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1
alpha cell tumor of the pancreas 2005:2010[pubdate] *count=100
483 results
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Items 1 to 100 of about 483
1.
Lackner C, Dlaska D, Fuchsbichler A, Stumptner C, Gogg-Kamerer M, Zatloukal K, Denk H:
p62 protein is expressed in pancreatic beta cells.
J Pathol
; 2005 Aug;206(4):402-8
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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
2.
Gotthardt M, Béhé MP, Grass J, Bauhofer A, Rinke A, Schipper ML, Kalinowski M, Arnold R, Oyen WJ, Behr TM:
Added value of gastrin receptor scintigraphy in comparison to somatostatin receptor scintigraphy in patients with carcinoids and other neuroendocrine tumours.
Endocr Relat Cancer
; 2006 Dec;13(4):1203-11
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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
3.
Pejcić I, Vrbić S, Filipović S, Sćekić M, Petković I, Pejcić L, Djenić N:
[Significance of serum tumor markers monitoring metastases in carcinomas of unknown primary site].
Vojnosanit Pregl
; 2010 Sep;67(9):723-31
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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
Advertisement
4.
Duell EJ, Casella DP, Burk RD, Kelsey KT, Holly EA:
Inflammation, genetic polymorphisms in proinflammatory genes TNF-A, RANTES, and CCR5, and risk of pancreatic adenocarcinoma.
Cancer Epidemiol Biomarkers Prev
; 2006 Apr;15(4):726-31
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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
5.
Chen X, Li SL, Wu T, Liu JD:
Proteasome inhibitor ameliorates severe acute pancreatitis and associated lung injury of rats.
World J Gastroenterol
; 2008 May 28;14(20):3249-53
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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
MedlinePlus Health Information.
consumer health - Lung Diseases
.
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.
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.
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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
6.
Shen SG, Zhang D, Hu HT, Li JH, Wang Z, Ma QY:
Effects of alpha-adrenoreceptor antagonists on apoptosis and proliferation of pancreatic cancer cells in vitro.
World J Gastroenterol
; 2008 Apr 21;14(15):2358-63
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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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.
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consumer health - Pancreatic Cancer
.
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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
7.
Rau BM, Krüger CM, Hasel C, Oliveira V, Rubie C, Beger HG, Schilling MK:
Effects of immunosuppressive and immunostimulative treatment on pancreatic injury and mortality in severe acute experimental pancreatitis.
Pancreas
; 2006 Aug;33(2):174-83
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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
8.
Qian ZY, Miao Y, Dai CC, Xu ZK, Liu XL:
[Combined multiple organ resection in 16 patients with adenocarcinoma of the body or tail of the pancreas].
Zhongguo Yi Xue Ke Xue Yuan Xue Bao
; 2005 Oct;27(5):572-4
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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
9.
Liao SY, Lerman MI, Stanbridge EJ:
Expression of transmembrane carbonic anhydrases, CAIX and CAXII, in human development.
BMC Dev Biol
; 2009 Mar 16;9:22
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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
10.
Marko PB, Miljković J, Zemljic TG:
Necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors.
Acta Dermatovenerol Alp Pannonica Adriat
; 2005 Dec;14(4):161-4, 166
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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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GLUCAGON
.
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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
11.
Nishida A, Andoh A, Inatomi O, Fujiyama Y:
Interleukin-32 expression in the pancreas.
J Biol Chem
; 2009 Jun 26;284(26):17868-76
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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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consumer health - Pancreatic Cancer
.
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NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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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
12.
Rizvi IA, Robinson K, McFadden DW, Riggs DR, Jackson BJ, Vona-Davis L:
Peptide YY reverses TNF-alpha induced transcription factor binding of interferon regulatory factor-1 and p53 in pancreatic acinar cells.
J Surg Res
; 2006 Nov;136(1):25-30
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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
13.
Aerts JM, Ottenhoff R, Powlson AS, Grefhorst A, van Eijk M, Dubbelhuis PF, Aten J, Kuipers F, Serlie MJ, Wennekes T, Sethi JK, O'Rahilly S, Overkleeft HS:
Pharmacological inhibition of glucosylceramide synthase enhances insulin sensitivity.
Diabetes
; 2007 May;56(5):1341-9
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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
MedlinePlus Health Information.
consumer health - Diabetes Medicines
.
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.
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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
14.
Chong MM, Metcalf D, Jamieson E, Alexander WS, Kay TW:
Suppressor of cytokine signaling-1 in T cells and macrophages is critical for preventing lethal inflammation.
Blood
; 2005 Sep 1;106(5):1668-75
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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
15.
de Herder WW:
Biochemistry of neuroendocrine tumours.
Best Pract Res Clin Endocrinol Metab
; 2007 Mar;21(1):33-41
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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
16.
Zhang XP, Lin Q, Zhou YF:
Progress of study on the relationship between mediators of inflammation and apoptosis in acute pancreatitis.
Dig Dis Sci
; 2007 May;52(5):1199-205
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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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[Cites]
Immunol Lett. 2001 Jun 1;77(2):79-85
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[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
17.
Chaw L, Krop TM, Hood AF:
What is your diagnosis? Necrolytic migratory erythema associated with a glucagonoma.
Cutis
; 2008 Jan;81(1):25, 30-2
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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
18.
Long C, Yin B, Lu Q, Zhou X, Hu J, Yang Y, Yu F, Yuan Y:
Promoter hypermethylation of the RUNX3 gene in esophageal squamous cell carcinoma.
Cancer Invest
; 2007 Dec;25(8):685-90
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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
19.
Cheung SS, Metzger DL, Wang X, Huang J, Tai J, Tingle AJ, Ou D:
Tumor necrosis factor-related apoptosis-inducing ligand and CD56 expression in patients with type 1 diabetes mellitus.
Pancreas
; 2005 Mar;30(2):105-14
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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
20.
Miettinen M, Lasota J:
Gastrointestinal stromal tumors: pathology and prognosis at different sites.
Semin Diagn Pathol
; 2006 May;23(2):70-83
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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
21.
Shen HC, Ylaya K, Pechhold K, Wilson A, Adem A, Hewitt SM, Libutti SK:
Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice.
Endocrinology
; 2010 Aug;151(8):4024-30
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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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.
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[Cites]
Development. 2000 Jun;127(11):2317-22
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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
22.
Yu G, Tang B, Yu PW, Peng ZH, Qian F, Sun G:
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.
Surg Endosc
; 2010 Nov;24(11):2860-70
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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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[
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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
23.
Zou GM, Maitra A:
Small-molecule inhibitor of the AP endonuclease 1/REF-1 E3330 inhibits pancreatic cancer cell growth and migration.
Mol Cancer Ther
; 2008 Jul;7(7):2012-21
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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
24.
Eastham LL, Mills CN, Niles RM:
PPARalpha/gamma expression and activity in mouse and human melanocytes and melanoma cells.
Pharm Res
; 2008 Jun;25(6):1327-33
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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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Melanoma Res. 2003 Oct;13(5):447-56
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[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
25.
Yang F, Shi P, Xi X, Yi S, Li H, Sun Q, Sun M:
Recombinant adenoviruses expressing TRAIL demonstrate antitumor effects on non-small cell lung cancer (NSCLC).
Med Oncol
; 2006;23(2):191-204
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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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.
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[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
26.
Stoeltzing O, Liu W, Fan F, Wagner C, Stengel K, Somcio RJ, Reinmuth N, Parikh AA, Hicklin DJ, Ellis LM:
Regulation of cyclooxygenase-2 (COX-2) expression in human pancreatic carcinoma cells by the insulin-like growth factor-I receptor (IGF-IR) system.
Cancer Lett
; 2007 Dec 18;258(2):291-300
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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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Pancreas. 2001 Apr;22(3):293-8
[
11291932.001
]
(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
27.
Lin YC, Lee PH, Yao YT, Hsiao JK, Sheu JC, Chen CH:
Alpha-fetoprotein-producing pancreatic acinar cell carcinoma.
J Formos Med Assoc
; 2007 Aug;106(8):669-72
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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
28.
Nishiuchi T, Imachi H, Murao K, Fujiwara M, Muraoka T, Kikuchi F, Nishiuchi Y, Kushida Y, Haba R, Ishida T:
Co-existence of glucagonoma with recurrent insulinoma in a patient with multiple endocrine neoplasia-type 1 (MEN-1).
Endocrine
; 2009 Aug;36(1):20-4
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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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.
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.
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.
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.
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.
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[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
29.
Serra S, Salahshor S, Fagih M, Niakosari F, Radhi JM, Chetty R:
Nuclear expression of E-cadherin in solid pseudopapillary tumors of the pancreas.
JOP
; 2007;8(3):296-303
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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
30.
Peracaula R, Tabarés G, López-Ferrer A, Brossmer R, de Bolós C, de Llorens R:
Role of sialyltransferases involved in the biosynthesis of Lewis antigens in human pancreatic tumour cells.
Glycoconj J
; 2005 Mar;22(3):135-44
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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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[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
31.
Cuzzocrea S, Malleo G, Genovese T, Mazzon E, Esposito E, Muià C, Abdelrahman M, Di Paola R, Thiemermann C:
Effects of glycogen synthase kinase-3beta inhibition on the development of cerulein-induced acute pancreatitis in mice.
Crit Care Med
; 2007 Dec;35(12):2811-21
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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
32.
Takahashi H, Funahashi H, Sawai H, Matsuo Y, Yamamoto M, Okada Y, Takeyama H, Manabe T:
Synthetic serine protease inhibitor, gabexate mesilate, prevents nuclear factor-kappaB activation and increases TNF-alpha-mediated apoptosis in human pancreatic cancer cells.
Dig Dis Sci
; 2007 Oct;52(10):2646-52
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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
Genetic Alliance.
consumer health - Pancreatic cancer
.
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.
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]
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[
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]
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Science. 1998 Sep 11;281(5383):1680-3
[
9733516.001
]
(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
33.
Granata R, Settanni F, Gallo D, Trovato L, Biancone L, Cantaluppi V, Nano R, Annunziata M, Campiglia P, Arnoletti E, Ghè C, Volante M, Papotti M, Muccioli G, Ghigo E:
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.
Diabetes
; 2008 Apr;57(4):967-79
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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
34.
He J, Haskins K:
Pathogenicity of T helper 2 T-cell clones from T-cell receptor transgenic non-obese diabetic mice is determined by tumour necrosis factor-alpha.
Immunology
; 2008 Jan;123(1):108-17
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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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[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
35.
Chamson-Reig A, Arany EJ, Summers K, Hill DJ:
A low protein diet in early life delays the onset of diabetes in the non-obese diabetic mouse.
J Endocrinol
; 2009 May;201(2):231-9
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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
36.
Barth BM, Gustafson SJ, Young MM, Fox TE, Shanmugavelandy SS, Kaiser JM, Cabot MC, Kester M, Kuhn TB:
Inhibition of NADPH oxidase by glucosylceramide confers chemoresistance.
Cancer Biol Ther
; 2010 Dec 1;10(11):1126-36
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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
37.
Matsuda T, Almasan A, Tomita M, Uchihara JN, Masuda M, Ohshiro K, Takasu N, Yagita H, Ohta T, Mori N:
Resistance to Apo2 ligand (Apo2L)/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis and constitutive expression of Apo2L/TRAIL in human T-cell leukemia virus type 1-infected T-cell lines.
J Virol
; 2005 Feb;79(3):1367-78
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[Title]
Resistance to Apo2 ligand (Apo2L)/
tumor
necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis and constitutive expression of Apo2L/TRAIL in human T-
cell
leukemia virus type 1-infected T-
cell
lines.
Adult T-
cell
leukemia (ATL), a CD4+-T-
cell
malignancy caused by human T-
cell
leukemia virus type 1 (HTLV-1), is difficult to cure, and novel treatments are urgently needed.
Apo2 ligand (Apo2L; also
tumor
necrosis factor-related apoptosis-inducing ligand [TRAIL]) has been implicated in antitumor therapy.
We found that HTLV-1-infected T-
cell
lines and primary ATL
cells
were more resistant to Apo2L-induced apoptosis than uninfected
cells
.
Interestingly, HTLV-1-infected T-
cell
lines and primary ATL
cells
constitutively expressed Apo2L mRNA.
Inducible expression of the viral oncoprotein Tax in a T-
cell
line up-regulated Apo2L mRNA.
NF-kappaB plays a crucial role in the pathogenesis and survival of ATL
cells
.
[MeSH-major]
Gene Expression Regulation. Gene Products, tax / metabolism. Human T-lymphotropic virus 1 / pathogenicity. Membrane Glycoproteins / metabolism. NF-kappa B / metabolism. T-Lymphocytes / virology.
Tumor
Necrosis Factor-
alpha
/ metabolism
[MeSH-minor]
Apoptosis. Apoptosis Regulatory Proteins.
Cell
Line. Humans. Leukemia-Lymphoma, Adult T-
Cell
. Ligands. TNF-Related Apoptosis-Inducing Ligand. Transcriptional Activation
Genetic Alliance.
consumer health - Human T-cell leukemia virus type 1
.
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[RetractionIn]
J Virol. 2011 Feb;85(3):1416
[
21228250.001
]
(PMID = 15650163.001).
[ISSN]
0022-538X
[Journal-full-title]
Journal of virology
[ISO-abbreviation]
J. Virol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
[Publication-country]
United States
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / Gene Products, tax; 0 / Ligands; 0 / Membrane Glycoproteins; 0 / NF-kappa B; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha
[Other-IDs]
NLM/ PMC544134
38.
Mastrandrea LD, Sessanna SM, Del Toro A, Laychock SG:
ATP-independent glucose stimulation of sphingosine kinase in rat pancreatic islets.
J Lipid Res
; 2010 Aug;51(8):2171-80
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[Title]
ATP-independent glucose stimulation of sphingosine kinase in rat
pancreatic
islets.
Sphingosine kinase (SPHK) catalyzes sphingosine 1-phosphate production, promoting
cell
survival and reducing apoptosis in isolated rat
pancreatic
islets.
Glucose, the primary
islet
beta-
cell
growth factor and insulin secretagogue, increased
islet
SPHK activity by 3- to 5-fold following acute (1 h) or prolonged (7 days) stimulation.
In contrast, 3-o-methylglucose (3-oMeG), which is transported but neither phosphorylated nor metabolized, did not increase
islet
SPHK activity.
Glyceraldehyde and
alpha
-ketoisocaproic acid (KIC), metabolites that stimulate glycolysis and the citric acid cycle, respectively, did not activate
islet
SPHK.
A role for SPHK activity in beta-
cell
growth was confirmed when small interfering (si)SPHK2 RNA transfection reduced rat insulinoma INS-1e
cell
SPHK levels and activity and
cell
growth.
Glucose induced an early and sustained increase in
islet
SPHK activity that was dependent on glucose phosphorylation, but independent of ATP generation or new protein biosynthesis.
Glucose-supported beta-
cell
growth appears to be in part mediated by SPHK activity.
[MeSH-major]
Adenosine Triphosphate. Glucose / pharmacology. Insulin-Secreting
Cells
/ drug effects. Insulin-Secreting
Cells
/ metabolism. Phosphotransferases (Alcohol Group Acceptor) / genetics. Phosphotransferases (Alcohol Group Acceptor) / metabolism
[MeSH-minor]
Animals.
Cell
Line,
Tumor
.
Cell
Proliferation / drug effects. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Enzymologic / genetics. Gene Knockdown Techniques. RNA, Small Interfering / genetics. Rats. Time Factors
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[ISSN]
1539-7262
[Journal-full-title]
Journal of lipid research
[ISO-abbreviation]
J. Lipid Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / RNA, Small Interfering; 8L70Q75FXE / Adenosine Triphosphate; EC 2.7.1.- / Phosphotransferases (Alcohol Group Acceptor); EC 2.7.1.- / sphingosine kinase; IY9XDZ35W2 / Glucose
[Other-IDs]
NLM/ PMC2903817
39.
Stone SP, Buescher LS:
Life-threatening paraneoplastic cutaneous syndromes.
Clin Dermatol
; 2005 May-Jun;23(3):301-6
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[Title]
Life-threatening paraneoplastic cutaneous
syndromes
.
Paraneoplastic
syndromes
are diseases or symptom complexes associated with malignancy, usually internal.
In this article, we discuss the link between malignancy and such dermatologic disorders as acanthosis nigricans, acrokeratosis paraneoplastica of Bazex, dermatomyositis, erythema gyratum repens, necrolytic migratory erythema (
glucagonoma syndrome
), and paraneoplastic pemphigus and discuss, where such information is known, the mechanism by which these paraneoplastic diseases occur.
[MeSH-major]
Paraneoplastic
Syndromes
/
diagnosis
. Skin Diseases /
diagnosis
[MeSH-minor]
Critical Illness. Erythema /
diagnosis
. Humans. Neoplasms /
diagnosis
. Pemphigus /
diagnosis
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(PMID = 15896545.001).
[ISSN]
0738-081X
[Journal-full-title]
Clinics in dermatology
[ISO-abbreviation]
Clin. Dermatol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
54
40.
Libé R, Chanson P:
[Endocrine tumors of the pancreas (EPTs) in multiple endocrine neoplasia (MEN1): up-date on prognostic factors, diagnostic procedures and treatment].
Ann Endocrinol (Paris)
; 2007 Jun;68 Suppl 1:1-8
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[Title]
[Endocrine
tumors
of the
pancreas
(EPTs) in multiple endocrine neoplasia (MEN1): up-date on prognostic factors, diagnostic procedures and treatment].
[Transliterated title]
Les tumeurs endocrines
du
pancréas lors
de
la néoplasie endocrinienne multiple type 1 (NEM1): actualités sur les facteurs pronostiques, l'imagerie et le traitement.
Endocrine
pancreatic tumors
(EPTs) are uncommon
tumors
, representing 1-2% of all
pancreatic
neoplasms.
They are categorized on the basis of their clinical features into functioning and non-functioning
tumors
.
EPTs may be part of the multiple endocrine neoplasia type 1 (MEN 1), an autosomal dominant
syndrome
due to inactivating germline mutation of the menin gene.
Among the different imaging techniques, echoendoscopy, computed tomography (CT) and magnetic resonance imaging (MRI) are indicated for the detection of the primary
tumor
, but (III)In-octreotide scintigraphy has the highest sensitivity for detecting metastases.
The choice of treatment is still debated and is different when
the tumor
occurs as a part of the MEN
syndrome
.
The medical treatment includes somatostatin analogues (SA), chemotherapy and interferon-
alpha
(IFN-
alpha
).
Chemotherapy, which is generally proposed as a combination of streptozotocin (STZ) and 5-fluorouracil (5-FU) or doxorubicin, is indicated when the
tumors
tend to grow.
Interferon-
alpha
(IFN-
alpha
) stimulates the immune system, blocks
the tumor
cells
in the G1/S-phase of the
cell
cycle, inhibits protein and hormone synthesis and inhibits angionenesis.
Treatment with IFN has been shown to produce symptomatic response in 40-60% of patients, a biochemical response in 30-60% and
tumor
shrinkage in 10-15%.
[MeSH-major]
Carcinoma,
Islet
Cell
. Multiple Endocrine Neoplasia Type 1
Genetic Alliance.
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.
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[ErratumIn]
Ann Endocrinol (Paris). 2008 Nov;69(5):459-60
(PMID = 17961653.001).
[ISSN]
0003-4266
[Journal-full-title]
Annales d'endocrinologie
[ISO-abbreviation]
Ann. Endocrinol. (Paris)
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
41.
Cheshire H, Stather P, Vorster J:
Acquired acrodermatitis enteropathica due to zinc deficiency in a patient with pre-existing Darier's disease.
J Dermatol Case Rep
; 2009 Nov 28;3(3):41-3
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[Title]
Acquired acrodermatitis enteropathica due to zinc deficiency in a patient with pre-existing Darier'
s disease
.
Typically these patches start near the body's orifices before migrating to other sites, however in this patient the presentation was atypical thus delaying the
diagnosis
.
OBSERVATIONS: We report a case of an atypical presentation of acrodermatitis enteropathica (AE) due to acquired zinc deficiency in a 65 year old female patient with a previous
diagnosis
of histologically confirmed Darier'
s disease
.
Acrodermatitis enteropathica typically presents in infants, either due to an autosomal recessive genetic
disorder
, or after the cessation of breast feeding.
In adults acquired zinc deficiency can be caused by
glucagonoma syndrome
, poor nutritional state, intestinal malabsorption, nephrotic
syndrome
and after major trauma (i.e. burns or significant surgery).
In our patient low zinc levels confirmed hypozincaemia and the
diagnosis
of acrodermatitis enteropathica.
CONCLUSION: We believe this to be an unusual presentation of acrodermatitis enteropathica due to a probable dietary zinc deficiency in a lady with pre-existing Darier'
s disease
which may possibly have influenced the uncharacteristic clinical presentation.
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[Cites]
Clin Dermatol. 2000 Nov-Dec;18(6):745-8
[
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[
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]
[Cites]
Br J Dermatol. 2009 Jul;161(1):184-6
[
19416256.001
]
(PMID = 21886729.001).
[ISSN]
1898-7249
[Journal-full-title]
Journal of dermatological case reports
[ISO-abbreviation]
J Dermatol Case Rep
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Poland
[Other-IDs]
NLM/ PMC3157796
[Keywords]
NOTNLM ; Darier's disease / acrodermatitis enteropathica / hair loss / mucous membranes / zinc
42.
Lewis RB, Lattin GE Jr, Paal E:
Pancreatic endocrine tumors: radiologic-clinicopathologic correlation.
Radiographics
; 2010 Oct;30(6):1445-64
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[Title]
Pancreatic
endocrine
tumors
: radiologic-clinicopathologic correlation.
Pancreatic
endocrine
tumors
(PETs) are primarily well-differentiated
tumors
composed of
cells
that resemble normal
islet cells
but that arise from
pancreatic
ductal
cells
.
They are classified as functioning or nonfunctioning according to their associated clinical symptoms; insulinoma, gastrinoma, and
glucagonoma
are the most common functioning PETs.
Most are sporadic, but some are associated with familial
syndromes
such as multiple endocrine neoplasia type 1, von Hippel-Lindau
syndrome
, and neurofibromatosis type 1.
At imaging, PETs typically appear as well-defined hypervascular masses,
a finding
indicative of their rich capillary network.
Cystic change, calcification, and necrosis are common in large
tumors
, which are associated with a poorer prognosis and a higher prevalence of local and vascular invasion and metastases than are smaller
tumors
.
Poorly differentiated PETs are rare and have an infiltrative appearance; patients with such
tumors
have a poor prognosis.
Knowledge of the characteristic clinical, pathologic, and radiologic features of PETs is important in the evaluation and management of patients with a suspected clinical
syndrome
or
a pancreatic
mass.
[MeSH-major]
Diagnostic Imaging.
Pancreatic
Neoplasms /
diagnosis
[MeSH-minor]
Adenoma
,
Islet
Cell
/
diagnosis
.
Adenoma
,
Islet
Cell
/ epidemiology.
Adenoma
,
Islet
Cell
/ pathology. Carcinoma,
Islet
Cell
/
diagnosis
. Carcinoma,
Islet
Cell
/ epidemiology. Carcinoma,
Islet
Cell
/ pathology.
Diagnosis
, Differential. Humans. Multiple Endocrine Neoplasia Type 1 / pathology. Neurofibromatosis 1 / pathology. Prevalence. von Hippel-Lindau
Disease
/ pathology
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[Copyright]
© RSNA, 2010.
(PMID = 21071369.001).
[ISSN]
1527-1323
[Journal-full-title]
Radiographics : a review publication of the Radiological Society of North America, Inc
[ISO-abbreviation]
Radiographics
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
43.
Shi Y, Sahu RP, Srivastava SK:
Triphala inhibits both in vitro and in vivo xenograft growth of pancreatic tumor cells by inducing apoptosis.
BMC Cancer
; 2008;8:294
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[Title]
Triphala inhibits both in vitro and in vivo xenograft growth of
pancreatic
tumor
cells
by inducing apoptosis.
This study elucidates the molecular mechanism of Triphala against human
pancreatic
cancer in the cellular and in vivo model.
METHODS: Growth-inhibitory effects of Triphala were evaluated in Capan-2, BxPC-3 and HPDE-6
cells
by Sulphoradamine-B assay.
Apoptosis was determined by
cell
death assay and western blotting.
Tumors
were analyzed by immunohistochemistry and western blotting.
RESULTS: Exposure of Capan-2
cells
to the aqueous extract of Triphala for 24 h resulted in the significant decrease in the survival of
cells
in a dose-dependent manner with an IC50 of about 50 microg/ml.
Triphala-mediated reduced
cell
survival correlated with induction of apoptosis, which was associated with reactive oxygen species (ROS) generation.
Triphala-induced apoptosis was linked with phosphorylation of p53 at Ser-15 and ERK at Thr-202/Tyr-204 in Capan-2
cells
.
Above mentioned effects were significantly blocked when the
cells
were pretreated with an antioxidant N-acetylcysteine (NAC), suggesting the involvement of ROS generation.
Pretreatment of
cells
with pifithrin-
alpha
or U0126, specific inhibitors of p53 or MEK-1/2, significantly attenuated Triphala-induced apoptosis.
Similarly, Triphala induced apoptosis in another
pancreatic
cancer
cell
line BxPC-3 by activating ERK.
On the other hand, Triphala failed to induce apoptosis or activate ERK or p53 in normal human
pancreatic
ductal epithelial (HPDE-6)
cells
.
Further, oral administration of 50 mg/kg or 100 mg/kg Triphala in PBS, 5 days/week significantly suppressed the growth of Capan-2
pancreatic
tumor
-xenograft.
Reduced
tumor
-growth in Triphala fed mice was due to increased apoptosis in the
tumors cells
, which was associated with increased activation of p53 and ERK.
CONCLUSION: Our preclinical studies demonstrate that Triphala is effective in inhibiting the growth of human
pancreatic
cancer
cells
in both cellular and in vivo model.
Our data also suggests that the growth inhibitory effects of Triphala is mediated by the activation of ERK and p53 and shows potential for the treatment and/or prevention of human
pancreatic
cancer.
[MeSH-major]
Antineoplastic Agents / pharmacology. Apoptosis / drug effects.
Pancreatic
Neoplasms / pathology. Plant Extracts / pharmacology
[MeSH-minor]
Animals.
Cell
Line,
Tumor
.
Cell
Survival / drug effects. DNA Damage. Enzyme Activation. Enzyme-Linked Immunosorbent Assay. Extracellular Signal-Regulated MAP Kinases / genetics. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Immunohistochemistry. Mice. Neoplasm Transplantation.
Pancreas
/ metabolism.
Pancreas
/ pathology. Reactive Oxygen Species / metabolism. Transplantation, Heterologous.
Tumor
Suppressor Protein p53 / genetics.
Tumor
Suppressor Protein p53 / metabolism
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[ISSN]
1471-2407
[Journal-full-title]
BMC cancer
[ISO-abbreviation]
BMC Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA106953
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Plant Extracts; 0 / Reactive Oxygen Species; 0 / Tumor Suppressor Protein p53; 0 / triphala; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
[Other-IDs]
NLM/ PMC2576337
44.
Esposito I, Penzel R, Chaib-Harrireche M, Barcena U, Bergmann F, Riedl S, Kayed H, Giese N, Kleeff J, Friess H, Schirmacher P:
Tenascin C and annexin II expression in the process of pancreatic carcinogenesis.
J Pathol
; 2006 Apr;208(5):673-85
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[Title]
Tenascin C and annexin II expression in the process of
pancreatic
carcinogenesis.
Cell
surface annexin II is a high-affinity receptor for large TNC splice variants.
The aim of this study was to analyse whether TNC and annexin II play a role in the development of
pancreatic
ductal adenocarcinoma (PDAC).
PDAC is characterized by a rich ECM populated by
pancreatic
stellate
cells
, which play a crucial role in
pancreatic
desmoplasia.
The mRNA and protein levels of TNC and of annexin II were analysed in
pancreatic
tissues by DNA array, quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR) and immunohistochemistry.
TNC and annexin II mRNA levels were significantly higher in
pancreatic
cancer tissues than in the normal
pancreas
.
TNC expression was detected with increased frequency in the progression from PanIN-1 lesions to PDAC, and a parallel switch from cytoplasmic to
cell
surface expression of annexin II was observed.
Large TNC transcripts were found in
pancreatic
cancer and in chronic pancreatitis, but not in the normal
pancreas
.
TNC expression was demonstrated in
pancreatic
stellate
cells
, where it could be induced by
tumour
necrosis factor
alpha
(TNFalpha), transforming growth factor beta1 (TGF-beta1) and by cancer
cell
supernatants supplemented with TGF-beta1.
In conclusion, the expression of TNC and
cell
surface annexin II increases in the progression from low-grade PanIN lesions to
pancreatic
cancer.
Pancreatic
stellate
cells
are identified as a source of TNC in
pancreatic
tissues, possibly under the influence of soluble factors released by the
tumour cells
.
[MeSH-major]
Adenocarcinoma / metabolism. Annexin A2 / metabolism.
Cell
Transformation, Neoplastic / metabolism.
Pancreatic
Neoplasms / metabolism. Tenascin / metabolism
[MeSH-minor]
Blotting, Western. Gene Expression Regulation, Neoplastic / drug effects. Humans. Immunoenzyme Techniques. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Pancreatitis, Chronic / metabolism. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Transforming Growth Factor beta / pharmacology. Transforming Growth Factor beta1.
Tumor
Cells
, Cultured.
Tumor
Necrosis Factor-
alpha
/ pharmacology
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(PMID = 16450333.001).
[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 / Annexin A2; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / TGFB1 protein, human; 0 / Tenascin; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha
45.
Sanlioglu AD, Griffith TS, Omer A, Dirice E, Sari R, Altunbas HA, Balci MK, Sanlioglu S:
Molecular mechanisms of death ligand-mediated immune modulation: a gene therapy model to prolong islet survival in type 1 diabetes.
J Cell Biochem
; 2008 Jun 1;104(3):710-20
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[Title]
Molecular mechanisms of death ligand-mediated immune modulation: a gene therapy model to prolong
islet
survival in type 1 diabetes.
Type 1 diabetes results from the T
cell
-mediated destruction of
pancreatic
beta
cells
.
Islet
transplantation has recently become a potential therapeutic approach for patients with type 1 diabetes.
However,
islet
-graft failure appears to be a challenging issue to overcome.
Thus, complementary gene therapy strategies are needed to improve the
islet
-graft survival following transplantation.
Immune modulation through gene therapy represents a novel way of attacking cytotoxic T
cells
targeting
pancreatic
islets.
The over-expression of TNF or FasL in
pancreatic
islets exacerbates the onset of type 1 diabetes generating lymphocyte infiltrates responsible for the inflammation.
Conversely, the lack of TRAIL expression results in higher degree of
islet
inflammation in
the pancreas
.
These results suggested that contrary to what was observed with TNF or FasL, adenovirus mediated TRAIL gene delivery into
pancreatic
islets is expected to be therapeutically beneficial in the setting of experimental models of type 1 diabetes.
[MeSH-minor]
Adenoviridae / genetics. Adenoviridae / metabolism. Animals. Fas Ligand Protein / metabolism. Gene Transfer Techniques. Humans. Islets of Langerhans / cytology. Rats. T-Lymphocytes, Cytotoxic / metabolism. Treatment Outcome.
Tumor
Necrosis Factor-
alpha
/ metabolism
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(PMID = 18247339.001).
[ISSN]
1097-4644
[Journal-full-title]
Journal of cellular biochemistry
[ISO-abbreviation]
J. Cell. Biochem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Fas Ligand Protein; 0 / Tumor Necrosis Factor-alpha
[Number-of-references]
70
46.
Kerem M, Bedirli A, Pasaoglu H, Unsal C, Yilmaz TU, Ofluoglu E, Sahin TT:
Role of ghrelin and leptin in predicting the severity of acute pancreatitis.
Dig Dis Sci
; 2007 Apr;52(4):950-5
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Ghrelin and leptin are the hormones that influence endocrine and exocrine functions of the
pancreas
and regulate feeding behaviors and energy metabolism.
After blood withdrawal,
the pancreas
was totally excised.
The levels of blood sugar, lipase, serum
tumor
necrosis factor-
alpha
(TNF-
alpha
), interleukin-1beta (IL-1beta), ghrelin, and leptin were investigated and histopathologic examination was performed.
The levels of TNF-
alpha
and IL-1beta in the AEP and ANP groups reached the peak level at 24 hr and then decreased to a level close to that of the control group at 48 hr.
While TNF-
alpha
and IL-1beta can be used as a prognostic factor in the first 24 hr, ghrelin and leptin can be used subsequently.
[MeSH-major]
Leptin / blood. Pancreatitis /
diagnosis
. Peptide Hormones / blood
[MeSH-minor]
Acute
Disease
. Animals. Biomarkers / blood. Blood Glucose / analysis. Ghrelin. Interleukin-1beta / blood. Lipase / blood. Male.
Pancreas
/ pathology. Pancreatitis, Acute Necrotizing /
diagnosis
. Prognosis. Rats. Rats, Wistar.
Tumor
Necrosis Factor-
alpha
/ analysis
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[Cites]
J Clin Endocrinol Metab. 2002 Jan;87(1):240-4
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]
(PMID = 17333355.001).
[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
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers; 0 / Blood Glucose; 0 / Ghrelin; 0 / Interleukin-1beta; 0 / Leptin; 0 / Peptide Hormones; 0 / Tumor Necrosis Factor-alpha; EC 3.1.1.3 / Lipase
47.
Stehr SN, Heller AR:
Omega-3 fatty acid effects on biochemical indices following cancer surgery.
Clin Chim Acta
; 2006 Nov;373(1-2):1-8
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Mechanisms accounting for these anti-
tumor
effects are reduced levels of PGE(2) and inducible NO synthase as well as an increased lipid peroxidation, or translation inhibition with subsequent
cell
cycle arrest.
Further, omega-3 eicosapentaenoic acid is capable of down-regulating the production and effect of a number of mediators of cachexia, such as IL-1, IL-6, TNF-
alpha
and proteolysis-inducing factor.
In patients undergoing
tumor
resection surgery we observed improvement of liver and
pancreas
biochemical indices when omega-3 fatty acids were administered.
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(PMID = 16796997.001).
[ISSN]
0009-8981
[Journal-full-title]
Clinica chimica acta; international journal of clinical chemistry
[ISO-abbreviation]
Clin. Chim. Acta
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Fatty Acids, Omega-3
[Number-of-references]
66
48.
Hoffmann AC, Mori R, Vallbohmer D, Brabender J, Klein E, Drebber U, Baldus SE, Cooc J, Azuma M, Metzger R, Hoelscher AH, Danenberg KD, Prenzel KL, Danenberg PV:
High expression of HIF1a is a predictor of clinical outcome in patients with pancreatic ductal adenocarcinomas and correlated to PDGFA, VEGF, and bFGF.
Neoplasia
; 2008 Jul;10(7):674-9
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[Title]
High expression of HIF1a is a predictor of clinical outcome in patients with
pancreatic
ductal adenocarcinomas and correlated to PDGFA, VEGF, and bFGF.
PURPOSE:
Pancreatic
cancer still has one of the worst prognoses in gastrointestinal cancers with a 5-year survival rate of 5%, making it necessary to find markers or gene sets that would further classify patients into different risk categories and thus allow more individually adapted multimodality treatment regimens.
EXPERIMENTAL DESIGN: Formalin-fixed paraffin-embedded tissue samples were obtained from 41 patients with
pancreatic
adenocarcinoma (age, 65; range, 34-85 years).
Tumor
size, P = .04, and high HIF1a mRNA expression (cutoff, 75th percentile) had a significant impact on survival, P = .009 (overall model fit, P = .02).
High HIF1a expression had a sensitivity of 87.1% and a specificity of 55.6% for the
diagnosis
short (<6 months) versus long (6-60 months) survival.
CONCLUSIONS: Measuring PDGFA, bFGF, and HIF1a expression may contribute to a better understanding of the prognosis of patients with
pancreatic
cancer and may even play a crucial role for the distribution of patients to multimodal therapeutic regimens.
[MeSH-major]
Carcinoma,
Pancreatic
Ductal /
diagnosis
. Fibroblast Growth Factor 2 / genetics. Hypoxia-Inducible Factor 1,
alpha
Subunit / genetics.
Pancreatic
Neoplasms /
diagnosis
. Platelet-Derived Growth Factor / genetics. Vascular Endothelial Growth Factors / genetics
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Biomarkers,
Tumor
/ genetics. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Middle Aged. Prognosis. Survival Analysis. Up-Regulation
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[ISSN]
1476-5586
[Journal-full-title]
Neoplasia (New York, N.Y.)
[ISO-abbreviation]
Neoplasia
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Canada
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Platelet-Derived Growth Factor; 0 / Vascular Endothelial Growth Factors; 0 / platelet-derived growth factor A; 103107-01-3 / Fibroblast Growth Factor 2
[Other-IDs]
NLM/ PMC2435004
49.
Marrache F, Tu SP, Bhagat G, Pendyala S, Osterreicher CH, Gordon S, Ramanathan V, Penz-Osterreicher M, Betz KS, Song Z, Wang TC:
Overexpression of interleukin-1beta in the murine pancreas results in chronic pancreatitis.
Gastroenterology
; 2008 Oct;135(4):1277-87
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[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
50.
Ma RY, Tam TS, Suen AP, Yeung PM, Tsang SW, Chung SK, Thomas MK, Leung PS, Yao KM:
Secreted PDZD2 exerts concentration-dependent effects on the proliferation of INS-1E cells.
Int J Biochem Cell Biol
; 2006;38(5-6):1015-22
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[Title]
Secreted PDZD2 exerts concentration-dependent effects on the proliferation of INS-1E
cells
.
PDZD2 (PDZ domain containing 2) is a multi-PDZ protein expressed in
pancreas
and many other tissues.
To understand the possible functional role of PDZD2 in
pancreas
, we investigated the cellular distribution of PDZD2 in adult
pancreas
using an antiserum that recognizes both the full-length and secreted forms of PDZD2.
Immunohistochemical analysis revealed a strong expression of PDZD2 in
pancreatic islet
beta
cells
but not
alpha
cells
.
Consistent with the beta-
cell
-enriched expression of PDZD2, immunoblot analysis indicated expression of both full-length PDZD2 and sPDZD2 in the insulinoma
cell
line INS-1E.
A recombinant sPDZD2 protein was synthesized for study of its functional effect on INS-1E
cells
.
In culture media with limiting serum, co-incubation with sPDZD2 stimulated the proliferation of INS-1E
cells
.
As a potential mitogen of beta-like
cells
, sPDZD2 may be useful for the optimization of beta-
cell
growth and differentiation in vitro.
[MeSH-minor]
Adaptor Proteins, Signal Transducing. Adult.
Cell
Line,
Tumor
.
Cell
Proliferation / drug effects. Humans. Insulin-Secreting
Cells
/ metabolism. Mitogens / pharmacology. Neoplasm Proteins.
Pancreas
/ metabolism
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(PMID = 16413998.001).
[ISSN]
1357-2725
[Journal-full-title]
The international journal of biochemistry & cell biology
[ISO-abbreviation]
Int. J. Biochem. Cell Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Adaptor Proteins, Signal Transducing; 0 / Intracellular Signaling Peptides and Proteins; 0 / Mitogens; 0 / Neoplasm Proteins; 0 / PDZD2 protein, human
51.
Ralhan R, Desouza LV, Matta A, Tripathi SC, Ghanny S, Datta Gupta S, Bahadur S, Siu KW:
Discovery and verification of head-and-neck cancer biomarkers by differential protein expression analysis using iTRAQ labeling, multidimensional liquid chromatography, and tandem mass spectrometry.
Mol Cell Proteomics
; 2008 06;7(6):1162-73
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Multidimensional LC-MS/MS has been used for the analysis of biological samples labeled with isobaric mass tags for relative and absolute quantitation (iTRAQ) to identify proteins that are differentially expressed in human head-and-neck squamous
cell
carcinomas (HNSCCs) in relation to non-cancerous head-and-neck tissues (controls) for cancer biomarker discovery.
Some of the proteins include stratifin (14-3-3sigma); YWHAZ (14-3-3zeta); three calcium-binding proteins of the S100 family, S100-A2, S100-A7 (psoriasin), and S100-A11 (calgizarrin); prothymosin
alpha
(PTHA); L-lactate dehydrogenase A chain; glutathione S-transferase Pi; APC-binding protein EB1; and fascin.
[MeSH-major]
Biomarkers,
Tumor
/ metabolism. Chromatography, Liquid / methods. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Head and Neck Neoplasms / metabolism. Proteomics / methods. Tandem Mass Spectrometry / methods
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NCI CPTC Antibody Characterization Program.
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]
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Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13015-20
[
11078522.001
]
(PMID = 18339795.001).
[ISSN]
1535-9484
[Journal-full-title]
Molecular & cellular proteomics : MCP
[ISO-abbreviation]
Mol. Cell Proteomics
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / 14-3-3 Proteins; 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / Neoplasm Proteins; 0 / S100 Proteins; 0 / S100A7 protein, human; EC 3.1.- / Exonucleases; EC 3.1.- / Exoribonucleases; EC 3.1.- / SFN protein, human
[Other-IDs]
NLM/ PMC2424195
52.
Dourakis SP, Alexopoulou A, Georgousi KK, Delladetsima JK, Tolis G, Archimandritis AJ:
Glucagonoma syndrome: survival 21 years with concurrent liver metastases.
Am J Med Sci
; 2007 Sep;334(3):225-7
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[Title]
Glucagonoma syndrome
: survival 21 years with concurrent liver metastases.
A patient who survived for 21 years since initial discovery of
glucagonoma
with concurrent liver metastases is described.
Psychiatric symptoms, weight loss, necrolytic migratory erythema, diarrhea, and diabetes mellitus developed gradually after
diagnosis
of the
tumor
.
The longevity of this patient may be related to the slow
tumor
growth expressed histologically by ischemic necrosis of the malignant
cells
and in imaging by extensive
tumor
calcifications, a very rare
finding
in this type of the
tumor
.
[MeSH-major]
Glucagonoma
/ pathology. Liver Neoplasms / secondary.
Pancreatic
Neoplasms / pathology
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.
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.
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.
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(PMID = 17873541.001).
[ISSN]
0002-9629
[Journal-full-title]
The American journal of the medical sciences
[ISO-abbreviation]
Am. J. Med. Sci.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
53.
Chow JY, Ban M, Wu HL, Nguyen F, Huang M, Chung H, Dong H, Carethers JM:
TGF-beta downregulates PTEN via activation of NF-kappaB in pancreatic cancer cells.
Am J Physiol Gastrointest Liver Physiol
; 2010 Feb;298(2):G275-82
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[Title]
TGF-beta downregulates PTEN via activation of NF-kappaB in
pancreatic
cancer
cells
.
TGF-beta utilizes receptor-activated SMAD signaling to mediate growth suppression; however, non-SMAD signaling that modulates the TGF-beta response in epithelial
cells
become apparent when the SMAD signaling is abrogated, a common occurrence in
pancreatic
cancers.
Here, we examined whether TGF-beta utilized NF-kappaB to downregulate PTEN, a gene that is rarely mutated in
pancreatic
cancers.
SMAD4-null BxPc3 and CAPAN-1
pancreatic
cancer
cells
were treated with TGF-beta (10 ng/ml) and lysed, and cellular proteins were analyzed by Western blots using p-IkappaB, p65, and PTEN antibodies.
Dominant negative p-IkappaB-
alpha
-M (NF-kappaB superrepressor) was used to block activation of NF-kappaB.
Cell
motility was assessed by Boyden chamber migration assay.
TGF-beta induced IkappaB-
alpha
phosphorylation followed by NF-kappaB p65 subunit nuclear translocation and increased NF-kappaB activity.
IkappaB-
alpha
-M blocked TGF-beta-induced NF-kappaB activity, reversed downregulated PTEN promoter activity and PTEN expression, and prevented augmentation
of cell
motility induced by TGF-beta.
Thus TGF-beta suppresses PTEN in
pancreatic
cancer
cells
through NF-kappaB activation and enhances
cell
motility and invasiveness in a SMAD4-independent manner that can be counteracted when TGF-beta-SMAD signaling is restored.
The TGF-beta/NF-kappaB/PTEN cascade may be a critical pathway for
pancreatic
cancer
cells
to proliferate and metastasize.
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11781575.001
]
(PMID = 19940030.001).
[ISSN]
1522-1547
[Journal-full-title]
American journal of physiology. Gastrointestinal and liver physiology
[ISO-abbreviation]
Am. J. Physiol. Gastrointest. Liver Physiol.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK067287; United States / NIDDK NIH HHS / DK / R01 DK067287-02; United States / NIDDK NIH HHS / DK / DK-067287; United States / NIDDK NIH HHS / DK / R24 DK080506; United States / NIDDK NIH HHS / DK / DK-073090; United States / NIDDK NIH HHS / DK / DK067287-02; United States / NIDDK NIH HHS / DK / R24 DK080506-01; United States / NIDDK NIH HHS / DK / DK-080506
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / I-kappa B Proteins; 0 / SMAD2 protein, human; 0 / SMAD3 protein, human; 0 / SMAD4 protein, human; 0 / Smad2 Protein; 0 / Smad3 Protein; 0 / Smad4 Protein; 0 / Transcription Factor RelA; 0 / Transforming Growth Factor beta; 139874-52-5 / NF-kappaB inhibitor alpha; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
[Other-IDs]
NLM/ PMC3774494
54.
Liu XN, Huo TT, Wang WZ:
[Protective effect of shenfu injection against ischemia-reperfusion injury due to pancreas transplantation in rats].
Zhongguo Zhong Xi Yi Jie He Za Zhi
; 2006 Jun;26 Suppl:111-5
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[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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consumer health - Pancreas Transplantation
.
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NITRIC OXIDE
.
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MALONALDEHYDE
.
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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
55.
Yubero S, Ramudo L, Manso MA, De Dios I:
Targeting peripheral immune response reduces the severity of necrotizing acute pancreatitis.
Crit Care Med
; 2009 Jan;37(1):240-5
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INTERVENTIONS: Retrograde infusion of 3.5% of sodium taurocholate into
pancreatic
-biliary duct was used to induce AP in rats.
MEASUREMENTS AND MAIN RESULTS: Dx and NAC treatments reduced the severity of AP in terms of amylasemia,
pancreatic
edema, and
pancreatic
and liver necrosis.
Dx, administered before or after AP, and NAC reduced the leukocytosis induced by AP and blocked the ability of circulating monocytes to produce
tumor
necrosis factor-
alpha
and monocyte chemoattractant protein-1; however none of them significantly reduced the overexpression of intercellular
cell
adhesion molecule-1 found in monocytes 6 hrs after inducing AP.
Leukocyte infiltration in
the pancreas
was attenuated in Dx-pretreated rats and significantly reduced 6 hrs after inducing AP in rats treated with NAC.
CONCLUSIONS: Our data demonstrated that treatments targeting the peripheral immune response reduced the severity of sodium taurocholate -induced AP attenuating
pancreatic
and liver injury, but they were not effective for limiting the spread of the inflammatory damage to the lung.
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.
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.
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(PMID = 19050604.001).
[ISSN]
1530-0293
[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 / Anti-Inflammatory Agents; 7S5I7G3JQL / Dexamethasone; WYQ7N0BPYC / Acetylcysteine
56.
Gibo J, Ito T, Kawabe K, Hisano T, Inoue M, Fujimori N, Oono T, Arita Y, Nawata H:
Camostat mesilate attenuates pancreatic fibrosis via inhibition of monocytes and pancreatic stellate cells activity.
Lab Invest
; 2005 Jan;85(1):75-89
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[Title]
Camostat mesilate attenuates
pancreatic
fibrosis via inhibition of monocytes and
pancreatic
stellate
cells
activity.
Our aim was to evaluate the therapeutic efficacy of CM in the experimental
pancreatic
fibrosis model induced by dibutyltin dichloride (DBTC), and we also determined the effect of CM on isolated monocytes and panceatic stellate
cells
(PSCs).
Thereafter, the effect of CM on monocyte chemoattractant protein-1 (MCP-1) and
tumor
necrosis factor-
alpha
(TNF-
alpha
) production from monocytes was examined.
In vivo, the oral administration of CM inhibited inflammation, cytokines expression and fibrosis in
the pancreas
.
The in vitro study revealed that CM inhibited both MCP-1 and TNF-
alpha
production from monocytes, and proliferation and MCP-1 production from PSCs.
These results suggest that CM attenuated DBTC-induced rat
pancreatic
fibrosis via inhibition of monocytes and PSCs activity.
[MeSH-major]
Fibrosis / drug therapy. Gabexate / analogs & derivatives. Gabexate / therapeutic use. Monocytes / pathology.
Pancreas
/ pathology. Pancreatitis / drug therapy. Protease Inhibitors / therapeutic use
[MeSH-minor]
Animals.
Cell
Proliferation / drug effects. Chemokine CCL2 / genetics. Chemokine CCL2 / metabolism.
Disease
Models, Animal. Dose-Response Relationship, Drug. Male. Organotin Compounds / toxicity. Procollagen / genetics. Procollagen / metabolism. RNA, Messenger / metabolism. Rats. Rats, Inbred Lew.
Tumor
Necrosis Factor-
alpha
/ genetics.
Tumor
Necrosis Factor-
alpha
/ metabolism
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(PMID = 15531908.001).
[ISSN]
0023-6837
[Journal-full-title]
Laboratory investigation; a journal of technical methods and pathology
[ISO-abbreviation]
Lab. Invest.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Ccl2 protein, rat; 0 / Chemokine CCL2; 0 / Organotin Compounds; 0 / Procollagen; 0 / Protease Inhibitors; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0FD207WKDU / camostat; 4V7M9137X9 / Gabexate; J4AQN88R8P / dibutyldichlorotin
57.
Miao Q, Sun Y, Wei T, Zhao X, Zhao K, Yan L, Zhang X, Shu H, Yang F:
Chymotrypsin B cached in rat liver lysosomes and involved in apoptotic regulation through a mitochondrial pathway.
J Biol Chem
; 2008 Mar 28;283(13):8218-28
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Although it was long recognized as a digestive protease exclusively secreted by the exocrine
pancreas
, our data support that it also expresses and intracellularly resides in rat liver lysosomes.
Translocation of lysosomal chymotrypsin B into cytosol was triggered by apoptotic stimuli such as
tumor
necrosis factor-
alpha
, and intracellular delivery of chymotrypsin B protein induced apoptotic
cell
death with a potency comparable with cathepsin B, suggestive of a lysosomal-mitochondrial pathway to apoptosis regulated by chymotrypsin B following its release.
Noteworthily, either knockdown of chymotrypsin B expression by RNA interference or pretreatment with chymotrypsin B inhibitor N-p-tosyl-L-phenylalanine chloromethyl ketone significantly reduced
tumor
necrosis factor-
alpha
-induce apoptosis.
These results demonstrate for the first time that chymotrypsin B is not only restricted to
the pancreas
but can function intracellularly as a pro-apoptotic protease.
[MeSH-minor]
Animals.
Cell
Line. Gene Expression Regulation, Enzymologic. Hepatocytes / enzymology. RNA, Messenger / genetics. Rats. Rats, Sprague-Dawley
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
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CHYMOTRYPSIN
.
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(PMID = 18211899.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / RNA, Messenger; EC 3.4.21.1 / Chymotrypsin; EC 3.4.21.1 / chymotrypsin B
58.
Gin VC, Zacharias M:
Glucagonoma: anaesthetic management.
Anaesth Intensive Care
; 2009 Mar;37(2):329-30
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[Title]
Glucagonoma
: anaesthetic management.
[MeSH-major]
Anesthesia, General / methods.
Glucagonoma
/ surgery.
Pancreatic
Neoplasms / surgery
[MeSH-minor]
Blood Glucose / analysis. Female.
Glucagon
/ blood. Humans. Middle Aged
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(PMID = 19400510.001).
[ISSN]
0310-057X
[Journal-full-title]
Anaesthesia and intensive care
[ISO-abbreviation]
Anaesth Intensive Care
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
Australia
[Chemical-registry-number]
0 / Blood Glucose; 9007-92-5 / Glucagon
59.
Büyükberber M, Savaş MC, Bağci C, Koruk M, Gülşen MT, Tutar E, Bilgiç T, Deveci R, Küçük C:
The beneficial effect of propolis on cerulein-induced experimental acute pancreatitis in rats.
Turk J Gastroenterol
; 2009 Jun;20(2):122-8
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Serum amylase and lipase levels, white blood
cell
count and serum
tumor
necrosis factor-
alpha
levels were measured and
pancreatic
tissue was evaluated histologically.
[MeSH-minor]
Acute
Disease
. Amylases / blood. Animals.
Disease
Models, Animal. Edema. Lipase / blood. Male.
Pancreas
/ drug effects.
Pancreas
/ pathology. Rats. Rats, Wistar. Treatment Outcome
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(PMID = 19530045.001).
[ISSN]
2148-5607
[Journal-full-title]
The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology
[ISO-abbreviation]
Turk J Gastroenterol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Turkey
[Chemical-registry-number]
0 / Anti-Infective Agents; 0 / Gastrointestinal Agents; 888Y08971B / Ceruletide; 9009-62-5 / Propolis; EC 3.1.1.3 / Lipase; EC 3.2.1.- / Amylases
60.
Baker AF, Koh MY, Williams RR, James B, Wang H, Tate WR, Gallegos A, Von Hoff DD, Han H, Powis G:
Identification of thioredoxin-interacting protein 1 as a hypoxia-inducible factor 1alpha-induced gene in pancreatic cancer.
Pancreas
; 2008 Mar;36(2):178-86
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[Title]
Identification of thioredoxin-interacting protein 1 as a hypoxia-inducible factor 1alpha-induced gene in
pancreatic
cancer.
OBJECTIVE: To investigate the expression of thioredoxin-interacting protein (TXNIP) during hypoxia and its dependency on hypoxia-inducible factor 1alpha (HIF-1alpha) in
pancreatic
cancer
cell
lines.
METHODS: MiaPaCa-2
pancreatic
cancer
cells
were transiently transfected with siRNA to HIF-1alpha and TXNIP protein measured after growth in normoxia or hypoxia.
In addition, HIF-1alpha dependency was assessed by transiently transfecting MiaPaCa-2
pancreatic
cancer
cells
with HIF-1alpha with a mutated oxygen degradation domain resulting in stable HIF-1alpha expression in normoxic conditions.
Panc-1
pancreatic
cancer
cells
with low endogenous TXNIP expression were stably transfected with TXNIP, and
cell
survival and response to platinum cancer agents were tested.
Quantitative immunohistochemistry was utilized to measure the expression of TXNIP and thioredoxin 1 in human
pancreatic
cancer tissues.
RESULTS: Thioredoxin-interacting protein was induced during hypoxia in
pancreatic
cancer
cells
in a HIF-1alpha-dependent manner.
Overexpression of TXNIP in the Panc-1
cells
resulted in a higher basal apoptosis and increased sensitivity to cisplatin and oxaliplatin.
A negative correlation was observed between TXNIP and thioredoxin 1 expression in human
pancreatic
cancer tissues.
CONCLUSIONS: Thioredoxin-interacting protein, a putative
tumor
suppressor gene, is induced in response to hypoxia in a HIF-1alpha-dependent manner in
pancreatic
cancer
cells
, resulting in increased apoptosis and increased sensitivity to platinum anticancer therapy.
[MeSH-major]
Carcinoma,
Pancreatic
Ductal / metabolism. Carrier Proteins / metabolism. Gene Expression Regulation, Neoplastic. Hypoxia-Inducible Factor 1,
alpha
Subunit / metabolism.
Pancreatic
Neoplasms / metabolism
[MeSH-minor]
Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Apoptosis.
Cell
Hypoxia.
Cell
Line,
Tumor
.
Cell
Survival / drug effects. Cisplatin / pharmacology. Cisplatin / therapeutic use. Humans. Immunohistochemistry. Mutation. Organoplatinum Compounds / pharmacology. Organoplatinum Compounds / therapeutic use. RNA Interference. RNA, Small Interfering / metabolism. Thioredoxins / metabolism. Tissue Array Analysis. Transfection. Up-Regulation
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(PMID = 18376310.001).
[ISSN]
1536-4828
[Journal-full-title]
Pancreas
[ISO-abbreviation]
Pancreas
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA077204; United States / NCI NIH HHS / CA / CA109552; United States / NCI NIH HHS / CA / CA90821
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Organoplatinum Compounds; 0 / RNA, Small Interfering; 0 / TXN protein, human; 0 / TXNIP protein, human; 04ZR38536J / oxaliplatin; 52500-60-4 / Thioredoxins; Q20Q21Q62J / Cisplatin
61.
Sbarra V, Ristorcelli E, Petit-Thévenin JL, Teissedre PL, Lombardo D, Vérine A:
In vitro polyphenol effects on activity, expression and secretion of pancreatic bile salt-dependent lipase.
Biochim Biophys Acta
; 2005 Sep 5;1736(1):67-76
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[Title]
In vitro polyphenol effects on activity, expression and secretion of
pancreatic
bile salt-dependent lipase.
In the present in vitro studies, we have evaluated and compared the effects of resveratrol, an active compound of red wine, and of a whole red wine polyphenolic extract (RWE) on the
pancreatic
bile salt-dependent lipase (BSDL).
Resveratrol and RWE also impaired the secretion of BSDL by the rat
pancreatic
AR4-2J
cells
used as secreting model.
This effect is reversed by the removal of resveratrol or RWE from
the cell
culture medium.
Further, resveratrol (but not RWE) affects the transcription of the gene encoding BSDL and dramatically diminishes the quantity of the enzyme that is expressed and secreted by AR4-2J
cells
.
[MeSH-major]
Flavonoids / physiology.
Pancreas
/ enzymology. Sterol Esterase / metabolism
[MeSH-minor]
Animals.
Cell
Line,
Tumor
. Humans. Phenols. Polyphenols. RNA, Messenger / metabolism. Rats. Stilbenes / pharmacology. Wine.
alpha
-Amylases / secretion
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(PMID = 16099206.001).
[ISSN]
0006-3002
[Journal-full-title]
Biochimica et biophysica acta
[ISO-abbreviation]
Biochim. Biophys. Acta
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; 0 / RNA, Messenger; 0 / Stilbenes; EC 3.1.1.- / bile salt-stimulated lipase; EC 3.1.1.13 / Sterol Esterase; EC 3.2.1.1 / alpha-Amylases; Q369O8926L / resveratrol
62.
Li YY, Li XJ, Lv S, Li K, Li YN, Gao ZR, Feng JY, Chen CJ, Schaefer C:
Ascitic fluid and serum from rats with acute pancreatitis injure rat pancreatic tissues and alter the expression of heat shock protein 60.
Cell Stress Chaperones
; 2010 Sep;15(5):583-91
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[Title]
Ascitic fluid and serum from rats with acute pancreatitis injure rat
pancreatic
tissues and alter the expression of heat shock protein 60.
After onset, extrapancreatic stimuli can induce the expression of cytokines in
pancreatic
acinar
cells
, thereby amplifying this inflammatory loop.
To further determine the role and mechanism of irritating agents in the pathogenesis of AP, rat
pancreatic
tissues were stimulated with ascitic fluid (APa) and serum (APs) from rats with AP or with lipopolysaccharide (LPS).
Rat
pancreas
was removed and meticulously snipped to fragments.
During this period, the tissue viability as well as amylase and TNF-
alpha
levels in the supernatant and the HSP60 expression in the
pancreatic
tissue before and after stimulation by APa, APs, and LPS were assayed time-dependently.
At different time-points during the culture, the viability and the amylase activity in the
pancreatic
tissue remained largely stable.
After stimulation with APa, APs, or LPS for 1 h, the
pancreatic
tissues showed some damage, and this was followed by a sharp decrease in the viability accompanied by increased levels of amylase and TNF-
alpha
in the culture medium 2 or 4 h after stimulation (p < 0.05).
APa, APs, or LPS induce injuries on isolated
pancreatic
tissues, accompanied by an altered HSP60 expression pattern in a time-dependent manner.
[MeSH-major]
Ascitic Fluid / chemistry. Chaperonin 60 / metabolism.
Pancreas
/ metabolism. Pancreatitis / blood. Pancreatitis / metabolism. Serum / chemistry
[MeSH-minor]
Amylases / metabolism. Animals. Immunohistochemistry. In Vitro Techniques. Lipopolysaccharides / pharmacology. RNA, Messenger. Rats. Reverse Transcriptase Polymerase Chain Reaction.
Tumor
Necrosis Factor-
alpha
/ metabolism
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[
10547198.001
]
(PMID = 20146106.001).
[ISSN]
1466-1268
[Journal-full-title]
Cell stress & chaperones
[ISO-abbreviation]
Cell Stress Chaperones
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Chaperonin 60; 0 / Lipopolysaccharides; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 3.2.1.- / Amylases
[Other-IDs]
NLM/ PMC3006631
63.
Tsao KC, Wu TL, Chang PY, Hong JH, Wu JT:
Detection of carcinomas in an asymptomatic Chinese population: advantage of screening with multiple tumor markers.
J Clin Lab Anal
; 2006;20(2):42-6
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[Title]
Detection of carcinomas in an asymptomatic Chinese population: advantage of screening with multiple
tumor
markers.
A total of 73,443 asymptomatic individuals were screened on a voluntary basis for cancer at Chang Gung Memorial Hospital in Taiwan using a panel
of tumor
markers, including
alpha
fetoprotein (AFP), CA 125, CA 15-3, CA 19-9, carcinoembryonic antigen (CEA), prostate specific antigen (PSA), chromogranin A (CgA), and squamous
cell
specific antigen (SCC).
A total of 210 cancers (approximately 0.3%) were detected, including cancers of the liver, lung, colon, prostate, stomach,
pancreas
, breast, cervix, ovary, and bladder.
Of the
tumor
markers monitored, elevated CA 19-9, CEA, and CA 125 were the most frequently detected in a variety of cancers.
It was surprising to find that many cancers were not detected by their dominant markers but by the elevation
of tumor
markers not recommended for monitoring their
tumor
activity.
Screening with multiple circulating
tumor
markers provides improved sensitivity for cancer detection in asymptomatic individuals before they reach the fatal advanced stage.
Screening with multiple
tumor
markers also allows cancers to be detected in the absence of their dominant markers.
If we had not measured the multiple
tumor
markers, these cancers would have gone undetected.
[MeSH-major]
Asian Continental Ancestry Group. Biomarkers,
Tumor
/ analysis. Carcinoma /
diagnosis
. Mass Screening / methods
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[Copyright]
(c) 2006 Wiley-Liss, Inc.
(PMID = 16538643.001).
[ISSN]
0887-8013
[Journal-full-title]
Journal of clinical laboratory analysis
[ISO-abbreviation]
J. Clin. Lab. Anal.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / CA-19-9 Antigen
64.
Izumi K, Ishikawa K, Tojigamori M, Matsui Y, Shiraishi N, Kitano S:
Liver metastasis and ICAM-1 mRNA expression in the liver after carbon dioxide pneumoperitoneum in a murine model.
Surg Endosc
; 2005 Aug;19(8):1049-54
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Little is known about intercellular adhesion molecule-1 (ICAM-1) and
tumor
necrosis factor-
alpha
(TNF-(
alpha
) mRNA expression in the liver after CO2 pneumoperitoneum.
METHODS: Forty-five male BALB/c mice were randomly divided into three groups after intra-splenic
tumor cell
(colon 26) inoculation and the following procedures were performed: CO2 pneumoperitoneum (n = 15), open laparotomy (n = 15), and anesthesia alone (n = 15).
On day 7 after each procedure, the livers were excised and the number and diameter of the
tumor
nodules and the cancer index score were determined.
After each procedure, the livers were excised on days 0, 1, 3, and ICAM-1 and TNF-
alpha
mRNA expression were examined by real-time RT-PCR using SYBR Green I.
RESULTS: The number
of tumor
nodules and the cancer index score were larger in the CO2 pneumoperitoneum group than in the control group (p < 0.05).
The mean diameter of the
tumor
nodules was not different among the three groups.
The expression of ICAM-1 in the CO2 pneumoperitoneum group was higher than that in the other groups on day 1 (p < 0.05), and the TNF-
alpha
mRNA was higher than that in the control group on day 1 (p < 0.05).
[MeSH-minor]
Animals.
Disease
Models, Animal. Male. Mice. Mice, Inbred BALB C
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[ISSN]
1432-2218
[Journal-full-title]
Surgical endoscopy
[ISO-abbreviation]
Surg Endosc
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / RNA, Messenger; 126547-89-5 / Intercellular Adhesion Molecule-1; 142M471B3J / Carbon Dioxide
65.
Kallichanda N, Tsai S, Stabile BE, Buslon V, Delgado DL, French SW:
Histogenesis of solid pseudopapillary tumor of the pancreas: the case for the centroacinar cell of origin.
Exp Mol Pathol
; 2006 Oct;81(2):101-7
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[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
66.
Prout TM, Taylor AJ:
Case of the season: glucagonoma syndrome.
Semin Roentgenol
; 2005 Jan;40(1):4-7
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[Title]
Case of the season:
glucagonoma syndrome
.
[MeSH-major]
Glucagonoma
/ radiography.
Pancreatic
Neoplasms / radiography
[MeSH-minor]
Diagnosis
, Differential. Female. Humans. Middle Aged.
Syndrome
. Tomography, X-Ray Computed
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(PMID = 15732554.001).
[ISSN]
0037-198X
[Journal-full-title]
Seminars in roentgenology
[ISO-abbreviation]
Semin Roentgenol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
67.
Bai J, Sui J, Demirjian A, Vollmer CM Jr, Marasco W, Callery MP:
Predominant Bcl-XL knockdown disables antiapoptotic mechanisms: tumor necrosis factor-related apoptosis-inducing ligand-based triple chemotherapy overcomes chemoresistance in pancreatic cancer cells in vitro.
Cancer Res
; 2005 Mar 15;65(6):2344-52
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[Title]
Predominant Bcl-XL knockdown disables antiapoptotic mechanisms:
tumor
necrosis factor-related apoptosis-inducing ligand-based triple chemotherapy overcomes chemoresistance in
pancreatic
cancer
cells
in vitro.
Pancreatic
cancer is lethal because of its invasiveness, rapid progression, and profound resistance to chemotherapy and radiation therapy.
To identify the molecular mechanisms underlying this, we have examined the expression and potency of three major death receptors:
tumor
necrosis factor receptor (TNF-R), TNF-related apoptosis-inducing ligand receptor (TRAIL-R), and Fas in mediating cytotoxicity in four invasive
pancreatic
cancer
cell
lines.
We have analyzed the expression of major antiapoptotic factors,
cell
cycle regulators and death receptor decoys (DcR) in comparison with normal
pancreas
tissues and five other human malignant
tumor cell
lines.
We have found that different
pancreatic
cancer
cell
lines coexpress high-level TRAIL-R, Fas, and TNF-R1 but are strongly resistant to apoptosis triggered by the death receptors.
DcR2 and DcR3 overexpression may partly contribute to the resistance of
pancreatic
cancer
cells
to TRAIL-R- and Fas-mediated cytotoxicity.
Bcl-XL and Bcl-2 are predominantly overexpressed in
pancreatic
cancer
cell
lines, respectively.
Bcl-XL is also predominantly overexpressed in prostate, colorectal, and intestinal cancer
cells
.
The knockdown of the predominant Bcl-XL overexpression significantly reduces the viability of
pancreatic
cancer
cells
to TNFalpha- and TRAIL-mediated apoptosis by sublethal-dose single and combined antitumor drugs, including geldanamycin, PS-341, Trichostatin A, and doxorubicine.
Bcl-XL plays a vital role in
pancreatic
cancer chemoresistance.
Geldanamycin, PS-341, and TRAIL triple combination may be a novel therapeutic strategy for
pancreatic
cancer.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / physiology.
Pancreatic
Neoplasms / drug therapy.
Pancreatic
Neoplasms / pathology. Proto-Oncogene Proteins c-bcl-2 / deficiency.
Tumor
Necrosis Factor-
alpha
/ pharmacology
[MeSH-minor]
Apoptosis Regulatory Proteins. Benzoquinones. Boronic Acids / administration & dosage. Boronic Acids / pharmacology. Bortezomib.
Cell
Line,
Tumor
. Doxorubicin / administration & dosage. Doxorubicin / pharmacology. Drug Synergism. Gene Expression Regulation, Neoplastic. Gene Silencing. HSP90 Heat-Shock Proteins / metabolism. Humans. Hydroxamic Acids / administration & dosage. Hydroxamic Acids / pharmacology. Lactams, Macrocyclic. Membrane Glycoproteins. Pyrazines / administration & dosage. Pyrazines / pharmacology. Quinones / administration & dosage. Quinones / pharmacology. TNF-Related Apoptosis-Inducing Ligand. bcl-X Protein
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(PMID = 15781649.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / BCL2L1 protein, human; 0 / Benzoquinones; 0 / Boronic Acids; 0 / HSP90 Heat-Shock Proteins; 0 / Hydroxamic Acids; 0 / Lactams, Macrocyclic; 0 / Membrane Glycoproteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Quinones; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / bcl-X Protein; 3X2S926L3Z / trichostatin A; 69G8BD63PP / Bortezomib; 80168379AG / Doxorubicin; Z3K3VJ16KU / geldanamycin
68.
Marogy G, De Man M, Verslype C:
Necrolytic migratory erythaema and glucagonoma syndrome.
Acta Clin Belg
; 2009 Jan-Feb;64(1):70-1
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[Title]
Necrolytic migratory erythaema and
glucagonoma syndrome
.
[MeSH-major]
Erythema / etiology.
Glucagonoma
/ pathology.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Female. Humans. Middle Aged.
Syndrome
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(PMID = 19317246.001).
[ISSN]
1784-3286
[Journal-full-title]
Acta clinica Belgica
[ISO-abbreviation]
Acta Clin Belg
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Belgium
69.
Oberg K:
Pancreatic endocrine tumors.
Semin Oncol
; 2010 Dec;37(6):594-618
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[Title]
Pancreatic
endocrine
tumors
.
Pancreatic
endocrine
tumors
have been steadily growing in incidence and prevalence during the last two decades, showing an incidence of 4-5/1,000,000 population.
They represent a heterogeneous group with very varying
tumor
biology and prognosis.
About half of the patients present clinical symptoms and
syndromes
related to substances released from the
tumors
(Zollinger-Ellison
syndrome
, insulinoma,
glucagonoma
, etc) and the other half are so-called nonfunctioning
tumors
mainly presenting with symptoms such as obstruction, jaundice, bleeding, and abdominal mass.
Ten percent to 15% of the
pancreatic
endocrine
tumors
are part of an inherited
syndrome
such as multiple endocrine neoplasia type 1 (MEN-1), von Hippel-Lindau (VHL), neurofibromatosis, or tuberousclerosis.
The
diagnosis
is based on histopathology demonstrating
neuroendocrine
features such as positive staining for chromogranin A and specific hormones such as gastrin, proinsulin, and
glucagon
.
Moreover, the biochemical
diagnosis
includes measurement of chromogranins A and B or specific hormones such as gastrin, insulin,
glucagon
, and vasoactive intestinal polypeptide (VIP) in the circulation.
Surgery is still one of the cornerstones in the management of
pancreatic
endocrine
tumors
, but curative surgery is rarely obtained in most cases because of metastatic
disease
.
Cytotoxic drugs, biological agents, such as somatostatin analogs,
alpha
interferons, mammalian target of rapamycin (mTOR) inhibitors and tyrosine kinase inhibitors are routinely used.
Tumor
-targeted radioactive treatment is available in many centres in Europe and is effective in patients with
tumors
that express high content of somatostatin receptors type 2 and 5.
In the future, treatment will be based on
tumor
biology and molecular genetics with the aim of so-called personalized medicine.
[MeSH-major]
Pancreatic
Neoplasms
[MeSH-minor]
Antineoplastic Agents / therapeutic use. Biological Therapy / methods. Biomarkers,
Tumor
. Humans. Neoplastic
Syndromes
, Hereditary /
diagnosis
. Neoplastic
Syndromes
, Hereditary / therapy. Pancreatectomy. Paraneoplastic Endocrine
Syndromes
/
diagnosis
. Paraneoplastic Endocrine
Syndromes
/ therapy
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[Copyright]
Copyright © 2010 Elsevier Inc. All rights reserved.
(PMID = 21167379.001).
[ISSN]
1532-8708
[Journal-full-title]
Seminars in oncology
[ISO-abbreviation]
Semin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Biomarkers, Tumor
70.
Lin YY, Viterbo D, Mueller CM, Stanek AE, Smith-Norowitz T, Drew H, Wadgaonkar R, Zenilman ME, Bluth MH:
Small-interference RNA gene knockdown of pancreatitis-associated proteins in rat acute pancreatitis.
Pancreas
; 2008 May;36(4):402-10
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METHODS: Pancreatitis-associated protein-specific siRNA was administered to AR42J
cell
cultures or rats induced with pancreatitis.
After 24 hours,
cells
and pancreata were harvested and assessed for PAP (PAP 1, PAP 2, PAP 3) gene expression and pancreatitis severity.
RESULTS: In vitro, PAP protein, and mRNA levels were reduced (PAP 1, 76%; PAP 2, 8%; PAP 3, 24%) in
cells
treated with PAP siRNA.
Serum amylase and lipase levels decreased (> or =50%) after administration of siRNA; interleukin (IL) 1beta, IL-4, and IL-6 increased, whereas C-reactive protein and
tumor
necrosis factor-
alpha
decreased when compared with vehicle control.
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[ISSN]
1536-4828
[Journal-full-title]
Pancreas
[ISO-abbreviation]
Pancreas
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / DK054511-05; United States / NIDDK NIH HHS / DK / R01 DK054511-05
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / pancreatitis-associated protein; 5E090O0G3Z / Taurocholic Acid
[Other-IDs]
NLM/ NIHMS109845; NLM/ PMC3151650
71.
Desgrosellier JS, Barnes LA, Shields DJ, Huang M, Lau SK, Prévost N, Tarin D, Shattil SJ, Cheresh DA:
An integrin alpha(v)beta(3)-c-Src oncogenic unit promotes anchorage-independence and tumor progression.
Nat Med
; 2009 Oct;15(10):1163-9
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[Title]
An integrin
alpha
(v)beta(3)-c-Src oncogenic unit promotes anchorage-independence and
tumor
progression.
Integrins regulate adhesion-dependent growth, survival and invasion
of tumor
cells
.
In particular, expression of integrin
alpha
(v)beta(3) is associated with progression of a variety of human
tumors
.
Here we reveal a previously undescribed adhesion-independent role for integrin
alpha
(v)beta(3) in
pancreatic
cancer and other carcinomas.
Specifically,
alpha
(v)beta(3) expressed in carcinoma
cells
enhanced anchorage-independent
tumor
growth in vitro and increased lymph node metastases in vivo.
These effects required recruitment of c-Src to the beta(3) integrin cytoplasmic tail, leading to c-Src activation, Crk-associated substrate (CAS) phosphorylation and
tumor cell
survival that, unexpectedly, was independent
of cell
adhesion or focal adhesion kinase (FAK) activation.
Pharmacological blockade of c-Src kinase activity or decreased expression of endogenous
alpha
(v)beta(3) integrin or c-Src not only inhibited anchorage-independent growth but also suppressed metastasis in vivo, yet these manipulations did not affect
tumor cell
migration or invasion.
These data define an unexpected role for an integrin as a mediator of anchorage independence, suggesting that an
alpha
(v)beta(3)-c-Src signaling module may account for the aggressive behavior of integrin
alpha
(v)beta(3)-expressing
tumors
in humans.
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[ISSN]
1546-170X
[Journal-full-title]
Nature medicine
[ISO-abbreviation]
Nat. Med.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA095262-06; United States / NCI NIH HHS / CA / CA129660-02; United States / NCI NIH HHS / CA / T32 CA121938; United States / NCI NIH HHS / CA / CA050286-20; United States / NCI NIH HHS / CA / R01 CA095262; United States / NCI NIH HHS / CA / R37 CA050286; United States / NCI NIH HHS / CA / R01 CA045726-23; United States / NCI NIH HHS / CA / CA123774; United States / NCI NIH HHS / CA / R37 CA050286-20; United States / NCI NIH HHS / CA / F32 CA123774; United States / NCI NIH HHS / CA / R21 CA129660; United States / NCI NIH HHS / CA / CA95262; United States / NCI NIH HHS / CA / R01 CA095262-06; United States / NCI NIH HHS / CA / CA129660; United States / NCI NIH HHS / CA / R21 CA129660-02; United States / NCI NIH HHS / CA / P01 CA078045-06A10004; United States / NCI NIH HHS / CA / P01 CA078045; United States / NHLBI NIH HHS / HL / HL57900; United States / NCI NIH HHS / CA / R01 CA045726; United States / NCI NIH HHS / CA / CA045726-23; United States / NHLBI NIH HHS / HL / P01 HL057900; United States / NCI NIH HHS / CA / CA78045; United States / NCI NIH HHS / CA / CA45726; United States / NCI NIH HHS / CA / CA078045-06A10004
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Fibronectins; 0 / Integrin alphaVbeta3; 0 / Ki-67 Antigen; 0 / RNA, Small Interfering; 147336-22-9 / Green Fluorescent Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.10.2 / src-Family Kinases
[Other-IDs]
NLM/ NIHMS125908; NLM/ PMC2759406
72.
Neutzner M, Lopez T, Feng X, Bergmann-Leitner ES, Leitner WW, Udey MC:
MFG-E8/lactadherin promotes tumor growth in an angiogenesis-dependent transgenic mouse model of multistage carcinogenesis.
Cancer Res
; 2007 Jul 15;67(14):6777-85
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[Title]
MFG-E8/lactadherin promotes
tumor
growth in an angiogenesis-dependent transgenic mouse model of multistage carcinogenesis.
The relevance of angiogenesis in
tumor
biology and as a therapeutic target is well established.
MFG-E8 (also termed lactadherin) and developmental endothelial locus 1 (Del1) constitute a two-gene family
of alpha
(v)beta(3)/beta(5) ligands that regulate angiogenesis.
After detecting MFG-E8 mRNA in murine
tumor cell
lines, we sought to determine if MFG-E8 influenced tumorigenesis in Rip1-Tag2 transgenic mice, a cancer model in which angiogenesis is critical.
MFG-E8 mRNA and protein were increased in angiogenic islets and
tumors
in Rip1-Tag2 mice compared with normal
pancreas
.
Frequencies of angiogenic islets and
tumor
burdens were decreased in MFG-E8-deficient Rip1-Tag2 mice compared with those in control Rip1-Tag2 mice.
Invasive carcinomas were modestly underrepresented in MFG-E8-deficient mice, but
tumor
frequencies and survivals were comparable in these two strains.
Absence of MFG-E8 also led to decreases in
tumor
vascular permeability without obvious changes in vascular morphology.
Decreased proliferation was noted in angiogenic islets and increases in apoptotic
cells
were detected in islets and
tumors
.
Compensatory increases in mRNA encoding proangiogenic proteins, including FGF2, in angiogenic islets, and Del1, in angiogenic islets and
tumors
, were also detected in MFG-E8-deficient mice.
[MeSH-major]
Antigens, Surface / genetics. Antigens, Surface / physiology.
Cell
Transformation, Neoplastic. Milk Proteins / genetics. Neovascularization, Pathologic
[MeSH-minor]
Animals. Apoptosis.
Cell
Proliferation. Female. Fibroblast Growth Factor 2 / metabolism. GTPase-Activating Proteins / physiology. Male. Mice. Mice, Knockout. Mice, Transgenic.
Pancreas
/ metabolism. RNA, Messenger / metabolism
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(PMID = 17638889.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[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 / Antigens, Surface; 0 / GTPase-Activating Proteins; 0 / Mfge8 protein, mouse; 0 / Milk Proteins; 0 / RNA, Messenger; 0 / Ralbp1 protein, mouse; 103107-01-3 / Fibroblast Growth Factor 2
73.
Hu HT, Ma QY, Zhang D, Shen SG, Han L, Ma YD, Li RF, Xie KP:
HIF-1alpha links beta-adrenoceptor agonists and pancreatic cancer cells under normoxic condition.
Acta Pharmacol Sin
; 2010 Jan;31(1):102-10
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[Title]
HIF-1alpha links beta-adrenoceptor agonists and
pancreatic
cancer
cells
under normoxic condition.
AIM: To examine whether beta-adrenoceptor (beta-AR) agonists can induce hypoxia-inducible factor (HIF)-1alpha accumulation which then up-regulate the expression of its target genes in
pancreatic
cancer
cells
at normoxia, and to further elucidate the mechanism involved.
METHODS: Pulse-chase assay, RT-PCR, and Western blot were employed to detect the effects of beta-AR agonists and antagonists, siRNA as well as several inhibitors of signal transduction pathways on MIA PaCa2 and BxPC-3
pancreatic
cancer
cells
.
RESULTS: Treatment of
pancreatic
cancer
cell
lines with beta-AR agonists led to accumulation of HIF-1alpha and then up-regulated expression of its target genes independently of oxygen levels.
Our data suggest a novel mechanism in
pancreatic
cancer
cells
that links beta-AR and HIF-1alpha signaling under normoxic conditions, with implications for the control of glucose transport, angiogenesis and metastasis.
[MeSH-major]
Adrenergic beta-Agonists / pharmacology. Hypoxia-Inducible Factor 1,
alpha
Subunit / drug effects.
Pancreatic
Neoplasms / metabolism
[MeSH-minor]
Adrenergic beta-1 Receptor Agonists. Adrenergic beta-2 Receptor Agonists. Blotting, Western.
Cell
Line,
Tumor
. Cyclic AMP-Dependent Protein Kinases / metabolism. Humans. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / metabolism. Receptor, Epidermal Growth Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Up-Regulation / drug effects
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[Cites]
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[
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]
(PMID = 20037603.001).
[ISSN]
1745-7254
[Journal-full-title]
Acta pharmacologica Sinica
[ISO-abbreviation]
Acta Pharmacol. Sin.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Adrenergic beta-1 Receptor Agonists; 0 / Adrenergic beta-2 Receptor Agonists; 0 / Adrenergic beta-Agonists; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Small Interfering; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
[Other-IDs]
NLM/ PMC4002695
74.
Wei D, Li J, Shen M, Jia W, Chen N, Chen T, Su D, Tian H, Zheng S, Dai Y, Zhao A:
Cellular production of n-3 PUFAs and reduction of n-6-to-n-3 ratios in the pancreatic beta-cells and islets enhance insulin secretion and confer protection against cytokine-induced cell death.
Diabetes
; 2010 Feb;59(2):471-8
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[Title]
Cellular production of n-3 PUFAs and reduction of n-6-to-n-3 ratios in the
pancreatic
beta-
cells
and islets enhance insulin secretion and confer protection against cytokine-induced
cell
death.
OBJECTIVE: To evaluate the direct impact of n-3 polyunsaturated fatty acids (n-3 PUFAs) on the functions and viability of
pancreatic
beta-
cells
.
RESEARCH DESIGN AND METHODS: We developed an mfat-1 transgenic mouse model in which endogenous production of n-3 PUFAs was achieved through overexpressing
a C
. elegans n-3 fatty acid desaturase gene, mfat-1.
The islets and INS-1
cells
expressing mfat-1 were analyzed for insulin secretion and viability in response to cytokine treatment.
Insulin secretion stimulated by glucose, amino acids, and
glucagon
-like peptide-1 (GLP-1) was significantly elevated in the transgenic islets.
When challenged with
tumor
necrosis factor-
alpha
(TNF-
alpha
), interleukin-1beta (IL-1beta), and gamma-interferon (IFN-gamma), the transgenic islets completely resisted cytokine-induced
cell
death.
Adenoviral transduction of mfat-1 gene in wild-type islets and in INS-1
cells
led to acute changes in the cellular levels of n-3- and n-6 PUFAs and recapitulated the results in the transgenic islets.
We further found that cytokine-induced activation of NF-kappaB and extracellular signal-related kinase 1/2 (ERK(1/2)) was significantly attenuated and that the expression of
pancreatic
duodenal hemeobox-1 (PDX-1), glucokinase, and insulin-1 was increased as a result of n-3 PUFA production.
CONCLUSIONS: Stable cellular production of n-3 PUFAs via mfat-1 can enhance insulin secretion and confers strong resistance to cytokine-induced beta-
cell
destruction.
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[Cites]
Int J Circumpolar Health. 2001 Nov;60(4):487-94
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Mol Cancer Ther. 2008 Oct;7(10):3203-11
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