 0 / Vimentin; EC 3.4.24.11 / Neprilysin

   

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

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

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

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

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

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

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

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

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

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

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

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(PMID = 15539431.001).

[ISSN] 0888-8809

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

[ISO-abbreviation] Mol. Endocrinol.

[Language] eng

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

[Publication-country] United States

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

   

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

[Title] [Protective effect of shenfu injection against ischemia-reperfusion injury due to pancreas transplantation in rats].

OBJECTIVE: To investigate the protective effect of Shenfu Injection against ischemia-reperfusion (I/R) injury due to pancreas transplantation in rats, and explore its possible mechanism.

Except I/R group, the rats in the other groups were intravenous injected with Shenfu Injection (SF,10 mg/kg), Hongshen Injection (HS, 9 mg/kg) and Fuzi Injection (FZ 1 mg/kg) respectively at the day and 30 minutes before pancreas transplantation performed in the SF group, HS group and FZ group, respectively.

The blood glucose was detected before and after reperfusion, and 2 hours later after reperfusion, the contents of serum nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha), the concentrations of malondialdehyde (MDA) , superoxide dismutase (SOD) , and myeloperoxidase (MPO) in the transplanted pancreas tissues were detected.

The cell apoptosis of the transplanted pancreas tissue was determined by TUNEL, and the bcl-2 and Bax protein expression was determined by Western blot.

RESULTS: After reperfusion, the levels of blood glucose and TNF-alpha decreased and the concentration of NO increased in the SF group, HS group and FZ group, compared with those in the I/R group.

CONCLUSION: Shenfu Injection can protect L/R injury due to pancreas transplantation in rats, the possible mechanism may be related to promoting activity of SOD, increasing synthesis of endogenous NO, decreasing the excretion of TNF-alpha, alleviating conglutination and aggregation of polymorphonuclear neutrophils (PMNs) in pancreas, as well as up-regulating Bcl-2 gene expression and down-regulating the Bax gene expression.

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(PMID = 17569364.001).

[ISSN] 1003-5370

[Journal-full-title] Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine

[ISO-abbreviation] Zhongguo Zhong Xi Yi Jie He Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Protective Agents; 0 / Shen-Fu; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide; 4Y8F71G49Q / Malondialdehyde; EC 1.15.1.1 / Superoxide Dismutase

   

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

[Title] Analysis of E-, N-cadherin, alpha-, beta-, and gamma-catenin expression in human pancreatic carcinoma cell lines.

OBJECTIVES: Cadherins are cell surface glycoproteins that mediate Ca2+-dependent, homophilic cell-cell adhesion.

The classic cadherins interact with either beta-catenin or gamma-catenin, which is bound to alpha-catenin that links the complex to the actin cytoskeleton.

The aim of this study was to analyze the expressions of E- and N-cadherins and catenins in human pancreatic cancer cell lines.

METHODS: We examined the expression of cadherins and catenins in 7 human pancreatic cancer cells by RT-PCR, Western blotting, and immunocytochemistry.

RESULTS: E-cadherin was expressed in all cell lines except for MIAPaCa-2, whereas N-cadherin was expressed in Capan-2, CFPAC-1, BxPC-3, and PANC-1.

The alpha-, beta-, and gamma-catenins were expressed and cadherins/beta-catenin interactions were detected in all cadherin-expressing cells.

CONCLUSION: The decreased or loss of cadherins and catenins expression could be involved in the tumor progression and metastasis, although these events may occur in in vivo conditions by interaction between cancer cells and extracellular matrices.

[MeSH-major] Adenocarcinoma / physiopathology. Cadherins / genetics. Catenins / genetics. Pancreatic Neoplasms / physiopathology

[MeSH-minor] Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Humans. RNA, Messenger / analysis. alpha Catenin / genetics. alpha Catenin / metabolism. beta Catenin / genetics. beta Catenin / metabolism. gamma Catenin / genetics. gamma Catenin / metabolism

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(PMID = 15714139.001).

[ISSN] 1536-4828

[Journal-full-title] Pancreas

[ISO-abbreviation] Pancreas

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Cadherins; 0 / Catenins; 0 / RNA, Messenger; 0 / alpha Catenin; 0 / beta Catenin; 0 / gamma Catenin

   

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

[Title] Elevation of tumor necrosis factor-alpha, interleukin-1beta and interleukin-6 levels in aortic intima of Chinese Guizhou minipigs with streptozotocin-induced diabetes.

BACKGROUND: Large animal models with toxin-mediated pancreatic damage have been used extensively in researches with respect to diabetes mellitus and cardiovascular diabetic complications.

The present study aimed to establish Chinese Guizhou minipig models with streptozotocin (STZ)-induced diabetes and characterize the animal models by analyzing inflammatory cytokine levels in aortic wall, such as tumor necrosis factor (TNF)-alpha, interleukin-1beta (IL-1beta) and interleukin-6 (IL-6).

Oral glucose tolerance test (OGTT) was performed before and one month after STZ administration and serum concentrations of alanine transaminase, asparagine transaminase, albumin, blood urea nitrogen, creatinine, lipids and white blood cell count were measured before and six months later.

Animals in both groups were euthanized after six months and pancreas was examined immunohistochemically for islet beta cells.

Aortic intima of diabetic minipigs and controls was analyzed for TNF-alpha level in tissue conditioned medium by Western blot.

TNF-alpha, IL-1beta and IL-6 mRNA levels in aortic intima were assayed by reverse transcription and polymerase chain reaction (RT-PCR).

The normal pancreas had many irregular sized islets and small clusters of islet beta cells, while in pancreas of diabetic minipigs islet beta cells almost disappeared.

Western blot demonstrated dramatically increased TNF-alpha level in aotic intima conditioned medium, and significant elevation of TNF-alpha, IL-1beta and IL-6 mRNA levels was revealed by RT-PCR.

Inflammatory cytokines (TNF-alpha, IL-1beta and IL-6) significantly elevated in aortic intima of diabetic minipigs.

[MeSH-major] Aorta / chemistry. Diabetes Mellitus, Experimental / immunology. Interleukin-1beta / blood. Interleukin-6 / blood. Tumor Necrosis Factor-alpha / blood

[MeSH-minor] Animals. Glucose Tolerance Test. Immunohistochemistry. Male. Pancreas / pathology. Streptozocin. Swine. Swine, Miniature

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(PMID = 17439741.001).

[ISSN] 0366-6999

[Journal-full-title] Chinese medical journal

[ISO-abbreviation] Chin. Med. J.

[Language] eng

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

[Publication-country] China

[Chemical-registry-number] 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 5W494URQ81 / Streptozocin

   

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

[Title] Anaplastic carcinoma of the pancreas with squamous features: report of a case and immunohistochemical study.

BACKGROUND: Anaplastic carcinomas of the pancreas are rare aggressive tumors with survival measurable in weeks.

Many terms have been applied used to describe these tumors, and anaplastic foci are identified in ductal adenocarcinomas and in ectopic pancreata, but are not the dominant pattern of growth.

We herein present our experience with a case of anaplastic carcinoma of the pancreas with squamous features in order that allowed us to delineate the clinicopathologic and immunohistochemical features of this rare entity.

CASE REPORT: According to imaging findings, the 77-year-old Japanese man was diagnosed as the malignant pancreatic tumor, and underwent a surgical resection.

Histopathologically, anaplastic tumor cells showed focal ductal and squamous features infiltrated into pancreatic parenchyma, extrapancreatic fatty tissue, and stomach.

The tumor cells showed strong reactivity for cytokeratin, alpha-SMA, vimentin, NSE, and S-100 protein.

Although immunoreactivity against p53 was negative, strong positive immunostaining for proliferating cell nuclear antigen and interleukin-1 receptor type I (IL-1RI) was observed in a the majority of tumor cells, while the alpha6 integrin subunit was predominantly strong expressed in the adenocarcinomatous lesion.

[MeSH-major] Biomarkers, Tumor / analysis. Carcinoma / diagnosis. Integrins / analysis. Pancreatic Neoplasms / diagnosis. Receptors, Interleukin-1 / analysis

[MeSH-minor] Aged. Carcinoma, Squamous Cell / diagnosis. Fatal Outcome. Humans. Immunohistochemistry. Male. Peritoneal Neoplasms / diagnosis. Peritoneal Neoplasms / secondary. Prognosis

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(PMID = 16258403.001).

[ISSN] 1234-1010

[Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research

[ISO-abbreviation] Med. Sci. Monit.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Poland

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Integrins; 0 / Receptors, Interleukin-1

   

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

[Title] Positive immunohistochemical staining of KIT in solid-pseudopapillary neoplasms of the pancreas is not associated with KIT/PDGFRA mutations.

Solid-pseudopapillary neoplasms of the pancreas are uncommon neoplasms of low malignant potential and of uncertain histogenesis.

A small percentage of patients develop metastatic disease and some succumb to disease.

The management of patients with metastatic disease or unresectable tumor, and patients who are just not good surgical candidates is problematic.

Successful treatment of metastatic and unresectable gastrointestinal stromal tumors with KIT kinase inhibitor, imatinib mesylate (Gleevec), makes it intriguing to look at the status of KIT in solid-pseudopapillary neoplasms of the pancreas.

Of the 50 (50%) solid-pseudopapillary neoplasms, 25 showed diffuse expression (in >50% neoplastic cells) of KIT and additional five (10%) cases showed focal staining (in 10-50% neoplastic cells).

Expression of KIT was not associated with tumor behavior and prognosis.

Experience in gastrointestinal stromal tumors and other tumors have shown that mutation-mediated activation of KIT or PDGFRA is a prerequisite for clinical response with imatinib mesylate.

Thus, lack of mutations in KIT or PDGFRA in solid-pseudopapillary neoplasms suggests that imatinib mesylate is less likely to be effective in the treatment for patients with metastatic disease or unresectable tumor, and patients who are just not good surgical candidates.

[MeSH-major] Carcinoma, Papillary / metabolism. Mutation. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins c-kit / metabolism. Receptor, Platelet-Derived Growth Factor alpha / metabolism

[MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / metabolism. Cell Count. Child. DNA Mutational Analysis. Female. Humans. Immunohistochemistry / methods. Male. Middle Aged. Survival Rate

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[Copyright] Published online 16 June 2006.

(PMID = 16778826.001).

[ISSN] 0893-3952

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

[ISO-abbreviation] Mod. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha

   

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

[Title] Nuclear expression of E-cadherin in solid pseudopapillary tumors of the pancreas.

CONTEXT: Solid pseudopapillary tumors of the pancreas are rare and have recently been shown to harbor mutations of the beta-catenin gene with resultant nuclear localization of beta-catenin protein to the nucleus.

OBJECTIVE: To explore the protein expression of E-cadherin in a series of solid pseudopapillary tumors of the pancreas.

PARTICIPANTS: Eighteen cases of solid pseudopapillary tumors of the pancreas.

Tissue cores from normal pancreas were used as controls and for orientation purposes.

MAIN OUTCOME MEASURES: The slides were stained with the following commercially available antibodies: CD10, CD56, vimentin, alpha-1-antitrypsin, alpha-1-antichymotrypsin, neuron-specific enolase, chromogranin, synaptophysin, beta-catenin and E-cadherin.

RESULTS: All the tumors were CD10, vimentin, alpha-1-antitrypsin and alpha-1-antichymotrypsin diffusely positive (50% or more of the tumor cells staining) and CD56 showed focal positivity in all cases with 5-10% of tumor cells displaying immunolabeling.

Similarly, E-cadherin protein was localized to the nucleus in all 18 cases, with loss of the characteristic membranous decoration of cells.

CONCLUSION: This study is the first demonstration of aberrant nuclear localization of E-cadherin protein in solid pseudopapillary tumors of the pancreas.

Whilst the exact mechanism is not know and nuclear E-cadherin is not related to tumor aggression, this staining pattern may be of diagnostic value in concert with beta-catenin staining.

[MeSH-major] Cadherins / analysis. Carcinoma, Papillary / chemistry. Cell Nucleus / chemistry. Pancreatic Neoplasms / chemistry

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(PMID = 17495358.001).

[ISSN] 1590-8577

[Journal-full-title] JOP : Journal of the pancreas

[ISO-abbreviation] JOP

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / Antigens, CD56; 0 / Cadherins; 0 / beta Catenin; EC 3.4.24.11 / Neprilysin

   

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

[Title] Cellular immune reaction in the pancreas is induced by constitutively active IkappaB kinase-2.

The aim of the present study was to analyse the consequences of ectopic IkappaB kinase-2 (IKK2) activation in the pancreas of mice.

METHODS: Transgenic mice were generated using an inducible genetic system (tet system) to conditionally overexpress a gain of function mutant of IKK2 (tetO-IKK2-EE) in the pancreas.

To achieve transgene expression in the pancreas, these animals were crossed with CMV-rtTA mice that are known to express the rtTA protein in the pancreas.

RESULTS: In these double transgenic animals, doxycycline treatment induced expression of IKK2-EE (IKK2(CA)) in pancreatic acinar cells resulting in moderate activation of the IkappaB kinase complex, as measured by the immune complex kinase assay, and up to 200-fold activation of the transgene expression cassette, as detected by luciferase assay.

IKK2(CA) expression in the pancreas had a mosaic appearance.

Increased mRNA levels of tumour necrosis factor alpha and RANTES were detected in pancreatic acinar cells.

However, only minor damage to pancreatic tissue was observed.

CONCLUSIONS: Our observations suggest that the role of IKK2 activation in pancreatic acini is to induce leucocyte infiltration, but at a moderate level of activation it is not sufficient to induce pancreatic damage in mice.

The IKK2(CA) induced infiltrations resemble those observed in autoimmune pancreatitis, indicating a role for IKK2/NF-kappaB in this disease.

IKK2(CA) in pancreatic acinar cells increases tissue damage of secretagogue induced experimental pancreatitis underlining the proinflammatory role of the IKK/NF-kappaB pathway in this disease.

[MeSH-major] I-kappa B Kinase / immunology. Immunity, Cellular / immunology. Pancreas / immunology

[MeSH-minor] Animals. B-Lymphocytes / immunology. Ceruletide / immunology. Chemokine CCL5 / analysis. Doxycycline / immunology. Enzyme Activation. Gene Expression / genetics. Immunohistochemistry / methods. Luciferases / metabolism. Macrophages / immunology. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Mice, Transgenic. NF-kappa B / genetics. NF-kappa B / metabolism. RNA, Messenger / analysis. Transgenes / immunology. Tumor Necrosis Factor-alpha / analysis

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(PMID = 16870717.001).

[ISSN] 0017-5749

[Journal-full-title] Gut

[ISO-abbreviation] Gut

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Chemokine CCL5; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 888Y08971B / Ceruletide; EC 1.13.12.- / Luciferases; EC 2.7.11.10 / I-kappa B Kinase; N12000U13O / Doxycycline

[Other-IDs] NLM/ PMC1856776