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[Title] p62 protein is expressed in pancreatic beta cells.

Furthermore, p62 has recently been detected as a component of intracytoplasmic protein aggregates (inclusion bodies), which are hallmarks of a variety of chronic degenerative disorders, such as Parkinson's disease and Alzheimer's disease, but also of steatohepatitis.

Here we report that p62 and insulin are co-expressed in a diffuse fashion in beta cells in normal human pancreas as well as in primary chronic pancreatitis and in normal pancreas from mouse and swine.

In contrast, p62 protein is absent from, or only focally and very weakly expressed in, insulinomas, glucagonomas or non-functioning pancreatic neuroendocrine tumours or carcinomas that express insulin or other pancreatic as well as extrapancreatic hormones.

Although the biological function of p62 in beta cells is unknown, the co-expression of p62 and insulin in non-neoplastic beta cells suggests that, in the beta cell, p62 may play a role in specific insulin-related signalling.

Since p62 may also be involved in pro-apototic signal transduction, the loss of p62 expression in neuroendocrine neoplasms of the pancreas may render the tumour cells less sensitive to pro-apototic signals.

Further research is necessary to elucidate the role of p62 in beta cell-specific signal transduction.

[MeSH-minor] Animals. Antibodies, Neoplasm / immunology. Carcinoma, Neuroendocrine / chemistry. Carcinoma, Neuroendocrine / genetics. Chronic Disease. Cross Reactions / immunology. Female. Gene Expression / genetics. Glucagonoma / chemistry. Glucagonoma / genetics. Humans. Immunohistochemistry / methods. Insulinoma / chemistry. Insulinoma / genetics. Male. Mice. Pancreatic Neoplasms / chemistry. Pancreatic Neoplasms / genetics. Swine

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[Copyright] Copyright 2005 Pathological Society of Great Britain and Ireland

(PMID = 15926199.001).

[ISSN] 0022-3417

[Journal-full-title] The Journal of pathology

[ISO-abbreviation] J. Pathol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antibodies, Neoplasm; 0 / SQSTM1 protein, human

   

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[Title] Added value of gastrin receptor scintigraphy in comparison to somatostatin receptor scintigraphy in patients with carcinoids and other neuroendocrine tumours.

As gastrin-binding CCK(2) receptors are also expressed on a variety of other neuroendocrine tumours (NET), we compared GRS to somatostatin receptor scintigraphy (SRS) in patients with NET.

SRS and GRS were performed within 21 days in a series of 60 consecutive patients with NET.

Of the 60 evaluable patients, 51 had carcinoid tumours, 3 gastrinomas, 2 glucagonomas, 1 insulinoma and 3 paragangliomas.

The overall tumour-detection rate was 73.7% for GRS and 82.1% for SRS.

Based on the number of tumour sites detected and the degree of uptake, GRS performed better than SRS in 13 patients (21.7%), equivalent images were obtained in 18 cases (30.0%) and SRS performed better in 24 (40.0%) cases.

In six of the SRS positive patients, 18 additional sites of tumour involvement could be detected.

Overall, GRS detected additional tumour sites in 20% of the patients.

GRS should be performed in selected patients as it may provide additional information in patients with NET with equivocal or absent somatostatin uptake.

[MeSH-major] Carcinoid Tumor / radionuclide imaging. Neuroendocrine Tumors / radionuclide imaging. Receptor, Cholecystokinin B / metabolism. Receptors, Somatostatin / metabolism

[MeSH-minor] Adult. Aged. Diagnosis, Differential. Female. Glucagonoma / radionuclide imaging. Humans. Indium Radioisotopes. Insulinoma / radionuclide imaging. Male. Middle Aged. Octreotide / analogs & derivatives. Paraganglioma / radionuclide imaging. Pentetic Acid / analogs & derivatives. Prognosis. Radiopharmaceuticals

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(PMID = 17158765.001).

[ISSN] 1351-0088

[Journal-full-title] Endocrine-related cancer

[ISO-abbreviation] Endocr. Relat. Cancer

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Indium Radioisotopes; 0 / Radiopharmaceuticals; 0 / Receptor, Cholecystokinin B; 0 / Receptors, Somatostatin; 142694-57-3 / SDZ 215-811; 7A314HQM0I / Pentetic Acid; RWM8CCW8GP / Octreotide

   

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[Title] [Significance of serum tumor markers monitoring metastases in carcinomas of unknown primary site].

BACKGROUND/AIM: Unknown primary tumors represent a heterogeneous group of malignancies that are indicative of ominous prognosis.

Cancer of unknown primary site (CUP) is defined as the lack of any detectable primary site after full evaluation, and accounts for approximately 3-5% of all newly diagnosed patients with malignancies.

The aim of this report was to present the prognostic and predictive value of 8 serum tumor markers in this group of patients.

On histological examination, all the patients were presented with metastatic tumors whose primary site (origin) could not be detected with noninvasive diagnostic techniques.

In all the cases we evaluated 8 serum tumor markers: alpha-fetoproteins (AFP), chronic gonadotrophin beta submit, human (beta-HCG), neuron specific enolase (NSE), marker of malignant ovarian tumors (CA 125), prostate-specific antigene (PSA), marker of malignant brest tumor (CA 15-3), marker of malignant pancreas tumor and gastrointestinal tumor (Ca 19-9), carcinoembryonic antigen (CEA) at the time of diagnosis.

The patients responding to chemotherapy with complete response (CR), partial response (PR) or stable disease (SD) had the markers determined after three-month periods until the time of relapse or progression.

Average tumor marker values before and after the chemotherapy were significantly lower for NSE and CA 125.

CONCLUSION: Increased values of serum tumor markers are very often in CUP.

The tumors show nonspecific overexpression of tumor markers.

However, a routine evaluation of commonly used serum tumor markers has not been proven of any prognostic and predictive assistance.

[MeSH-major] Adenocarcinoma / secondary. Biomarkers, Tumor / blood. Carcinoma / secondary. Carcinoma, Squamous Cell / secondary. Neoplasms, Unknown Primary / pathology

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(PMID = 20954411.001).

[ISSN] 0042-8450

[Journal-full-title] Vojnosanitetski pregled

[ISO-abbreviation] Vojnosanit Pregl

[Language] srp

[Publication-type] English Abstract; Journal Article

[Publication-country] Serbia

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

   

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[Title] Inflammation, genetic polymorphisms in proinflammatory genes TNF-A, RANTES, and CCR5, and risk of pancreatic adenocarcinoma.

Adenocarcinoma of the exocrine pancreas is the fourth leading cause of cancer-related death in men and women in the U.S.

Cytokines and other proinflammatory mediators have been implicated in inflammatory pancreatic diseases including pancreatitis and cancer.

We analyzed cytokine gene polymorphisms as risk factors for pancreatic cancer using questionnaire data obtained by in-person interviews and germ line DNA collected in a population-based case-control study of pancreatic cancer (532 cases and 1,701 controls) conducted in the San Francisco Bay Area.

We assessed potential interactions between these polymorphisms, proinflammatory conditions (e.g., pancreatitis, ulcer, and obesity), and smoking as risk factors for pancreatic cancer.

There was no overall association between pancreatic cancer risk and tumor necrosis factor-alpha (TNF-A -308G/A), regulated upon activation, normally T cell-expressed, and presumably secreted (RANTES -403G/A), and CC chemokine receptor 5 (CCR5-Delta32) polymorphisms.

There was a nearly 7-fold increased relative risk estimate for pancreatic cancer in individuals with a history of pancreatitis (adjusted OR, 6.9; 95% CI, 3.4-14.1).

Among patients with pancreatic cancer, pancreatitis was significantly associated with TNF-A -308 GA + AA (OR, 3.1; 95% CI, 1.3-7.4) and with RANTES -403 GA + AA (OR, 2.3; 95% CI, 1.0-5.4).

Our results lend support for the hypothesis that proinflammatory gene polymorphisms, in combination with proinflammatory conditions, may influence the development of pancreatic cancer.

[MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / genetics. Chemokine CCL5 / genetics. Genetic Predisposition to Disease. Inflammation / genetics. Pancreatic Neoplasms / etiology. Pancreatic Neoplasms / genetics. Polymorphism, Genetic. Receptors, CCR5 / genetics. Tumor Necrosis Factor-alpha / genetics

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(PMID = 16614115.001).

[ISSN] 1055-9965

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

[ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA108370; United States / NCI NIH HHS / CA / CA59706; United States / NCI NIH HHS / CA / CA89726; United States / NCI NIH HHS / CA / CA988889

[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 / Chemokine CCL5; 0 / Receptors, CCR5; 0 / Tumor Necrosis Factor-alpha

   

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A model of SAP was established by injection of 5% sodium taurocholate into the biliary-pancreatic duct of rats.

The changes in serum amylase, myeloperoxidase (MPO) activity of pancreatic and pulmonary tissue were measured.

The TNF-alpha level in pancreatic cytosolic fractions was assayed with an enzyme-linked immunosorbent assay (ELISA) kit.

Meanwhile, the pathological changes in both pancreatic and pulmonary tissues were also observed.

RESULTS: MG-132 significantly decreased serum amylase, pancreatic weight/body ratio, pancreatic TNF-alpha level, pancreatic and pulmonary MPO activity (P < 0.05).

Histopathological examinations revealed that pancreatic and pulmonary samples from rats pretreated with MG-132 demonstrated milder edema, cellular damage, and inflammatory activity (P < 0.05).

[MeSH-major] Cysteine Proteinase Inhibitors / pharmacology. Leupeptins / pharmacology. Lung / drug effects. Lung Diseases / prevention & control. Pancreas / drug effects. Pancreatitis / prevention & control. Proteasome Inhibitors

[MeSH-minor] Acute Disease. Amylases / blood. Animals. Disease Models, Animal. Enzyme-Linked Immunosorbent Assay. Male. Organ Size. Peroxidase / metabolism. Proteasome Endopeptidase Complex / metabolism. Rats. Rats, Sprague-Dawley. Severity of Illness Index. Taurocholic Acid. Tumor Necrosis Factor-alpha / metabolism

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(PMID = 18506934.001).

[ISSN] 1007-9327

[Journal-full-title] World journal of gastroenterology

[ISO-abbreviation] World J. Gastroenterol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Cysteine Proteinase Inhibitors; 0 / Leupeptins; 0 / Proteasome Inhibitors; 0 / Tumor Necrosis Factor-alpha; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 5E090O0G3Z / Taurocholic Acid; EC 1.11.1.7 / Peroxidase; EC 3.2.1.- / Amylases; EC 3.4.25.1 / Proteasome Endopeptidase Complex

[Other-IDs] NLM/ PMC2712861

   

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[Title] Effects of alpha-adrenoreceptor antagonists on apoptosis and proliferation of pancreatic cancer cells in vitro.

AIM: To discuss the expression of alpha-adrenoreceptors in pancreatic cancer cell lines PC-2 and PC-3 and the effects of alpha1- and alpha2-adrenoreceptor antagonists, yohimbine and urapidil hydrochloride, on the cell lines in vitro.

METHODS: We cultured the human ductal pancreatic adenocarcinoma cell lines PC-2 and PC-3 and analyzed the mRNA expression of alpha1- and alpha2-adrenergic receptors by reverse transcription polymerase chain reaction (RT-PCR).

The effects of yohimbine and urapidil hydrochloride on cell proliferation were assessed by 3-(4,5-dimethylthiasol-2-yl)-2,4,-diphenyltetrazolium bromide (MTT) assay.

MTT assays showed that urapidil hydrochloride had no effect on PC-3 cell lines.

However, exposure to urapidil hydrochloride increased DNA synthesis in PC-2 cell lines as compared to the control group.

PC-2 cell lines were sensitive to both drugs.

The proliferation of the 2 cell lines was inhibited by yohimbine.

Cell proliferation was inhibited by yohimbine via apoptosis induction.

CONCLUSION: The expression of alpha1- and alpha2-adrenoreceptors is different in PC-2 and PC-3 cell lines, which might be indicative of their different functions.

The alpha2-adrenoceptor antagonist, yohimbine, can inhibit the proliferation of both cell lines and induce their apoptosis, suggesting that yohimbine can be used as an anticancer drug for apoptosis of PC-2 and PC-3 cells.

[MeSH-major] Adrenergic alpha-2 Receptor Antagonists. Adrenergic alpha-Antagonists / pharmacology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Proliferation / drug effects. Pancreatic Neoplasms / pathology. Yohimbine / pharmacology

[MeSH-minor] Adrenergic alpha-1 Receptor Antagonists. Cell Line, Tumor. DNA Replication / drug effects. Dose-Response Relationship, Drug. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. In Situ Nick-End Labeling. Piperazines / pharmacology. RNA, Messenger / metabolism. Receptors, Adrenergic, alpha-1 / metabolism. Receptors, Adrenergic, alpha-2 / genetics. Receptors, Adrenergic, alpha-2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 18416462.001).

[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 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-2 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Antineoplastic Agents; 0 / Piperazines; 0 / RNA, Messenger; 0 / Receptors, Adrenergic, alpha-1; 0 / Receptors, Adrenergic, alpha-2; 2Y49VWD90Q / Yohimbine; A78GF17HJS / urapidil

[Other-IDs] NLM/ PMC2705090

   

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[Title] Effects of immunosuppressive and immunostimulative treatment on pancreatic injury and mortality in severe acute experimental pancreatitis.

Enhanced cell death by apoptosis during the postacute course was reduced in FK506-treated animals only.

Pancreatic interleukin (IL) 1beta messenger RNA up-regulation occurred early and was slightly suppressed in both treatment groups; tumor necrosis factor alpha (TNF-alpha) and IL-2 messenger RNA expression paralleled the onset of apoptosis and was markedly decreased in IFN-gamma- and FK506-treated rats.

The 2 therapeutic regimens had similar effects on intrapancreatic and systemic IL-1beta and TNF-alpha protein release; however, the profiles of both cytokines were differently influenced.

Whereas IFN-gamma and FK506 treatment lead to an enhanced intrapancreatic and systemic TNF-alpha protein release during the early course, IL-1beta concentrations were significantly reduced within the late intervals.

CONCLUSIONS: Severe acute pancreatitis is associated with early alterations of the immune response comprising overt T-cell activation and impaired monocyte/macrophage function alike.

Targeting either immunologic derangement improves local pancreatic damage and systemic severity.

[MeSH-major] Adjuvants, Immunologic / pharmacology. Immunosuppressive Agents / pharmacology. Pancreas / drug effects. Pancreatitis, Acute Necrotizing / prevention & control

[MeSH-minor] Animals. Apoptosis. Disease Models, Animal. Gene Expression Regulation. Interferon-gamma / pharmacology. Interleukin-1beta / genetics. Interleukin-1beta / metabolism. Interleukin-2 / genetics. Interleukin-2 / metabolism. Male. Necrosis. RNA, Messenger / metabolism. Rats. Rats, Wistar. Tacrolimus / pharmacology. Taurocholic Acid. Time Factors. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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(PMID = 16868484.001).

[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 / Adjuvants, Immunologic; 0 / Immunosuppressive Agents; 0 / Interleukin-1beta; 0 / Interleukin-2; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 5E090O0G3Z / Taurocholic Acid; 82115-62-6 / Interferon-gamma; WM0HAQ4WNM / Tacrolimus

   

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[Title] [Combined multiple organ resection in 16 patients with adenocarcinoma of the body or tail of the pancreas].

OBJECTIVE: To investigate the feasibility and therapeutic results of multiple organ resection in patients with tumor of the body and tail of pancreas.

METHODS: The clinical and pathological data were analysed in 16 consecutive patients with neoplasm of the body and tail of pancreas from 1999 to 2004 retrospectively.

RESULTS: Multiple organ resection was performed in 6 cases of primary pancreatic adenocarcinoma of the body and tail (3 cases of pancreatic cancer, 2 cases of malignant glucagonoma, and 1 case of well-differentiated pancreatic stromal sarcoma) and 10 cases of extrapancreatic malignancy (4 cases of gastric cancer, 2 cases of gastric leiomyosarcoma, 1 case of duodenal cancer, and 3 cases of colon cancer of hepatic flexure).

Patients with primary pancreatic cancer or pancreatic stromal sarcoma died within 1 year.

Two patients with malignant glucagonoma died 51 and 39 months later.

[MeSH-major] Adenocarcinoma / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery

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(PMID = 16274034.001).

[ISSN] 1000-503X

[Journal-full-title] Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae

[ISO-abbreviation] Zhongguo Yi Xue Ke Xue Yuan Xue Bao

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

   

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BACKGROUND: Transmembrane CAIX and CAXII are members of the alpha carbonic anhydrase (CA) family.

Expression of CAIX and CAXII proteins in tumor tissues is primarily induced by hypoxia and this is particularly true for CAIX, which is regulated by the transcription factor, hypoxia inducible factor-1 (HIF-1).

Their distributions in normal adult human tissues are restricted to highly specialized cells that are not always hypoxic.

RESULTS: The co-localization of CAIX and HIF-1alpha was limited to certain cell types in embryonic and early fetal tissues.

Those cells comprised the primitive mesenchyma or involved chondrogenesis and skin development.

Transient CAIX expression was limited to immature tissues of mesodermal origin and the skin and ependymal cells.

The only tissues that persistently expressed CAIX protein were coelomic epithelium (mesothelium) and its remnants, the epithelium of the stomach and biliary tree, glands and crypt cells of duodenum and small intestine, and the cells located at those sites previously identified as harboring adult stem cells in, for example, the skin and large intestine.

CAXII expression is restricted to cells involved in secretion and water absorption such as parietal cells of the stomach, acinar cells of the salivary glands and pancreas, epithelium of the large intestine, and renal tubules.

3) CAIX and CAXII expression is closely related to cell origin and secretory activity involving proton transport, respectively.

The intriguing finding of rare CAIX-expressing cells in those sites corresponding to stem cell niches requires further investigation.

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(PMID = 19291313.001).

[ISSN] 1471-213X

[Journal-full-title] BMC developmental biology

[ISO-abbreviation] BMC Dev. Biol.

[Language] ENG

[Grant] United States / NCI NIH HHS / CO / N01-CO-56000; United States / Intramural NIH HHS / /

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

[Publication-country] England

[Chemical-registry-number] EC 4.2.1.1 / Carbonic Anhydrases

[Other-IDs] NLM/ PMC2666674

   

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

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

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

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

The serum glucagon level was markedly increased.

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

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

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

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

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

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

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(PMID = 16435046.001).

[ISSN] 1318-4458

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

[ISO-abbreviation] Acta Dermatovenerol Alp Pannonica Adriat

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Slovenia

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

   

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[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

   

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[Title] Peptide YY reverses TNF-alpha induced transcription factor binding of interferon regulatory factor-1 and p53 in pancreatic acinar cells.

Transcription factors interferon regulatory factor-1 (IRF-1) and the tumor suppressor gene p53 collaborate to enhance p21 related cell cycle regulation during pathological disease progression.

However, little is known about their role in the pancreas after cytokine challenge.

Our laboratory has previously shown that TNF-alpha induces the binding of many transcription factors, including NF-kappa B, and treatment with the gut hormone, Peptide YY (PYY), ameliorates the effects.

We hypothesized that TNF-alpha would induce IRF-1 and p53 protein binding in pancreatic acinar cells and that PYY would attenuate the effect.

MATERIALS AND METHODS: Rat pancreatic acinar AR42J cells were treated with rat recombinant TNF-alpha (200 ng/ml).

To verify that our model was inducing pancreatitis, alpha-amylase activity was measured in the cell culture supernatant by fluorescence spectroscopy.

PYY [3-36] was added at 500 pM 30 min post-TNF treatment; cells were harvested at 2 h for extraction of nuclear protein.

RESULTS: Amylase enzyme activity was significantly (P < 0.05) elevated in the TNF-alpha-treated cells by 2 h.

Induction by TNF-alpha increased IRF-1 protein binding 3.5-fold, while binding levels of p53 protein increased six-fold.

The addition of PYY to TNF-treated cells reduced IRF-1 and p53 binding to control levels.

CONCLUSIONS: We have shown for the first time that short-term exposure to TNF-alpha induces the binding activity of transcription factors IRF-1 and p53 in rat pancreatic acinar cells, and that addition of PYY reduces it.

[MeSH-major] Interferon Regulatory Factor-1 / metabolism. Pancreas, Exocrine / metabolism. Peptide YY / metabolism. Tumor Necrosis Factor-alpha / metabolism. Tumor Suppressor Protein p53 / metabolism

[MeSH-minor] Acute Disease. Amylases / metabolism. Animals. Cell Line. Oligonucleotide Array Sequence Analysis. Pancreatitis / metabolism. Protein Binding / drug effects. Rats. Transcription Factors / genetics. Transcription Factors / metabolism

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(PMID = 16978650.001).

[ISSN] 0022-4804

[Journal-full-title] The Journal of surgical research

[ISO-abbreviation] J. Surg. Res.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Interferon Regulatory Factor-1; 0 / Transcription Factors; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 106388-42-5 / Peptide YY; EC 3.2.1.- / Amylases

   

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In cultured 3T3-L1 adipocytes, the iminosugar derivative N-(5'-adamantane-1'-yl-methoxy)-pentyl-1-deoxynojirimycin (AMP-DNM) counteracted tumor necrosis factor-alpha-induced abnormalities in glycosphingolipid concentrations and concomitantly reversed abnormalities in insulin signal transduction.

[MeSH-minor] 3T3 Cells. Animals. Ceramides / metabolism. Glucose Intolerance / blood. Glucosylceramides / metabolism. Glycosphingolipids / metabolism. Humans. Liver / drug effects. Liver / physiology. Mice. Mice, Inbred C57BL. Mice, Obese. Pancreas / drug effects. Pancreas / physiology. Signal Transduction

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(PMID = 17287460.001).

[ISSN] 1939-327X

[Journal-full-title] Diabetes

[ISO-abbreviation] Diabetes

[Language] eng

[Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / JF16994; United Kingdom / Wellcome Trust / /

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

[Publication-country] United States

[Chemical-registry-number] 0 / Ceramides; 0 / Enzyme Inhibitors; 0 / Glucosylceramides; 0 / Glycosphingolipids; 0 / Insulin; 0 / N-(5-adamantane-1-yl-methoxy-pentyl)deoxynojirimycin; 19130-96-2 / 1-Deoxynojirimycin; EC 2.4.1.- / Glucosyltransferases; EC 2.4.1.80 / ceramide glucosyltransferase; PJY633525U / Adamantane

[Other-IDs] NLM/ EMS61739; NLM/ PMC4298701

   

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[Title] Suppressor of cytokine signaling-1 in T cells and macrophages is critical for preventing lethal inflammation.

Here, cre/loxP deletion of Socs1 was used to investigate the contribution of specific cells/tissues to inflammatory disease.

Mice with SOCS-1 deficiency in myeloid and lymphoid cells, but not lymphoid alone, became ill at 50 to 250 days of age.

These mice developed splenomegaly and T-cell/macrophage infiltration of many organs, including liver, lung, pancreas, and muscle.

There were also abnormally high levels of the proinflammatory cytokines interferon gamma (IFN-gamma), tumor necrosis factor (TNF), and interleukin-12 (IL-12), and activated T cells circulating in these mice.

Socs1(null) T cells were found to be hypersensitive to multiple cytokines, including IL-1, IL-2, and IL-12, resulting in IFN-gamma production without requiring T-cell receptor (TCR) ligation.

A dysregulated cytokine network between T cells and macrophages is thus associated with this inflammatory disease.

These findings indicate that SOCS-1 is critical in both T cells and macrophages for preventing uncontrolled inflammation.

[MeSH-minor] Animals. Cell Lineage / drug effects. Cell Lineage / immunology. Dose-Response Relationship, Drug. Interferon-gamma / pharmacology. Lipopolysaccharides / pharmacology. Mice. Mice, Transgenic. Myeloid Progenitor Cells / drug effects. Myeloid Progenitor Cells / immunology. Suppressor of Cytokine Signaling Proteins. Tumor Necrosis Factor-alpha / pharmacology

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(PMID = 15899915.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Carrier Proteins; 0 / Lipopolysaccharides; 0 / Repressor Proteins; 0 / Socs1 protein, mouse; 0 / Suppressor of Cytokine Signaling Proteins; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma

   

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[Title] Biochemistry of neuroendocrine tumours.

Several circulating or urinary tumour markers can be used for the diagnosis and follow-up of functioning and clinically non-functioning neuroendocrine tumours of the pancreatic islet cells and intestinal tract.

Among the specific tumour markers are serotonin and its metabolites--e.g.

5-hydroxyindoleacetic acid (5-HIAA)--in carcinoid tumours and the carcinoid syndrome, insulin and its precursors or breakdown products in insulinoma, and gastrin in gastrinoma.

Plasma vasointestinal polypeptide (VIP) determinations have been used in the diagnosis of VIPoma, plasma glucagon for glucagonoma, and serum somatostatin for somatostatinoma.

Among the tumour-non-specific markers are: chromogranins, neuron-specific enolase (NSE), alpha-subunits of the glycoprotein hormones, catecholamines, pancreatic polypeptide (PP), ghrelin and adrenomedullin.

[MeSH-major] Biomarkers, Tumor / analysis. Neuroendocrine Tumors / diagnosis

[MeSH-minor] Biomarkers / analysis. Carcinoid Tumor / diagnosis. Gastrinoma / diagnosis. Gastrins / analysis. Humans. Insulin / analysis. Insulin / metabolism. Insulinoma / diagnosis. Malignant Carcinoid Syndrome / diagnosis. Pancreatic Neoplasms / diagnosis. Serotonin / analysis. Serotonin / metabolism

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(PMID = 17382264.001).

[ISSN] 1521-690X

[Journal-full-title] Best practice & research. Clinical endocrinology & metabolism

[ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers; 0 / Biomarkers, Tumor; 0 / Gastrins; 0 / Insulin; 333DO1RDJY / Serotonin

[Number-of-references] 49

   

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As an important pathological feature of acute pancreatitis, apoptosis may occur in multiple organs and relate directly to the progression of disease.

We summarize here the roles of the main inflammatory mediators (e.g., NO, TNF-alpha, TGF-beta1, IL-10, NF-kappaB) during the pathologic process of acute pancreatitis.

[MeSH-minor] Acute Disease. Animals. Humans. Interleukin-10 / metabolism. NF-kappa B / metabolism. Nitric Oxide / metabolism. Transforming Growth Factor beta1 / metabolism. Tumor Necrosis Factor-alpha / metabolism

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(PMID = 17372825.001).

[ISSN] 0163-2116

[Journal-full-title] Digestive diseases and sciences

[ISO-abbreviation] Dig. Dis. Sci.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Inflammation Mediators; 0 / NF-kappa B; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 31C4KY9ESH / Nitric Oxide

[Number-of-references] 74

   

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

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

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

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(PMID = 18306843.001).

[ISSN] 0011-4162

[Journal-full-title] Cutis

[ISO-abbreviation] Cutis

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

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

   

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[Title] Promoter hypermethylation of the RUNX3 gene in esophageal squamous cell carcinoma.

Alteration in transforming growth factor-beta (TGF-beta) signaling pathway is one of the main causes of esophageal squamous cell carcinoma (ESCC).

Hypermethylation of RUNX3 promoter was frequently found in gastrointestinal cancers, including those of stomach, liver, colon and pancreas.

The aim of this study was to determine whether promoter methylation of the RUNX3 gene correlates with ESCC tumor progression.Accordingly, we first determined RUNX3 mRNA expression and methylation status of its promoter region in 42 primary tumors with ESCC and Eca-109, an ESCC cell line.

Loss of RUNX3 mRNA expression was detected by RT-PCR in 23 out of 42 (54.8%) ESCC specimens and Eca-109 cells.

The Promoter hypermethylation was detected by Methylation Specific Polymerase Chain Reaction (MS-PCR) in 27 out of 42 (64.3%) ESCC specimen and Eca-109 cells.

Importantly, we found positive correlations, not only between the promoter hypermethylation and tumor clinical pathologic stages (P = 0.003), but also between the loss of RUNX3 mRNA expression and the tumor progression (P = 0.016).

Finally, we observed that the loss of RUNX3 mRNA expression is statistically correlated with the promoter hypermethylation in these tumors (P < 0.001).

[MeSH-major] Carcinoma, Squamous Cell / genetics. Core Binding Factor Alpha 3 Subunit / genetics. DNA Methylation. Esophageal Neoplasms / genetics. Promoter Regions, Genetic

[MeSH-minor] Aged. Azacitidine / pharmacology. Cell Line, Tumor. Female. Humans. Male. Middle Aged. RNA, Messenger / analysis. Signal Transduction. Transforming Growth Factor beta / physiology

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(PMID = 18058463.001).

[ISSN] 1532-4192

[Journal-full-title] Cancer investigation

[ISO-abbreviation] Cancer Invest.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factor Alpha 3 Subunit; 0 / RNA, Messenger; 0 / Runx3 protein, human; 0 / Transforming Growth Factor beta; M801H13NRU / Azacitidine

   

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[Title] Tumor necrosis factor-related apoptosis-inducing ligand and CD56 expression in patients with type 1 diabetes mellitus.

OBJECTIVES: Our previous report showed that beta-cell antigen-specific CD56+ T-cells and cytokine TRAIL mediate destruction of human pancreatic [beta] cells in vitro.

To determine whether CD56 and TRAIL are present during islet cell destruction at the onset of clinical symptoms of type 1 diabetes mellitus (T1D), we studied cell marker and cytokine expression in the pancreatic islets of 2 children who died at presentation of acute-onset T1D and in T-cell lines derived from a group of children with new-onset T1D.

METHODS: TRAIL, CD56, and other T-cell markers and cytokine expression were studied using immunohistochemistry on pancreatic sections from 2 children with acute-onset T1D.

TRAIL and CD56 expression was analyzed by flow cytometry in the antigen-activated T-cell lines derived from 29 children with new-onset T1D.

RESULTS: TRAIL+, CD56+, CD45RO+, and CD3+ cells were present in the islets of acute-onset T1D patients, while none were present in the normal islets.

T-cell lines from new-onset T1D expressed TRAIL and CD56 in response to stimulation with beta-cell antigens GAD, IA-2 and insulin beta chain.

CONCLUSION: The presence of TRAIL and CD56 markers is part of the T-cell response repertoire in beta-cell destruction.

[MeSH-major] Antigens, CD56 / metabolism. Apoptosis / immunology. Apoptosis Regulatory Proteins / metabolism. Biomarkers. Diabetes Mellitus, Type 1 / immunology. Diabetes Mellitus, Type 1 / metabolism. Membrane Glycoproteins / metabolism. Tumor Necrosis Factor-alpha / metabolism

[MeSH-minor] Adolescent. Adult. Child. Female. Humans. Immunohistochemistry. Immunophenotyping. Insulin-Secreting Cells / immunology. Insulin-Secreting Cells / metabolism. Insulin-Secreting Cells / pathology. Interferon-gamma / metabolism. Male. Receptors, TNF-Related Apoptosis-Inducing Ligand. Receptors, Tumor Necrosis Factor / metabolism. T-Lymphocytes / immunology. T-Lymphocytes / pathology. TNF-Related Apoptosis-Inducing Ligand

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(PMID = 15714132.001).

[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 / Antigens, CD56; 0 / Apoptosis Regulatory Proteins; 0 / Biomarkers; 0 / Membrane Glycoproteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma

   

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[Title] Gastrointestinal stromal tumors: pathology and prognosis at different sites.

Gastrointestinal (GI) stromal tumors (GISTs) are the most common mesenchymal tumors specific to the GI tract, generally defined as KIT (CD117)-positive tumors with a characteristic set of histologic features.

These tumors, derived from Cajal cells or their precursors, most commonly occur at the age >50 years in the stomach (60%), jejunum and ileum (30%), duodenum (4-5%), rectum (4%), colon and appendix (1-2%), and esophagus (<1%), and rarely as apparent primary extragastrointestinal tumors in the vicinity of stomach or intestines.

Their overall incidence has been estimated as 10 to 20 per million, including incidental minimal tumors.

GISTs contain a spectrum from minute indolent tumors to sarcomas at all sites of occurrence.

Their gross patterns are diverse, including nodular, cystic, and diverticular tumors.

External involvement of pancreas and liver can simulate primary tumor in these organs.

In general, gastric tumors have a more favorable prognosis than the intestinal ones with similar parameters.

Gastric GISTs can be divided into histologic subgroups including 4 spindle cell and 4 epithelioid variants.

Immunohistochemical demonstration of KIT, CD34, or protein kinase theta positivity helps to properly identify these tumors.

[MeSH-major] Biomarkers, Tumor / analysis. Gastrointestinal Stromal Tumors / pathology. Gastrointestinal Tract / pathology. Neurofibromatosis 1 / complications

[MeSH-minor] Adolescent. Animals. Child. Humans. Immunohistochemistry. Muscle Cells / metabolism. Neurons / metabolism. Prognosis. Receptor, Platelet-Derived Growth Factor alpha / metabolism

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(PMID = 17193820.001).

[ISSN] 0740-2570

[Journal-full-title] Seminars in diagnostic pathology

[ISO-abbreviation] Semin Diagn Pathol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

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

[Number-of-references] 91

   

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[Title] Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice.

The pancreatic alpha- and beta-cells are critical components in regulating blood glucose homeostasis via secretion of glucagon and insulin, respectively.

Both cell types are typically localized in the islets of Langerhans.

The lack of suitable cell lines to study alpha- and beta-cells interactions have led us to develop an alpha-cell-specific Cre-expressing transgenic line utilizing a glucagon promoter sequence, the Glu-Cre transgenic mouse.

Here, we demonstrate that the Glu-Cre could specifically and efficiently excise floxed target genes in adult islet alpha-cells.

We further showed that deletion of the tumor suppressor gene, multiple endocrine neoplasia type 1 (Men1), in alpha-cells led to tumorigenesis.

However, to our surprise, the lack of Men1 in alpha-cells did not result in glucagonomas but rather beta-cell insulinomas.

Because deletion of the Men1 alleles was only present in alpha-cells, our data suggested that cross communication between alpha- and beta-cells contributes to tumorigenesis in the absence of Men1.

Together, we believed that the new model systems described here will allow future studies to decipher cellular interactions between islet alpha- and beta-cells in a physiological context.

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(PMID = 20555035.001).

[ISSN] 1945-7170

[Journal-full-title] Endocrinology

[ISO-abbreviation] Endocrinology

[Language] ENG

[Grant] United States / Intramural NIH HHS / /

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

[Publication-country] United States

[Chemical-registry-number] 0 / Men1 protein, mouse; 0 / Proto-Oncogene Proteins; 9007-92-5 / Glucagon

[Other-IDs] NLM/ PMC2940531

   

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[Title] Systemic and peritoneal inflammatory response after laparoscopic-assisted gastrectomy and the effect of inflammatory cytokines on adhesion of gastric cancer cells to peritoneal mesothelial cells.

We designed this trial to investigate the effects of the inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) on the interaction between gastric cancer cells and mesothelial cells, and to evaluate differences in both the peritoneal and systemic cytokine (IL-1β and TNF-α) concentrations after laparoscopic and conventional surgical approaches, thus offering another possible advantage of laparoscopic procedures for treatment of gastric cancer.

EXPERIMENTAL DESIGN: A reproducible human in vitro assay was developed to study adhesion of SGC-7901 and MKN-45 human gastric cancer cells to monolayers of primary cultured human peritoneal mesothelial cells (HPMCs).

Tumor cell adhesion to a mesothelial monolayer was assessed after preincubation of the monolayer with IL-1β and TNF-α using flow cytometry.

RESULTS: Preincubation of the mesothelial monolayer with IL-1β and TNF-α resulted in enhanced tumor cell adhesion of SGC-7901 and MKN-45 cells.

Mesothelial cells showed significant enhancement of expression of ICAM-1, VCAM-1, and CD44 after stimulation with IL-1β and TNF-α.

Meanwhile their counterparts (LFA-1, VLA-4, and CD44) were identified in gastric cancer cells.

CONCLUSIONS: The presented results prove that IL-1β and TNF-α are significant stimulating factors in gastric cancer cell adhesion in vitro and may therefore partly account for local tumor recurrence and peritoneal metastasis in vivo.

[MeSH-major] Cell Adhesion Molecules / metabolism. Gastrectomy. Inflammation Mediators / pharmacology. Interleukin-1beta / pharmacology. Laparoscopy. Peritoneum / physiopathology. Stomach Neoplasms / physiopathology. Stomach Neoplasms / surgery. Tumor Necrosis Factor-alpha / pharmacology. Tumor Necrosis Factor-alpha / physiology

[MeSH-minor] Ascitic Fluid / chemistry. Cell Adhesion / drug effects. Cell Line, Tumor. Cell Proliferation. Cell Survival. Epithelial Cells / physiology. Humans. Peritoneal Neoplasms / secondary. Tumor Cells, Cultured

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(PMID = 20419322.001).

[ISSN] 1432-2218

[Journal-full-title] Surgical endoscopy

[ISO-abbreviation] Surg Endosc

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Inflammation Mediators; 0 / Interleukin-1beta; 0 / Tumor Necrosis Factor-alpha

   

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[Title] Small-molecule inhibitor of the AP endonuclease 1/REF-1 E3330 inhibits pancreatic cancer cell growth and migration.

APE1 is overexpressed in several human cancers, and disruption of APE1 function has detrimental effects on cancer cell viability.

In the present study, we used E3330, a small-molecule inhibitor of APE1 redox domain function, to interrogate the functional relevance of sustained redox function in pancreatic cancer.

We show that E3330 significantly reduces the growth of human pancreatic cancer cells in vitro.

This phenomenon was further confirmed by a small interfering RNA experiment to knockdown APE1 expression in pancreatic cancer cells.

E3330 exposure promotes endogenous reactive oxygen species formation in pancreatic cancer cells, and the resulting oxidative stress is associated with higher levels of oxidized, and hence inactive, SHP-2, an essential protein tyrosine phosphatase that promotes cancer cell proliferation in its active state.

Finally, E3330 treatment inhibits pancreatic cancer cell migration as assessed by in vitro chemokine assays.

E3330 shows anticancer properties at multiple functional levels in pancreatic cancer, such as inhibition of cancer cell growth and migration.

Inhibition of the APE1 redox function through pharmacologic means has the potential to become a promising therapeutic strategy in this disease.

[MeSH-major] Benzoquinones / pharmacology. Cell Movement / drug effects. DNA-(Apurinic or Apyrimidinic Site) Lyase / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / pathology. Propionates / pharmacology

[MeSH-minor] Antigens, CD44 / metabolism. Cell Hypoxia / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Chemokine CXCL12 / metabolism. DNA, Neoplasm / metabolism. Enzyme Activation / drug effects. Epithelial Cells / drug effects. Epithelial Cells / pathology. G1 Phase / drug effects. G2 Phase / drug effects. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Models, Biological. Oxidation-Reduction / drug effects. Pancreas / pathology. Protein Tyrosine Phosphatase, Non-Receptor Type 11 / metabolism. Reactive Oxygen Species / metabolism

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(PMID = 18645011.001).

[ISSN] 1535-7163

[Journal-full-title] Molecular cancer therapeutics

[ISO-abbreviation] Mol. Cancer Ther.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA006973

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD44; 0 / Benzoquinones; 0 / Chemokine CXCL12; 0 / DNA, Neoplasm; 0 / Enzyme Inhibitors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Propionates; 0 / Reactive Oxygen Species; 136164-66-4 / E 3330; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 4.2.99.18 / APEX1 protein, human; EC 4.2.99.18 / DNA-(Apurinic or Apyrimidinic Site) Lyase

[Other-IDs] NLM/ NIHMS436971; NLM/ PMC3569736

   

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[Title] PPARalpha/gamma expression and activity in mouse and human melanocytes and melanoma cells.

PURPOSE: We examined the expression of PPARs and the effects of PPARalpha and PPARgamma agonists on growth of mouse and human melanocytes and melanoma cells.

METHODS: PPARalpha,beta, and PPARgamma mRNA qualitative expression in melan-a mouse melanocytes, B16 mouse melanoma, human melanocytes, and A375 and SK-mel28 human melanoma cells was determined by RT-PCR, while quantitative PPARalpha mRNA levels were determined by QuantiGene assay.

The effect of natural and synthetic PPAR ligands on cell growth was determined by either hemocytometer counting or crystal violet assay.

RESULTS: Both mouse and human melanoma cells produced more PPARalpha and PPARgamma protein compared to melanocytes.

PPARalpha mRNA levels were elevated in human melanoma cells, but not in mouse melanoma cells relative to melanocytes.

Silencing of PPARalpha in human melanoma cells did not alter cell proliferation or morphology.

PPARgamma-selective agonists inhibited the growth of both mouse and human melanoma cells, while PPARalpha-selective agonists had limited effects.

[MeSH-major] Melanocytes / metabolism. Melanoma / metabolism. PPAR alpha / physiology. PPAR gamma / physiology

[MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Humans. Mice. RNA, Messenger / analysis. Transcriptional Activation

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(PMID = 18172578.001).

[ISSN] 0724-8741

[Journal-full-title] Pharmaceutical research

[ISO-abbreviation] Pharm. Res.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA59530; United States / NCI NIH HHS / CA / CA59539/S; United States / NCRR NIH HHS / RR / P20 RR20180

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

[Publication-country] United States

[Chemical-registry-number] 0 / PPAR alpha; 0 / PPAR gamma; 0 / RNA, Messenger

   

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[Title] Recombinant adenoviruses expressing TRAIL demonstrate antitumor effects on non-small cell lung cancer (NSCLC).

INTRODUCTION: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in a variety of malignant cells, but not in normal cells.

This preferential toxicity to the abnormal cells renders TRAIL potentially a very powerful therapeutic weapon against cancer.

However, a requirement for large quantities of TRAIL to suppress tumor growth in vivo is one of the major factors that has hindered it from being widely applied clinically.

To overcome this, we constructed a replication-deficient adenovirus that carries a human full-length TRAIL gene (Ad-TRAIL) and tested its efficacy against a lung cancer model system in comparison to that of the recombinant soluble TRAIL protein.

METHODS: To investigate the antitumor activity and therapeutic value of the Ad-TRAIL on the non-small cell lung cancer (NSCLC), four NSCLC cell lines, namely, YTMLC, GLC, A549, and H460 cells, were used.

Cell viability was analyzed by proliferation assay, and DNA ladder and cell-cycle analysis were used to identify apoptosis.

To further evaluate the effect of Ad-TRAIL in vivo, YTMLC cells were inoculated to the subcutis of nude mice.

The Ad-TRAIL was subsequently administered into the established tumors.

Tumor growth and the TRAIL toxicity were evaluated after treatment.

RESULTS: YTMLC cells infected with Ad-TRAIL showed decreased cell viability and a higher percentage of apoptosis.

Similar, Ad-TRAIL treatment also significantly suppressed tumor growth in vivo.

[MeSH-major] Adenoviridae. Apoptosis. Apoptosis Regulatory Proteins / biosynthesis. Carcinoma, Non-Small-Cell Lung / therapy. Genetic Therapy. Lung Neoplasms / therapy. Membrane Glycoproteins / biosynthesis. Tumor Necrosis Factor-alpha / biosynthesis

[MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. Neoplasms, Experimental / therapy. Neoplasms, Experimental / ultrastructure. TNF-Related Apoptosis-Inducing Ligand

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(PMID = 16720919.001).

[ISSN] 1357-0560

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

[ISO-abbreviation] Med. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tnfsf10 protein, mouse; 0 / Tumor Necrosis Factor-alpha

   

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[Title] Regulation of cyclooxygenase-2 (COX-2) expression in human pancreatic carcinoma cells by the insulin-like growth factor-I receptor (IGF-IR) system.

Both the insulin-like growth factor-I receptor (IGF-IR) and cyclooxygenase-2 (COX-2) are frequently overexpressed in pancreatic cancer.

Pancreatic cancer cells (L3.6pl) were stably transfected with a dominant-negative receptor (IGF-IR DN) construct or empty vector (pcDNA).

Cells were stimulated with IGF-I to determine activated signaling intermediates and induction of COX-2.

In addition, IGF-IR DN cells showed a marked decrease in constitutive COX-2 and a blunted response to IGF-I.

Similarly, treatment with an anti-IGF-IR antibody effectively inhibited IGF-IR and MAPK/Erk activation and decreased COX-2 in parental cells.

In conclusion, activation of IGF-IR mediates COX-2 expression in human pancreatic cancer cells.

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(PMID = 17950526.001).

[ISSN] 0304-3835

[Journal-full-title] Cancer letters

[ISO-abbreviation] Cancer Lett.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA009599-15; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA16672; United States / PHS HHS / / T-32 09599; United States / NCI NIH HHS / CA / T32 CA009599-15; United States / NCI NIH HHS / CA / T32 CA009599

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

[Publication-country] Ireland

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Enzyme Inhibitors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / IRS1 protein, human; 0 / Insulin Receptor Substrate Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 67763-96-6 / Insulin-Like Growth Factor I; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3

[Other-IDs] NLM/ NIHMS35362; NLM/ PMC2147684

   

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[Title] Alpha-fetoprotein-producing pancreatic acinar cell carcinoma.

A 47-year-old man with chronic hepatitis B had progressive elevated alpha-fetoprotein of 2 years' duration.

A pancreatic tail tumor, instead of liver tumor, was detected.

He underwent elective distal pancreatectomy and splenectomy and the pathology turned out to be acinar cell carcinoma of the pancreas.

Serum level of alpha-fetoprotein returned to normal soon after surgery.

Alpha-fetoprotein is commonly used as a tumor marker to screen for hepatocellular carcinoma in high-risk patients.

However, elevated alpha-fetoprotein could occur in a much rarer disease, acinar cell carcinoma of the pancreas.

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(PMID = 17711801.001).

[ISSN] 0929-6646

[Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi

[ISO-abbreviation] J. Formos. Med. Assoc.

[Language] ENG

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

[Publication-country] Singapore

[Chemical-registry-number] 0 / alpha-Fetoproteins

   

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[Title] Co-existence of glucagonoma with recurrent insulinoma in a patient with multiple endocrine neoplasia-type 1 (MEN-1).

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterized by tumors of the parathyroid glands, the anterior pituitary, and the endocrine pancreas.

He was admitted to our hospital because of recurrent hypoglycemia and a growth of pancreatic tumors.

He subsequently underwent surgery for the pancreatic tumors.

The majority of these tumor cells were immunohistochemically positive for insulin and negative for glucagon.

A few nodules showed immunohistochemical staining positivity for glucagon but they were negative for insulin.

Although it is uncommon for patients with MEN1 to exhibit insulinoma and glucagonoma, this case suggests the need for careful analysis of pancreatic tumors in patients with MEN1.

[MeSH-major] Glucagonoma / pathology. Insulinoma / pathology. Multiple Endocrine Neoplasia Type 1 / pathology. Pancreatic Neoplasms / pathology

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(PMID = 19350420.001).

[ISSN] 1355-008X

[Journal-full-title] Endocrine

[ISO-abbreviation] Endocrine

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins

   

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[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

   

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[Title] Role of sialyltransferases involved in the biosynthesis of Lewis antigens in human pancreatic tumour cells.

The sialylated carbohydrate antigens, sialyl-Lewisx and sialyl-Lewisa, are expressed in pancreatic tumour cells and are related to their metastatic potential.

While the action of the fucosyltransferases involved in the synthesis of these antigens has already been investigated, no studies have been carried out on the activity and expression of the alpha 2,3-sialyltransferases in pancreatic tumour cells.

We describe the sialyltransferase (ST) activity, mRNA expression, and analysis of the cell carbohydrate structures in four human pancreatic adenocarcinoma cell lines of a wide range of neoplastic differentiation stages and in normal human pancreatic tissues.

Total ST activity measured on asialofetuin, employing a CMP fluorescent sialic acid, varied among the pancreatic cell lines and could be correlated to the expression of their cell surface antigens.

However, in some of the pancreatic cell lines, no relationship could be established with their ST3Gal III and IV mRNA expression.

Human pancreatic tissues also showed ST expression and activity.

In conclusion, ST activity levels in pancreatic cells could be correlated to their expression of sialylated epitopes, which indicates their involvement in the formation of the sialyl-Lewis antigens, in addition to fucosyltransferase activities.

[MeSH-major] Adenocarcinoma / enzymology. Antigens, Tumor-Associated, Carbohydrate / metabolism. Lewis Blood-Group System / biosynthesis. Sialyltransferases / metabolism

[MeSH-minor] Enzyme-Linked Immunosorbent Assay. Fucosyltransferases / metabolism. Gene Expression Regulation, Neoplastic. Humans. Middle Aged. Pancreas / enzymology. Pancreatic Neoplasms / enzymology. RNA, Messenger / metabolism. Tumor Cells, Cultured

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(PMID = 16133834.001).

[ISSN] 0282-0080

[Journal-full-title] Glycoconjugate journal

[ISO-abbreviation] Glycoconj. J.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Lewis Blood-Group System; 0 / RNA, Messenger; EC 2.4.1.- / Fucosyltransferases; EC 2.4.99.- / Sialyltransferases; EC 2.4.99.4 / beta-galactoside alpha-2,3-sialyltransferase

   

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TDZD-8 significantly reduced the degree of pancreas injury, amylase, and lipase serum levels (p < .01); nuclear factor-kappaB activation (p < .01); the production of tumor necrosis factor-alpha and interleukin-1beta (p < .01); the expression of adhesion molecules and neutrophil accumulation (p < .01); the formation of oxygen and nitrogen-derived radicals (p < .01); the degree of lipid peroxidation (p < .01); the expression of transforming growth factor-beta and vascular endothelial growth factor (p < .01); and-ultimately-the mortality rate (p < .01).

[MeSH-minor] Acute Disease. Animals. Cell Adhesion Molecules / drug effects. Ceruletide. Cytokines / drug effects. Male. Mice. Mice, Inbred Strains. NF-kappa B / drug effects. Neutrophil Activation / drug effects. Oxidative Stress / drug effects. Prospective Studies. Random Allocation. Survival Analysis

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[CommentIn] Crit Care Med. 2007 Dec;35(12):2874-5 [18043215.001]

(PMID = 18074481.001).

[ISSN] 0090-3493

[Journal-full-title] Critical care medicine

[ISO-abbreviation] Crit. Care Med.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione; 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / NF-kappa B; 0 / Thiadiazoles; 888Y08971B / Ceruletide; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3

   

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[Title] Synthetic serine protease inhibitor, gabexate mesilate, prevents nuclear factor-kappaB activation and increases TNF-alpha-mediated apoptosis in human pancreatic cancer cells.

Gabexate mesilate (GM), a synthetic serine protease inhibitor, suppresses nuclear factor-kappaB (NF-kappaB) activity in human monocytes or human umbilical vein endothelial cells (HUVECs).

In this study we examine whether GM also suppresses NF-kappaB activation and induces apoptosis in human pancreatic cancer cell lines.

The addition of tumor necrosis factor alpha (TNF-alpha) did not change the rates of growth of BxPC-3 and MIA PaCa-2.

However, in the presence of GM and TNF-alpha, proliferation decreased in a dose-dependent manner.

GM- and TNF-alpha-treated cells exhibited morphologic changes indicative of apoptosis, including chromatin condensation and nuclear fragmentation.

The NF-kappaB activity of both cell lines was increased by the addition of TNF-alpha, while TNF-alpha-induced NF-kappaB activity was suppressed by prestimulation with GM in a dose-dependent manner.

Caspase 3 and 7 activity was significantly increased by TNF-alpha with GM stimulation.

Furthermore, GM also suppressed the invasive potential of both cell lines.

These results indicate that GM inhibits TNF-alpha-induced NF-kappaB activation and enhances apoptosis in human pancreatic cancer cell lines.

[MeSH-major] Apoptosis / drug effects. Gabexate / pharmacology. NF-kappa B / drug effects. Pancreatic Neoplasms / drug therapy. Serine Proteinase Inhibitors / pharmacology. Tumor Necrosis Factor-alpha / pharmacology

[MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Humans

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(PMID = 17357832.001).

[ISSN] 0163-2116

[Journal-full-title] Digestive diseases and sciences

[ISO-abbreviation] Dig. Dis. Sci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / NF-kappa B; 0 / Serine Proteinase Inhibitors; 0 / Tumor Necrosis Factor-alpha; 4V7M9137X9 / Gabexate

   

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[Title] Obestatin promotes survival of pancreatic beta-cells and human islets and induces expression of genes involved in the regulation of beta-cell mass and function.

We investigated obestatin effect on survival of beta-cells and human pancreatic islets and the underlying signaling pathways.

RESEARCH DESIGN AND METHODS: beta-Cells and human islets were used to assess obestatin effect on cell proliferation, survival, apoptosis, intracellular signaling, and gene expression.

RESULTS: Obestatin showed specific binding on HIT-T15 and INS-1E beta-cells, bound to glucagon-like peptide-1 receptor (GLP-1R), and recognized ghrelin binding sites.

Obestatin exerted proliferative, survival, and antiapoptotic effects under serum-deprived conditions and interferon-gamma/tumor necrosis factor-alpha/interleukin-1 beta treatment, particularly at pharmacological concentrations.

Ghrelin receptor antagonist [D-Lys(3)]-growth hormone releasing peptide-6 and anti-ghrelin antibody prevented obestatin-induced survival in beta-cells and human islets. beta-Cells and islet cells released obestatin, and addition of anti-obestatin antibody reduced their viability.

Obestatin increased beta-cell cAMP and activated extracellular signal-related kinase 1/2 (ERK1/2) and phosphatidylinositol 3-kinase (PI 3-kinase)/Akt; its antiapoptotic effect was blocked by inhibition of adenylyl cyclase/cAMP/protein kinase A (PKA), PI 3-kinase/Akt, and ERK1/2 signaling.

The GLP-1R antagonist exendin-(9-39) reduced obestatin effect on beta-cell survival.

In human islets, obestatin, whose immunoreactivity colocalized with that of ghrelin, promoted cell survival and blocked cytokine-induced apoptosis through cAMP increase and involvement of adenylyl cyclase/cAMP/PKA signaling.

2) stimulated insulin secretion and gene expression; and 3) upregulated GLP-1R, IRS-2, pancreatic and duodenal homeobox-1, and glucokinase mRNA.

CONCLUSIONS: These results indicate that obestatin promotes beta-cell and human islet cell survival and stimulates the expression of main regulatory beta-cell genes, identifying a new role for this peptide within the endocrine pancreas.

[MeSH-major] Cell Survival / drug effects. Gene Expression Regulation / drug effects. Insulin-Secreting Cells / cytology. Islets of Langerhans / cytology. Peptide Hormones / pharmacology

[MeSH-minor] Caspase 3 / metabolism. Cell Culture Techniques. Cell Division / drug effects. Cell Membrane / drug effects. Cell Membrane / physiology. Cyclic AMP / metabolism. Ghrelin / secretion. Glucagon-Like Peptide 1 / secretion. Humans. Insulin Receptor Substrate Proteins. Intracellular Signaling Peptides and Proteins / drug effects. Intracellular Signaling Peptides and Proteins / metabolism. Phosphoproteins / drug effects. Phosphoproteins / metabolism

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(PMID = 18162507.001).

[ISSN] 1939-327X

[Journal-full-title] Diabetes

[ISO-abbreviation] Diabetes

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Ghrelin; 0 / IRS2 protein, human; 0 / Insulin Receptor Substrate Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Peptide Hormones; 0 / Phosphoproteins; 0 / obestatin, human; 89750-14-1 / Glucagon-Like Peptide 1; E0399OZS9N / Cyclic AMP; EC 3.4.22.- / Caspase 3

   

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[Title] Pathogenicity of T helper 2 T-cell clones from T-cell receptor transgenic non-obese diabetic mice is determined by tumour necrosis factor-alpha.

Although T cells producing Th2 cytokines are generally thought to counter a Th1 response, there have been reports of Th2 T-cell clones with pathogenic activity, including one previously reported by us in which the Th2 T-cell clone was derived from a T-cell receptor transgenic (TCR-Tg) mouse bearing pathogenic TCR.

In this study, our goal was to determine whether Th2 T-cell clones derived from a TCR-Tg in which the autoantigen was absent would be pathogenic and if so, to investigate possible mechanisms by which the Th2 T-cell clone could promote disease.

We found that a Th2 T-cell clone derived from the 6.9 TCR-Tg/non-obese diabetic (NOD).C6 mouse in which 6.9 T cells do not encounter autoantigen, produced Th2 cytokines but not interferon-gamma.

This Th2 T-cell clone, like the previous one we had isolated from the 2.5 TCR-Tg/NOD mouse, also turned out to be pathogenic.

Intracellular staining revealed that these Th2 T-cell clones produce low levels of tumour necrosis factor-alpha (TNF-alpha) in vitro, and after adoptive transfer, they migrate to the pancreas where they produce TNF-alpha as well as Th2 cytokines (interleukin (IL)-4, IL-10).

Induction of disease was prevented by administration of soluble TNF-alpha receptor to recipient mice, suggesting that the diabetogenicity of these Th2 T-cell clones is caused by their low level production of TNF-alpha.

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(PMID = 17983440.001).

[ISSN] 1365-2567

[Journal-full-title] Immunology

[ISO-abbreviation] Immunology

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / R01 DK050561; United States / NIDDK NIH HHS / DK / R56 DK050561; United States / NIDDK NIH HHS / DK / R01DK50561

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

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Cytokines; 0 / Icos protein, mouse; 0 / Inducible T-Cell Co-Stimulator Protein; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Tumor Necrosis Factor; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 31C4KY9ESH / Nitric Oxide

[Other-IDs] NLM/ PMC2433281

   

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Dietary insult in early life can affect the development and future function of the endocrine pancreas.

Serum insulin and pancreatic insulin content were reduced in LP-fed NOD offspring at 8 weeks, as were serum interferon gamma and pancreatic tumor necrosis factor alpha, while the number of pancreatic islets demonstrating peri-insulitis, and the degree of invasiveness were reduced.

To determine if LP caused early morphometric changes in the pancreas, we measured mean islet area at days 3 and 21.

Mean islet size did not differ with diet, but by 8 weeks of age LP-fed NOD females exhibited a significantly reduced islet number and mean islet area, and a lower fractional area of pancreas occupied by both alpha- and beta-cells than control-fed mice.

The mechanism is likely to involve both altered beta-cell morphology and function and changes in cytotoxic cytokines.

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(PMID = 19228796.001).

[ISSN] 1479-6805

[Journal-full-title] The Journal of endocrinology

[ISO-abbreviation] J. Endocrinol.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Insulin

   

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The bioactive sphingolipid ceramide induces oxidative stress by disrupting mitochondrial function and stimulating NADPH oxidase (NOX) activity, both implicated in cell death mechanisms.

Many anticancer chemotherapeutics (anthracyclines, Vinca alkaloids, paclitaxel, and fenretinide), as well as physiological stimuli such as tumor necrosis factor α (TNFα), stimulate ceramide accumulation and increase oxidative stress in malignant cells.

Consequently, ceramide metabolism in malignant cells and, in particular the up-regulation of glucosylceramide synthase (GCS), has gained considerable interest in contributing to chemoresistance.

We further showed, in both glioblastoma and neuroblastoma cells that glucosylceramide directly interfered with NOX assembly, hence delineating a direct resistance mechanism.

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(PMID = 20935456.001).

[ISSN] 1555-8576

[Journal-full-title] Cancer biology & therapy

[ISO-abbreviation] Cancer Biol. Ther.

[Language] ENG

[Grant] United States / NIGMS NIH HHS / GM / R01 GM077391; United States / NINDS NIH HHS / NS / U54 NS041069; United States / NIGMS NIH HHS / GM / GM77391; United States / NINDS NIH HHS / NS / U54 NS41069

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

[Publication-country] United States

[Chemical-registry-number] 0 / Glucosylceramides; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / Tumor Necrosis Factor-alpha; 80168379AG / Doxorubicin; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; EC 1.6.3.1 / NADPH Oxidase; EC 2.4.1.- / Glucosyltransferases; EC 2.4.1.80 / ceramide glucosyltransferase

[Other-IDs] NLM/ PMC3047104