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1
alpha cell neoplasm 2005:2010[pubdate] *count=100
24948 results
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Expand the query
'
neoplasm
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3 meanings
. Choose the one you intended:
Concept C0027651: neoplasm morphologic abnormality;
details
Concept C1882062: neoplastic disease disorder;
details
Concept C2981607: send neoplasm;
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alpha cell
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Items 1 to 100 of about 24948
1.
Kostakis GC, Papadogeorgakis N, Koumaki V, Kamakari S, Koumaki D, Alexandridis C:
Absence of hotspot mutations in exons 9 and 20 of the PIK3CA gene in human oral squamous cell carcinoma in the Greek population.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
; 2010 May;109(5):e53-8
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[Title]
Absence of hotspot mutations in exons 9 and 20 of the PIK3CA gene in human oral squamous
cell
carcinoma in the Greek population.
Recent studies have reported high frequencies of somatic hotspot mutations in the phosphatidylinositol-3 kinase catalytic
alpha
(PIK3CA) gene, which encodes for one of these kinases, in several human solid
tumors
,
including
oral squamous
cell
carcinoma (OSCC).
STUDY DESIGN: Eighty-six formalin-fixed and paraffin-embedded primary
tumor
specimens were analyzed by direct genomic DNA sequencing.
RESULTS
: No hotspot mutations were detected in any of the samples.
[MeSH-major]
Biomarkers,
Tumor
/ genetics. Carcinoma, Squamous
Cell
/ enzymology. Exons / genetics. Mouth
Neoplasms
/ enzymology. Mutation / genetics. Phosphatidylinositol 3-Kinases / genetics
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Case-Control Studies. Cytosine. Female. Gingival
Neoplasms
/ enzymology. Gingival
Neoplasms
/ genetics. Greece. Guanine. Humans. Introns / genetics. Male. Mandibular
Neoplasms
/ enzymology. Mandibular
Neoplasms
/ genetics. Middle Aged. Mouth Mucosa / pathology.
Neoplasm
Staging. Polymerase Chain Reaction. Polymorphism, Genetic / genetics. Sequence Analysis, DNA. Thymine. Tongue
Neoplasms
/ enzymology. Tongue
Neoplasms
/ genetics. Young Adult
Genetic Alliance.
consumer health - Carcinoma, Squamous Cell
.
Genetic Alliance.
consumer health - Oral squamous cell carcinoma
.
MedlinePlus Health Information.
consumer health - Oral Cancer
.
Hazardous Substances Data Bank.
GUANINE
.
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[Copyright]
Copyright (c) 2010 Mosby, Inc. All rights reserved.
(PMID = 20416519.001).
[ISSN]
1528-395X
[Journal-full-title]
Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
[ISO-abbreviation]
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 5Z93L87A1R / Guanine; 8J337D1HZY / Cytosine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; QR26YLT7LT / Thymine
2.
Wang YA, Shen K, Ishida Y, Wang Y, Kakizuka A, Brooks SC:
Induction of murine leukemia and lymphoma by dominant negative retinoic acid receptor alpha.
Mol Carcinog
; 2005 Dec;44(4):252-61
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[Title]
Induction of murine leukemia and lymphoma by dominant negative retinoic acid receptor
alpha
.
Acute promyelocytic leukemia (APL) is invariably associated with chromosomal translocation to retinoic acid receptor
alpha
(RARalpha) locus.
It was thought that the fusion protein PML-RARalpha acts
as a
double dominant negative mutant to inhibit the PML and RARalpha signaling.
In an attempt to study the physiological role of retinoic acid in mammary gland development, we created a transgenic model system expressing a dominant negative RARalpha under the regulation of murine mammary
tumor
viral promoter.
Retinoic acid blocked
tumor
development ex vivo through induction of apoptosis.
Thus, our
results
suggested that disruption of RARalpha signaling was the first essential step in the development of APL in vivo.
[MeSH-major]
Gene Expression Regulation / physiology. Genes, Dominant. Precursor
Cell
Lymphoblastic Leukemia-Lymphoma / etiology. Receptors, Retinoic Acid / genetics
[MeSH-minor]
Acute
Disease
. Animals. Apoptosis.
Cell
Proliferation. Female. Humans. Male. Mammary
Tumor
Virus, Mouse / genetics. Mice. Mice, Transgenic. Survival Rate. Tretinoin / pharmacology.
Tumor Cells
, Cultured
Hazardous Substances Data Bank.
ALL-TRANS-RETINOIC ACID
.
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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(PMID = 16273555.001).
[ISSN]
0899-1987
[Journal-full-title]
Molecular carcinogenesis
[ISO-abbreviation]
Mol. Carcinog.
[Language]
eng
[Grant]
United States / NIEHS NIH HHS / ES / P30 ES06639; United States / NCI NIH HHS / CA / R01 CA89526
[Publication-type]
Comparative Study; 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 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha; 5688UTC01R / Tretinoin
3.
Shen R, Tao L, Xu Y, Chang S, Van Brocklyn J, Gao JX:
Reversibility of aberrant global DNA and estrogen receptor-alpha gene methylation distinguishes colorectal precancer from cancer.
Int J Clin Exp Pathol
; 2009;2(1):21-33
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[Title]
Reversibility of aberrant global DNA and estrogen receptor-
alpha
gene methylation distinguishes colorectal precancer from cancer.
Recently we have identified
a new type of
cancer
cell
called precancerous stem
cells
(pCSCs) and proposed that cancer may arise from a lengthy development process
of tumor
initiating
cells
(TICs) --> pCSCs --> cancer stem
cells
(CSCs) --> cancer, which is in parallel to histological changes of hyperplasia (TICs) --> precancer (pCSCs) --> carcinoma (CSCs/cancer
cells
), accompanied by clonal evolutionary epigenetic and genetic alterations.
In this study, we investigated whether aberrant DNA methylation can be used
as a
biomarker for the differentiation between premalignant
and malignant
lesions in the colorectum.
The profile of global DNA and estrogen receptor (ER)-
alpha
gene methylation during cancer development was determined by analysis of 5-methylcytosine (5-MeC) using immunohistochemical (IHC) staining, dot blot analysis or a quantitative gene methylation assay (QGMA).
Herein we show that global DNA hypomethylation and ER-
alpha
gene hypermethylation are progressively enhanced from hyperplastic
polyps
(HPs) --> adenomatous
polyps
(APs) --> adenomatous carcinoma (AdCa).
In normal colorectal mucosa, while global DNA methylation was not affected by aging, ER-
alpha
gene methylation was significantly increased with aging.
Taken together, reversibility of aberrant global DNA and ER-
alpha
gene methylation distinguishes colorectal precancer from cancer.
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[
11016626.001
]
[Cites]
Gut. 2006 Oct;55(10):1467-74
[
16469793.001
]
(PMID = 18830381.001).
[ISSN]
1936-2625
[Journal-full-title]
International journal of clinical and experimental pathology
[ISO-abbreviation]
Int J Clin Exp Pathol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Keywords]
NOTNLM ; DNA methylation / Precancer / cancer progression / colorectal cancer / epigenetic / estrogen receptor-α / nonsteroidal anti-inflammatory drugs / tumor initiation
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4.
Li MY, Yuan H, Ma LT, Kong AW, Hsin MK, Yip JH, Underwood MJ, Chen GG:
Roles of peroxisome proliferator-activated receptor-alpha and -gamma in the development of non-small cell lung cancer.
Am J Respir Cell Mol Biol
; 2010 Dec;43(6):674-83
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[Title]
Roles of peroxisome proliferator-activated receptor-
alpha
and -gamma in the development
of non
-small
cell
lung cancer.
Peroxisome proliferator-activated receptor (PPAR)-α and PPARγ participate in
cell
proliferation and apoptosis.
The roles of PPARα and -γ were investigated in the development of pulmonary
tumors
induced in the adult A/J mouse by treatment with 4-(methylnitrosamino)-l-(3-pyridyl)-lbutanone (NNK).
Compared with the normal lung tissues, PPARγ expression was much higher in the NNK-induced lung
tumor
tissues.
Along with the alteration of PPARγ and its endogenous ligands, the level of PPARα and its activity were increased in the NNK-induced mouse lung
tumors
.
Treatment of mice with the synthetic PPARγ ligand, pioglitazone, significantly inhibited the formation of mouse lung
tumors
induced by NNK.
Our study demonstrated that the reduction of endogenous PPARγ ligands and increased PPARα occurred before the formation of lung
tumors
, indicating that the molecular changes play a role in lung carcinogenesis.
The
results
suggest that the enhancement of PPARγ activity with its ligands, and the suppression of PPARα with its inhibitors, may prevent the formation of lung
tumors
, as well as accelerate the therapy of lung cancer.
Our
findings
may also reveal the possibility of using the level of endogenous PPARγ ligands and the activities of PPARγ or PPARα
as tumor
markers for lung cancer.
[MeSH-major]
Carcinoma,
Non
-Small-
Cell
Lung / metabolism. Lung
Neoplasms
/ metabolism. PPAR
alpha
/ metabolism. PPAR gamma / metabolism. Precancerous Conditions / pathology
[MeSH-minor]
Animals.
Disease
Progression. Female. Gene Expression Regulation,
Neoplastic
/ drug effects. Humans. Hydroxyeicosatetraenoic Acids / metabolism. Ligands. Linoleic Acids / metabolism. Lipid Metabolism / drug effects. Lipid Metabolism / genetics. Male. Mice. Nitrosamines. Retinoid X Receptor
alpha
/ metabolism. Signal Transduction / drug effects. Signal Transduction / genetics. Thiazolidinediones / pharmacology. Transcription, Genetic / drug effects
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.
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.
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consumer health - Lung Cancer
.
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PIOGLITAZONE
.
Hazardous Substances Data Bank.
4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone
.
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Mouse Genome Informatics (MGI)
.
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(PMID = 20081051.001).
[ISSN]
1535-4989
[Journal-full-title]
American journal of respiratory cell and molecular biology
[ISO-abbreviation]
Am. J. Respir. Cell Mol. Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Hydroxyeicosatetraenoic Acids; 0 / Ligands; 0 / Linoleic Acids; 0 / Nitrosamines; 0 / PPAR alpha; 0 / PPAR gamma; 0 / Retinoid X Receptor alpha; 0 / Thiazolidinediones; 5204-88-6 / 13-hydroxy-9,11-octadecadienoic acid; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; 73945-47-8 / 15-hydroxy-5,8,11,13-eicosatetraenoic acid; X4OV71U42S / pioglitazone
5.
Blank C, Brown I, Kacha AK, Markiewicz MA, Gajewski TF:
ICAM-1 contributes to but is not essential for tumor antigen cross-priming and CD8+ T cell-mediated tumor rejection in vivo.
J Immunol
; 2005 Mar 15;174(6):3416-20
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[Title]
ICAM-1 contributes to but is not essential for
tumor
antigen cross-priming and CD8+ T
cell
-mediated
tumor
rejection in vivo.
ICAM-1 has been described to provide both adhesion and costimulatory functions during T
cell
activation.
In the setting of antitumor immunity, ICAM-1/LFA-1 interactions could be important at the level
of T
cell
priming by APCs in draining lymph nodes as well as for transendothelial migration
and tumor
cell
recognition at the
tumor
site.
To determine the contribution of ICAM-1 to
tumor
rejection in vivo, we performed adoptive transfer of 2C TCR-transgenic/RAG2(-/-)
T cells
into TCRalpha(-/-) vs ICAM(-/-)/TCRalpha(-/-) recipient animals.
ICAM-1-deficient mice successfully rejected HTR.
C tumors
expressing Ld recognized by the 2C TCR, albeit with a kinetic delay.
Inasmuch as HTR.
C tumor cells
themselves express ICAM-1, a second model was pursued using B16-F10 melanoma
cells
that lack ICAM-1 expression.
These
cells
were transduced to express the SIYRYYGL peptide recognized by the 2C TCR in the context of Kb, which is cross-presented by APCs in H-2b mice in vivo.
These
tumors
also grew more slowly but were eventually rejected by the majority of ICAM-1(-/-)/TCRalpha(-/-) recipients.
Delayed rejection in ICAM-1(-/-) mice was associated with diminished T
cell
priming as assessed by ELISPOT.
In contrast, T
cell
penetration into the
tumor
was comparable in wild-
type and
ICAM-1(-/-) hosts, and adoptively transferred primed effector 2C
cells
rejected normally in ICAM-1(-/-) recipients.
Our
results
suggest that ICAM-1 contributes to but is not absolutely required for CD8+ T
cell
-mediated
tumor
rejection in vivo and dominantly acts at the level of priming rather than the effector phase of the antitumor immune response.
[MeSH-major]
Antigens,
Neoplasm
. CD8-Positive T-Lymphocytes / immunology. Intercellular Adhesion Molecule-1 / immunology
[MeSH-minor]
Adoptive Transfer. Animals. Antigen Presentation.
Cell
Line,
Tumor
. In Vitro Techniques. Mice. Mice, Knockout. Mice, Transgenic.
Neoplasm
Transplantation.
Neoplasms
, Experimental / immunology. Receptors, Antigen, T-
Cell
,
alpha
-beta / deficiency. Receptors, Antigen, T-
Cell
,
alpha
-beta / genetics
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(PMID = 15749875.001).
[ISSN]
0022-1767
[Journal-full-title]
Journal of immunology (Baltimore, Md. : 1950)
[ISO-abbreviation]
J. Immunol.
[Language]
eng
[Grant]
United States / NIGMS NIH HHS / GM / 5 T32 GM07281; United States / NCI NIH HHS / CA / P01CA97296
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Receptors, Antigen, T-Cell, alpha-beta; 126547-89-5 / Intercellular Adhesion Molecule-1
6.
Mirzoeva S, Kim ND, Chiu K, Franzen CA, Bergan RC, Pelling JC:
Inhibition of HIF-1 alpha and VEGF expression by the chemopreventive bioflavonoid apigenin is accompanied by Akt inhibition in human prostate carcinoma PC3-M cells.
Mol Carcinog
; 2008 Sep;47(9):686-700
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[Title]
Inhibition of HIF-1
alpha
and VEGF expression by the chemopreventive bioflavonoid apigenin is accompanied by Akt inhibition in human prostate carcinoma PC3-
M cells
.
Progression of cancer leads to hypoxic solid
tumors
that mount specific
cell
signaling responses to low oxygen conditions.
An important objective of anti-cancer therapy is the development
of new
drugs that suppress hypoxic responses in solid
tumors
.
Apigenin is a natural flavone that has been shown to have chemopreventive and/or anti-cancer properties against a number
of tumor
types.
In this study, we have investigated the effects of apigenin on expression of hypoxia-inducible factor-1 (HIF-1) in human metastatic prostate PC3-M cancer
cells
.
We found that hypoxia induced a time-dependent increase in the level of HIF-1alpha subunit protein in PC3-
M cells
, and treatment with apigenin markedly decreased HIF-1alpha expression under both normoxic and hypoxic conditions.
Further, apigenin prevented the activation of the HIF-1 downstream target gene vascular endothelial
growth
factor (VEGF).
We also found that apigenin inhibited Akt and GSK-3beta phosphorylation in PC3-
M cells
.
Taken together, our
results
identify apigenin
as a
bioflavonoid that inhibits hypoxia-activated pathways linked to cancer progression in human prostate cancer, in particular the PI3K/Akt/GSK-3 pathway.
Further studies on the mechanism of action of apigenin will likely provide
new
insight into its applicability for pharmacologic targeting of HIF-1alpha for cancer therapeutic or chemopreventive purposes.
[MeSH-major]
Apigenin / pharmacology. Flavonoids / pharmacology. Hypoxia-Inducible Factor 1,
alpha
Subunit / genetics. Prostatic
Neoplasms
/ pathology. Vascular Endothelial
Growth
Factor A / genetics
[MeSH-minor]
Cell
Hypoxia.
Cell
Line,
Tumor
. Gene Expression Regulation,
Neoplastic
/ drug effects. Humans. Male.
Neoplasm
Metastasis
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(PMID = 18240292.001).
[ISSN]
1098-2744
[Journal-full-title]
Molecular carcinogenesis
[ISO-abbreviation]
Mol. Carcinog.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P50 CA90386; United States / PHS HHS / / T32-0700085
[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 / Flavonoids; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 7V515PI7F6 / Apigenin
7.
Carlson CB, Mowery P, Owen RM, Dykhuizen EC, Kiessling LL:
Selective tumor cell targeting using low-affinity, multivalent interactions.
ACS Chem Biol
; 2007 Feb 20;2(2):119-27
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[Title]
Selective
tumor
cell
targeting using low-affinity, multivalent interactions.
This report highlights the advantages of low-affinity, multivalent interactions to recognize one
cell
type
over another.
Our goal was to devise a strategy to mediate selective killing
of tumor cells
, which are often distinguished from normal
cells
by their higher levels of particular
cell
surface receptors.
To test whether multivalent interactions could lead to highly specific
cell
targeting, we used a chemically synthesized small-molecule ligand composed of two distinct motifs:.
(1) an Arg-Gly-Asp (RGD) peptidomimetic that binds tightly (Kd approximately 10(-9)M) to alphavbeta3 integrins and (2) the galactosyl-
alpha
(1-3)galactose (
alpha
-Gal epitope), which is recognized by human anti-
alpha
-galactosyl antibodies (anti-Gal).
Importantly, anti-Gal binding requires a multivalent presentation of carbohydrate residues; anti-Gal antibodies interact weakly with the monovalent oligosaccharide (Kd approximately 10(-5)M) but bind tightly (Kd approximately 10(-11) M) to multivalent displays of
alpha
-Gal epitopes.
Such a display is generated when the bifunctional conjugate decorates a
cell
possessing a high level of alphavbeta3 integrin; the resulting
cell
surface, which presents many
alpha
-Gal epitopes, can recruit anti-Gal, thereby triggering complement-mediated lysis.
Only those
cells
with high levels of the integrin receptor are killed.
In contrast, doxorubicin tethered to the RGD-based ligand affords indiscriminate
cell
death.
These
results
highlight the advantages of exploiting the
type of
the multivalent recognition processes used by physiological systems to discriminate between
cells
.
Our
results
have implications for the treatment of cancer and other diseases characterized by the presence of deleterious
cells
.
[MeSH-major]
Antineoplastic Agents / chemical synthesis. Disaccharides / metabolism.
Neoplasms
/ drug therapy. Oligopeptides / metabolism
[MeSH-minor]
Cell
Line,
Tumor
. Complement System Proteins / physiology. Doxorubicin / pharmacology. Drug Design. Humans. Integrin alphaVbeta3 / analysis. Integrin alphaVbeta3 / metabolism. Molecular Weight
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.
The Lens.
Cited by Patents in
.
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(PMID = 17291050.001).
[ISSN]
1554-8937
[Journal-full-title]
ACS chemical biology
[ISO-abbreviation]
ACS Chem. Biol.
[Language]
eng
[Grant]
United States / NIAID NIH HHS / AI / AI55258; United States / NCI NIH HHS / CA / CA14520; United States / NIGMS NIH HHS / GM / GM07215
[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 / Antineoplastic Agents; 0 / Disaccharides; 0 / Integrin alphaVbeta3; 0 / Oligopeptides; 13168-24-6 / galactosyl-(1-3)galactose; 80168379AG / Doxorubicin; 9007-36-7 / Complement System Proteins; 99896-85-2 / arginyl-glycyl-aspartic acid
8.
Tchinda VH, Tadem AD, Tako EA, Tene G, Fogako J, Nyonglema P, Sama G, Zhou A, Leke RG:
Severe malaria in Cameroonian children: correlation between plasma levels of three soluble inducible adhesion molecules and TNF-alpha.
Acta Trop
; 2007 Apr;102(1):20-8
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[Title]
Severe malaria in Cameroonian children: correlation between plasma levels of three soluble inducible adhesion molecules and TNF-
alpha
.
Plasma levels of three soluble inducible adhesion molecules, namely: intercellular adhesion molecule-1 (sICAM-1), vascular
cell
adhesion molecule-1 (sVCAM-1) and endothelial leucocyte adhesion molecule-1 (sELAM-1) or
sE
-selectin and the pro-inflammatory cytokine,
tumour
necrosis factor-
alpha
(TNF-
alpha
) were measured in well-defined clinical groups of children with severe and uncomplicated malaria.
Results
showed significantly increased plasma concentrations of sICAM-1, sVCAM-1
and sE
-selectin in children with severe malaria compared to those with uncomplicated malaria and healthy children (P<0.001).
TNF-
alpha
levels increased significantly in children with severe malaria, approximately 2-folds compared to those with uncomplicated malaria and about 3-folds compared to healthy children (P<0.001).
More importantly, levels of TNF-
alpha
strongly correlated with those of the three adhesion molecules and were significantly associated with increased risk of death (P=0.03).
In addition, children who died from severe malaria showed higher mean levels of all measured factors compared to those who recovered, with significant differences observed with sICAM-1 (P<0.001)
and sE
-selectin (P=0.002).
Taken together, these
results
confirm the role of TNF-
alpha
and the three adhesion molecules in pathogenic processes associated with severe malaria in children, and suggest an association between sICAM-1 and severe malarial anemia.
[MeSH-major]
Cell
Adhesion Molecules / blood. Malaria, Falciparum / immunology. Malaria, Falciparum / physiopathology. Plasmodium falciparum / pathogenicity. Severity of Illness Index.
Tumor
Necrosis Factor-
alpha
/ blood
[MeSH-minor]
Animals. Cameroon / epidemiology. Child. Child, Preschool. E-Selectin / blood. Female. Humans. Infant. Intercellular Adhesion Molecule-1 / blood. Malaria, Cerebral / epidemiology. Malaria, Cerebral / immunology. Malaria, Cerebral / parasitology. Malaria, Cerebral / physiopathology. Male. Solubility. Up-Regulation. Vascular
Cell
Adhesion Molecule-1 / blood
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(PMID = 17397790.001).
[ISSN]
0001-706X
[Journal-full-title]
Acta tropica
[ISO-abbreviation]
Acta Trop.
[Language]
eng
[Grant]
United States / FIC NIH HHS / TW / 5D43 TW01264
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Cell Adhesion Molecules; 0 / E-Selectin; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1
9.
Farkas A, Tonel G, Nestle FO:
Interferon-alpha and viral triggers promote functional maturation of human monocyte-derived dendritic cells.
Br J Dermatol
; 2008 May;158(5):921-9
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[Title]
Interferon-
alpha
and viral triggers promote functional maturation of human monocyte-derived dendritic
cells
.
BACKGROUND:
Type I
interferons (IFNs) play an important role in the pathogenesis of many autoimmune disorders
including
psoriasis.
In the presence of IFN-
alpha
and granulocyte/macrophage colony-stimulating factor (GM-CSF), monocytes differentiate into dendritic
cells
(DCs) referred to as IFN-DCs.
OBJECTIVES: Recently, it was shown that single-stranded RNA (ssRNA) triggers TLR7 and TLR8; therefore we studied ssRNA,
as a
surrogate for ssRNA viruses and their impact on IFN-DCs.
METHODS: We established culture conditions for IFN-DCs, generated from plastic adherent monocytes using GM-CSF plus IFN-
alpha
.
The ability of IFN-DCs to stimulate allogeneic T-
cell
proliferation was evaluated in a mixed leucocyte reaction.
RESULTS
: We found that IFN-DCs express mRNA for TLR7 and TLR8 and that ssRNA stimulation significantly improves their costimulatory molecule expression, stabilizes their phenotype and enhances their capacity to stimulate naive T-
cell
proliferation.
In contrast, ssRNA stimulation led to a significant production of IL-12p70, IL-1beta, IL-6
and tumour
necrosis factor
alpha
.
CONCLUSIONS: Our study sheds light on a potential role for IFN-
alpha
and viral infections in triggering DC populations in psoriasis.
These
results
provide additional data for the better understanding of human autoimmune and antiviral responses and may also have implications for strategies developing cancer immunotherapy.
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(PMID = 18371115.001).
[ISSN]
0007-0963
[Journal-full-title]
The British journal of dermatology
[ISO-abbreviation]
Br. J. Dermatol.
[Language]
ENG
[Grant]
United States / NIAMS NIH HHS / AR / AR040065-17; United States / NIAMS NIH HHS / AR / R01 AR040065-17
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Cytokines; 0 / Interferon-alpha; 0 / RNA, Messenger; 0 / Toll-Like Receptor 7; 0 / Toll-Like Receptor 8; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
[Other-IDs]
NLM/ NIHMS152059; NLM/ PMC2829135
10.
Trent JT, Kerdel FA:
Tumor necrosis factor alpha inhibitors for the treatment of dermatologic diseases.
Dermatol Nurs
; 2005 Apr;17(2):97-107
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[Title]
Tumor
necrosis factor
alpha
inhibitors for the treatment of dermatologic diseases.
Tumor
necrosis factor
alpha
(TNFalpha) is involved in
cell
differentiation, mitogenesis, cytotoxic responses, inflammation, immunomodulation, and wound healing.
Because of its numerous roles, it was thought that inhibition of TNF may aid in the treatment of certain dermatologic diseases such as psoriasis, hidradentitis suppurativa, pyoderma gangrenosum, Behcet '
s syndrome
, and graft versus host
disease
.
The efficacy of these agents has proven impressive and short-term side effects have been few and relatively
benign
.
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(PMID = 15916184.001).
[ISSN]
1060-3441
[Journal-full-title]
Dermatology nursing
[ISO-abbreviation]
Dermatol Nurs
[Language]
ENG
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Dermatologic Agents; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab; OP401G7OJC / Etanercept
[Number-of-references]
57
11.
Carlisle DL, Liu X, Hopkins TM, Swick MC, Dhir R, Siegfried JM:
Nicotine activates cell-signaling pathways through muscle-type and neuronal nicotinic acetylcholine receptors in non-small cell lung cancer cells.
Pulm Pharmacol Ther
; 2007;20(6):629-41
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[Title]
Nicotine activates
cell
-signaling pathways through muscle-
type and
neuronal nicotinic acetylcholine receptors in
non
-small
cell
lung cancer
cells
.
Nicotinic acetylcholine receptors (nAChR) are expressed on
non
-neuronal
cell
types,
including
normal bronchial epithelial
cells
, and nicotine has been reported to cause Akt activation in cultured normal airway
cells
.
This study documents mRNA and protein expression of subunits known to form a muscle-
type
nAChR in
non
-small
cell
lung cancer (NSCLC)
cell
lines.
In one NSCLC examined, mRNA and protein for a heteropentamer neuronal-
type
alpha3beta2 nAChR was detected in addition to a muscle-
type
receptor.
Protein for the alpha5 nAChR was also detected in NSCLC
cells
.
Although, mRNA for the alpha7 nAChR subunit was observed in all
cell
lines, alpha7 protein was not detectable by immunoblot in NSCLC
cell
extracts.
Immunohistochemistry (IHC) of NSCLC primary tissues from 18 patients demonstrated protein expression of nAChR alpha1 and beta1 subunits, but not alpha7 subunit, in lung
tumors
, indicating preferential expression of the muscle-
type
receptor.
In addition, the beta1 subunit showed significantly increased expression in lung
tumors as
compared to
non
-
tumor
bronchial tissue.
The alpha1 subunit also showed evidence of high expression in lung
tumors
.
Inhibition was observed at 100 nM
alpha
-bungarotoxin (
alpha
-BTX) or 10 microM hexamethonium (HEX); maximal inhibition was achieved using a combination of
alpha
-BTX and HEX.
Akt was also phosphorylated in NSCLC
cells
after exposure to nicotine; this effect was inhibited by the PI3K inhibitor LY294002 and antagonists to the neuronal-
type
nAChR, but not to the muscle-
type
receptor.
Nicotine triggered influx of calcium in the 273T NSCLC
cell
line, suggesting that L-
type
calcium channels were activated.
273T
cells
also showed greater activation of p44/42 MAPK than of Akt in response to nicotine.
Cultures treated with nicotine and the EGFR tyrosine kinase inhibitor gefitinib showed a significant increase in the number of surviving
cells
compared to gefitinib alone.
These data indicate that the muscle-
type
nAChR, rather than the alpha7
type
, is highly expressed in NSCLC and leads to downstream activation of the p44/42 MAPK pathway.
Neuronal-
type
receptors are also present and functional, as evidenced by antagonist studies, although, the expression levels are lower than muscle-
type
nAChR.
Nicotine may play a role in regulating survival of NSCLC
cells and
endogenous acetylcholine released locally in the lung and/or chronic nicotine exposure might play a role in NSCLC development.
[MeSH-major]
Ganglionic Stimulants / pharmacology. Gene Expression Regulation,
Neoplastic
/ drug effects. Nicotine / pharmacology. Nicotinic Agonists / pharmacology. Protein Subunits / genetics. Receptors, Nicotinic / genetics
[MeSH-minor]
Acetylcholine / metabolism. Calcium Channels, L-
Type
/ drug effects. Calcium Channels, L-
Type
/ metabolism. Carcinoma,
Non
-Small-
Cell
Lung / genetics. Carcinoma,
Non
-Small-
Cell
Lung / metabolism.
Cell
Line,
Tumor
.
Cell
Survival / drug effects. Humans. Lung
Neoplasms
/ genetics. Lung
Neoplasms
/ metabolism. Mitogen-Activated Protein Kinase 1 / metabolism. Phosphorylation. Proto-Oncogene Proteins c-akt / drug effects. Proto-Oncogene Proteins c-akt / metabolism. RNA, Messenger / metabolism. Receptor, Epidermal
Growth
Factor / antagonists & inhibitors. Signal Transduction / drug effects. alpha7 Nicotinic Acetylcholine Receptor
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(PMID = 17015027.001).
[ISSN]
1094-5539
[Journal-full-title]
Pulmonary pharmacology & therapeutics
[ISO-abbreviation]
Pulm Pharmacol Ther
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P50 CA090440
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / CHRNA1 protein, human; 0 / CHRNB1 protein, human; 0 / Calcium Channels, L-Type; 0 / Chrna7 protein, human; 0 / Ganglionic Stimulants; 0 / Nicotinic Agonists; 0 / Protein Subunits; 0 / RNA, Messenger; 0 / Receptors, Nicotinic; 0 / alpha7 Nicotinic Acetylcholine Receptor; 6M3C89ZY6R / Nicotine; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; N9YNS0M02X / Acetylcholine
12.
Yamazaki M, Fukushima H, Shin M, Katagiri T, Doi T, Takahashi T, Jimi E:
Tumor necrosis factor alpha represses bone morphogenetic protein (BMP) signaling by interfering with the DNA binding of Smads through the activation of NF-kappaB.
J Biol Chem
; 2009 Dec 18;284(51):35987-95
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[Title]
Tumor
necrosis factor
alpha
represses bone morphogenetic protein (BMP) signaling by interfering with the DNA binding of Smads through the activation of NF-kappaB.
Bone morphogenetic proteins (BMPs) induce not only bone formation in vivo but also osteoblast differentiation of mesenchymal
cells
in vitro.
Tumor
necrosis factor
alpha
(TNFalpha) inhibits both osteoblast differentiation and bone formation induced by BMPs.
In this study, we found that TNFalpha inhibited the alkaline phosphatase activity and markedly reduced BMP2- and Smad-induced reporter activity in MC3T3-E1
cells
.
These
results
suggest that TNFalpha inhibits BMP signaling by interfering with the DNA binding of Smads through the activation of NF-kappaB.
[MeSH-major]
Bone Morphogenetic Protein 2 / metabolism.
Cell
Nucleus / metabolism. Signal Transduction / physiology. Smad Proteins / metabolism. Transcription Factor RelA / metabolism.
Tumor
Necrosis Factor-
alpha
/ metabolism
[MeSH-minor]
Active Transport,
Cell
Nucleus / drug effects. Animals.
Cell
Line. Mice. Mice, Knockout. Nitriles / pharmacology. Sulfones / pharmacology
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]
(PMID = 19854828.001).
[ISSN]
1083-351X
[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 / 3-(4-methylphenylsulfonyl)-2-propenenitrile; 0 / Bmp2 protein, mouse; 0 / Bone Morphogenetic Protein 2; 0 / Nitriles; 0 / Rela protein, mouse; 0 / Smad Proteins; 0 / Sulfones; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha
[Other-IDs]
NLM/ PMC2791026
13.
Bartolomé RA, Wright N, Molina-Ortiz I, Sánchez-Luque FJ, Teixidó J:
Activated G(alpha)13 impairs cell invasiveness through p190RhoGAP-mediated inhibition of RhoA activity.
Cancer Res
; 2008 Oct 15;68(20):8221-30
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[Title]
Activated G(
alpha
)13 impairs
cell
invasiveness through p190RhoGAP-mediated inhibition of RhoA activity.
The GTPase RhoA is a downstream target of heterotrimeric G(13) proteins and plays key roles in
cell
migration and invasion.
Here, we show that expression in human melanoma
cells of
a constitutively active, GTPase-deficient Galpha(13) form (G(
alpha
)(13)QL) or lysophosphatidylcholine (LPC)-promoted signaling through G(
alpha
)(13)-coupled receptors led to a blockade of chemokine-stimulated RhoA activation and
cell
invasion that was rescued by active RhoA.
Melanoma
cells
expressing G(
alpha
)(13)QL or
cells
stimulated with LPC displayed an increase in p190RhoGAP activation, and defects in RhoA activation and invasion were recovered by knocking down p190RhoGAP expression, thus identifying this GTPase-activating protein (GAP) protein
as a
downstream G(
alpha
)(13) target that is responsible for these inhibitory responses.
In addition, defective stress fiber assembly and reduced migration speed underlay inefficient invasion of G(
alpha
)(13)QL melanoma
cells
.
Importantly, G(
alpha
)(13)QL expression in melanoma
cells
led to impairment in lung metastasis associated with prolonged survival in SCID mice.
The data indicate that G(
alpha
)(13)-dependent downstream effects on RhoA activation and invasion tightly depend on
cell
type
-specific GAP activities and that G(
alpha
)(13)-p190RhoGAP signaling might represent a potential target for intervention in melanoma metastasis.
[MeSH-major]
GTP-Binding Protein
alpha
Subunits, G12-G13 / physiology. Guanine Nucleotide Exchange Factors / physiology. Melanoma / pathology. Repressor Proteins / physiology. rhoA GTP-Binding Protein / antagonists & inhibitors
[MeSH-minor]
Animals.
Cell
Line,
Tumor
. Chemokine CXCL12 / pharmacology. GTP-Binding Protein
alpha
Subunits, Gi-Go / physiology. Humans. Lung
Neoplasms
/ prevention & control. Lung
Neoplasms
/ secondary. Lysophosphatidylcholines / pharmacology. Mice. Mice, SCID.
Neoplasm
Invasiveness. Proto-Oncogene Proteins c-vav / metabolism. Signal Transduction. Swiss 3T3
Cells
. Thromboxane A2 / physiology
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.
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(PMID = 18922893.001).
[ISSN]
1538-7445
[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 / ARHGAP35 protein, human; 0 / Chemokine CXCL12; 0 / Guanine Nucleotide Exchange Factors; 0 / Lysophosphatidylcholines; 0 / Proto-Oncogene Proteins c-vav; 0 / Repressor Proteins; 0 / VAV2 protein, human; 57576-52-0 / Thromboxane A2; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, G12-G13; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go; EC 3.6.5.2 / rhoA GTP-Binding Protein
14.
Kota RS, Ramana CV, Tenorio FA, Enelow RI, Rutledge JC:
Differential effects of lipoprotein lipase on tumor necrosis factor-alpha and interferon-gamma-mediated gene expression in human endothelial cells.
J Biol Chem
; 2005 Sep 2;280(35):31076-84
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[Title]
Differential effects of lipoprotein lipase on
tumor
necrosis factor-
alpha
and interferon-gamma-mediated gene expression in human endothelial
cells
.
In vascular diseases, such as atherosclerosis, inflammation plays an important role in the pathogenesis of the
disease
.
We examined the role of LPL in modulating
tumor
necrosis factor-
alpha
(TNF-
alpha
)- and interferon-gamma (IFN-gamma)-mediated inflammatory cytokine signal transduction pathways in human aortic endothelial
cells
(HAECs).
LPL significantly suppressed TNF-
alpha
-induced gene expression, and this suppression was reversed by tetrahydrolipstatin and heparinase.
The anti-inflammatory response of LPL in suppressing TNF-
alpha
-induced gene expression was a result of its inhibition of NF-kappaB activity by the abrogation of IkappaB-
alpha
degradation and phosphorylation of the p65 subunit.
[MeSH-major]
Endothelial
Cells
/ physiology. Gene Expression Regulation. Interferon-gamma / metabolism. Lipoprotein Lipase / metabolism.
Tumor
Necrosis Factor-
alpha
/ metabolism
[MeSH-minor]
Aorta / cytology. Cholesterol, VLDL / metabolism. Culture Media, Serum-Free. Cytokines / metabolism. DNA-Binding Proteins / metabolism. E-Selectin / metabolism. Enzyme Inhibitors / metabolism. Heparin Lyase / metabolism. Humans. Intercellular Adhesion Molecule-1 / genetics. Intercellular Adhesion Molecule-1 / metabolism. Lactones / metabolism. NF-kappa B / metabolism. Phosphatidylinositol 3-Kinases / metabolism. STAT1 Transcription Factor. Signal Transduction / physiology. Trans-Activators / metabolism. Vascular
Cell
Adhesion Molecule-1 / metabolism
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(PMID = 15994321.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Grant]
United States / NHLBI NIH HHS / HL / HL55667; United States / NHLBI NIH HHS / HL / HL58660; United States / NHLBI NIH HHS / HL / HL70816; United States / NHLBI NIH HHS / HL / HL78615
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Cholesterol, VLDL; 0 / Culture Media, Serum-Free; 0 / Cytokines; 0 / DNA-Binding Proteins; 0 / E-Selectin; 0 / Enzyme Inhibitors; 0 / Lactones; 0 / NF-kappa B; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / Trans-Activators; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 82115-62-6 / Interferon-gamma; 95M8R751W8 / orlistat; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.1.34 / Lipoprotein Lipase; EC 4.2.2.7 / Heparin Lyase
15.
Haugaard SB, Andersen O, Pedersen SB, Dela F, Deacon CF, Holst JJ, Iversen J, Madsbad S:
Glucose-stimulated prehepatic insulin secretion is associated with circulating alanine, triglyceride, glucagon, lactate and TNF-alpha in patients with HIV-lipodystrophy.
HIV Med
; 2006 Apr;7(3):163-72
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[Title]
Glucose-stimulated prehepatic insulin secretion is associated with circulating alanine, triglyceride,
glucagon
, lactate and TNF-
alpha
in patients with HIV-lipodystrophy.
The prehepatic insulin secretion rate was estimated by deconvolution
of C
-peptide concentrations, and insulin sensitivity (SIRd) was estimated by the glucose clamp technique.
The disposition index (Di=ISREG0-10 min x SIRd) was calculated to estimate the beta-
cell
response relative to insulin sensitivity.
RESULTS
: FISR was increased by 69% (P<0.001), whereas median Di was decreased by 75% (P<0.01), primarily
as a
result
of a
reduction of SI(Rd) by 60% (P<0.001) in LIPO patients compared with controls.
Four LIPO patients displayed high FISR [+3 standard deviations (SD), P<0.001], high ISREG0-10 min (+3 SD, P<0.001) and low SIRd (P<0.01), suggesting an intact B-
cell
capacity to compensate insulin resistance; six LIPO patients exhibited high FISR (+3SD, P<0.001), low ISREG0-10min (-1 SD, P=0.01), and low SIRd (P<0.01), suggesting depletion of readily releasable insulin stores; the remaining eight LIPO patients and controls displayed identical FISR and ISREG0-10 min.
Increased concentrations of the nonglucose insulin secretagogues triglyceride (+124%), alanine (+35%)
and glucagon
(+88%), and also lactate (+96%)
and tumour
necrosis factor (TNF)-
alpha
(+62%) were observed in the 10 LIPO patients with aberrations in FISR and ISREG0-10 min compared with the remaining HIV-infected patients (all P<0.05).
CONCLUSION: Plasma triglyceride, alanine,
glucagon
, lactate and TNF-
alpha
may be associated with alterations in the first-phase prehepatic insulin secretion response to intravenous glucose in normoglycaemic lipodystrophic HIV-infected patients.
[MeSH-major]
Glucose. HIV-1. HIV-Associated Lipodystrophy
Syndrome
/ metabolism. Insulin / secretion. Insulin Resistance
[MeSH-minor]
Adult. Alanine / blood. C-Peptide / analysis. Case-Control Studies.
Glucagon
/ blood. Glucose Clamp Technique. Humans. Infusions, Intravenous. Insulin-
Secreting Cells
/ secretion. Lactates / blood. Male. Middle Aged. Stimulation, Chemical. Triglycerides / blood.
Tumor
Necrosis Factor-
alpha
/ analysis
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(PMID = 16494630.001).
[ISSN]
1464-2662
[Journal-full-title]
HIV medicine
[ISO-abbreviation]
HIV Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / C-Peptide; 0 / Insulin; 0 / Lactates; 0 / Triglycerides; 0 / Tumor Necrosis Factor-alpha; 9007-92-5 / Glucagon; IY9XDZ35W2 / Glucose; OF5P57N2ZX / Alanine
16.
Volante M, Saviozzi S, Rapa I, Ceppi P, Cappia S, Calogero R, Novello S, Borasio P, Papotti M, Scagliotti GV:
Epidermal growth factor ligand/receptor loop and downstream signaling activation pattern in completely resected nonsmall cell lung cancer.
Cancer
; 2007 Sep 15;110(6):1321-8
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[Title]
Epidermal
growth
factor ligand/receptor loop and downstream signaling activation pattern in completely resected nonsmall
cell
lung cancer.
BACKGROUND: In recent years, molecular insights shed light on the role of the epidermal
growth
factor receptor (EGFR) in nonsmall
cell
lung cancer (NSCLC),
and new
therapeutic agents, such as the EGFR tyrosine kinase inhibitors, were tested successfully, with responsiveness to those agents more likely in those patients with specific EGFR gene alterations.
The objective of the current study was to investigate the protein profiles of EGFR, c-erb-B2, transforming
growth
factor
alpha
(TGF-
alpha
) (one of the EGFR ligands commonly expressed in NSCLC), and some downstream molecules, potentially to detect a subset
of tumors
with an activated autocrine loop that is responsible for higher intracellular signaling.
METHODS: One hundred twelve consecutive patients with resected NSCLC were analyzed by immunohistochemistry for EGFR, the c-erb-B2 receptor, TGF-
alpha
, and pivotal molecules downstream from EGFR activation.
RESULTS
: EGFR, c-erb-B2, TGF-
alpha
and downstream molecule expression, per
se
, was not correlated significantly with any clinicopathologic variables, with the exception
of a
significant correlation between squamous histology and EGFR and between adenocarcinoma and TGF-
alpha
.
However, nearly 30% of NSCLCs demonstrated coexpression of both TGF-
alpha
and EGFR, and this molecular status was associated positively with a statistically significant expression of phosphatidylinositol 3 kinase and an inversely with mitogen-activated protein kinase expression.
CONCLUSIONS: The presence
of a
subgroup of NSCLCs with an activated autocrine loop may help to explain the mechanisms that lead to the relative ineffectiveness of the EGFR tyrosine kinase inhibitor and may support
new
clinical trials to define whether the subgroup of patients with these
tumors
reasonably may benefit from higher doses of such inhibitors or from the simultaneous inhibition of EGFR downstream signaling targets.
[MeSH-major]
Biomarkers,
Tumor
/ metabolism. Carcinoma,
Non
-Small-
Cell
Lung / metabolism. Carcinoma,
Non
-Small-
Cell
Lung / surgery. Lung
Neoplasms
/ metabolism. Lung
Neoplasms
/ surgery. Receptor, Epidermal
Growth
Factor / metabolism
[MeSH-minor]
Aged. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation,
Neoplastic
. Humans. Immunohistochemistry. Italy. Male. Middle Aged. Mitogen-Activated Protein Kinases / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Receptor, ErbB-2 / metabolism. Retrospective Studies. Signal Transduction. Transforming
Growth
Factor
alpha
/ metabolism
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[Copyright]
(c) 2007 American Cancer Society.
(PMID = 17647268.001).
[ISSN]
0008-543X
[Journal-full-title]
Cancer
[ISO-abbreviation]
Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Transforming Growth Factor alpha; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
17.
Li M, Li H, Li C, Zhou S, Guo L, Liu H, Jiang W, Liu X, Li P, McNutt MA, Li G:
Alpha fetoprotein is a novel protein-binding partner for caspase-3 and blocks the apoptotic signaling pathway in human hepatoma cells.
Int J Cancer
; 2009 Jun 15;124(12):2845-54
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[Title]
Alpha
fetoprotein is a novel protein-binding partner for caspase-3 and blocks the apoptotic signaling pathway in human hepatoma
cells
.
Although there is increasing evidence that
alpha
fetoprotein (AFP) may function as regulatory factor in the
growth of tumor cells
, the precise mechanism is still unclear.
Our
results
showed that low doses of TNF-related apoptosis-inducing ligand (TRAIL) elevated the activity of caspase-8, but not caspase-3.
Caspase-3 colocalized and interacted with AFP in the cytoplasm of Bel 7402
cells
, and translocated into nuclei in association with the occurrence of apoptosis while
cells
were under cotreatment with all-trans retinoic acid (ATRA) or TRAIL.
Knockdown of AFP increased the sensitivity of Bel 7402
cells
to TRAIL, and thereby, triggered caspase-3 signaling.
The effect of AFP on caspase-3 was further confirmed by transfection of the AFP gene into HLE
cells
(AFP negative).
Therefore, it is possible that the combination of AFP gene silencing together with ATRA/TRAIL cotreatment will benefit the enhancement of the chemotherapeutic efficiency of these agents on
tumors
.
[MeSH-major]
Apoptosis / physiology. Carcinoma, Hepatocellular / metabolism. Caspase 3 / metabolism. Liver
Neoplasms
/ metabolism. Signal Transduction.
alpha
-Fetoproteins / metabolism
[MeSH-minor]
Antineoplastic Agents / pharmacology. Blotting, Western. Caspase 8 / metabolism.
Cell
Proliferation / drug effects. Electrophoresis, Polyacrylamide Gel. Flow Cytometry. Fluorescence Resonance Energy Transfer. Humans. Immunoprecipitation. Protein Transport. RNA, Small Interfering / pharmacology. TNF-Related Apoptosis-Inducing Ligand / pharmacology. Tretinoin / pharmacology.
Tumor Cells
, Cultured
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[Copyright]
Copyright 2008 UICC.
(PMID = 19267404.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / RNA, Small Interfering; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / alpha-Fetoproteins; 5688UTC01R / Tretinoin; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8
18.
Lin CC, Hwang JM, Tsai MT, Su WW, Chen LM, Lai TY, Hsu HH, Yen SK, Huang CY, Liu JY:
Protein kinase C alpha location and the expression of phospho-MEK and MDR1 in hepatitis virus-related hepatocellular carcinoma biopsies.
Chin J Physiol
; 2010 Apr 30;53(2):112-8
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[Title]
Protein kinase C
alpha
location and the expression of phospho-MEK and MDR1 in hepatitis virus-related hepatocellular carcinoma biopsies.
The purpose of this study was to elucidate the function of protein kinase C (PKC)
alpha
in human hepatocellular carcinoma (HCC).
Expression of PKCalpha, phospho-MEK and MDR1 was significantly increased in the region of HCC location compared with the
non
-
tumor
location.
The HCC tissues were classified as cytosolic
type
, where PKCalpha was deposited in the cytoplasm in > 50%
of cells
, or membranous
type
for others.
The
results
showed that the higher expression levels of phospho-MEK and MDR1 in HCC location were significantly associated with those patients whose
cells
were of the membranous
type
.
The
results
indicate that elevated expression of MDR1 in HCC patients with
non
-HCV infection may be mediated through PKC signaling pathway.
[MeSH-major]
Carcinoma, Hepatocellular / metabolism. Hepatitis B / complications. Hepatitis C / complications. Liver
Neoplasms
/ metabolism. Mitogen-Activated Protein Kinase Kinases / metabolism. P-Glycoprotein / metabolism. Protein Kinase C-
alpha
/ metabolism
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Biopsy.
Cell
Membrane / metabolism. Cytoplasm / metabolism. Female. Humans. Male. Middle Aged. Retrospective Studies. Signal Transduction / physiology
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(PMID = 21793318.001).
[ISSN]
0304-4920
[Journal-full-title]
The Chinese journal of physiology
[ISO-abbreviation]
Chin J Physiol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China (Republic : 1949- )
[Chemical-registry-number]
0 / P-Glycoprotein; EC 2.7.11.13 / Protein Kinase C-alpha; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
19.
Pozharisskiĭ KM, Leenman EE, Arzumanov AA:
[Achievements in morphological diagnosis of prostatic cancer: alpha-methylacyl-coenzyme-A-racemase--a new marker of malignant cell transformation].
Arkh Patol
; 2005 Sep-Oct;67(5):15-9
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[Title]
[Achievements in morphological diagnosis of prostatic cancer:
alpha
-methylacyl-coenzyme-A-racemase--
a new
marker
of malignant
cell
transformation].
Gene P504S is considered as the most specific for prostatic carcinoma and its protein (
alpha
-methylacyl coenzyme A racemaze (AMACR/P504S) is higly sensitive and specific marker not only for adenocarcinoma
cells
but also for preceding changes - prostatic intraepithelial
neoplasm
(PIN).
AMACR/P504S seems to be the first marker
of malignant
transformation
and tumor
progression.
Use of immunohistochemical method for revealing this marker together with methods of basal prostatic
cells
observation (cytokeratin
of a
high molecular weight, cytokeratin 5/6, p63) improves morphological diagnosis of prostatic carcinoma, particularly on the material of needle biopsies.
This combination allows one to identify
neoplastic
nature of some difficult lesions.
[MeSH-major]
Biomarkers,
Tumor
/ analysis.
Cell
Transformation,
Neoplastic
. Prostatic Intraepithelial
Neoplasia
/ diagnosis. Prostatic
Neoplasms
/ diagnosis. Racemases and Epimerases / analysis
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(PMID = 16323473.001).
[ISSN]
0004-1955
[Journal-full-title]
Arkhiv patologii
[ISO-abbreviation]
Arkh. Patol.
[Language]
rus
[Publication-type]
Editorial; English Abstract
[Publication-country]
Russia (Federation)
[Chemical-registry-number]
0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
20.
Crane-Godreau MA, Wira CR:
Effects of estradiol on lipopolysaccharide and Pam3Cys stimulation of CCL20/macrophage inflammatory protein 3 alpha and tumor necrosis factor alpha production by uterine epithelial cells in culture.
Infect Immun
; 2005 Jul;73(7):4231-7
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[Title]
Effects of estradiol on lipopolysaccharide and Pam3Cys stimulation of CCL20/macrophage inflammatory protein 3
alpha
and tumor
necrosis factor
alpha
production by uterine epithelial
cells
in culture.
We have previously demonstrated that rat uterine epithelial
cells
(UEC) produce CCL20/macrophage inflammatory protein 3
alpha
(MIP3alpha)
and tumor
necrosis factor
alpha
(TNF-
alpha
) in response to live and heat-killed Escherichia coli and to the pathogen-associated molecular patterns (PAMP) lipopolysaccharide (LPS) and Pam3Cys.
To determine whether estradiol (E2) modulates PAMP-induced CCL20/MIP3alpha and TNF-
alpha
secretion, primary cultures of rat UEC were incubated with E2 for 24 h and then treated with LPS or Pam3Cys or not treated for an additional 12 h.
E2 inhibited the constitutive secretion of TNF-
alpha
and CCL20/MIP3alpha into culture media.
In contrast, and at the same time, E2 lowered the TNF-
alpha
response to both PAMP.
To determine whether estrogen receptors (ER) mediated the effects of E2, epithelial
cells
were incubated with E2 and/or ICI 182,780, a known ER antagonist.
ICI 182,780 had no effect on E2 inhibition of constitutive TNF-
alpha
and CCL20/MIP3alpha secretion.
In contrast, ICI 182,780 reversed the stimulatory effect of E2 on LPS- and/or Pam3Cys-induced CCL20/MIP3alpha secretion as well as partially reversed the inhibitory effect of E2 on TNF-
alpha
production by epithelial
cells
.
Overall, these
results
indicate that E2 regulates the production of TNF-
alpha
and CCL20/MIP3alpha by UEC in the absence as well as presence of PAMP.
Since CCL20/MIP3alpha has antimicrobial activity and is chemotactic for immune
cells
, these studies suggest that regulation of CCL20/MIP3alpha and TNF-
alpha
by E2 and PAMP may have profound effects on innate and adaptive immune responses to microbial challenge in the female reproductive tract.
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(PMID = 15972514.001).
[ISSN]
0019-9567
[Journal-full-title]
Infection and immunity
[ISO-abbreviation]
Infect. Immun.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / AI-13541; United States / NIAID NIH HHS / AI / R01 AI013541; United States / NIAID NIH HHS / AI / R37 AI013541; United States / NIAID NIH HHS / AI / P01 AI051877; United States / NIAID NIH HHS / AI / AI-51877
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Ccl20 protein, rat; 0 / Chemokine CCL20; 0 / Chemokines, CC; 0 / Lipopolysaccharides; 0 / Lipoproteins; 0 / Macrophage Inflammatory Proteins; 0 / Tumor Necrosis Factor-alpha; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol; 87420-41-5 / 2,3-bis(palmitoyloxy)-2-propyl-1-palmitoylcysteine; K848JZ4886 / Cysteine
[Other-IDs]
NLM/ PMC1168574
21.
Kanda H, Ishii K, Ogura Y, Imamura T, Kanai M, Arima K, Sugimura Y:
Naftopidil, a selective alpha-1 adrenoceptor antagonist, inhibits growth of human prostate cancer cells by G1 cell cycle arrest.
Int J Cancer
; 2008 Jan 15;122(2):444-51
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[Title]
Naftopidil, a selective
alpha
-1 adrenoceptor antagonist, inhibits
growth of
human prostate cancer
cells
by G1
cell
cycle arrest.
Alpha
-1 adrenoceptor antagonists are generally prescribed for
benign
prostate hyperplasia with lower urinary tract symptoms.
Naftopidil, a selective
alpha
-1 adrenoceptor antagonist, is frequently used in Japan because it has fewer side effects.
Here we demonstrate for the first time that naftopidil has
growth
inhibitory effect in androgen-sensitive and -insensitive human prostate cancer
cell
lines.
The concentrations causing 50% inhibition (IC50) of cancer
cell
growth
were 22.2 +/- 4.0 microM in androgen-sensitive LNCaP
cells and
33.2 +/- 1.1 microM in androgen-insensitive PC-3
cells
.
FACS analysis revealed that
cell
growth
inhibition by naftopidil was due to the arrest of the G1
cell
cycle.
Expressions of p27(kip1) and p21(cip1) were significantly increased in LNCaP
cells
treated with naftopidil.
In PC-3
cells
, naftopidil induced p21(cip1) but not p27(kip1).
In vivo, oral administration of naftopidil to nude mice inhibited the
growth of
PC-3
tumors as
compared to vehicle-treated controls.
These
results
suggest that naftopidil may be useful in the chemoprevention of prostate cancer and the intervention of hormone refractory prostate cancer.
[MeSH-major]
Adrenergic
alpha
-1 Receptor Antagonists. G1 Phase / drug effects. Naphthalenes / pharmacology. Piperazines / pharmacology. Prostatic
Neoplasms
/ drug therapy. Prostatic
Neoplasms
/ metabolism
[MeSH-minor]
Adrenergic
alpha
-Antagonists / pharmacology. Animals.
Cell
Line,
Tumor
.
Cell
Proliferation.
Cell
Separation. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27. Flow Cytometry. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Male. Mice. Mice, Nude.
Neoplasm
Transplantation. Receptors, Adrenergic,
alpha
-1 / metabolism
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[Copyright]
Copyright 2007 Wiley-Liss, Inc.
(PMID = 17918159.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / CDKN1A protein, human; 0 / CDKN1B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Intracellular Signaling Peptides and Proteins; 0 / Naphthalenes; 0 / Piperazines; 0 / Receptors, Adrenergic, alpha-1; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; R9PHW59SFN / naftopidil
22.
Meilleur MA, Akpovi CD, Pelletier RM, Vitale ML:
Tumor necrosis factor-alpha-induced anterior pituitary folliculostellate TtT/GF cell uncoupling is mediated by connexin 43 dephosphorylation.
Endocrinology
; 2007 Dec;148(12):5913-24
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[Title]
Tumor
necrosis factor-
alpha
-induced anterior pituitary folliculostellate TtT/GF
cell
uncoupling is mediated by connexin 43 dephosphorylation.
The anterior pituitary folliculostellate (FS)
cells
are key elements of the paracrine control of the pituitary function.
These
cells
are the source and the target
of growth
factors and cytokines, and are connected to other pituitary
cells
via Cx43-mediated gap junctions.
Here, we show that acute treatment of the FS TtT/GF
cell
line with TNF-
alpha
caused a transient
cell
uncoupling that was accompanied by the dephosphorylation of Cx43 in Ser368.
These TNF-
alpha
-evoked effects were dependent on protein phosphatase 2A (PP2A) and protein kinase C (PKC) activities.
TNF-
alpha
did not affect total
cell
Cx43-PP2A catalytic subunit interaction, but it did induce PP2A catalytic subunit recruitment to the Triton X-100 insoluble subcellular fraction, in which Cx43-gap junction plaques are recovered.
Cx43 did not interact with the conventional PKC-
alpha
, but it did interact with the atypical PKC-zeta.
Moreover, this interaction was weakened by TNF-
alpha
.
The temporary closure of gap junctions during acute TNF-
alpha
challenge may constitute a protective mechanism to limit or confine the spread of inflammatory signals among the FS
cells
.
[MeSH-major]
Connexin 43 / metabolism. Pituitary Gland, Anterior / drug effects. Signal Transduction / drug effects.
Tumor
Necrosis Factor-
alpha
/ pharmacology
[MeSH-minor]
Animals. Blotting, Western.
Cell
Communication / drug effects.
Cell
Line. Gap Junctions / drug effects. Gap Junctions / metabolism. Isoenzymes / metabolism. Mice. Microscopy, Fluorescence. Phosphoprotein Phosphatases / metabolism. Phosphorylation / drug effects. Protein Binding. Protein Kinase C / metabolism. Protein-Serine-Threonine Kinases / metabolism. Time Factors. Tyrosine / metabolism
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(PMID = 17872368.001).
[ISSN]
0013-7227
[Journal-full-title]
Endocrinology
[ISO-abbreviation]
Endocrinology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Connexin 43; 0 / Isoenzymes; 0 / Tumor Necrosis Factor-alpha; 42HK56048U / Tyrosine; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.13 / Protein Kinase C; EC 3.1.3.16 / Phosphoprotein Phosphatases
23.
Fiorentino S, Chopin M, Dastot H, Boissel N, Reboul M, Legrès L, Janin A, Aplan P, Sigaux F, Regnault A:
Disruption of T cell regulatory pathways is necessary for immunotherapeutic cure of T cell acute lymphoblastic leukemia in mice.
Eur Cytokine Netw
; 2005 Dec;16(4):300-8
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[Title]
Disruption
of T
cell
regulatory pathways is necessary for immunotherapeutic cure
of T
cell
acute lymphoblastic leukemia in mice.
In recent years, the outcome has been globally improved by current therapies, but it remains poor in patients with high, persistent residual
disease
following the first course of chemotherapy, prompting evaluation of the possible beneficial effects of immunotherapy protocols.
In this study, we hypothesized that the disruption of two immunoregulatory pathways controlling the auto-reactive T
cell
response might synergize with dendritic
cell
-based immunotherapy of the
disease
, which is considered to be poorly immunogenic.
In this study, we used TAL1xLMO1 leukemia
cells
adoptively transferred in mice, to generate murine leukemia with poorly immunogenic
cells as
a model for human T-ALL.
We compared the efficiency
of a
classical, dendritic
cell
-based immunotherapy (injection of dendritic
cells
loaded with
tumor
-derived antigenic products), to a combined treatment associating injection of antigen-loaded dendritic
cells and
disruption of the two immunoregulatory pathways: CD25+ suppressive
T cells
and cytotoxic T lymphocyte-associated antigens (CTLA-4).
We show that this combined treatment resulted in cure, concomitantly with in vivo generation of immune memory, and TNF-
alpha
secretion.
This study demonstrates that the disruption of these two immunoregulatory pathways synergized with immunostimulation by dendritic
cells
loaded with
tumor
-derived antigens, and paves the way for the testing of this combination in clinical trials.
[MeSH-major]
Immunotherapy, Adoptive. Precursor T-
Cell
Lymphoblastic Leukemia-Lymphoma / immunology. Precursor T-
Cell
Lymphoblastic Leukemia-Lymphoma / therapy. Signal Transduction / immunology. T-Lymphocytes / immunology
[MeSH-minor]
Animals. Antigens, CD / metabolism. Antigens,
Neoplasm
/ administration & dosage. CTLA-4 Antigen.
Cell
Line,
Tumor
. Dendritic
Cells
/ immunology. Dendritic
Cells
/ metabolism. Dendritic
Cells
/ transplantation.
Disease
Models, Animal. Immunologic Memory. Interleukin-2 Receptor
alpha
Subunit / biosynthesis. Lymphocyte Depletion. Mice. Mice, Inbred C3H. Mice, Inbred C57BL. T-Lymphocytes, Regulatory / immunology. T-Lymphocytes, Regulatory / metabolism.
Tumor
Necrosis Factor-
alpha
/ secretion
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(PMID = 16464745.001).
[ISSN]
1148-5493
[Journal-full-title]
European cytokine network
[ISO-abbreviation]
Eur. Cytokine Netw.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
France
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / Ctla4 protein, mouse; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Tumor Necrosis Factor-alpha
24.
Singh RR, Barnes CJ, Talukder AH, Fuqua SA, Kumar R:
Negative regulation of estrogen receptor alpha transactivation functions by LIM domain only 4 protein.
Cancer Res
; 2005 Nov 15;65(22):10594-601
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[Title]
Negative regulation of estrogen receptor
alpha
transactivation functions by LIM domain only 4 protein.
LIM domain only 4 (LMO4), a member of the LIM-only family of transcriptional coregulatory proteins, consists of two LIM protein-protein interaction domains that enable it to function
as a
linker protein in multiprotein complexes.
Here, we have identified estrogen receptor
alpha
(ERalpha) and its corepressor, metastasis
tumor
antigen 1 (MTA1), as two novel binding partners of LMO4.
Interestingly, LMO4 exhibited binding with both ERalpha and MTA1 and existed
as a
complex with ERalpha, MTA1, and histone deacetylases (HDAC), implying that LMO4 was a component of the MTA1 corepressor complex.
These
findings
suggested that LMO4 was an integral part of the molecular machinery involved in the negative regulation of ERalpha transactivation function in breast
cells
.
Because LMO4 is up-regulated in human breast cancers, repression of ERalpha transactivation functions by LMO4 might contribute to the process of breast cancer progression by allowing the development of ERalpha-negative phenotypes, leading to increased aggressiveness of breast cancer
cells
.
[MeSH-major]
Estrogen Receptor
alpha
/ physiology. Homeodomain Proteins / metabolism. Transcription Factors / metabolism. Transcriptional Activation / physiology
[MeSH-minor]
Adaptor Proteins, Signal Transducing. Breast
Neoplasms
/ genetics. Breast
Neoplasms
/ metabolism.
Cell
Line,
Tumor
. Chromatin / genetics. Chromatin / metabolism. Estrogen Receptor beta / metabolism. Gene Expression Regulation,
Neoplastic
/ physiology. Histone Deacetylases / metabolism. Humans. LIM Domain Proteins. Repressor Proteins / metabolism
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(PMID = 16288053.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA098823; United States / NCI NIH HHS / CA / CA90970
[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 / Adaptor Proteins, Signal Transducing; 0 / Chromatin; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / LMO4 protein, human; 0 / Repressor Proteins; 0 / Transcription Factors; EC 3.5.1.- / Mta1 protein, human; EC 3.5.1.98 / Histone Deacetylases
25.
Shan L, Aster JC, Sklar J, Sunday ME:
Notch-1 regulates pulmonary neuroendocrine cell differentiation in cell lines and in transgenic mice.
Am J Physiol Lung Cell Mol Physiol
; 2007 Feb;292(2):L500-9
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[Title]
Notch-1 regulates pulmonary neuroendocrine
cell
differentiation in
cell
lines and in transgenic mice.
The notch gene family encodes transmembrane receptors that regulate
cell
differentiation by interacting with surface ligands on adjacent
cells
.
Previously, we demonstrated that
tumor
necrosis factor-
alpha
(TNF) induces neuroendocrine (
NE
)
cell
differentiation in H82, but not H526, undifferentiated small
cell
lung carcinoma lines.
We now test the hypothesis that TNF mediates
NE
cell
differentiation in part by altering Notch gene expression.
First, using RT-PCR, we determined that TNF treatment of H82, but not H526, transiently decreases notch-1 mRNA in parallel with induction of gene expression for the
NE
-specific marker DOPA decarboxylase (DDC).
After 7 days of Notch-1 antisense treatment, neural
cell
adhesion molecule (NCAM) immunoreactivity is induced in H82 but not H526.
Third, we generated transgenic mice bearing notch-1 driven by the neural/
NE
-specific calcitonin promoter, which express activated Notch-1 in developing lung epithelium.
Newborn NotchCal mouse lungs have high levels of hes1 mRNA, reflecting increased activated Notch, compared with wild-
type
.
NotchCal lungs have decreased CGRP-positive
NE cells
, decreased protein gene product 9.5 (PGP9.5)-positive
NE cells
, and decreased gastrin-releasing peptide (GRP), CGRP, and DDC mRNA levels compared with normal littermates.
Cumulatively, these observations provide further support for a role for Notch-1 signaling in regulating pulmonary
NE
cell
differentiation.
[MeSH-major]
Cell
Differentiation. Lung / cytology. Neurosecretory Systems / cytology. Receptor, Notch1 / metabolism
[MeSH-minor]
Animals. Animals, Newborn. Calcitonin / genetics. Carcinoma, Small
Cell
/ genetics. Carcinoma, Small
Cell
/ pathology.
Cell
Line,
Tumor
. Dopa Decarboxylase / genetics. Gastrin-Releasing Peptide / genetics. Gastrin-Releasing Peptide / metabolism. Gene Expression / drug effects. Gene Expression Regulation,
Neoplastic
/ drug effects. Humans. Lung
Neoplasms
/ genetics. Lung
Neoplasms
/ pathology. Mice. Mice, Transgenic. Neural
Cell
Adhesion Molecules / metabolism. Oligonucleotides, Antisense / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Signal Transduction / drug effects.
Tumor
Necrosis Factor-
alpha
/ pharmacology
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.
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(PMID = 17028268.001).
[ISSN]
1040-0605
[Journal-full-title]
American journal of physiology. Lung cellular and molecular physiology
[ISO-abbreviation]
Am. J. Physiol. Lung Cell Mol. Physiol.
[Language]
eng
[Grant]
United States / NHLBI NIH HHS / HL / R01-HL-44984
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Neural Cell Adhesion Molecules; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Tumor Necrosis Factor-alpha; 80043-53-4 / Gastrin-Releasing Peptide; 9007-12-9 / Calcitonin; EC 4.1.1.- / Dopa Decarboxylase
26.
Villa-Bellosta R, Levi M, Sorribas V:
Vascular smooth muscle cell calcification and SLC20 inorganic phosphate transporters: effects of PDGF, TNF-alpha, and Pi.
Pflugers Arch
; 2009 Oct;458(6):1151-61
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[Title]
Vascular smooth muscle
cell
calcification and SLC20 inorganic phosphate transporters: effects of PDGF, TNF-
alpha
, and Pi.
Pi transport by vascular smooth muscle
cells
(VSMC) has been proposed to play an important role in the pathogenesis of vascular calcification.
In this study, we have determined the correlation between calcification induced by Pi, platelet-derived
growth
factor (PDGF)-BB,
and tumor
necrosis factor-
alpha
and Pi transport activity in primary cultures of rat aortic VSMC.
Only PDGF increased Pi transport when it was expressed per unit of DNA, as PDGF also increased total
cell
protein by 100%, while DNA content and number
of cells
were not modified.
PDGF increased the expression of the Pi transporter, Pit-1, but membrane protein biotinylation showed that Pit-1 abundance was not modified in the
cell
surface.
Immunofluorescence revealed that, under basal conditions, Pit-1 is only slightly expressed at the
cell
membrane, but strongly expressed inside the
cell
.
The intracellular signal colocalizes with endoplasmic reticulum (ER) markers, and PDGF increases Pit-1 expression in the ER but not the
cell
membrane.
In conclusion, Pi transport across the plasma membrane does not correlate directly with calcification, but the expression of Pit-1 in the ER opens
new
possibilities for the study of the pathogenesis of vascular calcification.
[MeSH-major]
Muscle, Smooth, Vascular / metabolism. Phosphates / pharmacology. Platelet-Derived
Growth
Factor / pharmacology. Sodium-Phosphate Cotransporter Proteins,
Type
III / physiology.
Tumor
Necrosis Factor-
alpha
/ pharmacology
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[Cites]
Circ Res. 2005 Jul 22;97(2):105-14
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18655772.001
]
(PMID = 19506901.001).
[ISSN]
1432-2013
[Journal-full-title]
Pflugers Archiv : European journal of physiology
[ISO-abbreviation]
Pflugers Arch.
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / 1 R01 DK066029
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Phosphates; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / Slc20a1 protein, rat; 0 / Sodium-Phosphate Cotransporter Proteins, Type III; 0 / Tumor Necrosis Factor-alpha; 1B56C968OA / becaplermin
27.
Studebaker AW, Storci G, Werbeck JL, Sansone P, Sasser AK, Tavolari S, Huang T, Chan MW, Marini FC, Rosol TJ, Bonafé M, Hall BM:
Fibroblasts isolated from common sites of breast cancer metastasis enhance cancer cell growth rates and invasiveness in an interleukin-6-dependent manner.
Cancer Res
; 2008 Nov 1;68(21):9087-95
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[Title]
Fibroblasts isolated from common sites of breast cancer metastasis enhance cancer
cell
growth
rates and invasiveness in an interleukin-6-dependent manner.
Common sites of breast cancer metastasis include the lung, liver, and bone, and of these secondary metastatic sites, estrogen receptor
alpha
(ERalpha)-positive breast cancer often favors bone.
Within secondary organs, cancer
cells
would predictably encounter tissue-specific fibroblasts or their soluble factors, yet our understanding of how tissue-specific fibroblasts directly affect cancer
cell
growth
rates and survival remains largely unknown.
Therefore, we tested the hypothesis that mesenchymal fibroblasts isolated from common sites of breast cancer metastasis provide a more favorable microenvironment with respect to
tumor growth
rates.
We found a direct correlation between the ability of breast, lung, and bone fibroblasts to enhance ERalpha-positive breast cancer
cell
growth and
the level of soluble interleukin-6 (IL-6) produced by each organ-specific fibroblast, and fibroblast-mediated
growth
enhancement was inhibited by the removal or inhibition of IL-6.
Interestingly, mice coinjected with MCF-7 breast
tumor cells
and senescent skin fibroblasts, which secrete IL-6, developed
tumors
, whereas mice coinjected with presenescent skin fibroblasts that produce little to no IL-6 failed to form xenograft
tumors
.
We subsequently determined that IL-6 promoted
growth and
invasion of breast cancer
cells
through signal transducer and activator of transcription 3-dependent up-regulation of Notch-3, Jagged-1, and carbonic anhydrase IX.
These data suggest that tissue-specific fibroblasts and the factors they produce can promote breast cancer
disease
progression and may represent attractive targets for development
of new
therapeutics.
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(PMID = 18974155.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA109451; United States / NCI NIH HHS / CA / R01 CA109451; United States / NCI NIH HHS / CA / RC1 CA146381; United States / NCI NIH HHS / CA / P50 CA116199; United States / NCI NIH HHS / CA / CA-116199
[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 / Culture Media, Conditioned; 0 / Interleukin-6; 0 / STAT3 Transcription Factor
28.
Li YT, He B, Wang YZ:
Exposure to cigarette smoke upregulates AP-1 activity and induces TNF-alpha overexpression in mouse lungs.
Inhal Toxicol
; 2009 Jun;21(7):641-7
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[Title]
Exposure to cigarette smoke upregulates AP-1 activity and induces TNF-
alpha
overexpression in mouse lungs.
Cigarette smoke-triggered inflammation is important in the pathophysiology of chronic obstructive pulmonary
disease
, and involves overexpression of many proinflammatory genes.
Transcription factors regulating expression of inflammatory mediators may play a key role in characterizing the
disease
.
The levels of inflammatory mediators
tumor
necrosis factor (TNF)-
alpha
, interleukin(IL)-6, and IL-8 in bronchoalveolar lavage fluid (BALF) were measured using enzyme-linked immunosorbent assay (ELISA).
Compared to the control group, smoke exposure induced a notable increase in TNF-
alpha
in BALF.
These data demonstrated that subacute smoke-triggered lung inflammation was accompanied by inflammatory
cell
influx, AP-1 activation, and proinflammatory gene overexpression in mouse lungs.
[MeSH-major]
Gene Expression Regulation / physiology. Lung / metabolism. Smoking / metabolism. Transcription Factor AP-1 / biosynthesis.
Tumor
Necrosis Factor-
alpha
/ biosynthesis. Up-Regulation / physiology
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(PMID = 19235541.001).
[ISSN]
1091-7691
[Journal-full-title]
Inhalation toxicology
[ISO-abbreviation]
Inhal Toxicol
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / Inflammation Mediators; 0 / Transcription Factor AP-1; 0 / Tumor Necrosis Factor-alpha
29.
Yang DI, Chen S, Ezekiel UR, Xu J, Wu Y, Hsu CY:
Antisense RNA to inducible nitric oxide synthase reduces cytokine-mediated brain endothelial cell death.
Ann N Y Acad Sci
; 2005 May;1042:439-47
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[Title]
Antisense RNA to inducible nitric oxide synthase reduces cytokine-mediated brain endothelial
cell
death.
We test whether inhibition of inducible nitric oxide synthase (iNOS) can exert a cytoprotective effect on cerebral endothelial
cells
upon stimulation by pro-inflammatory cytokines.
Mouse brain endothelial
cells
were stably transfected to express an antisense RNA against iNOS driven by an endothelium-specific von Willebrand factor (vWF) promoter.
Upon stimulation with
tumor
necrosis factor-
alpha
(TNF-
alpha
) plus interferon-gamma (IFN-gamma), antisense transfectants showed less iNOS enzymatic activity with less nitric oxide (NO) when compared to the sense control
cells
.
Correspondingly, the antisense
cells
showed a reduced LDH release and less cytosolic content of oligonucleosomes.
These
findings
establish a
cell
-specific antisense strategy and confirm the cytotoxic role of iNOS expression in cultured cerebral endothelial
cells
.
[MeSH-major]
Brain / cytology. Brain / metabolism. Cytokines / pharmacology. Endothelial
Cells
/ cytology. Endothelial
Cells
/ metabolism. Nitric Oxide Synthase
Type
II / metabolism. RNA, Antisense / genetics
[MeSH-minor]
Animals.
Cell
Death / drug effects.
Cell
Line. Mice
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(PMID = 15965090.001).
[ISSN]
0077-8923
[Journal-full-title]
Annals of the New York Academy of Sciences
[ISO-abbreviation]
Ann. N. Y. Acad. Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Cytokines; 0 / RNA, Antisense; EC 1.14.13.39 / Nitric Oxide Synthase Type II
30.
Birraux J, Kirby JA, Thomason JM, Taylor JJ:
The effect of cyclosporin on cell division and apoptosis in human oral keratinocytes.
J Periodontal Res
; 2006 Aug;41(4):297-302
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[Title]
The effect of cyclosporin on
cell
division and apoptosis in human oral keratinocytes.
The objective of the present study was to investigate the effects of CsA on the
growth of
oral epithelial
cells
in vitro and to test the hypothesis that CsA influences apoptosis in these
cells
.
MATERIAL AND METHODS: Cyclosporin was cocultured with an immortalized normal human oral keratinocyte
cell
line (HOK-16B), an epitheloid cervical carcinoma
cell
line (HeLa) and primary oral keratinocytes.
Cell
division was quantified using a CyQUANT kit.
Apoptosis was induced using
tumour
necrosis factor-
alpha
(TNF-
alpha
) and assayed by analysis of caspase-3 activity.
RESULTS
: CsA exhibited a dose- and time-dependent inhibition of
cell
division in all three keratinocyte
cell
cultures.
Significantly, HOK-16B
cells
treated with high doses of CsA (10 alphag/ml) did not recover their proliferative capacity 3 d after withdrawal of CsA, indicating that CsA-induced inhibition
of growth
is not temporary.
Concentrations of CsA that inhibited
cell
division (1 microg/ml) did not have any effect on constitutive or TNF-
alpha
-induced apoptosis or Bcl-2 expression in HOK-16B
cells
.
CONCLUSION: CsA inhibits oral epithelial
cell
division and this effect is not associated with changes in apoptosis in these
cells
.
The action of CsA on oral epithelial
cells
may be associated with a long-lasting stress signal, which might account for some of the pathological effects of this drug.
[MeSH-minor]
Caspase 3. Caspases / metabolism.
Cell
Line, Transformed.
Cell
Proliferation / drug effects. HeLa
Cells
. Humans. Proto-Oncogene Proteins c-bcl-2 / biosynthesis
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(PMID = 16827723.001).
[ISSN]
0022-3484
[Journal-full-title]
Journal of periodontal research
[ISO-abbreviation]
J. Periodont. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Immunosuppressive Agents; 0 / Proto-Oncogene Proteins c-bcl-2; 83HN0GTJ6D / Cyclosporine; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
31.
Zhao YF, Feng DD, Chen C:
Contribution of adipocyte-derived factors to beta-cell dysfunction in diabetes.
Int J Biochem Cell Biol
; 2006;38(5-6):804-19
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[Title]
Contribution of adipocyte-derived factors to beta-
cell
dysfunction in diabetes.
In addition to serving as an energy reservoir, the adipocyte has been characterized as an endocrine
cell
,
secreting
many bioactive factors which influence energy homeostasis.
Being overweight, with excessive adipose tissue, is considered to be part of the pathogenesis
of type
2 diabetes.
Insulin resistance and beta-
cell
dysfunction are two major pathophysiological changes seen in
type
2 diabetes.
In addition to inducing insulin resistance in insulin-responsive tissues, adipocyte-derived factors play an important role in the pathogenesis of beta-
cell
dysfunction.
Leptin, free fatty acids, adiponectin,
tumor
necrosis factor-
alpha
and interleukin-6 are all produced and secreted by adipocytes, and may directly influence aspects of beta-
cell
function,
including
insulin synthesis and secretion, insulin
cell
survival and apoptosis.
During the progression from normal weight to obesity and on to overt diabetes, the adipocyte-derived factors contribute to the occurrence and development of beta-
cell
dysfunction
and type
2 diabetes.
[MeSH-major]
Adipocytes / physiology. Diabetes Mellitus / physiopathology. Insulin-
Secreting Cells
/ drug effects
[MeSH-minor]
Adiponectin / physiology. Animals. Fatty Acids, Nonesterified / physiology. Humans. Interleukin-6 / physiology. Leptin / physiology.
Tumor
Necrosis Factor-
alpha
/ physiology
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(PMID = 16378747.001).
[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; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Adiponectin; 0 / Fatty Acids, Nonesterified; 0 / Interleukin-6; 0 / Leptin; 0 / Tumor Necrosis Factor-alpha
[Number-of-references]
155
32.
Moll R, Sievers E, Hämmerling B, Schmidt A, Barth M, Kuhn C, Grund C, Hofmann I, Franke WW:
Endothelial and virgultar cell formations in the mammalian lymph node sinus: endothelial differentiation morphotypes characterized by a special kind of junction (complexus adhaerens).
Cell Tissue Res
; 2009 Jan;335(1):109-41
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[Title]
Endothelial and virgultar
cell
formations in the mammalian lymph node sinus: endothelial differentiation morphotypes characterized by a special kind of junction (complexus adhaerens).
The lymph node sinus are channel structures of unquestionable importance in immunology and pathology, specifically in the filtering of the lymph, the transport and processing of antigens, the adhesion and migration of immune
cells
, and the spread of metastatic cancer
cells
.
Our knowledge of the
cell
and molecular biology of the sinus-forming
cells
is still limited, and the origin and biological nature of these
cells
have long been a matter of debate.
Here, we review the relevant literature and present our own experimental
results
, in particular concerning molecular markers of intercellular junctions and
cell
differentiation.
We show that both the monolayer
cells
lining the sinus walls and the intraluminal virgultar
cell
meshwork are indeed different morphotypes of the same basic endothelial
cell
character, as demonstrated by the presence
of a
distinct spectrum of general and lymphatic endothelial markers, and we therefore refer to these
cells as
sinus endothelial/virgultar
cells
(SEVCs).
These
cells
are connected by unique adhering junctions, termed complexus adhaerentes, characterized by the transmembrane glycoprotein VE-cadherin, combined with the desmosomal plaque protein desmoplakin, several adherens junction plaque proteins
including
alpha
- and beta-catenin and p120 catenin, and components of the tight junction ensemble, specifically claudin-5 and JAM-A, and the plaque protein ZO-1.
Overall, the SEVC system might be considered
as a
local and specific modification of the general lymphatic vasculature system.
Finally, physiological and pathological alterations of the SEVC system will be presented, and the possible value of the molecular markers described in histological diagnoses of autochthonous lymph node
tumors
will be discussed.
[MeSH-major]
Adherens Junctions / metabolism. Desmosomes / metabolism. Endothelial
Cells
/ metabolism. Lymph Nodes / metabolism. Lymphatic Vessels / metabolism. Tight Junctions / metabolism
[MeSH-minor]
Animals. Antigens, Differentiation. Biological Transport.
Cell
Adhesion.
Cell
Differentiation.
Cell
Movement. Cytoskeletal Proteins / metabolism. Humans. Lymph / metabolism. Membrane Glycoproteins / metabolism.
Neoplasm
Metastasis.
Neoplasms
/ metabolism.
Neoplasms
/ pathology
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(PMID = 19015886.001).
[ISSN]
1432-0878
[Journal-full-title]
Cell and tissue research
[ISO-abbreviation]
Cell Tissue Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Antigens, Differentiation; 0 / Cytoskeletal Proteins; 0 / Membrane Glycoproteins
[Number-of-references]
202
33.
Liu R, Li Z, Bai S, Zhang H, Tang M, Lei Y, Chen L, Liang S, Zhao YL, Wei Y, Huang C:
Mechanism of cancer cell adaptation to metabolic stress: proteomics identification of a novel thyroid hormone-mediated gastric carcinogenic signaling pathway.
Mol Cell Proteomics
; 2009 Jan;8(1):70-85
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[Title]
Mechanism of cancer
cell
adaptation to metabolic stress: proteomics identification
of a
novel thyroid hormone-mediated gastric carcinogenic signaling pathway.
To determine the mechanism of adaptation to metabolic stress in cancer
cells
, we used gastric cancer
as a
model system to reveal the potential signaling pathways involved.
Two-dimensional polyacrylamide gel electrophoresis coupled with ESI-Q-TOF MS/MS analysis was used to identify differentially expressed proteins between gastric
tumor
tissues and the corresponding noncancerous tissues.
T(3)-induced expression of HIF1-
alpha
and vascular endothelial
growth
factor was further verified using a gastric cancer
cell
line and in vivo mouse model.
Because the early accumulation of HIF1-
alpha
was found to be independent
of de
novo transcription, we also found that the cytosolic cascade phosphatidylinositol 3-kinase/Akt pathway sensitive to T(3) stimulus was involved.
Furthermore we demonstrated that T(3)-induced overexpression of HIF1-
alpha
was mediated by fumarate accumulation and could be enhanced by fumarate hydratase inactivation but inhibited by 2-oxoglutarate.
These
results
provide evidence for alteration of metabolic proteins and dysfunction of thyroid hormone regulation in gastric
tumors
,
and a
novel thyroid hormone-mediated tumorigenic signaling pathway is proposed.
Our
findings
are considered a significant step toward a better understanding of adaptations to metabolic stress in gastric carcinogenesis.
[MeSH-major]
Adaptation, Physiological. Proteomics. Signal Transduction. Stomach
Neoplasms
/ metabolism. Stress, Physiological. Thyroid Hormones / metabolism
[MeSH-minor]
Animals.
Cell
Line,
Tumor
. Citrates / metabolism. Electrophoresis, Gel, Two-Dimensional. Fumarate Hydratase / metabolism. Fumarates / metabolism. Gene Expression Profiling. Gene Expression Regulation,
Neoplastic
/ drug effects. Humans. Hypoxia-Inducible Factor 1,
alpha
Subunit / genetics. Hypoxia-Inducible Factor 1,
alpha
Subunit / metabolism. Mass Spectrometry. Mice.
Neoplasm
Proteins / chemistry.
Neoplasm
Proteins / genetics.
Neoplasm
Proteins / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Reproducibility
of Results
. Triiodothyronine / metabolism. Up-Regulation / drug effects. Vascular Endothelial
Growth
Factor A / genetics. Vascular Endothelial
Growth
Factor A / metabolism
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.
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.
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(PMID = 18723843.001).
[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 / Citrates; 0 / Fumarates; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Neoplasm Proteins; 0 / Thyroid Hormones; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 06LU7C9H1V / Triiodothyronine; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 4.2.1.2 / Fumarate Hydratase
34.
Choi IY, Kim SJ, Jeong HJ, Park SH, Song YS, Lee JH, Kang TH, Park JH, Hwang GS, Lee EJ, Hong SH, Kim HM, Um JY:
Hesperidin inhibits expression of hypoxia inducible factor-1 alpha and inflammatory cytokine production from mast cells.
Mol Cell Biochem
; 2007 Nov;305(1-2):153-61
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[Title]
Hesperidin inhibits expression of hypoxia inducible factor-1
alpha
and inflammatory cytokine production from mast
cells
.
The citrus unshiu peel has been used traditionally
as a
medicine to improve bronchial and asthmatic conditions or cardiac and blood circulation in Korea, China, and Japan.
Here, we report the effects of citrus unshiu peel water extract (CPWE) on the phorbol myristate acetate (PMA)+calcium ionophore A23187-induced hypoxia-inducible factor-1alpha (HIF-1alpha) activation and inflammatory cytokine production from the human mast
cell
line, HMC-1
cells
.
CPWE and hesperidin inhibited the PMA+A23187-induced HIF-1alpha expression and the subsequent production of vascular endothelial
growth
factor (VEGF).
We also show that the increased cytokines interleukin (IL)-1beta, IL-8,
and tumor
necrosis factor (TNF)-
alpha
level was significantly inhibited by treatment of CPWE or hesperidin.
In the present study, we report that CPWE and hesperidin are inhibitors of HIF-1alpha and cytokines on the mast
cell
-mediated inflammatory responses.
[MeSH-major]
Cytokines / metabolism. Hesperidin / pharmacology. Hypoxia-Inducible Factor 1,
alpha
Subunit / genetics. Inflammation Mediators / metabolism. Mast
Cells
/ drug effects. Mast
Cells
/ metabolism
[MeSH-minor]
Calcimycin / pharmacology.
Cell
Survival / drug effects.
Cells
, Cultured. Citrus / chemistry. Drugs, Chinese Herbal / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Gene Expression / drug effects. HL-60
Cells
. HeLa
Cells
. Humans. Ionophores / pharmacology. Tetradecanoylphorbol Acetate / pharmacology. Vascular Endothelial
Growth
Factor A / metabolism
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(PMID = 17629775.001).
[ISSN]
0300-8177
[Journal-full-title]
Molecular and cellular biochemistry
[ISO-abbreviation]
Mol. Cell. Biochem.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Cytokines; 0 / Drugs, Chinese Herbal; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Inflammation Mediators; 0 / Ionophores; 0 / Vascular Endothelial Growth Factor A; 37H9VM9WZL / Calcimycin; E750O06Y6O / Hesperidin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; NI40JAQ945 / Tetradecanoylphorbol Acetate
35.
Bigley NJ, Perymon H, Bowman GC, Hull BE, Stills HF, Henderson RA:
Inflammatory cytokines and cell adhesion molecules in a rat model of decompression sickness.
J Interferon Cytokine Res
; 2008 Feb;28(2):55-63
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[Title]
Inflammatory cytokines and
cell
adhesion molecules in a rat model of decompression sickness.
Early blood and tissue markers predictive of DCS include inflammatory cytokines and
cell
adhesion molecules (CAMs).
Increased levels of inflammatory cytokines, especially
tumor
necrosis factor-
alpha
(TNF-
alpha
), interleukin-6 (IL-6), and interferon-gamma (IFN-gamma), were detected in the circulation 6 h after decompression.
Compared with control animals maintained at 1 atmospheres absolute pressure ATA (101 kPascal), significant increases in expression
of E
-selectin, and L-selectin, as well as intercellular adhesion molecule-1 (ICAM-1), were observed immunohistochemically in the lungs and brains of the rats 6 h after exposure to 2 (203 kPascal), 3 (303 kPascal), or 4 (404 kPascal) ATA, followed by rapid decompression.
In contrast to the observations in brain, greater increases in expression
of E
-selectin and L-selectin around vessels and connective tissue were seen at 24 h after decompression in the quadriceps of rats exposed to either 3 or 4 ATA.
This study demonstrated that rapid decompression induces the release of mediators of inflammation and resulting tissue inflammation cascades, as well
as a
protective anti-inflammatory response.
[MeSH-major]
Cell
Adhesion Molecules / metabolism. Cytokines / metabolism. Decompression Sickness / immunology
[MeSH-minor]
Animals. Brain / immunology.
Disease
Models, Animal. E-Selectin / metabolism. Female. Inflammation Mediators / metabolism. Intercellular Adhesion Molecule-1 / metabolism. Interferon-gamma / blood. Interferon-gamma / metabolism. Interleukin-6 / blood. Interleukin-6 / metabolism. L-Selectin / metabolism. Lung / immunology. Muscle, Skeletal / immunology. Rats. Rats, Sprague-Dawley. Receptor, Adenosine A2A / metabolism.
Tumor
Necrosis Factor-
alpha
/ blood.
Tumor
Necrosis Factor-
alpha
/ metabolism
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(PMID = 18279101.001).
[ISSN]
1079-9907
[Journal-full-title]
Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
[ISO-abbreviation]
J. Interferon Cytokine Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / E-Selectin; 0 / Inflammation Mediators; 0 / Interleukin-6; 0 / Receptor, Adenosine A2A; 0 / Tumor Necrosis Factor-alpha; 126547-89-5 / Intercellular Adhesion Molecule-1; 126880-86-2 / L-Selectin; 82115-62-6 / Interferon-gamma
36.
Pasche S, Wenger B, Ischer R, Giazzon M, Angeloni S, Voirin G:
Integrated optical biosensor for in-line monitoring of cell cultures.
Biosens Bioelectron
; 2010 Dec 15;26(4):1478-85
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[Title]
Integrated optical biosensor for in-line monitoring of
cell
cultures.
An analytical detection platform was developed to evaluate the induced toxicity in
cell
cultures exposed to foreign agents like
growth
factors or nanoparticles.
Connecting a biosensing detection device to the
cell
culture flasks allows analyzing the composition of
cell
medium in real-time.
The analysis relies on the quantification of inflammatory cytokines released by
cells
into the
cell
culture medium, by means of solid-phase immunoassays analyzed with the wavelength interrogated optical sensing (WIOS) instrument.
A fluidic system for in situ measurements allows detecting cytokines in real-time, with a sensitivity of 1-100
ng
/mL depending on the cytokine.
In addition, integration of an in-line optical absorbance measurement unit, in combination with the standard AB
cell
proliferation assay, provides information on the
cell
viability in the culture.
Fluidic connections between the
cell
culture flasks, the optical biosensor and the absorbance measurement unit simultaneously allow quantifying up to three cytokines (interleukin 8, interleukin 6 and the monocyte chemotactic protein), assessing cellular proliferation, and thus discriminating between naïve
cells and cells
exposed to foreign agents such
as growth
factors (
tumor
necrosis factor
alpha
) or nanoparticles.
[MeSH-major]
Biosensing Techniques / instrumentation.
Cell
Culture Techniques / instrumentation. Computer Systems
[MeSH-minor]
Cell
Line.
Cell
Proliferation / drug effects.
Cell
Survival. Culture Media / analysis. Cytokines / analysis. Cytokines / biosynthesis. Humans. Immunoassay / methods. Nanoparticles / toxicity. Optical Processes. Spectrophotometry.
Tumor
Necrosis Factor-
alpha
/ pharmacology
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[Copyright]
Copyright © 2010 Elsevier B.V. All rights reserved.
(PMID = 20732803.001).
[ISSN]
1873-4235
[Journal-full-title]
Biosensors & bioelectronics
[ISO-abbreviation]
Biosens Bioelectron
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Culture Media; 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha
37.
Zhang W, Liu J, Wu Y, Xiao F, Wang Y, Wang R, Yang H, Wang G, Yang J, Deng H, Li J, Wen Y, Wei Y:
Immunotherapy of hepatocellular carcinoma with a vaccine based on xenogeneic homologous alpha fetoprotein in mice.
Biochem Biophys Res Commun
; 2008 Nov 7;376(1):10-4
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[Title]
Immunotherapy of hepatocellular carcinoma with a vaccine based on xenogeneic homologous
alpha
fetoprotein in mice.
alpha
-Fetoprotein (AFP) is a diagnostic marker for the presence of hepatocellular carcinoma,
and a
potential target for immunotherapy.
In the present study, we used AFP
as a
model antigen to explore the feasibility of the immunotherapy of AFP-positive liver cancer by the breaking of immune tolerance against AFP in a cross-reaction between the xenogeneic homologues and self molecules.
Recombinant rat AFP was prepared
as a
vaccine, and mouse AFP was prepared
as a
control.
Both humoral and cellular immune responses may be responsible for the antitumor activity against AFP-positive
tumor cells
, and no marked side effects were observed in the immunized mice.
[MeSH-major]
Cancer Vaccines / immunology. Cancer Vaccines / therapeutic use. Carcinoma, Hepatocellular / therapy. Liver
Neoplasms
/ therapy.
alpha
-Fetoproteins / immunology.
alpha
-Fetoproteins / therapeutic use
[MeSH-minor]
Animals. Antibodies,
Neoplasm
/ blood. Antibodies,
Neoplasm
/ immunology.
Cell
Line,
Tumor
. Immune Tolerance. Immunotherapy / methods. Mice. Mice, Inbred C57BL. Rats. Recombinant Proteins / genetics. Recombinant Proteins / immunology. Recombinant Proteins / therapeutic use
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(PMID = 18725206.001).
[ISSN]
1090-2104
[Journal-full-title]
Biochemical and biophysical research communications
[ISO-abbreviation]
Biochem. Biophys. Res. Commun.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Neoplasm; 0 / Cancer Vaccines; 0 / Recombinant Proteins; 0 / alpha-Fetoproteins
38.
He C, Deng LF, Yang QM, Shen W, Feng W, Zhang Y, Zhu YP:
[Experiment on induction of fibroblasts on 3-D cell-foam structures to express osteoblastic phenotype and its mechanism].
Zhonghua Wai Ke Za Zhi
; 2006 Feb 15;44(4):271-4
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[Title]
[Experiment on induction of fibroblasts on 3-D
cell
-foam structures to express osteoblastic phenotype and its mechanism].
OBJECTIVE: To study the feasibility of osteogenic phenotype expression by human skin fibroblasts induced in polyglycolic acid (PGA) foams and the effect
of tumor
necrosis factor-
alpha
(TNF-
alpha
) on the expression of bone morphogenetic protein (BMP) receptors.
The
cell
-PGA complexes were cultured in RCCS for 6 weeks, in the media of TNF-
alpha
(50 U/ml) and BMP-2 (0.1 microg/ml).
1 d, 3 and 6 weeks later,
cells and
extracellular matrix were investigated by electron microscopic and histochemistry observation respectively.
Secretion of osteogenic markers were analyzed by biochemical methods. (2) Fibroblasts were seeded on the glass fragments or culture flasks and treated with TNF-
alpha
(50 U/ml) in different usage (one-time, all-time).
The RT-PCR method and the immunohistochemistry fluorescence staining were used to examine the influence of TNF-
alpha
on the mRNA expression and the protein expression of the
type I
BMP receptors at 2, 4, 6, 8 d after treatment.
RESULTS
: Fibroblasts seeded on the PGA foams formed 3-dimensional matrix 3 weeks after seeding, which was demonstrated as osteo-tissue by tetracycline labeling and ARS staining.
Cells
secreted much more bone-specific alkaline phosphatase (B-AKP) and osteocalcin (OCN) into supernatant than the
cells
that were cultured in the media without TNF-
a and
BMP2.
Eight days after all-time usage, the TNF-
alpha
(50 U/ml) increased the expression of the mRNA and protein of the
type
IB BMP receptor.
CONCLUSIONS: Fibroblasts on 3-D
cell
-foam structures can express osteoblastic phenotype under certain inducing conditions.
The numerous fibroblasts in
body
would be a promising resource for
cell
seeds candidate of tissue- engineered bone.
TNF-
alpha
provides the essential condition for BMP2's target effect on fibroblasts, and combined use of TNF-
alpha
and BMP2 is one of the regulating factors.
[MeSH-major]
Bone Morphogenetic Protein Receptors,
Type I
/ genetics. Bone Morphogenetic Protein Receptors,
Type
II / genetics. Bone Morphogenetic Proteins / pharmacology. Fibroblasts / cytology. Fibroblasts / drug effects. Transforming
Growth
Factor beta / pharmacology.
Tumor
Necrosis Factor-
alpha
/ pharmacology
[MeSH-minor]
Bone Morphogenetic Protein 2.
Cell
Culture Techniques / methods.
Cell
Differentiation / drug effects.
Cells
, Cultured. Drug Synergism. Humans. Phenotype. Polyglycolic Acid
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(PMID = 16635375.001).
[ISSN]
0529-5815
[Journal-full-title]
Zhonghua wai ke za zhi [Chinese journal of surgery]
[ISO-abbreviation]
Zhonghua Wai Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / BMP2 protein, human; 0 / Bone Morphogenetic Protein 2; 0 / Bone Morphogenetic Proteins; 0 / TNF protein, human; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 26009-03-0 / Polyglycolic Acid; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type I; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type II
39.
Belyaev NN, Bogdanov AY, Savvulidi PG, Krasnoshtanov VK, Tleulieva RT, Alipov GK, Sekine I, Bae JS, Lee JB, Min YK, Yang HM:
The Influence of Alpha-fetoprotein on Natural Suppressor Cell Activity and Ehrlich Carcinoma Growth.
Korean J Physiol Pharmacol
; 2008 Aug;12(4):193-7
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[Title]
The Influence of
Alpha
-fetoprotein on Natural Suppressor
Cell
Activity and Ehrlich Carcinoma
Growth
.
The influence of
alpha
-fetoprotein (AFP) on the bone marrow (BM) natural suppressor (NS)
cells of
intact Ehrlich carcinoma -bearing CBA mice was studied.
Bone marrow NS
cells
were fractionated into three fractions by isopycnic centrifugation on percoll gradients: NS1 (rho=1.080 g/ml), NS2 (rho=1.090 g/ml) and NS3 (1.100>rho>1.090 g/ml).
These fractions were highly different in their sensitivity to known NS
cell
inductors (interleukin (IL)-2, IL-3 or histamine).
None of the NS fractions isolated from the intact mice spontaneously produced antiproliferative activity, however, they showed a high level of NS (antiproliferative and natural killer
cell
inhibitory) activity under the influence of AFP.
A single injection of AFP to intact mice led to an increase of spontaneous NS activity and the inhibition of natural killer
cell
activity.
NS activity, especially NS2, was increased in when
tumor cells
were subcutaneously inoculated three days after AFP injection.
In the AFP-treated mice, the
tumor
mass at 14 days was 60% larger than that in the untreated mice.
Our data confirmed that AFP is
a tumor
marker that can inhibit cancer immunity and plays a role in cancer pathogenesis.
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[Cites]
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Adv Exp Med Biol. 1995;383:255-69
[
8644510.001
]
(PMID = 19967055.001).
[ISSN]
2093-3827
[Journal-full-title]
The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology
[ISO-abbreviation]
Korean J. Physiol. Pharmacol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Korea (South)
[Other-IDs]
NLM/ PMC2788635
[Keywords]
NOTNLM ; Alpha-fetoprotein (AFP) / Ehrlich carcinoma (EC) / Natural killer cells / Natural suppressor (NS) cells
40.
Taura M, Fukuda R, Suico MA, Eguma A, Koga T, Shuto T, Sato T, Morino-Koga S, Kai H:
TLR3 induction by anticancer drugs potentiates poly I:C-induced tumor cell apoptosis.
Cancer Sci
; 2010 Jul;101(7):1610-7
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[Title]
TLR3 induction by anticancer drugs potentiates poly I:C-induced
tumor
cell
apoptosis.
Toll-like receptor 3 (TLR3) has gained recognition
as a
novel molecular target for cancer therapy because TLR3 activation by its synthetic ligand poly I:C directly causes
tumor
cell
death.
Recently, we reported that
tumor
suppressor p53 increases the expression of TLR3 in several
tumor
cell
lines.
Another study also showed that interferon-
alpha
(IFN-
alpha
) up-regulates TLR3 expression.
We thus hypothesized that various anticancer drugs such as p53-activating reagents and IFNs may potentiate poly I:C-induced
tumor
cell
death through the up-regulation of TLR3 expression.
Here, we screened several anticancer drugs that, together with poly I:C, effectively cause
tumor
cell
death in colon carcinoma HCT116
cells
.
We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+)
cells
but had only minimal effect in p53(-/-)
cells
, indicating a p53-dependent pathway.
On the other hand, IFN-
alpha
increased poly I:C-induced apoptosis and the TLR3 mRNA level in HCT116 p53(+/+) and p53(-/-)
cell
lines.
Furthermore, the combination of poly I:C, 5-FU and IFN-
alpha
induced the highest apoptosis in HCT116 p53(+/+) and p53(-/-)
cells
.
Considering that the p53 status in
malignant cells
is heterogeneous, this combination approach may provide a highly effective
tumor
therapy.
[MeSH-minor]
Adenocarcinoma / genetics. Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use.
Cell
Cycle / drug effects.
Cell
Death / drug effects.
Cell
Line.
Cell
Line,
Tumor
. Colorectal
Neoplasms
/ genetics. DNA Damage / drug effects. Fluorouracil / pharmacology. Humans. Interferon-
alpha
/ pharmacology. Interferon-beta / pharmacology. Kidney. Lung
Neoplasms
/ genetics. Mice
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.
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(PMID = 20367642.001).
[ISSN]
1349-7006
[Journal-full-title]
Cancer science
[ISO-abbreviation]
Cancer Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / TLR3 protein, human; 0 / Toll-Like Receptor 3; 24939-03-5 / Poly I-C; 77238-31-4 / Interferon-beta; U3P01618RT / Fluorouracil
41.
Sapey E, Wood AM, Ahmad A, Stockley RA:
Tumor necrosis factor-{alpha} rs361525 polymorphism is associated with increased local production and downstream inflammation in chronic obstructive pulmonary disease.
Am J Respir Crit Care Med
; 2010 Jul 15;182(2):192-9
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[Title]
Tumor
necrosis factor-{
alpha
} rs361525 polymorphism is associated with increased local production and downstream inflammation in chronic obstructive pulmonary
disease
.
RATIONALE: Chronic obstructive pulmonary
disease
(COPD) has a genetic component, explaining susceptibility.
Tumor
necrosis factor (TNF)-
alpha
polymorphisms have been associated with COPD, but it is unclear if genotype influences clinical phenotype, protein expression, and bioactivity.
OBJECTIVES: To determine if a functional polymorphism was important by assessing TNF-
alpha
expression and activity and its association with clinical severity over time.
TNF-
alpha
, its antagonists, and downstream mediators were measured in plasma and sputum.
To determine TNF-
alpha
bioactivity, IL-8 secretion from primary bronchial epithelial
cells
(PBECs) was measured, and neutrophil migration was assessed using sputum from both subject groups in the presence and absence of TNF-
alpha
antibody.
MEASUREMENTS AND MAIN
RESULTS
: Patients with polymorphism had more chronic bronchitis, a lower
body
mass index,
and a
greater annual decline in FEV(1) than patients with COPD without rs361525 polymorphism.
TNF-
alpha
concentrations were 100-fold higher in airway secretions from the patients with the rs361525 polymorphism, with no difference in TNF-
alpha
antagonists.
These effects could be abrogated by TNF-
alpha
antibody, demonstrating the bioactivity of TNF-
alpha
in lung secretions from this group.
CONCLUSIONS: This TNF-
alpha
polymorphism is associated with clinical features
of disease including
progression.
There is clear evidence of TNF-
alpha
overexpression and bioactivity with neutrophilic inflammation.
The polymorphism is likely to be a factor that influences a COPD
disease
phenotype and its progression.
[MeSH-major]
Polymorphism, Genetic. Pulmonary
Disease
, Chronic Obstructive / genetics.
Tumor
Necrosis Factor-
alpha
/ genetics
[MeSH-minor]
Adult. Aged.
Body
Mass Index. Bronchi / cytology. Bronchitis / epidemiology. Case-Control Studies.
Cell
Movement.
Disease
Progression. Epithelial
Cells
/ metabolism. Female. Forced Expiratory Volume. Genotype. Humans. Interleukin-8 / metabolism. Interleukin-8 / secretion. Male. Middle Aged. Neutrophils / physiology. Peroxidase / metabolism. Phenotype. Severity of Illness Index. Sputum / metabolism
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(PMID = 20299531.001).
[ISSN]
1535-4970
[Journal-full-title]
American journal of respiratory and critical care medicine
[ISO-abbreviation]
Am. J. Respir. Crit. Care Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Interleukin-8; 0 / Tumor Necrosis Factor-alpha; EC 1.11.1.7 / Peroxidase
42.
Bolick DT, Srinivasan S, Kim KW, Hatley ME, Clemens JJ, Whetzel A, Ferger N, Macdonald TL, Davis MD, Tsao PS, Lynch KR, Hedrick CC:
Sphingosine-1-phosphate prevents tumor necrosis factor-{alpha}-mediated monocyte adhesion to aortic endothelium in mice.
Arterioscler Thromb Vasc Biol
; 2005 May;25(5):976-81
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[Title]
Sphingosine-1-phosphate prevents
tumor
necrosis factor-{
alpha
}-mediated monocyte adhesion to aortic endothelium in mice.
Sphingosine-1-phosphate (S1P) is a sphingolipid that binds to G protein-coupled receptors on endothelial
cells
(ECs).
METHODS
AND RESULTS
: We injected C57BL/6J mice intravenously with
tumor
necrosis factor (TNF)-
alpha
in the presence and absence of the S1P1 receptor agonist SEW2871 and examined monocyte adhesion.
Aortas from TNF-
alpha
-injected mice had a 4-fold increase in the number of monocytes bound, whereas aortas from TNF-
alpha
plus SEW2871-treated mice had few monocytes bound (P<0.0001).
Using siRNA, we found that inhibiting the S1P1 receptor in vascular ECs blocked the ability of S1P to prevent monocyte-EC interactions in response to TNF-
alpha
.
We examined signaling pathways downstream of S1P1 and found that 100 nM S1P increased phosphorylation of Akt and decreased activation
of c
-jun.
CONCLUSIONS: Thus, we provide the first evidence that S1P signaling through the endothelial S1P1 receptor protects the vasculature against TNF-
alpha
-mediated monocyte-EC interactions in vivo.
[MeSH-major]
Cell
Adhesion / drug effects. Endothelium, Vascular / cytology. Lysophospholipids / pharmacology. Monocytes / cytology. Sphingosine / analogs & derivatives.
Tumor
Necrosis Factor-
alpha
/ metabolism. Vasculitis / drug therapy
[MeSH-minor]
Animals. Aorta / cytology. Aorta / immunology.
Cells
, Cultured. Chemokines / metabolism. E-Selectin / metabolism. Intercellular Adhesion Molecule-1 / metabolism. Mice. Mice, Inbred C57BL. Oxadiazoles / pharmacology. Receptors, Lysosphingolipid / agonists. Receptors, Lysosphingolipid / metabolism. Signal Transduction / drug effects. Signal Transduction / immunology. Thiophenes / pharmacology. Vascular
Cell
Adhesion Molecule-1 / metabolism
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(PMID = 15761190.001).
[ISSN]
1524-4636
[Journal-full-title]
Arteriosclerosis, thrombosis, and vascular biology
[ISO-abbreviation]
Arterioscler. Thromb. Vasc. Biol.
[Language]
eng
[Grant]
United States / NIGMS NIH HHS / GM / F31 GM064101; United States / NIGMS NIH HHS / GM / R01 GM067958; United States / NHLBI NIH HHS / HL / R01 HL079621
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Chemokines; 0 / E-Selectin; 0 / Lysophospholipids; 0 / Oxadiazoles; 0 / Receptors, Lysosphingolipid; 0 / SEW2871; 0 / Thiophenes; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 26993-30-6 / sphingosine 1-phosphate; NGZ37HRE42 / Sphingosine
43.
Doedens AL, Stockmann C, Rubinstein MP, Liao D, Zhang N, DeNardo DG, Coussens LM, Karin M, Goldrath AW, Johnson RS:
Macrophage expression of hypoxia-inducible factor-1 alpha suppresses T-cell function and promotes tumor progression.
Cancer Res
; 2010 Oct 1;70(19):7465-75
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[Title]
Macrophage expression of hypoxia-inducible factor-1
alpha
suppresses T-
cell
function and promotes
tumor
progression.
T cells
can inhibit
tumor growth
, but their function in the
tumor
microenvironment is often suppressed.
Many solid
tumors
exhibit abundant macrophage infiltration and low oxygen tension, yet how hypoxic conditions may affect innate immune
cells and
their role in
tumor
progression is poorly understood.
Targeted deletion of the hypoxia-responsive transcription factor hypoxia-inducible factor-1α (HIF-1α) in macrophages in a progressive murine model of breast cancer resulted in reduced
tumor growth
, although vascular endothelial
growth
factor-A levels and vascularization were unchanged.
Tumor
-associated macrophages can suppress
tumor
-infiltrating
T cells
by several mechanisms, and we found that hypoxia powerfully augmented macrophage-mediated T-
cell
suppression in vitro in a manner dependent on macrophage expression of HIF-1α.
Our
findings
link the innate immune hypoxic response to
tumor
progression through induction
of T
-
cell
suppression in the
tumor
microenvironment.
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[Copyright]
© 2010 AACR.
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[
18523649.001
]
[Cites]
Nature. 2008 Dec 11;456(7223):814-8
[
18997773.001
]
[Cites]
Genes Dev. 2010 Mar 1;24(5):491-501
[
20194441.001
]
[Cites]
Transgenic Res. 1999 Aug;8(4):265-77
[
10621974.001
]
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Cancer Res. 2000 Aug 1;60(15):4010-5
[
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]
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[
11257139.001
]
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Nature. 2001 Apr 26;410(6832):1107-11
[
11323675.001
]
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J Biol Chem. 2001 May 11;276(19):15881-5
[
11278602.001
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[
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J Immunol. 2003 Jan 1;170(1):270-8
[
12496409.001
]
(PMID = 20841473.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA118165; United States / NCI NIH HHS / CA / R01 CA082515; United States / NCI NIH HHS / CA / R01 CA130980; United States / NIAID NIH HHS / AI / R01 AI072117; United States / NCI NIH HHS / CA / R01 CA118165; United States / NCI NIH HHS / CA / R01 CA130980-03
[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 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse
[Other-IDs]
NLM/ NIHMS226663; NLM/ PMC2948598
44.
Posypanova GA, Gorokhovets NV, Makarov VA, Savvateeva LV, Kireeva NN, Severin SE, Severin ES:
Recombinant alpha-fetoprotein C-terminal fragment: the new recombinant vector for targeted delivery.
J Drug Target
; 2008 May;16(4):321-8
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[Title]
Recombinant
alpha
-fetoprotein C-terminal fragment: the
new
recombinant vector for targeted delivery.
The specific receptor of
alpha
-fetoprotein (AFP) is a universal
tumor
marker, being expressed on the surface of many
tumor cells
, but not in normal human tissues.
AFP enters the
cell
by receptor-mediated endocytosis; its receptor-binding site is hypothetically localized in the third domain of AFP.
A recombinant C-terminal AFP fragment, which contains all the third
and a
part of the second domains of hAFP, was produced.
This AFP fragment was bound specifically to the AFP receptor on the surface
of tumor cells and
was accumulated by them with the same efficiency as the full-size hAFP.
Similar to hAFP, the recombinant C-terminal fragment inhibited the estradiol-induced
growth of
hormone-dependent MCF-7
cells
in vitro.
Hence, the recombinant C-terminal AFP fragment can be used
as a
protein vector for the targeted delivery of cytostatic drugs to
tumor cells
.
[MeSH-major]
Drug Carriers / pharmacology.
alpha
-Fetoproteins / pharmacology
[MeSH-minor]
Antineoplastic Agents / administration & dosage. Bacteria / drug effects. Bacteria / genetics.
Cell
Line,
Tumor
. DNA, Complementary / biosynthesis. DNA, Complementary / genetics. Escherichia coli / metabolism. Estradiol / pharmacology. Female. Fluorescein-5-isothiocyanate. Fluorescent Dyes. Humans. Lymphocytes / drug effects. Lymphocytes / metabolism. Microscopy, Fluorescence. Protein Folding. Receptors, Peptide / metabolism. Recombinant Proteins / pharmacology
Hazardous Substances Data Bank.
ESTRADIOL
.
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(PMID = 18446611.001).
[ISSN]
1061-186X
[Journal-full-title]
Journal of drug targeting
[ISO-abbreviation]
J Drug Target
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / DNA, Complementary; 0 / Drug Carriers; 0 / Fluorescent Dyes; 0 / Receptors, Peptide; 0 / Recombinant Proteins; 0 / alpha-Fetoproteins; 0 / alpha-fetoprotein receptor, human; 4TI98Z838E / Estradiol; I223NX31W9 / Fluorescein-5-isothiocyanate
45.
Unursaikhan S, Xu X, Zeng F, Zhang L:
Antitumor activities of O-sulfonated derivatives of (1-->3)-alpha-D-glucan from different Lentinus edodes.
Biosci Biotechnol Biochem
; 2006 Jan;70(1):38-46
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[Title]
Antitumor activities
of O
-sulfonated derivatives of (1-->3)-
alpha
-D-glucan from different Lentinus edodes.
Four water-insoluble (1-->3)-
alpha
-D-glucans, coded L-II1, L-II2, L-II3 and L-II4, with different molecular weights were isolated from four kinds of fruiting bodies of Lentinus Edodes.
The four
alpha
-D-glucans were O-sulfonated to obtain derivatives (SL-II) having degrees of substitution (DS) from 0.9 to 2.1 respectively.
The
structure of
the samples was analyzed by infrared spectra, elemental analysis, and 13C NMR.
The weight-average molecular weight (Mw), radii of gyration (<s2>z1/2) and intrinsic viscosity ([eta]) of the native
alpha
-D-glucans
and O
-sulfonated derivatives were measured by size-exclusion chromatography combined with laser light scattering (SEC-LLS), LLS, and viscometry in 0.2 M aqueous NaCl and in dimethyl sulfoxide (DMSO) containing 0.25 M LiCl at 25 degrees C respectively.
The Mw values of the O-sulfonated derivatives were much lower than those of the native
alpha
-D-glucans.
The experimental
results
indicate that the O-sulfonated derivatives are water-soluble and exist as an expanded flexible chain in aqueous solution owing to intramolecular hydrogen bonding or interaction between charge groups.
The in vivo and in vitro antitumor activities of the native
alpha
-D-glucans and their O-sulfonated derivatives against solid
tumor
Sarcoma 180
cells
were evaluated and compared.
The
results
reveal that the effect
of O
-sulfonation of the
alpha
-D-glucan on the improvement of their antitumor activities was considerable.
[MeSH-minor]
Animals.
Cell
Line,
Tumor
.
Cell
Proliferation / drug effects. Magnetic Resonance Spectroscopy. Mice. Mice, Inbred BALB C. Molecular Weight. Spectroscopy, Fourier Transform Infrared. Viscosity
Hazardous Substances Data Bank.
Sulfur, Elemental
.
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(PMID = 16428819.001).
[ISSN]
0916-8451
[Journal-full-title]
Bioscience, biotechnology, and biochemistry
[ISO-abbreviation]
Biosci. Biotechnol. Biochem.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Glucans; 70FD1KFU70 / Sulfur; 9051-95-0 / alpha-1,3-glucan
46.
Brooksbank R, Woodiwiss AJ, Sliwa K, Badenhorst D, Deftereos D, Wadee AA, Essop MR, Sareli P, Norton GR:
Endotoxin-independent white cell cytokine production in haemodynamically stable patients with idiopathic dilated cardiomyopathy.
Cardiovasc J S Afr
; 2005 Sep-Oct;16(5):260-5
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[Title]
Endotoxin-independent white
cell
cytokine production in haemodynamically stable patients with idiopathic dilated cardiomyopathy.
INTRODUCTION: In heart failure, increased circulating white
cell
tumour
necrosis factor-
alpha
production could be attributed to elevated plasma endotoxin concentrations or an increase in white
cell
sensitivity to endotoxin.
AIMS: To ascertain whether, in patients with IDC, circulating white
cell
TNF-
alpha
production is also mediated through endotoxin-independent mechanisms.
METHODS: Whole blood production of TNF-
alpha
, both with and without the presence of an endotoxin stimulus, was evaluated in 89 controls and in 60 patients with IDC in
New
York Heart Association functional class I, II or III heart failure and without evidence of oedema, reduced peripheral perfusion or elevated plasma endotoxin concentrations.
RESULTS
: In patients compared to controls, IgG (p < 0.01) (IgG1 and IgG3), but not IgM concentrations were elevated, and plasma TNF-
alpha
and TGF-beta concentrations were raised (p < 0.001, p < 0.02 respectively).
In addition, endotoxin-free cultured whole blood TNF-
alpha
production (p < 0.0005) was increased.
Against a role for endotoxin-mediated pre-activation of white
cells
in patients, the sensitivity of white
cells
to endotoxin, as determined from the excitatory endotoxin concentration producing 50% maximal TNF-
alpha
production was unchanged.
Moreover, in favour
of non
-endotoxin-mediated white
cell
activation, the calcineurin inhibitor, cyclosporin-A, which did not alter endotoxin-induced TNF-
alpha
production, decreased TNF-
alpha
produced by unstimulated cultured
cells
in patients to values not significantly greater than those in controls.
CONCLUSIONS: We concluded that circulating white
cell
cytokine over-production can occur through both endotoxin- dependent and -independent mechanisms in IDC.
[MeSH-major]
Cardiomyopathy, Dilated / blood. Endotoxins / pharmacology. Leukocytes / metabolism.
Tumor
Necrosis Factor-
alpha
/ biosynthesis
[MeSH-minor]
Female. Humans. Immunoglobulin G / blood. Immunoglobulin M / blood. In Vitro Techniques. Lymphotoxin-
alpha
/ blood. Male. Middle Aged
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(PMID = 16307158.001).
[Journal-full-title]
Cardiovascular journal of South Africa : official journal for Southern Africa Cardiac Society [and] South African Society of Cardiac Practitioners
[ISO-abbreviation]
Cardiovasc J S Afr
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
South Africa
[Chemical-registry-number]
0 / Endotoxins; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Lymphotoxin-alpha; 0 / Tumor Necrosis Factor-alpha
47.
Keslacy S, Tliba O, Baidouri H, Amrani Y:
Inhibition of tumor necrosis factor-alpha-inducible inflammatory genes by interferon-gamma is associated with altered nuclear factor-kappaB transactivation and enhanced histone deacetylase activity.
Mol Pharmacol
; 2007 Feb;71(2):609-18
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[Title]
Inhibition
of tumor
necrosis factor-
alpha
-inducible inflammatory genes by interferon-gamma is associated with altered nuclear factor-kappaB transactivation and enhanced histone deacetylase activity.
Airway smooth muscle (ASM)
cells
can act as effector
cells
in the initiation and/or perpetuation of airway inflammation in asthma by producing various inflammatory chemokines or cytokines.
Previous studies from our laboratory and others showed that the combination
of tumor
necrosis factor-
alpha
(TNFalpha) and interferon-gamma (IFNgamma) or endogenous IFNbeta
results
in a synergistic induction of various pro-inflammatory genes,
including
CD38 and regulated upon activation normal T-
cell
expressed and secreted (RANTES), in ASM
cells
.
[MeSH-major]
Gene Expression Regulation / drug effects. Histone Deacetylases / metabolism. Inflammation / genetics. Interferon-gamma / pharmacology. NF-kappa B / genetics.
Tumor
Necrosis Factor-
alpha
/ pharmacology
[MeSH-minor]
Cells
, Cultured. Chemokine CCL11. Chemokines, CC / biosynthesis. Dose-Response Relationship, Drug. Drug Synergism. Humans. Interleukin-6 / biosynthesis. Interleukin-8 / biosynthesis. Myocytes, Smooth Muscle / cytology. Trachea / cytology. Transcriptional Activation
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 17108260.001).
[ISSN]
0026-895X
[Journal-full-title]
Molecular pharmacology
[ISO-abbreviation]
Mol. Pharmacol.
[Language]
eng
[Grant]
United States / NHLBI NIH HHS / HL / HL064063
[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 / CCL11 protein, human; 0 / Chemokine CCL11; 0 / Chemokines, CC; 0 / Interleukin-6; 0 / Interleukin-8; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 3.5.1.98 / Histone Deacetylases
48.
Kelly K, Kittelson J, Franklin WA, Kennedy TC, Klein CE, Keith RL, Dempsey EC, Lewis M, Jackson MK, Hirsch FR, Bunn PA, Miller YE:
A randomized phase II chemoprevention trial of 13-CIS retinoic acid with or without alpha tocopherol or observation in subjects at high risk for lung cancer.
Cancer Prev Res (Phila)
; 2009 May;2(5):440-9
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[Title]
A randomized phase II chemoprevention trial of 13-
CIS
retinoic acid with or without
alpha
tocopherol or observation in subjects at high risk for lung cancer.
We evaluated the effect of 13-
cis
retinoic acid (13-
cis
RA), with or without
alpha
tocopherol,
as a
lung cancer chemoprevention agent in a phase II randomized controlled clinical trial of adult subjects at high risk for lung cancer as defined by the presence of sputum atypia, history of smoking, and airflow obstruction, or a prior surgically cured nonsmall
cell
lung cancer (
disease
free, >3 years).
Subjects were randomly assigned to receive either 13-
cis
RA, 13-
cis
RA plus
alpha
tocopherol (13-
cis
RA/
alpha
toco) or observation for 12 months.
Seventy-five subjects were randomized (27/22/26 to observations/13-
cis
RA/13-
cis
RA/
alpha
toco); 59 completed the trial; 55 had both baseline and follow-up bronchoscopy.
The risk of treatment failure was 55.6% (15 of 27) and 50% (24 of 48) in the observation and combined (13
cis
RA plus 13
cis
RA/
alpha
toco) treatment arms, respectively (odds ratio adjusted for baseline histology, 0.97; 95% confidence interval, 0.36-2.66; P = 0.95).
Similar (nonsignificant)
results
were observed for treatment effects on endobronchial proliferation as assessed by Ki-67 immunolabeling.
Twelve-month treatment with 13-
cis
RA produced nonsignificant changes in bronchial histology, consistent with
results
in other trials.
The addition of
alpha
tocopherol did not affect toxicity.
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.
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(PMID = 19401528.001).
[ISSN]
1940-6215
[Journal-full-title]
Cancer prevention research (Philadelphia, Pa.)
[ISO-abbreviation]
Cancer Prev Res (Phila)
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50 CA058187; United States / NCI NIH HHS / CA / P50 CA058187-14; United States / NCI NIH HHS / CA / CA058187-14; United States / NCI NIH HHS / CA / P30 CA046934; United States / NCI NIH HHS / CA / P30 CA 46934; United States / NCI NIH HHS / CA / P50 CA 058187
[Publication-type]
Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 1406-66-2 / Tocopherols; EH28UP18IF / Isotretinoin
[Other-IDs]
NLM/ NIHMS268583; NLM/ PMC3103211
49.
Kretschmar C, Kleinberg L, Greenberg M, Burger P, Holmes E, Wharam M:
Pre-radiation chemotherapy with response-based radiation therapy in children with central nervous system germ cell tumors: a report from the Children's Oncology Group.
Pediatr Blood Cancer
; 2007 Mar;48(3):285-91
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[Title]
Pre-radiation chemotherapy with response-based radiation therapy in children with central nervous system germ
cell
tumors
: a report from the Children'
s Oncology
Group.
BACKGROUND: This Phase II study was designed to determine response to chemotherapy and survival after response-based radiation (RT) in children with CNS germ
cell
tumors
.
Children with nongerminomatous
tumors
or with abnormal markers received doubled doses of cisplatin and CPM.
For germinoma patients in complete response (
CR
), RT was decreased from 50.4 to 30.6 Gy.
High-risk patients received neuraxis RT: 50.4 Gy local + 30.6 Gy neuraxis in
CR
; 54 Gy local + 36 Gy if less than
CR
.
RESULTS
: Of 12 germinoma patients, 4 had cerebrospinal fluid (CSF) human chorionic gonadotropin (HCG) 6.9-21 mIU/ml.
Of 14 nongerminomatous patients, HCG in serum or CSF was >50 mIU/ml in 9,
alpha
-fetoprotein (AFP) abnormal in 9.
Four germinoma patients attained
CR
, six
PR
, one SD, one not evaluable after resection.
Two nongerminomatous patients had
CR
, three
PR
, three SD, one PD, four not evaluable after resection; one inadequately treated patient had progressive
disease
(PD).
Eleven germinoma patients are PF at median 66 months; one patient in
CR
refused RT, had PD at 10 months, received RT, and was PF at 56 months.
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[Copyright]
(c) 2006 Wiley-Liss, Inc.
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Cancer. 1985 Oct 1;56(7 Suppl):1841-6
[
4027923.001
]
(PMID = 16598761.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA006973
[Publication-type]
Clinical Trial, Phase II; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin; 0 / alpha-Fetoproteins; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin
[Other-IDs]
NLM/ NIHMS582771; NLM/ PMC4086720
50.
Han ZB, Ren H, Zhao H, Chi Y, Chen K, Zhou B, Liu YJ, Zhang L, Xu B, Liu B, Yang R, Han ZC:
Hypoxia-inducible factor (HIF)-1 alpha directly enhances the transcriptional activity of stem cell factor (SCF) in response to hypoxia and epidermal growth factor (EGF).
Carcinogenesis
; 2008 Oct;29(10):1853-61
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[Title]
Hypoxia-inducible factor (HIF)-1
alpha
directly enhances the transcriptional activity of stem
cell
factor (SCF) in response to hypoxia and epidermal
growth
factor (EGF).
Stem
cell
factor (SCF) plays important roles in
tumor growth
and angiogenesis.
Here, we report that hypoxia upregulated the expression of SCF in MCF-7 breast cancer
cells
in both messenger RNA and protein levels.
When hypoxia-inducible factor (HIF)-1
alpha
expression was knocked down by RNA interference, the MCF-7
cell
expression of SCF was decreased significantly.
Furthermore, the SCF receptor, c-kit phosphorylation was significantly strengthened by the condition culture media from hypoxic MCF-7 and MCF-7-
c cells
.
The survival of A549
cells
was more dependent on SCF under hypoxia.
Chromatin immunoprecipitation assay demonstrated that HIF-1
alpha
directly bound to this region under normoxia, and this binding activity was significantly enhanced under hypoxia.
Overexpression of HIF-1
alpha
significantly upregulated the expression of luciferase reporter gene under control of the SCF promoters in both MCF-7
cells and
human embryonic kidney 293
cells
, but mutation of the HRE site completely blocked this effect.
Epidermal
growth
factor was also able to enhance the SCF expression under normoxia in MCF-7
cells
, which was dependent on HIF-1
alpha
.
Taken together, our data demonstrated that HIF-1
alpha
was a key regulator of SCF expression in breast cancer
cells
.
Hypoxia and epidermal
growth
factor receptor signal coexisted in the
tumor
microenvironment and might promote angiogenesis through HIF-1
alpha
-mediated upregulation of SCF and other angiogenic factors.
[MeSH-major]
Cell
Hypoxia. Epidermal
Growth
Factor / pharmacology. Hypoxia-Inducible Factor 1,
alpha
Subunit / physiology. Stem
Cell
Factor / physiology. Transcription, Genetic
[MeSH-minor]
Cell
Line,
Tumor
. Humans. Neovascularization, Pathologic / etiology. Promoter Regions, Genetic. Proto-Oncogene Proteins c-kit / physiology. Signal Transduction
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(PMID = 18339685.001).
[ISSN]
1460-2180
[Journal-full-title]
Carcinogenesis
[ISO-abbreviation]
Carcinogenesis
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Stem Cell Factor; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
51.
Stier S, Totzke G, Gruewald E, Neuhaus T, Fronhoffs S, Schoneborn S, Vetter H, Ko Y:
Identification of p54(nrb) and the 14-3-3 Protein HS1 as TNF-alpha-inducible genes related to cell cycle control and apoptosis in human arterial endothelial cells.
J Biochem Mol Biol
; 2005 Jul 31;38(4):447-56
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[Title]
Identification of p54(nrb) and the 14-3-3 Protein HS1 as TNF-
alpha
-inducible genes related to
cell
cycle control and apoptosis in human arterial endothelial
cells
.
TNF-
alpha
plays a pivotal role in inflammation processes which are mainly regulated by endothelial
cells
.
While TNF-
alpha
induces apoptosis of several
cell
types like
tumor cells
, endothelial
cells
are resistant to TNFa mediated
cell
death.
The cytotoxic effects of TNF-
alpha
on most
cells
are only evident if RNA or protein synthesis is inhibited, suggesting that
de
novo RNA or protein synthesis protect
cells
from TNF-
alpha
cytotoxicity, presumably by NF-kappaB mediated induction of protective genes.
However, the cytoprotective genes involved in NF-kappaB dependent endothelial
cell
survival have not been sufficiently identified.
In the present study, the suppression subtractive hybridization (SSH) method was employed to identify rarely transcribed TNF-
alpha
inducible genes in human arterial endothelial
cells
related to
cell
survival and
cell
cycle.
The TNF-
alpha
-induced expression of the RNA binding protein p54(nrb) and the 14-3-3 protein HS1 as shown here for the first time may contribute to the TNF-
alpha
mediated
cell
protection of endothelial
cells
.
These genes have been shown to play pivotal roles in
cell
survival and
cell
cycle control in different experimental settings.
The concerted expression of these genes together with other genes related to
cell
protection and
cell
cycle like DnaJ, p21(cip1) and the ubiquitin activating enzyme E1 demonstrates the identification
of new
genes in the context of TNF-
alpha
induced gene expression patterns mediating the prosurvival effect of TNF-
alpha
in endothelial
cells
.
[MeSH-major]
Apoptosis / drug effects. Blood Proteins / metabolism.
Cell
Cycle / drug effects. Endothelium, Vascular / metabolism. Nuclear Matrix-Associated Proteins / metabolism. Octamer Transcription Factors / metabolism. RNA-Binding Proteins / metabolism.
Tumor
Necrosis Factor-
alpha
/ pharmacology
[MeSH-minor]
Cells
, Cultured. Humans. NF-kappa B / metabolism. Nucleic Acid Hybridization. Subtraction Technique. Umbilical Cord
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(PMID = 16053712.001).
[ISSN]
1225-8687
[Journal-full-title]
Journal of biochemistry and molecular biology
[ISO-abbreviation]
J. Biochem. Mol. Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Blood Proteins; 0 / HCLS1 protein, human; 0 / NF-kappa B; 0 / NONO protein, human; 0 / Nuclear Matrix-Associated Proteins; 0 / Octamer Transcription Factors; 0 / RNA-Binding Proteins; 0 / Tumor Necrosis Factor-alpha
52.
Prasad S, Mathur A, Gupta N, Jaggi M, Singh AT, Rajendran P, Sanna VK, Datta K, Mukherjee R:
Bombesin analogs containing alpha-amino-isobutyric acid with potent anticancer activity.
J Pept Sci
; 2007 Jan;13(1):54-62
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[Title]
Bombesin analogs containing
alpha
-amino-isobutyric acid with potent anticancer activity.
Six octapeptide bombesin (BN) analogs were synthesized by substituting
alpha
-aminoisobutyric acid (Aib), in place of Ala9 or Gly11, or both, in the [D-Phe6, desMet14]-BN (6-14) sequence: D-Phe6-Gln7-Trp8-Ala9-Val10-Gly11-His12-Leu13-NH2 (P0).
The antiproliferative activity of the analogs was tested in vitro on human
pancreatic
(MiaPaCa-2) and colon cancer (SW620, HT29 and PTC)
cell
lines using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.
The analogs demonstrated anticancer activity in the above
cell
lines at concentrations ranging from 0.01 nM to 1 microM.
One of the analogs, P6, was evaluated for in vivo
tumor
regression in a xenograft model of human primary colon cancer in athymic nude mice and was found to cause significant reduction in
tumor
volume.
NMR and molecular dynamics (MD) simulation studies for this analog revealed the presence
of a
mixed 3(10)/
alpha
-helical
structure
.
[MeSH-major]
Aminoisobutyric Acids / chemistry. Antineoplastic Agents / pharmacology. Bombesin / pharmacology.
Cell
Proliferation / drug effects
[MeSH-minor]
Amino Acid Sequence. Animals.
Cell
Line,
Tumor
. Dose-Response Relationship, Drug. HT29
Cells
. Humans. Magnetic Resonance Spectroscopy. Mice. Mice, Inbred BALB C. Mice, Nude. Models, Molecular. Molecular
Structure
.
Structure
-Activity Relationship. Thermodynamics. Xenograft Model Antitumor Assays / methods
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[Copyright]
(c) 2006 European Peptide Society and John Wiley & Sons, Ltd.
(PMID = 17031871.001).
[ISSN]
1075-2617
[Journal-full-title]
Journal of peptide science : an official publication of the European Peptide Society
[ISO-abbreviation]
J. Pept. Sci.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Aminoisobutyric Acids; 0 / Antineoplastic Agents; 1E7ZW41IQU / 2-aminoisobutyric acid; PX9AZU7QPK / Bombesin
53.
Ting HJ, Stice JP, Schaff UY, Hui DY, Rutledge JC, Knowlton AA, Passerini AG, Simon SI:
Triglyceride-rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to tumor necrosis factor-alpha.
Circ Res
; 2007 Feb 16;100(3):381-90
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[Title]
Triglyceride-rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to
tumor
necrosis factor-
alpha
.
TGRL isolated from human plasma during the postprandial state was examined for its capacity to bind to cultured human aortic endothelial
cells
(HAECs) and alter the acute inflammatory response to
tumor
necrosis factor-
alpha
.
This was reflected by increased mitogen-activated protein kinase activation, nuclear translocation of NF-kappaB, amplified expression of endothelial selectin and VCAM-1,
and a
subsequent increase in monocyte-specific recruitment under shear flow as quantified in a microfabricated vascular mimetic device.
[MeSH-major]
Aortic Diseases / etiology. Arteriosclerosis / etiology. Arteritis / etiology. Dietary Fats / adverse effects. Endothelial
Cells
/ drug effects. Hypertriglyceridemia / complications. LDL-Receptor Related Proteins / metabolism. Lipoproteins, HDL / toxicity. Lipoproteins, LDL / toxicity. Lipoproteins, VLDL / toxicity. Low Density Lipoprotein Receptor-Related Protein-1 / metabolism. Membrane Transport Proteins / metabolism. Receptors, LDL / metabolism. Triglycerides / toxicity.
Tumor
Necrosis Factor-
alpha
/ pharmacology
[MeSH-minor]
Aorta. Apolipoprotein C-III / metabolism. Apolipoprotein C-III / pharmacology.
Cell
Adhesion / drug effects.
Cell
Adhesion Molecules / metabolism.
Cells
, Cultured / drug effects.
Cells
, Cultured / metabolism. Chylomicrons / blood. E-Selectin / biosynthesis. E-Selectin / genetics. Endocytosis. Endothelium, Vascular / cytology. Fat Emulsions, Intravenous / pharmacology. Gene Expression Regulation / drug effects. Humans. Hypoglycemia. Intercellular Adhesion Molecule-1 / biosynthesis. Intercellular Adhesion Molecule-1 / genetics. LDL-Receptor Related Protein-Associated Protein / pharmacology. Leukocytes / cytology. Leukocytes / drug effects. Lipopolysaccharides / pharmacology. Models, Cardiovascular. Monocytes / cytology. Monocytes / drug effects. NF-kappa B / metabolism. Oxidative Stress. Rheology. Signal Transduction / drug effects. Vascular
Cell
Adhesion Molecule-1 / biosynthesis. Vascular
Cell
Adhesion Molecule-1 / genetics. p38 Mitogen-Activated Protein Kinases / metabolism
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[CommentIn]
Circ Res. 2007 Apr 13;100(7):e81
[
17431191.001
]
[CommentIn]
Circ Res. 2007 Feb 16;100(3):299-301
[
17307968.001
]
(PMID = 17234968.001).
[ISSN]
1524-4571
[Journal-full-title]
Circulation research
[ISO-abbreviation]
Circ. Res.
[Language]
eng
[Grant]
United States / NIA NIH HHS / AG / AG19327; United States / NIAID NIH HHS / AI / AI47294; United States / NHLBI NIH HHS / HL / HL077281; United States / NHLBI NIH HHS / HL / HL55667; United States / NHLBI NIH HHS / HL / HL61332
[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 / Apolipoprotein C-III; 0 / Cell Adhesion Molecules; 0 / Chylomicrons; 0 / Dietary Fats; 0 / E-Selectin; 0 / Fat Emulsions, Intravenous; 0 / HDL-triglyceride; 0 / LDL-Receptor Related Protein-Associated Protein; 0 / LDL-Receptor Related Proteins; 0 / Lipopolysaccharides; 0 / Lipoproteins, HDL; 0 / Lipoproteins, LDL; 0 / Lipoproteins, VLDL; 0 / Low Density Lipoprotein Receptor-Related Protein-1; 0 / Membrane Transport Proteins; 0 / NF-kappa B; 0 / Receptors, LDL; 0 / SORL1 protein, human; 0 / Triglycerides; 0 / Tumor Necrosis Factor-alpha; 0 / VLDL receptor; 0 / Vascular Cell Adhesion Molecule-1; 0 / low density lipoprotein triglyceride; 0 / very low density lipoprotein triglyceride; 126547-89-5 / Intercellular Adhesion Molecule-1; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
54.
Milner CM, Tongsoongnoen W, Rugg MS, Day AJ:
The molecular basis of inter-alpha-inhibitor heavy chain transfer on to hyaluronan.
Biochem Soc Trans
; 2007 Aug;35(Pt 4):672-6
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[Title]
The molecular basis of inter-
alpha
-inhibitor heavy chain transfer on to hyaluronan.
The inflammation-associated protein TSG-6 (the product
of tumour
necrosis factor-stimulated gene-6) can form covalent complexes with the heavy chains (HC1 and HC2) of IalphaI (inter-
alpha
-inhibitor); namely, TSG-6.HC1 and TSG-6.HC2, which act as intermediates in the covalent transfer of HCs on to the GAG (glycosaminoglycan) HA (hyaluronan).
HC.HA, which is formed for example in the synovial fluids of arthritis patients, is more aggregated than unmodified HA and has altered mechanical and
cell
-binding properties.
It has been shown recently that TSG-6-mediated HC.HA formation is essential for the formation of HA-rich pericellular matrix and for
cell
migration in a model of wound healing.
In contrast, in this model, the formation of
cell
-associated HA cable-like structures, although requiring the transfer of HCs on to HA, might not involve TSG-6.
[MeSH-major]
Alpha
-Globulins / metabolism. Hyaluronic Acid / metabolism
Hazardous Substances Data Bank.
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.
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(PMID = 17635118.001).
[ISSN]
0300-5127
[Journal-full-title]
Biochemical Society transactions
[ISO-abbreviation]
Biochem. Soc. Trans.
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / MC/ U138274352
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Alpha-Globulins; 39346-44-6 / inter-alpha-inhibitor; 9004-61-9 / Hyaluronic Acid
[Number-of-references]
18
55.
O'Connor JC, Julian J, Lim SD, Carson DD:
MUC1 expression in human prostate cancer cell lines and primary tumors.
Prostate Cancer Prostatic Dis
; 2005;8(1):36-44
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[Title]
MUC1 expression in human prostate cancer
cell
lines and primary
tumors
.
MUC1 expression was evaluated in normal prostate epithelial
cells
(PrEC), and prostate cancer
cell
lines in response to dihydrotestosterone (DHT), interferon-gamma (IFN-gamma)
and tumor
necrosis factor-
alpha
(TNF-
alpha
) treatment.
Expression of MUC1 core protein was stimulated in PrEC and PC-3
cells
after cytokine treatment, but was highly and constitutively expressed by
DU
-145
cells
.
MUC1 was not expressed by LNCaP, C4-2 or C4-2B
cells
under any condition.
DHT alone or in combination with cytokines had no effect on MUC1 expression in any
cell
line tested.
Using antibodies capable of detecting all isoforms of MUC1 core protein independent of their glycosylation state, immunohistochemical staining of tissue microarrays containing both nontumor
and tumor
tissue revealed that only 17%
of tumor
tissues and 41% of nontumor tissues stained positively for MUC1.
Staining patterns in
tumor
tissue varied from focal apical staining to diffuse cytoplasmic staining.
Furthermore, IFN-gamma and TNF-
alpha
strongly induce MUC1 expression in both normal prostate epithelia and certain prostate
tumor
cell
lines and may exacerbate pathologies associated with MUC1-positive prostate cancers.
[MeSH-major]
Gene Expression Profiling. Mucin-1 / biosynthesis. Prostatic
Neoplasms
/ genetics. Prostatic
Neoplasms
/ immunology
[MeSH-minor]
Blotting, Western. Cytokines / pharmacology. Dihydrotestosterone / pharmacology. Humans. Immunohistochemistry. Male.
Neoplasm
Staging.
Tumor Cells
, Cultured
Genetic Alliance.
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(PMID = 15477874.001).
[ISSN]
1365-7852
[Journal-full-title]
Prostate cancer and prostatic diseases
[ISO-abbreviation]
Prostate Cancer Prostatic Dis.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P01 CA098912
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / Cytokines; 0 / Mucin-1; 08J2K08A3Y / Dihydrotestosterone
56.
Suriano AR, Sanford AN, Kim N, Oh M, Kennedy S, Henderson MJ, Dietzmann K, Sullivan KE:
GCF2/LRRFIP1 represses tumor necrosis factor alpha expression.
Mol Cell Biol
; 2005 Oct;25(20):9073-81
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[Title]
GCF2/LRRFIP1 represses
tumor
necrosis factor
alpha
expression.
Tumor
necrosis factor
alpha
(TNF-
alpha
) is an important mediator of inflammation, apoptosis, and the development of secondary lymphoid structures.
The TNF-
alpha
-308 promoter polymorphism is a G-to-A transition which has been statistically associated with various autoimmune disorders.
Some studies have found that it may directly mediate the increased transcription of TNF-
alpha
in some circumstances.
GCF2/LRRFIP1 appears to act
as a
repressor and occupies the -308 site in
cells
that do not make TNF-
alpha
.
Cells
competent to produce TNF-
alpha
have Ets-1 bound to the -308 promoter site.
Active transcription is accompanied by NF-kappaB
and c
-Jun binding to the proximal promoter.
Thus, dynamic changes on the TNF-
alpha
promoter, particularly at the -308 site, accompany the transition from repressed to active transcription.
GCF2/LRRFIP1 is the first TNF-
alpha
repressor identified.
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[Cites]
J Biol Chem. 1998 Aug 21;273(34):21594-602
[
9705290.001
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Arthritis Rheum. 1997 Dec;40(12):2207-11
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(PMID = 16199883.001).
[ISSN]
0270-7306
[Journal-full-title]
Molecular and cellular biology
[ISO-abbreviation]
Mol. Cell. Biol.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / R21 AI090914; United States / NIAID NIH HHS / AI / R01 AI44127; United States / NIAID NIH HHS / AI / R01 AI051323; United States / NIAMS NIH HHS / AR / R29 AR/AI43172; United States / NIAID NIH HHS / AI / R01 AI044127
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / ETS1 protein, human; 0 / LRRFIP1 protein, human; 0 / Proto-Oncogene Protein c-ets-1; 0 / RNA-Binding Proteins; 0 / Repressor Proteins; 0 / Tumor Necrosis Factor-alpha; 9007-49-2 / DNA
[Other-IDs]
NLM/ PMC1265793
57.
El-Obeid A, Al-Harbi S, Al-Jomah N, Hassib A:
Herbal melanin modulates tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6) and vascular endothelial growth factor (VEGF) production.
Phytomedicine
; 2006 May;13(5):324-33
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[Title]
Herbal melanin modulates
tumor
necrosis factor
alpha
(TNF-
alpha
), interleukin 6 (IL-6) and vascular endothelial
growth
factor (VEGF) production.
Recent studies have indicated that cytokines can enhance immunogenicity and promote
tumor
regression.
In this study we report the effects
of a
herbal melanin, extracted from Nigella sativa L., on the production of three cytokines [
tumor
necrosis factor
alpha
(TNF-
alpha
), interleukin 6 (IL-6) and vascular endothelial
growth
factor (VEGF)], by human monocytes, total peripheral blood mononuclear
cells
(PBMC) and THP-1
cell
line.
Cells
were treated with variable concentrations of melanin and the expression of TNF-
alpha
, IL-6 and VEGF mRNA in
cell
lysates and secretion of proteins in the supernatants were detected by RT-PCR and ELISA.
Melanin induced TNF-
alpha
, IL-6 and VEGF mRNA expression by the monocytes, PBMC and THP-1
cell
line.
On the protein level, melanin significantly induced TNF-
alpha
and IL-6 protein production and inhibited VEGF production by monocytes and PBMC.
In the THP-1
cell
line melanin induced production of all three cytokine proteins.
[MeSH-minor]
Actins / analysis. Adult.
Cell
Line. DNA Primers / chemistry. Gene Expression / drug effects. Humans. Interleukin-6 / biosynthesis. Interleukin-6 / genetics. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / immunology. Middle Aged. RNA, Messenger / analysis. Seeds / chemistry. Toxicity Tests, Acute / methods.
Tumor
Necrosis Factor-
alpha
/ biosynthesis.
Tumor
Necrosis Factor-
alpha
/ drug effects.
Tumor
Necrosis Factor-
alpha
/ genetics. Vascular Endothelial
Growth
Factor A / biosynthesis. Vascular Endothelial
Growth
Factor A / drug effects. Vascular Endothelial
Growth
Factor A / genetics
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 16635740.001).
[ISSN]
0944-7113
[Journal-full-title]
Phytomedicine : international journal of phytotherapy and phytopharmacology
[ISO-abbreviation]
Phytomedicine
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Actins; 0 / Cytokines; 0 / DNA Primers; 0 / Interleukin-6; 0 / Melanins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Endothelial Growth Factor A
58.
Kato T, Madono K, Saito J, Kakuta Y, Tanigawa G, Yazawa K, Hosomi M, Ito K:
[Successful preoperative interferon-alpha therapy of advanced renal cell carcinoma with tumor thrombus extending into the inferior vena cava: a case report].
Hinyokika Kiyo
; 2008 Feb;54(2):119-22
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[Title]
[Successful preoperative interferon-
alpha
therapy of advanced renal
cell
carcinoma with
tumor
thrombus extending into the inferior vena cava: a case report].
We report a case of renal
cell
carcinoma in which interferon-a therapy was effective in reducing the
tumor
thrombus extending into the inferior vena cava.
We made a diagnosis
of a
left renal
cell
carcinoma with
tumor
thrombus by imaging examination.
Twenty-two months after the start of interferon-a therapy, the
tumor
thrombus was markedly reduced in size, and the clinical response was evaluated as partial response by the response criteria for urological cancer treatrment.
Because of improvement of the performance status and downsizing
of tumor
thrombus, we performed radical nephrectomy.
Pathological examinations revealed that viable renal
cell
carcinomas were found in the primary lesion and the
tumor
thrombus.
In some cases, interferon-
alpha
therapy is useful and safe in the treatment of the
tumor
thrombus.
Furthermore, radical nephrectomy and complete resection of the
tumor
thrombus prolongs postoperative survival.
[MeSH-major]
Carcinoma, Renal
Cell
/ drug therapy. Interferon-
alpha
/ therapeutic use. Kidney
Neoplasms
/ drug therapy.
Neoplastic Cells
, Circulating / pathology. Thrombosis / pathology. Vena Cava, Inferior / pathology
Genetic Alliance.
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.
MedlinePlus Health Information.
consumer health - Blood Clots
.
MedlinePlus Health Information.
consumer health - Kidney Cancer
.
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(PMID = 18323170.001).
[ISSN]
0018-1994
[Journal-full-title]
Hinyokika kiyo. Acta urologica Japonica
[ISO-abbreviation]
Hinyokika Kiyo
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Interferon-alpha
[Number-of-references]
9
59.
Cameron AJ, Procyk KJ, Leitges M, Parker PJ:
PKC alpha protein but not kinase activity is critical for glioma cell proliferation and survival.
Int J Cancer
; 2008 Aug 15;123(4):769-79
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[Title]
PKC
alpha
protein but not kinase activity is critical for glioma
cell
proliferation and survival.
Protein kinase C
alpha
(PKCalpha) has been implicated in
tumor
development with high levels of PKCalpha expression being associated with various malignancies
including
glioblastomas
and tumors
of the breast and prostate.
To account for its upregulation in these cancers, studies have suggested that PKCalpha plays a role in promoting
cell
survival.
Here we show by siRNA depletion in U87MG glioma
cells
that a critical threshold level of PKCalpha protein expression is essential for their
growth
in the presence of serum and for their survival following serum deprivation.
Derivation of PKCalpha wt and KO mouse embryo fibroblast
cell
lines confirms a role for PKCalpha in protecting
cells
from apoptosis induced by serum deprivation.
Notably, PKCalpha was found to mediate chemo-protection in these fibroblastic
cell
lines.
In U87MG
cells
PKCalpha does not confer chemoprotection though this likely reflects
growth
arrest associated with its depletion.
In contrast to loss of PKCalpha protein, inhibition of PKC kinase activity in glioma
cell
lines does not significantly inhibit
growth
or survival.
These
results
indicate an essential pro-proliferative and pro-survival role for PKCalpha in glioma but question the use of ATP competitive inhibitors as therapeutics, either alone, or in combination with chemotoxic agents.
[MeSH-major]
Glioblastoma / enzymology. Protein Kinase C-
alpha
/ metabolism
[MeSH-minor]
Adenosine Triphosphate / metabolism. Animals.
Cell
Cycle / physiology.
Cell
Growth
Processes / drug effects.
Cell
Growth
Processes / physiology.
Cell
Line,
Tumor
.
Cell
Survival / drug effects.
Cell
Survival / physiology.
Cells
, Cultured. Culture Media, Serum-Free. Fibroblasts / cytology. Fibroblasts / enzymology. Humans. Indoles / pharmacology. Maleimides / pharmacology. Mice. Mice, Knockout. Naphthalenes / pharmacology. Protein Kinase Inhibitors / pharmacology. RNA, Small Interfering / genetics. Rats
Genetic Alliance.
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.
Hazardous Substances Data Bank.
CALPHOSTIN C
.
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[Copyright]
(c) 2008 Wiley-Liss, Inc.
(PMID = 18508315.001).
[ISSN]
1097-0215
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / 2-(1-(3-dimethylaminopropyl)-5-methoxyindol-3-yl)-3-(1H-indol-3-yl)maleimide; 0 / Culture Media, Serum-Free; 0 / Indoles; 0 / Maleimides; 0 / Naphthalenes; 0 / Protein Kinase Inhibitors; 0 / RNA, Small Interfering; 121263-19-2 / calphostin C; 133052-90-1 / bisindolylmaleimide I; 8L70Q75FXE / Adenosine Triphosphate; EC 2.7.11.13 / Protein Kinase C-alpha
60.
Yoshida T, Park JS, Yokosuka K, Jimbo K, Yamada K, Sato K, Nagata K:
Effect of a nonprotein bioactive agent on the reduction of cyclooxygenase-2 and tumor necrosis factor-alpha in human intervertebral disc cells in vitro.
J Neurosurg Spine
; 2008 Nov;9(5):411-8
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[Title]
Effect
of a
nonprotein bioactive agent on the reduction of cyclooxygenase-2
and tumor
necrosis factor-
alpha
in human intervertebral disc
cells
in vitro.
In the present study the authors sought to clarify the focal antiinflammatory effects of Neurotropin in intervertebral disc
cells
, and these effects were compared with those induced by the selective cyclooxygenase (COX)-2 inhibitor 6-methoxy-2-naphthylacetic acid (nabumetone).
Cells
were stimulated with 500 pg/ml of interleukin (IL)-1beta in the presence of various concentrations of Neurotropin (0, 10(-5), 10(-4), and 10(-3) Neurotropin Units/ml) or 50 microg/ml of nabumetone for 3 hours.
The mRNA was extracted for polymerase chain reaction (PCR), and real-time PCR was used to quantify the mRNA levels of COX- 2,
tumor
necrosis factor (TNF)-
alpha
, and phospholipase A2.
RESULTS
: Neurotropin was found to significantly suppress the expression of COX-2 and TNFalpha at mRNA levels as well as the concentration of COX-2 at protein levels in a dose-dependent manner.
CONCLUSIONS:
Results
in this study suggest that Neurotropin has an analgesic effect through the suppression of COX-2 and TNFalpha in a focal area, and nabumetone shows this same effect through the suppression of PGE2 production.
[MeSH-major]
Analgesics / pharmacology. Cyclooxygenase 2 / metabolism. Intervertebral Disc / drug effects. Lumbar Vertebrae. Polysaccharides / pharmacology.
Tumor
Necrosis Factor-
alpha
/ metabolism
[MeSH-minor]
Adult. Butanones.
Cell
Culture Techniques. Dinoprostone / metabolism. Female. Humans. Interleukin-1beta. Intervertebral Disc Displacement / metabolism. Intervertebral Disc Displacement / pathology. Intervertebral Disc Displacement / surgery. Male. Phospholipases A2 / genetics. Phospholipases A2 / metabolism. RNA, Messenger / metabolism
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(PMID = 18976171.001).
[ISSN]
1547-5654
[Journal-full-title]
Journal of neurosurgery. Spine
[ISO-abbreviation]
J Neurosurg Spine
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Analgesics; 0 / Butanones; 0 / Interleukin-1beta; 0 / Polysaccharides; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 42924-53-8 / nabumetone; 57657-35-9 / neurotropin; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.1.1.4 / Phospholipases A2; K7Q1JQR04M / Dinoprostone
61.
Stigliano A, Cerquetti L, Borro M, Gentile G, Bucci B, Misiti S, Piergrossi P, Brunetti E, Simmaco M, Toscano V:
Modulation of proteomic profile in H295R adrenocortical cell line induced by mitotane.
Endocr Relat Cancer
; 2008 Mar;15(1):1-10
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[Title]
Modulation of proteomic profile in H295R adrenocortical
cell
line induced by mitotane.
In this
type of
cancer, the biological mechanism induced by this treatment remains still unknown.
In this study, we have already shown a greater impairment in the first steps of the steroidogenesis and recognized a little effect on
cell
cycle.
We also evaluated the variation of proteomic profile of the H295R ACC
cell
line, either in total
cell
extract or in mitochondria-enriched fraction after treatment with mitotane.
In total
cell
extracts, triose phosphate isomerase,
alpha
-enolase, D-3-phosphoglycerate dehydrogenase, peroxiredoxin II and VI, heat shock protein 27, prohibitin, histidine triad nucleotide-binding protein, and profilin-1 showed a different expression.
It permits to identify some protein classes affected by the drug involved in energetic metabolism, stress response, cytoskeleton
structure
, and tumorigenesis.
[MeSH-major]
Adrenal Cortex
Neoplasms
/ metabolism. Adrenocortical Carcinoma / metabolism. Antineoplastic Agents, Hormonal / pharmacology. Biomarkers,
Tumor
/ metabolism. Mitotane / pharmacology.
Neoplasm
Proteins / metabolism. Proteomics
[MeSH-minor]
Blotting, Western.
Cell
Cycle / drug effects.
Cell
Proliferation / drug effects. Electrophoresis, Gel, Two-Dimensional. Humans. Hydrocortisone / metabolism. Mitochondria / drug effects. Mitochondria / metabolism. Progesterone / metabolism. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. Testosterone / metabolism.
Tumor Cells
, Cultured / drug effects
COS Scholar Universe.
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.
Hazardous Substances Data Bank.
HYDROCORTISONE
.
Hazardous Substances Data Bank.
MITOTANE
.
Hazardous Substances Data Bank.
PROGESTERONE
.
Hazardous Substances Data Bank.
TESTOSTERONE
.
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(PMID = 18310271.001).
[ISSN]
1351-0088
[Journal-full-title]
Endocrine-related cancer
[ISO-abbreviation]
Endocr. Relat. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 3XMK78S47O / Testosterone; 4G7DS2Q64Y / Progesterone; 78E4J5IB5J / Mitotane; WI4X0X7BPJ / Hydrocortisone
62.
Kawaguchi K, Honda M, Yamashita T, Shirota Y, Kaneko S:
Differential gene alteration among hepatoma cell lines demonstrated by cDNA microarray-based comparative genomic hybridization.
Biochem Biophys Res Commun
; 2005 Apr 1;329(1):370-80
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[Title]
Differential gene alteration among hepatoma
cell
lines demonstrated by cDNA microarray-based comparative genomic hybridization.
We assayed chromosomal abnormalities in hepatoma
cell
lines using the microarray-based comparative genomic hybridization (array-CGH) method and investigated the relationship between genomic copy number alterations and expression profiles in these hepatoma
cell
lines.
We modified a cDNA array-CGH assay to compare genomic DNAs from seven hepatoma
cell
lines, as well as DNA from two
non
-hepatoma
cell
lines and from normal
cells
.
We predominantly found alterations of apoptosis-related genes in Hep3B and HepG2,
cell
adhesion and receptor molecules in HLE, and cytokine-related genes in PLC/PRF/5.
Hierarchical clustering analysis showed that the expression of these genes allows differentiation between
alpha
-fetoprotein (AFP)-producing and AFP-negative
cell
lines. cDNA array-CGH is a sensitive method that can be used to detect alterations in genomic copy number in
tumor cells
.
Differences in DNA copy alterations between AFP-producing and AFP-negative
cells
may lead to differential gene expression and may be related to the phenotype of these
cells
.
[MeSH-major]
Gene Expression Profiling / methods. Gene Expression Regulation,
Neoplastic
. Liver
Neoplasms
/ genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis / methods
[MeSH-minor]
Apoptosis. Blotting, Southern. Carcinoma, Hepatocellular / metabolism.
Cell
Adhesion.
Cell
Line,
Tumor
. Chromosome Mapping. Cluster Analysis. DNA, Complementary / metabolism. Gene Deletion. Humans. Phenotype. Protein Binding. RNA, Messenger / metabolism.
alpha
-Fetoproteins / metabolism
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(PMID = 15721316.001).
[ISSN]
0006-291X
[Journal-full-title]
Biochemical and biophysical research communications
[ISO-abbreviation]
Biochem. Biophys. Res. Commun.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Complementary; 0 / RNA, Messenger; 0 / alpha-Fetoproteins
63.
Kreckler LM, Gizewski E, Wan TC, Auchampach JA:
Adenosine suppresses lipopolysaccharide-induced tumor necrosis factor-alpha production by murine macrophages through a protein kinase A- and exchange protein activated by cAMP-independent signaling pathway.
J Pharmacol Exp Ther
; 2009 Dec;331(3):1051-61
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[Title]
Adenosine suppresses lipopolysaccharide-induced
tumor
necrosis factor-
alpha
production by murine macrophages through a protein kinase A- and exchange protein activated by cAMP-independent signaling pathway.
Adenosine is generated during tissue hypoxia and stress, which reduces inflammation by suppressing the activity of most immune
cells
.
Among its various actions, adenosine suppresses the production of proinflammatory cytokines
including tumor
necrosis factor (TNF)-
alpha
, through the cAMP-elevating A(2A) adenosine receptor (AR) subtype.
In this study, we examined the signaling mechanisms by which A(2A)AR activation inhibits TNF-
alpha
production in thioglycollate-elicited mouse peritoneal macrophages.
Pretreating murine macrophages with the nonselective AR agonist adenosine-5'-N-ethylcarboxamide (NECA), the A(2A)AR agonist 2-[p-(2-carboxyethyl)phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS 21680), or the cAMP-elevating agent forskolin reduced TNF-
alpha
production in response to lipopolysaccharide (LPS) by greater than 60%.
However, we were surprised to find that treating macrophages with three different PKA inhibitors or small interfering RNA-mediated knockdown of the exchange protein activated by cAMP (Epac-1) failed to block the suppressive actions of NECA or forskolin on LPS-induced TNF-
alpha
release.
Subsequent studies showed that NECA and forskolin decreased LPS-induced steady-state TNF-
alpha
mRNA levels; this effect was due to a decreased rate of transcription based on assays examining the rate of generation of primary TNF-
alpha
transcripts.
Treatment with NECA or forskolin did not interfere with LPS-induced translocation or DNA binding of the RelA/p65 subunit of nuclear factor-kappaB or phosphorylation of inhibitor of nuclear factor-kappaB-
alpha
, extracellular signal-regulated kinase 1/2, c-Jun NH(2)-terminal kinase, or p38 kinase.
Our
results
suggest that AR activation inhibits LPS-induced TNF-
alpha
production by murine macrophages at the level of gene transcription through a unique cAMP-dependent, but PKA- and Epac-independent, signaling pathway involving protein phosphatase activity.
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(PMID = 19749080.001).
[ISSN]
1521-0103
[Journal-full-title]
The Journal of pharmacology and experimental therapeutics
[ISO-abbreviation]
J. Pharmacol. Exp. Ther.
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / R01 HL077707; United States / NHLBI NIH HHS / HL / R01-HL60051; United States / NHLBI NIH HHS / HL / HL077707-04; United States / NHLBI NIH HHS / HL / R01 HL060051; United States / NHLBI NIH HHS / HL / R01 HL077707-04; United States / NHLBI NIH HHS / HL / R01 HL077707-05; United States / NHLBI NIH HHS / HL / R01-HL077707
[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 / Adenosine A2 Receptor Agonists; 0 / Epac protein, mouse; 0 / Guanine Nucleotide Exchange Factors; 0 / Lipopolysaccharides; 0 / Receptor, Adenosine A2A; 0 / Tumor Necrosis Factor-alpha; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; K72T3FS567 / Adenosine
[Other-IDs]
NLM/ PMC2784717
64.
Decker WK, Li S, Xing D, Robinson SN, Yang H, Steiner D, Komanduri KV, Bollard CM, Shpall EJ:
Deficient T(H)-1 responses from TNF-alpha-matured and alpha-CD40-matured dendritic cells.
J Immunother
; 2008 Feb-Mar;31(2):157-65
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[Title]
Deficient T(H)-1 responses from TNF-
alpha
-matured and
alpha
-CD40-matured dendritic
cells
.
The ultimate success of dendritic
cell
(DC) vaccination for the active immunotherapy
of neoplasia
is thought to be dependent on a very large number of variables,
including
DC generation protocol, loading methodology, dose, route of administration, and maturation method.
Although the use
of a
maturation cocktail comprising interleukin (IL)-1beta,
tumor
necrosis factor-
alpha
, IL-6, and prostaglandin E2 (ITIP) has recently appeared in the literature, much of the data in the basic and clinical literature have been generated using DCs matured with the single inflammatory cytokine TNF-
alpha
.
Here, we demonstrate that DCs matured with TNF-
alpha
alone or in combination with CD40 agonism are highly deficient, both physiologically and functionally, in comparison with DCs matured with IL-1beta, TNF-
alpha
, IL-6, and prostaglandin E2.
Empirically, the data suggest that DCs matured with these agents are deficient in the induction
of type
1 T-helper responses.
[MeSH-major]
Antigens, CD40 / agonists.
Cell
Differentiation / drug effects. Dendritic
Cells
/ drug effects.
Tumor
Necrosis Factor-
alpha
/ pharmacology
[MeSH-minor]
Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / pharmacology. Antigens, CD / metabolism. CD8-Positive T-Lymphocytes / cytology. CD8-Positive T-Lymphocytes / drug effects. CD8-Positive T-Lymphocytes / immunology.
Cell
Proliferation / drug effects. Dinoprostone / pharmacology. Humans. Interferon-gamma / metabolism. Interleukin-10 / metabolism. Interleukin-12 / metabolism. Interleukin-1beta / pharmacology. Interleukin-6 / pharmacology. Lymphocyte Activation / drug effects. Lymphocyte Activation / immunology. T-Lymphocytes / immunology. T-Lymphocytes / metabolism
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(PMID = 18481385.001).
[ISSN]
1524-9557
[Journal-full-title]
Journal of immunotherapy (Hagerstown, Md. : 1997)
[ISO-abbreviation]
J. Immunother.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / 5 R01 CA061508-13
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, CD40; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma; K7Q1JQR04M / Dinoprostone
65.
He J, King Y, Jiang J, Safavi KE, Spångberg LS, Zhu Q:
Enamel matrix derivative inhibits TNF-alpha-induced apoptosis in osteoblastic MC3T3-E1 cells.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
; 2005 Jun;99(6):761-7
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[Title]
Enamel matrix derivative inhibits TNF-
alpha
-induced apoptosis in osteoblastic MC3T3-E1
cells
.
OBJECTIVE: The purpose of this study was to examine the effect of enamel matrix derivative (EMD) on TNF-
alpha
-induced apoptosis in osteoblastic MC3T3-E1
cells
.
STUDY DESIGN: MC3T3-E1
cells
were cultured at an initial density of 5000/cm 2 in Dulbecco's modified eagle medium (DMEM) with 10% fetal bovine serum (FBS) and allowed to adhere for 24 hours.
After 16 hours,
cells
were treated with EMD (100 microg/mL) alone,
tumor
necrosis factor
alpha
(TNF-
alpha
) (20
ng
/mL) alone, transforming
growth
factor beta 1 (TGF-beta1) (10
ng
/mL) alone, TNF-
alpha
plus TGF-beta1, or TNF-
alpha
plus EMD.
Cells
cultured with DMEM and 0.5% FBS served as control.
Following 24-hour incubation, apoptosis was assessed by terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) assay, and quantified by
cell
death enzyme-linked immunosorbent assay (ELISA).
RESULTS
: Both TUNEL assay and
cell
death ELISA show that TNF-
alpha
induces apoptosis in MC3T3-E1
cells
.
TNF-
alpha
increases
cell
death by approximately 2-fold, which is attenuated by both EMD and TGF-beta1.
[MeSH-minor]
3T3
Cells
. Animals. Enzyme-Linked Immunosorbent Assay / methods. In Situ Nick-End Labeling. Mice. Transforming
Growth
Factor beta / pharmacology. Transforming
Growth
Factor beta1.
Tumor
Necrosis Factor-
alpha
/ pharmacology
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(PMID = 15897865.001).
[ISSN]
1528-395X
[Journal-full-title]
Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
[ISO-abbreviation]
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
[Language]
eng
[Grant]
United States / NIDCR NIH HHS / DE / DE14126
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Dental Enamel Proteins; 0 / Tgfb1 protein, mouse; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 0 / enamel matrix proteins
66.
Yu H, Jiang X, Shen C, Karunakaran KP, Jiang J, Rosin NL, Brunham RC:
Chlamydia muridarum T-cell antigens formulated with the adjuvant DDA/TDB induce immunity against infection that correlates with a high frequency of gamma interferon (IFN-gamma)/tumor necrosis factor alpha and IFN-gamma/interleukin-17 double-positive CD4+ T cells.
Infect Immun
; 2010 May;78(5):2272-82
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[Title]
Chlamydia muridarum T-
cell
antigens formulated with the adjuvant DDA/TDB induce immunity against infection that correlates with a high frequency of gamma interferon (IFN-gamma)/
tumor
necrosis factor
alpha
and IFN-gamma/interleukin-17 double-positive CD4+
T cells
.
Major impediments to developing a Chlamydia vaccine lie in identifying immunologically relevant T-
cell
antigens and delivery in a manner to stimulate protective immunity.
Using an immunoproteomic approach, we previously identified three immunodominant Chlamydia T-
cell
antigens (PmpG-1, PmpE/F-2, and RplF).
Therefore, in this study, we evaluated protection against Chlamydia infection in the genital tract in C57BL/6 mice immunized with Chlamydia-specific membrane proteins PmpG-1, PmpE/F-2, and major outer membrane protein (MOMP;
as a reference
) or a combination of them formulated with one of three adjuvants, CpG oligodeoxynucleotide (CpG-ODN), AbISCO-100 (AbISCO), or DDA/TDB (dimethyldioctadecylammonium bromide/D-(+)-trehalose 6,6'-dibehenate).
The
results
show that immunization with the CpG-ODN formulation failed to provide protection against Chlamydia infection; the AbISCO formulation conferred moderate protection, and the DDA/TDB formulation showed the highest degree of protective efficacy.
We measured
cell
-mediated immune cytokine responses in mice immunized with PmpG-1 mixed with each of the three adjuvants.
The
results
demonstrate that mice immunized with the DDA/TDB formulation induced the strongest gamma interferon (IFN-gamma) and interleukin-17 (IL-17) responses, characterized by the highest frequency of IFN-gamma/
tumor
necrosis factor
alpha
(TNF-
alpha
) and IFN-gamma/IL-17 double-positive CD4(+)
T cells
.
In conclusion, a Chlamydia vaccine based on the recombinant proteins PmpG-1, PmpE/F-2, and MOMP delivered in a DDA/TDB adjuvant conferred protection against infection that correlated with IFN-gamma/TNF-
alpha
and IFN-gamma/IL-17 double-positive CD4(+)
T cells
.
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(PMID = 20231405.001).
[ISSN]
1098-5522
[Journal-full-title]
Infection and immunity
[ISO-abbreviation]
Infect. Immun.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / R01 AI076483; United States / NIAID NIH HHS / AI / R01AI076483
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Adjuvants, Immunologic; 0 / Antigens, Bacterial; 0 / Bacterial Vaccines; 0 / Interleukin-17; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
[Other-IDs]
NLM/ PMC2863536
67.
Poli UR, Swarnalata G, Maturi R, Rao ST:
Recurrent alpha-fetoprotein secreting Sertoli-Leydig cell tumor of ovary with an unusual presentation.
Indian J Cancer
; 2009 Jan-Mar;46(1):64-6
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[Title]
Recurrent
alpha
-fetoprotein
secreting
Sertoli-Leydig
cell
tumor of
ovary with an unusual presentation.
Alpha
-fetoprotein
secreting
(AFP) Sertoli-Leydig
cell
tumors of
ovary (SLCT) are now identified
as a
distinct entity among the uncommon group of sex cord
tumors of
ovary.
We report an unusual case of recurrent AFP
secreting
ovarian
tumors and
as ileocecal mesenteric
cyst
in a 25-year-old patient resulting in difficulty in initial diagnosis of AFP producing SLCT.
Although six recurrent cases were described out of the 25 reported cases of AFP
secreting
SLCTs, this patient with an unusual presentation of recurrence is the second case in the literature to the best of our knowledge.
[MeSH-major]
Cecal
Neoplasms
/ pathology. Ileal
Neoplasms
/ pathology. Leydig
Cell
Tumor
/ metabolism. Mesenteric
Cyst
/ pathology.
Neoplasm
Recurrence, Local / pathology. Ovarian
Neoplasms
/ metabolism. Sertoli
Cell
Tumor
/ metabolism.
alpha
-Fetoproteins / metabolism
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.
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.
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(PMID = 19282570.001).
[ISSN]
0019-509X
[Journal-full-title]
Indian journal of cancer
[ISO-abbreviation]
Indian J Cancer
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
India
[Chemical-registry-number]
0 / alpha-Fetoproteins
68.
Oehadian A, Koide N, Mu MM, Hassan F, Islam S, Yoshida T, Yokochi T:
Interferon (IFN)-beta induces apoptotic cell death in DHL-4 diffuse large B cell lymphoma cells through tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
Cancer Lett
; 2005 Jul 8;225(1):85-92
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[Title]
Interferon (IFN)-beta induces apoptotic
cell
death in DHL-4 diffuse large B
cell
lymphoma
cells
through
tumor
necrosis factor-related apoptosis-inducing ligand (TRAIL).
The effect of interferon (IFN)-
alpha
, beta and gamma on the
growth of
DHL-4 diffuse large B
cell
lymphoma
cells
was studied.
IFN-beta significantly inhibited the
cell
growth
, and the effect was stronger than that of IFN-
alpha
.
IFN-gamma did not inhibit the
cell
growth
because of lack of IFN-gamma receptors.
IFN-beta caused apoptotic
cell
death which was accompanied by DNA fragmentation, caspase 3 activation and annexin V binding.
IFN-beta lead to the expression
of tumor
necrosis factor-related apoptosis-inducing ligand (TRAIL) mRNA.
It was suggested that IFN-beta might cause apoptosis in DHL-4
cells
through TRAIL.
[MeSH-major]
Antineoplastic Agents / pharmacology. Apoptosis. Interferon-beta / pharmacology. Lymphoma, B-
Cell
/ pathology. Lymphoma, Large B-
Cell
, Diffuse / pathology. Membrane Glycoproteins / biosynthesis. Membrane Glycoproteins / physiology.
Tumor
Necrosis Factor-
alpha
/ biosynthesis.
Tumor
Necrosis Factor-
alpha
/ physiology
[MeSH-minor]
Apoptosis Regulatory Proteins.
Cell
Proliferation. DNA Damage. Gene Expression Profiling. Humans. Interferon-
alpha
/ pharmacology. Interferon-gamma / pharmacology. TNF-Related Apoptosis-Inducing Ligand.
Tumor Cells
, Cultured
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(PMID = 15922860.001).
[ISSN]
0304-3835
[Journal-full-title]
Cancer letters
[ISO-abbreviation]
Cancer Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Interferon-alpha; 0 / Membrane Glycoproteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 77238-31-4 / Interferon-beta; 82115-62-6 / Interferon-gamma
69.
Huang TT, Chen JY, Tseng CE, Su YC, Ho HC, Lee MS, Chang CT, Wong YK, Chen HR:
Decreased GRP78 protein expression is a potential prognostic marker of oral squamous cell carcinoma in Taiwan.
J Formos Med Assoc
; 2010 May;109(5):326-37
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[Title]
Decreased GRP78 protein expression is a potential prognostic marker of oral squamous
cell
carcinoma in Taiwan.
BACKGROUND/PURPOSE: Oral squamous
cell
carcinoma (OSCC) is an aggressive
tumor and
its occurrence in Taiwan is closely related to chronic smoking, alcohol consumption, and especially to betel quid chewing.
It became the fourth most common
malignant tumor
of Taiwanese men in 2006.
Unfortunately, there are few biomarkers for diagnosis and treatment of this
disease
.
METHODS: To find potential markers, two domestic
cell
lines (OC2 and OCSL) derived from different grades of OSCC were established and their proteins were compared by global proteomic analysis.
The expression differences of GRP78 protein in these two
cell
lines and clinical samples from OSCC patients were verified.
RESULTS
: Of the 11 candidate proteins expressed differentially in both
cell
lines, six [heat shock protein 90 kDa beta member 1 (94 kDa glucose-regulated protein; GRP94), protein disulfide-isomerase precursor, vimentin, tubulin beta-2C chain, 78 kDa glucose-regulated protein precursor (GRP78), and annexin A2] were increased in OC2
cells
(low-grade OSCC), and five (heat shock protein 90-beta, annexin A1, stress-induced phosphoprotein 1, elongation factor-2, and integrin
alpha
-3 precursor) were increased in OCSL
cells
(high-grade OSCC).
Some of these proteins have been previously associated with
malignant tumors
, but no previous association of GRP78 with OSCC has been reported.
GRP78 protein expression in these two OSCC
cell
lines was confirmed by Western blotting.
Immunohistochemical staining of clinical samples from OSCC patients revealed that decreased GRP78 protein expression was significantly correlated with advance
tumor
stage (p < 0.001) and neck lymph node metastasis (p = 0.001).
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[Copyright]
Copyright 2010 Formosan Medical Association & Elsevier. Published by Elsevier B.V. All rights reserved.
(PMID = 20497865.001).
[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]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Singapore
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Heat-Shock Proteins; 0 / molecular chaperone GRP78
70.
Russell MR, Liu Q, Lei H, Kazlauskas A, Fatatis A:
The alpha-receptor for platelet-derived growth factor confers bone-metastatic potential to prostate cancer cells by ligand- and dimerization-independent mechanisms.
Cancer Res
; 2010 May 15;70(10):4195-203
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[Title]
The
alpha
-receptor for platelet-derived
growth
factor confers bone-metastatic potential to prostate cancer
cells
by ligand- and dimerization-independent mechanisms.
Metastatic dissemination requires a complex series of coordinated events that result in
cells
that escape from the primary
tumor
into the circulation and eventually colonize a distant organ.
The ability of these
cells
to evolve into macroscopic metastases depends strongly on their compatibility with, and ability to utilize, this
new
microenvironment.
We previously showed that bone-metastatic prostate cancer
cells
exposed to human bone marrow respond by activation of
cell
survival pathways, such as phosphoinositide 3-kinase/Akt, and that these events are mediated by the
alpha
-receptor for platelet-derived
growth
factor (PDGFRalpha).
Our studies show that this truncated PDGFRalpha is able to restore bone-metastatic potential of prostate cancer
cells as
effectively as the full-length form of the receptor.
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.
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[Copyright]
(c)2010 AACR.
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[
12941962.001
]
[Cites]
Mol Cancer Ther. 2005 Mar;4(3):369-79
[
15767546.001
]
(PMID = 20442296.001).
[ISSN]
1538-7445
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
ENG
[Grant]
United States / NEI NIH HHS / EY / EY012509; United States / NEI NIH HHS / EY / R01 EY012509; United States / NCI NIH HHS / PC / PC080987; United States / NEI NIH HHS / EY / EY012509-10A1; United States / NEI NIH HHS / EY / R01 EY012509-10A1
[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 / Ligands; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
[Other-IDs]
NLM/ NIHMS190973; NLM/ PMC2875778
71.
Elgqvist J, Andersson H, Bäck T, Claesson I, Hultborn R, Jensen H, Johansson BR, Lindegren S, Olsson M, Palm S, Warnhammar E, Jacobsson L:
Alpha-radioimmunotherapy of intraperitoneally growing OVCAR-3 tumors of variable dimensions: Outcome related to measured tumor size and mean absorbed dose.
J Nucl Med
; 2006 Aug;47(8):1342-50
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[Title]
Alpha
-radioimmunotherapy of intraperitoneally growing OVCAR-3
tumors of
variable dimensions: Outcome related to measured
tumor
size and mean absorbed dose.
(b) image the
tumor growth
on the peritoneum; and (c) calculate the specific energy and mean absorbed dose to
tumors and
critical organs.
METHODS: Two experiments with 5-wk-old nude mice (n = 100 + 93), intraperitoneally inoculated with approximately 1 x 10(7) NIH:OVCAR-3
cells
, were done.
At the time of treatment 29 animals were sacrificed and biopsies were taken for determination
of tumor
sizes using scanning electron microscopy (SEM).
Eight weeks after each treatment the animals were sacrificed and the presence of macro- and microscopic
tumors and
ascites was determined.
The specific energy and mean absorbed dose to
tumors
were calculated.
RESULTS
: When given treatment 1, 3, 4, 5, or 7 wk after
cell
inoculation the
tumor
-free fraction (TFF) was 95%, 68%, 58%, 47%, 26%, and 100%, 80%, 20%, 20%, and 0% when treated with 211At-MX35 F(ab')2 or 211At-Rituximab F(ab')2, respectively.
The SEM images revealed maximum
tumor
radius of approximately 30 mum 1 wk after
cell
inoculation, increasing to approximately 340 mum at 7 wk.
Specific energy to
cell
nuclei varied between 0 and approximately 540 Gy, depending on assumptions regarding activity distribution
and tumor
size.
CONCLUSION: Treatment with 211At-MX35 F(ab')2 or 211At-Rituximab F(ab')2 resulted in a TFF of 95%-100% when the
tumor
radius was < or =30 microm.
The TFF was decreased (TFF < or = 20%) for 211At-Rituximab F(ab')2 when the
tumor
radius exceeded the range of the
alpha
-particles.
The specific antibody gave for these
tumor
sizes a significantly better TFF, explained by a high mean absorbed dose (>22 Gy) from the activity bound to the
tumor
surface and probably some contribution from penetrating activity.
[MeSH-major]
Ovarian
Neoplasms
/ radionuclide imaging. Ovarian
Neoplasms
/ therapy. Radioimmunotherapy / methods
[MeSH-minor]
Alpha
Particles. Animals. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Agents / therapeutic use.
Cell
Line,
Tumor
. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Microscopy, Electron.
Neoplasm
Transplantation. Rituximab. Treatment Outcome
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[CommentIn]
J Nucl Med. 2006 Aug;47(8):1238-40
[
16882999.001
]
(PMID = 16883015.001).
[ISSN]
0161-5505
[Journal-full-title]
Journal of nuclear medicine : official publication, Society of Nuclear Medicine
[ISO-abbreviation]
J. Nucl. Med.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
72.
Shahid M, Francis J, Majid DS:
Tumor necrosis factor-alpha induces renal vasoconstriction as well as natriuresis in mice.
Am J Physiol Renal Physiol
; 2008 Dec;295(6):F1836-44
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[Title]
Tumor
necrosis factor-
alpha
induces renal vasoconstriction as well as natriuresis in mice.
Tumor
necrosis factor-
alpha
(TNF-
alpha
) has been implicated in the pathogenesis of hypertension and renal injury.
However, the direct effects of TNF-
alpha
on renal hemodynamic and excretory function are not yet clearly defined.
We examined the renal responses to infusion of TNF-
alpha
(0.33
ng
.g(-1).min(-1)) in anesthetized mice.
Following the 60-min control clearance period, TNF-
alpha
infusion was initiated and 15 min were given for stabilization followed by another 60-min clearance period.
TNF-
alpha
alone (n = 7) caused decreases in RBF (7.9 +/- 0.3 to 6.4 +/- 0.3 ml.min(-1).g(-1)) and GFR (1.04 +/- 0.06 to 0.62 +/- 0.08 ml.min(-1).g(-1)) as well as increases in absolute (0.8 +/- 0.3 to 1.4 +/- 0.3 micromol.min(-1).g(-1)) and fractional excretion of sodium (0.5 +/- 0.2 to 1.5 +/- 0.4%) without affecting arterial pressure.
TNF-
alpha
also increased 8-isoprostane excretion (8.10 +/- 1.09 to 11.13 +/- 1.34 pg.min(-1).g(-1)).
Pretreatment with TNF-
alpha
blocker etanercept (5 mg/kg sc; 24 and 3 h before TNF-
alpha
infusion; n = 6) abolished these responses.
However, TNF-
alpha
induced an increase in RBF and caused attenuation of the GFR reduction in mice pretreated with superoxide (O(2)(-)) scavenger tempol (2 microg.g(-1).min(-1); n = 6).
Pretreatment with nitric oxide (NO) synthase inhibitor nitro-l-arginine methyl ester (0.1 microg.g(-1).min(-1); n = 6) resulted in further enhancement in vasoconstriction while natriuresis remained unaffected in response to TNF-
alpha
.
These data suggest that TNF-
alpha
induces renal vasoconstriction and hypofiltration via enhancing the activity
of O
(2)(-) and thus reducing the activity of NO.
The natriuretic response to TNF-
alpha
is related to its direct effects on tubular sodium reabsorption.
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Annu Rev Physiol. 2000;62:515-34
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10845101.001
]
(PMID = 18922887.001).
[ISSN]
1931-857X
[Journal-full-title]
American journal of physiology. Renal physiology
[ISO-abbreviation]
Am. J. Physiol. Renal Physiol.
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / HL-66432
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Tumor Necrosis Factor-alpha; 27415-26-5 / 8-epi-prostaglandin F2alpha; 9NEZ333N27 / Sodium; B7IN85G1HY / Dinoprost; RWP5GA015D / Potassium
[Other-IDs]
NLM/ PMC2604828
73.
Sondarva G, Kundu CN, Mehrotra S, Mishra R, Rangasamy V, Sathyanarayana P, Ray RS, Rana B, Rana A:
TRAF2-MLK3 interaction is essential for TNF-alpha-induced MLK3 activation.
Cell Res
; 2010 Jan;20(1):89-98
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[Title]
TRAF2-MLK3 interaction is essential for TNF-
alpha
-induced MLK3 activation.
Mixed lineage kinase 3 (MLK3) is a mitogen-activated protein kinase kinase kinase that is activated by
tumor
necrosis factor-
alpha
(TNF-
alpha
) and specifically activates c-Jun N-terminal kinase (JNK) on TNF-
alpha
stimulation.
The mechanism by which TNF-
alpha
activates MLK3 is still not known.
TNF receptor-associated factors (TRAFs) are adapter molecules that are recruited to cytoplasmic end of TNF receptor and mediate the downstream signaling,
including
activation of JNK.
Endogenous TRAF2 and MLK3 associate with each other in response to TNF-
alpha
treatment in a time-dependent manner.
The association between MLK3 and TRAF2 mediates MLK3 activation and competition with the TRAF2 deletion mutant that binds to MLK3 attenuates MLK3 kinase activity in a dose-dependent manner, on TNF-
alpha
treatment.
Furthermore the downstream target of MLK3, JNK was activated by TNF-
alpha
in a TRAF2-dependent manner.
Hence, our data show that the direct interaction between TRAF2 and MLK3 is required for TNF-
alpha
-induced activation of MLK3 and its downstream target, JNK.
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(PMID = 19918265.001).
[ISSN]
1748-7838
[Journal-full-title]
Cell research
[ISO-abbreviation]
Cell Res.
[Language]
ENG
[Grant]
United States / NIGMS NIH HHS / GM / GM055835-07A3; United States / NCI NIH HHS / CA / R21 CA121221; United States / NIGMS NIH HHS / GM / GM55835; United States / NCI NIH HHS / CA / CA121221; United States / NIGMS NIH HHS / GM / R01 GM055835-07A3; United States / NIGMS NIH HHS / GM / R01 GM055835
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
England
[Chemical-registry-number]
0 / TNF Receptor-Associated Factor 2; 0 / TNF Receptor-Associated Factor 5; 0 / TNF Receptor-Associated Factor 6; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / mitogen-activated protein kinase kinase kinase 11
[Other-IDs]
NLM/ NIHMS149286; NLM/ PMC2801772
74.
Koschmieder S, D'Alò F, Radomska H, Schöneich C, Chang JS, Konopleva M, Kobayashi S, Levantini E, Suh N, Di Ruscio A, Voso MT, Watt JC, Santhanam R, Sargin B, Kantarjian H, Andreeff M, Sporn MB, Perrotti D, Berdel WE, Müller-Tidow C, Serve H, Tenen DG:
CDDO induces granulocytic differentiation of myeloid leukemic blasts through translational up-regulation of p42 CCAAT enhancer binding protein alpha.
Blood
; 2007 Nov 15;110(10):3695-705
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[Title]
CDDO induces granulocytic differentiation of myeloid leukemic blasts through translational up-regulation of p42 CCAAT enhancer binding protein
alpha
.
2-Cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO) induces differentiation and apoptosis
of tumor cells
in vitro and in vivo.
Here we assessed the effects of CDDO on CCAAT enhancer-binding protein
alpha
(CEBPA), a transcription factor critical for granulocytic differentiation.
In HL60 acute myeloid leukemia (AML)
cells
, CDDO (0.01 to 2 muM) induces apoptosis in a dose-dependent manner.
Conversely, subapoptotic doses of CDDO promote phagocytic activity and granulocytic-monocytic differentiation of HL60
cells
through increased
de
novo synthesis of p42 CEBPA protein.
In concordance with these
results
, CDDO induces a CEBPA ratio change and differentiation of primary blasts from patients with acute myeloid leukemia (AML).
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(PMID = 17671235.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / 2P30-CA 16672; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / R01 CA095512; United States / NCI NIH HHS / CA / R01 CA089346; United States / NCI NIH HHS / CA / 1 P50 CA100632; United States / NCI NIH HHS / CA / R01 CA89346; United States / NCI NIH HHS / CA / CA095512; United States / NCI NIH HHS / CA / P01 CA55164; United States / NCI NIH HHS / CA / P01 CA055164
[Publication-type]
Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Eukaryotic Initiation Factor-2; 0 / Eukaryotic Initiation Factor-4E; 6SMK8R7TGJ / Oleanolic Acid
[Other-IDs]
NLM/ PMC2077317
75.
Bellezza G, Colella R, Sidoni A, Del Sordo R, Ferri I, Cioccoloni C, Cavaliere A:
Immunohistochemical expression of Galectin-3 and HBME-1 in granular cell tumors: a new finding.
Histol Histopathol
; 2008 09;23(9):1127-30
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[Title]
Immunohistochemical expression of Galectin-3 and HBME-1 in granular
cell
tumors
:
a new finding
.
Granular
cell
tumor
(GCT) is a relatively rare
neoplasm
, usually located in the upper aerodigestive tract, skin and soft tissue.
Because of its uncertain histogenesis, GCT has been the object of many immunohistochemical and ultrastructural studies that have suggested a Schwann
cell
origin.
Our recent observation
of a
case of GCT immunoreactive for Galectin-3 and HBME-1 led us to further investigate the immunohistochemical profile of these
neoplasms
.
We evaluated the immunohistochemical expression of the traditional markers for GCT (S-100, CD68) along with
new
markers (Galectin-3, HBME-1, Calretinina and Inhibin-
alpha
) in 22 granular
cell
tumors
.
Our
results
showed, in all cases, a constant diffuse positivity for S-100 protein, CD68 and Galectin-3.
The present study gives
a new
immunophenotypic profile for GCT, which could help pathologists in distinguishing morphologically ambiguous granular lesions in unusual sites.
[MeSH-major]
Biomarkers,
Tumor
/ metabolism. Galectin 3 / metabolism. Granular
Cell
Tumor
/ metabolism. Head and Neck
Neoplasms
/ metabolism. Skin
Neoplasms
/ metabolism
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(PMID = 18581283.001).
[ISSN]
1699-5848
[Journal-full-title]
Histology and histopathology
[ISO-abbreviation]
Histol. Histopathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Spain
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Galectin 3; 0 / HBME-1 antigen
76.
Charerntantanakul W, Platt R, Roth JA:
Effects of porcine reproductive and respiratory syndrome virus-infected antigen-presenting cells on T cell activation and antiviral cytokine production.
Viral Immunol
; 2006;19(4):646-61
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[Title]
Effects of porcine reproductive and respiratory
syndrome
virus-infected antigen-presenting
cells
on T
cell
activation and antiviral cytokine production.
The ability of porcine reproductive and respiratory
syndrome
virus (PRRSV) to suppress T
cell
expression of CD25 (
alpha
chain of interleukin [IL]-2 receptor), interferon-gamma (IFN-gamma),
and tumor
necrosis factor-
alpha
(TNF-
alpha
) was determined by flow cytometry in naive porcine
T cells
in response to mitogen (concanavalin A) and cytokine inducers (phorbol 12-myristate 13-acetate plus ionomycin [PMA/I]).
Four PRRSV isolates of varying clinical virulence and three different types of porcine myeloid antigen-presenting
cells
(APCs) were used.
T cells
cultured with monocytes infected with virulent PRRSV (VR-2385, SDSU-73, and VR-2332), but not with a vaccine strain (Ingelvac PRRS MLV; Boehringer Ingelheim Vetmedica, St. Joseph, MO), demonstrated significantly reduced CD25 expression (%CD25(+)) and IFN-gamma expression (%IFN-gamma (+)) compared with
T cells
incubated with uninoculated monocyte cultures.
T cells
cultured with monocytes infected with all four PRRSV isolates demonstrated significantly reduced %TNF-
alpha
(+).
The significant reduction of %CD25(+), %IFN-gamma (+), and %TNF-
alpha
(+) was not detected in
T cells
cultured with monocyte-derived macrophages (MDMs) and immature monocyte-derived dendritic
cells
(MDCs) infected with any PRRSV isolates.
Heat-inactivated PRRSV did not induce significantly reduced T
cell
responses in any APC cultures.
The reduction
of T
cell
response in monocyte cultures was not due to PRRSV-induced T
cell
death.
Increased IL-10 gene expression contributed to significantly reduced %IFN-gamma (+) and %TNF-
alpha
(+), but not %CD25(+), as determined by IL-10 neutralization assay.
This study reports that PRRSV has the ability to suppress T
cell
responses.
[MeSH-major]
Porcine Reproductive and Respiratory
Syndrome
/ immunology. Porcine respiratory and reproductive
syndrome
virus / physiology. T-Lymphocytes / immunology
[MeSH-minor]
Animals. Antigen-Presenting
Cells
/ immunology.
Cells
, Cultured. Coculture Techniques. Dendritic
Cells
/ virology. Down-Regulation. Gene Expression. Interferon-gamma / biosynthesis. Interferon-gamma / metabolism. Interleukin-10 / genetics. Interleukin-2 Receptor
alpha
Subunit / metabolism. Macrophages / virology. Monocytes / physiology. Monocytes / virology. Swine.
Tumor
Necrosis Factor-
alpha
/ biosynthesis. Virulence
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(PMID = 17201660.001).
[ISSN]
0882-8245
[Journal-full-title]
Viral immunology
[ISO-abbreviation]
Viral Immunol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Interleukin-2 Receptor alpha Subunit; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 82115-62-6 / Interferon-gamma
77.
Roomi MW, Monterrey JC, Kalinovsky T, Niedzwiecki A, Rath M:
Modulation of MMP-2 and MMP-9 by cytokines, mitogens and inhibitors in lung cancer and malignant mesothelioma cell lines.
Oncol Rep
; 2009 Dec;22(6):1283-91
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[Title]
Modulation of MMP-2 and MMP-9 by cytokines, mitogens and inhibitors in lung cancer
and malignant
mesothelioma
cell
lines.
Matrix metalloproteinases (MMPs) secreted by lung cancer (LC)
and malignant
mesothelioma (MM), especially MMP-2 and MMP-9, play crucial roles in
tumor
invasion and metastasis.
We examined the effect of cytokines, mitogens and inhibitors on MMP-2 and MMP-9 expression in LC and MM
cell
lines.
Human LC (A-549) and MM (MSTO-211H)
cell
lines were cultured in appropriate media.
At near confluence, the
cells
were washed with PBS and incubated in serum-free medium with various concentrations of several cytokines, mitogens and inhibitors.
TNF-
alpha
, IL-1beta, LPS and PMA, stimulated MMP-2 in LC and inhibited MMP-2 in MM, but had no effect on MMP-9.
Doxycycline, EGCG and NM inhibited MMP-2 and MMP-9 expression, in both
cell
lines.
Actinomycin-D, cyclohexamide, retinoic acid and dexamethasone inhibited MMP-2 in both cancer
cell
lines and inhibited MMP-9 in MM.
Our
results
show that cytokines and inhibitors have an up- or down-regulatory effect on MMP-2 and MMP-9 expression in LC and MM, suggesting the clinical value of targeting these proteases for management of LC and MM and their pathogenesis.
[MeSH-major]
Gene Expression Regulation, Enzymologic. Gene Expression Regulation,
Neoplastic
. Lung
Neoplasms
/ metabolism. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / metabolism. Mesothelioma / metabolism
[MeSH-minor]
Antineoplastic Agents / pharmacology.
Cell
Line,
Tumor
. Culture Media / pharmacology. Cytokines / metabolism. Humans. Lipopolysaccharides / pharmacology.
Neoplasm
Metastasis. Tetradecanoylphorbol Acetate / pharmacology. Time Factors
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.
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.
MedlinePlus Health Information.
consumer health - Mesothelioma
.
Hazardous Substances Data Bank.
12-O-TETRADECANOYLPHORBOL-13-ACETATE
.
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(PMID = 19885578.001).
[ISSN]
1791-2431
[Journal-full-title]
Oncology reports
[ISO-abbreviation]
Oncol. Rep.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Culture Media; 0 / Cytokines; 0 / Lipopolysaccharides; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; NI40JAQ945 / Tetradecanoylphorbol Acetate
78.
Xu G, Tan X, Wang H, Sun W, Shi Y, Burlingame S, Gu X, Cao G, Zhang T, Qin J, Yang J:
Ubiquitin-specific peptidase 21 inhibits tumor necrosis factor alpha-induced nuclear factor kappaB activation via binding to and deubiquitinating receptor-interacting protein 1.
J Biol Chem
; 2010 Jan 8;285(2):969-78
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[Title]
Ubiquitin-specific peptidase 21 inhibits
tumor
necrosis factor
alpha
-induced nuclear factor kappaB activation via binding to and deubiquitinating receptor-interacting protein 1.
Ubiquitination and deubiquitination of receptor-interacting protein 1 (RIP1) play an important role in the positive and negative regulation of the
tumor
necrosis factor
alpha
(TNFalpha)-induced nuclear factor kappaB (NF-kappaB) activation.
Using a combination of functional genomic and proteomic approaches, we have identified ubiquitin-specific peptidase 21 (USP21)
as a
deubiquitinase for RIP1.
Notably, knockdown of USP21 in HeLa
cells
enhances TNFalpha-induced RIP1 ubiquitination, IkappaB kinase beta (IKKbeta), and NF-kappaB phosphorylation, inhibitor of NF-kappaB
alpha
(IkappaB
alpha
) phosphorylation and ubiquitination, as well as NF-kappaB-dependent gene expression.
Therefore, our
results
demonstrate that USP21 plays an important role in the down-regulation of TNFalpha-induced NF-kappaB activation through deubiquitinating RIP1.
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(PMID = 19910467.001).
[ISSN]
1083-351X
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / P30 DK079638; United States / NCI NIH HHS / CA / R21 CA106513; United States / NCI NIH HHS / CA / 1R21CA106513-01A2; United States / NIDDK NIH HHS / DK / DK079638
[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 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.1 / RIPK1 protein, human; EC 2.7.11.1 / Receptor-Interacting Protein Serine-Threonine Kinases; EC 2.7.11.1 / Ripk1 protein, mouse; EC 2.7.11.10 / I-kappa B Kinase; EC 3.1.2.15 / USP21 protein, human; EC 3.1.2.15 / Ubiquitin Thiolesterase
[Other-IDs]
NLM/ PMC2801298
79.
Frick LR, Arcos ML, Rapanelli M, Zappia MP, Brocco M, Mongini C, Genaro AM, Cremaschi GA:
Chronic restraint stress impairs T-cell immunity and promotes tumor progression in mice.
Stress
; 2009 Mar;12(2):134-43
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[Title]
Chronic restraint stress impairs T-
cell
immunity and promotes
tumor
progression in mice.
The T-
cell
response is an important component of anti-tumoral immunity.
Hence, impairment of the immune function induced by a chronic stressor has been postulated to alter the immunosurveillance
of tumors
, thus leading to a worse
neoplastic
prognosis.
Here, we show that chronic restraint stress affects T-
cell
mediated immunity in mice.
This was evidenced by a decrease of mitogen-induced T-
cell
proliferation, a reduction in CD4(+)T lymphocyte number
and a
decrease
of tumor
necrosis factor-
alpha
(TNF-
alpha
) and Interferon-gamma (IFN-gamma) production in stressed mice.
Additionally, mice subjected to chronic restraint stress displayed an enhancement
of tumor growth
in a syngeneic lymphoma model, i.e. an increase
of tumor
proliferation
and a
reduction of animal survival.
Finally, stressed mice had a reduced specific cytotoxic response against these
tumor cells
.
These
results
suggest that chronic exposure to stress promotes cancer establishment and subsequent progression, probably by depressing T-
cell
mediated immunity.
The T-
cell
immunity impairment as well as the
tumor
progression enhancement emphasize the importance of the therapeutic management of stress to improve the prognosis of cancer patients.
[MeSH-major]
Lymphoma, T-
Cell
/ immunology. Stress, Psychological / immunology. T-Lymphocytes / immunology
[MeSH-minor]
Animals. Behavior, Animal. CD4-Positive T-Lymphocytes / immunology.
Cell
Proliferation. Female. Interferon-gamma / biosynthesis. Killer
Cells
, Natural / immunology. Mice. Mice, Inbred BALB C. Restraint, Physical.
Tumor
Necrosis Factor-
alpha
/ biosynthesis
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.
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(PMID = 18609297.001).
[ISSN]
1607-8888
[Journal-full-title]
Stress (Amsterdam, Netherlands)
[ISO-abbreviation]
Stress
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
80.
Castillo-Avila W, Piulats JM, Garcia Del Muro X, Vidal A, Condom E, Casanovas O, Mora J, Germà JR, Capellà G, Villanueva A, Viñals F:
Sunitinib inhibits tumor growth and synergizes with cisplatin in orthotopic models of cisplatin-sensitive and cisplatin-resistant human testicular germ cell tumors.
Clin Cancer Res
; 2009 May 15;15(10):3384-95
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[Title]
Sunitinib inhibits
tumor growth
and synergizes with cisplatin in orthotopic models of cisplatin-sensitive and cisplatin-resistant human testicular germ
cell
tumors
.
PURPOSE: Germ
cell
tumors
(GCT) of the testis are highly curable, but those patients who are refractory to cisplatin (CDDP)-based combination chemotherapy have a poor prognosis.
Therefore, identifying
new
alternatives for treatment remains a priority.
EXPERIMENTAL DESIGN: Mice were implanted with four different testicular
tumors
: a yolk sac, two choriocarcinomas,
and a
CDDP-resistant choriocarcinoma variant induced in mice by continuous exposure to CDDP.
Mice were treated with vehicle, CDDP, sunitinib, or the combination of both drugs and their effects on
tumors
were analyzed.
RESULTS
: We observed a significant inhibition in
tumor growth
accompanied by longer survival after sunitinib treatment.
Sunitinib induced apoptosis, reduced
tumor
cell
proliferation
and tumor
vasculature, and inhibited vascular endothelial
growth
factor receptor 1, 2, and 3 and platelet-derived
growth
factor receptor
alpha
phosphorylation without affecting phosphorylation of other tyrosine kinase receptors.
More importantly,
tumor growth
inhibition induced by sunitinib was also observed in the induced CDDP-resistant choriocarcinoma model.
CONCLUSIONS: Taken together, these
results
suggest that sunitinib might be
a new
alternative for treatment of CDDP-refractory patients.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Indoles / therapeutic use.
Neoplasms
, Germ
Cell
and Embryonal / drug therapy. Pyrroles / therapeutic use. Testicular
Neoplasms
/ drug therapy. Xenograft Model Antitumor Assays
[MeSH-minor]
Angiogenesis Inhibitors / administration & dosage. Angiogenesis Inhibitors / pharmacology. Angiogenesis Inhibitors / therapeutic use. Animals. Apoptosis / drug effects. Blotting, Western.
Cell
Line,
Tumor
.
Cell
Proliferation / drug effects.
Cell
Survival / drug effects. Cisplatin / administration & dosage. Cisplatin / pharmacology. Drug Resistance,
Neoplasm
. Drug Synergism. Humans. Male. Mice. Mice, Nude. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / prevention & control. Receptors, Platelet-Derived
Growth
Factor / genetics. Receptors, Platelet-Derived
Growth
Factor / metabolism. Receptors, Vascular Endothelial
Growth
Factor / genetics. Receptors, Vascular Endothelial
Growth
Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis.
Tumor
Burden / drug effects
MedlinePlus Health Information.
consumer health - Testicular Cancer
.
Hazardous Substances Data Bank.
CIS-DIAMINEDICHLOROPLATINUM
.
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(PMID = 19417025.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Angiogenesis Inhibitors; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; Q20Q21Q62J / Cisplatin
81.
Xiang J, Munegowda MA, Deng Y:
Transgene expression of alpha tumor necrosis factor with mutations D142N and A144R under control of human telomerase reverse transcriptase promoter eradicates well-established tumors and induces long-term antitumor immunity.
Cancer Gene Ther
; 2009 May;16(5):430-8
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[Title]
Transgene expression of
alpha
tumor
necrosis factor with mutations D142N and A144R under control of human telomerase reverse transcriptase promoter eradicates well-established
tumors and
induces long-term antitumor immunity.
Recombinant adenoviral vectors (AdVTNF-
alpha
) expressing
alpha
tumor
necrosis factor (TNF-
alpha
) under control of cytomegalovirus (CMV) promoter have been used in cancer gene therapy.
To reduce its cytotoxicity, we constructed a recombinant AdV(TERT)mTNF-
alpha
expressing a mutant TNF-
alpha
(mTNF-
alpha
) with mutations at D142N and A144R under control of human telomerase reverse transcriptase (hTERT) promoter for treatment of well-established ovalbumin (OVA)-expressing murine B16 melanoma (BL6-10(OVA)) (6 mm in diameter).
We demonstrated that the mTNF-
alpha
with mutations at D142N and A144R has less in vitro cytotoxicity, but maintains its functional effect in the stimulation
of T
-
cell
proliferation.
The in vitro and in vivo transgene expressions under control of hTERT promoter are highly restricted in
tumor cells
compared with those under the control of the CMV promoter.
AdV(TERT)mTNF-
alpha
gene therapy by intratumoral injection of AdV(TERT)mTNF-
alpha
vector (2 x 10(9) PFU) expressing the mutant mTNF-
alpha
under control of hTERT promoter reduces its in vivo toxicity, eradicates well-established BL6-10(OVA)
tumors
in 4/10
tumor
-bearing mice, and induces OVA-specific CD8(+) T-
cell
-mediated long-term antitumor immunity.
Therefore, AdV(TERT)mTNF-
alpha
gene therapy may be very useful in the immunotherapy of cancer.
[MeSH-major]
Gene Expression Regulation. Genetic Therapy. Mutation / genetics. Promoter Regions, Genetic. Telomerase / genetics. Transgenes / genetics.
Tumor
Necrosis Factor-
alpha
/ genetics
[MeSH-minor]
Animals. Antineoplastic Agents / immunology. Antineoplastic Agents / pharmacology. CD8-Positive T-Lymphocytes / cytology. CD8-Positive T-Lymphocytes / immunology.
Cell
Proliferation.
Disease
Models, Animal. Female. Humans. Immunotherapy. Mice. Mice, Inbred C57BL.
Tumor Cells
, Cultured / drug effects
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.
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(PMID = 19096444.001).
[ISSN]
1476-5500
[Journal-full-title]
Cancer gene therapy
[ISO-abbreviation]
Cancer Gene Ther.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Tumor Necrosis Factor-alpha; EC 2.7.7.49 / Telomerase
82.
Liu YP, Lin HI, Tzeng SF:
Tumor necrosis factor-alpha and interleukin-18 modulate neuronal cell fate in embryonic neural progenitor culture.
Brain Res
; 2005 Aug 30;1054(2):152-8
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[Title]
Tumor
necrosis factor-
alpha
and interleukin-18 modulate neuronal
cell
fate in embryonic neural progenitor culture.
Neural progenitor
cells
(NPCs) in developing and adult CNS are capable of giving rise to various neuronal and glial
cell
populations.
Yet, little is known about the effect of microglia-derived factors on the
cell
fate of embryonic NPCs.
Treatment with pentoxifylline (PTX), an inhibitor for
tumor
necrosis factor-
alpha
(TNF-
alpha
) secretion from LPS-activated microglia, blocked the reduction of betaIII-tubulin+
cells
in NPC culture.
Furthermore, treatment of NPCs with interleukin-18 (IL-18), a recently discovered proinflammatory cytokine, also decreased the number of betaIII-tubulin+
cells
in a dose- and time-dependent manner.
Surprisingly, we also observed that the remaining betaIII-tubulin+
cells
in the LPS/M-CM-treated culture exhibited more branching neurites.
Thus, the activated microglia-derived cytokines, TNF-
alpha
and IL-18, may either inhibit the neuronal differentiation or induce neuronal
cell
death in the NPC culture, whereas these
cells
may also produce factors to improve the neurite branching in the NPC culture.
[MeSH-major]
Interleukin-18 / metabolism. Neurons / physiology. Stem
Cells
/ physiology.
Tumor
Necrosis Factor-
alpha
/ metabolism
[MeSH-minor]
Animals. Animals, Newborn. Blotting, Western / methods.
Cell
Count / methods.
Cell
Death / drug effects.
Cell
Death / physiology.
Cell
Differentiation / drug effects.
Cell
Differentiation / physiology.
Cells
, Cultured. Dose-Response Relationship, Drug. Embryo, Mammalian. Immunohistochemistry / methods. Lipopolysaccharides / pharmacology. Microglia / drug effects. Microglia / physiology. Pertussis Toxin / pharmacology. Rats. Rats, Sprague-Dawley. Tubulin / metabolism
MedlinePlus Health Information.
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.
COS Scholar Universe.
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.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 16054598.001).
[ISSN]
0006-8993
[Journal-full-title]
Brain research
[ISO-abbreviation]
Brain Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Interleukin-18; 0 / Lipopolysaccharides; 0 / Tubb3 protein, rat; 0 / Tubulin; 0 / Tumor Necrosis Factor-alpha; EC 2.4.2.31 / Pertussis Toxin
83.
Amigó M, Payá M, De Rosa S, Terencio MC:
Antipsoriatic effects of avarol-3'-thiosalicylate are mediated by inhibition of TNF-alpha generation and NF-kappaB activation in mouse skin.
Br J Pharmacol
; 2007 Oct;152(3):353-65
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[Title]
Antipsoriatic effects of avarol-3'-thiosalicylate are mediated by inhibition of TNF-
alpha
generation and NF-kappaB activation in mouse skin.
EXPERIMENTAL APPROACH: Human neutrophils and monocytes as well as the human keratinocyte
cell
line HaCaT were used to study the effect of TA on oxidative stress, the arachidonic acid pathway,
tumour
necrosis factor-
alpha
(TNF-
alpha
) release and nuclear factor-kappaB (NF-kappaB) activation.
All these parameters were also determined in vivo using the zymosan induced mouse
air
pouch model and the 12-O-tetradecanoylphorbol-13-acetate (TPA) induced mouse epidermal hyperplasia model.
KEY
RESULTS
: TA showed antioxidant properties in human neutrophils and in the hypoxanthine/xanthine oxidase assay.
This compound reduced, in a concentration-dependent manner, leukotriene B(4), prostaglandin E(2) and TNF-
alpha
production in activated leukocytes.
Oral and intrapouch administration of TA in the mouse
air
pouch model produced a dose-dependent reduction of all these inflammatory mediators.
In TPA-induced mouse epidermal hyperplasia, topical administration of TA reduced oedema, leukocyte infiltration, eicosanoid levels and TNF-
alpha
in skin.
[MeSH-major]
Antioxidants / pharmacology. NF-kappa B / drug effects. Psoriasis / drug therapy. Salicylates / pharmacology. Sesquiterpenes / pharmacology.
Tumor
Necrosis Factor-
alpha
/ drug effects
[MeSH-minor]
Animals. Arachidonic Acid / metabolism.
Cell
Line.
Disease
Models, Animal. Dose-Response Relationship, Drug. Female. Humans. Hyperplasia / drug therapy. Hyperplasia / physiopathology. Inflammation Mediators / metabolism. Keratinocytes / drug effects. Keratinocytes / metabolism. Mice. Monocytes / drug effects. Monocytes / metabolism. Neutrophils / drug effects. Neutrophils / metabolism. Oxidative Stress / drug effects. Protein Transport / drug effects
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.
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(PMID = 17641670.001).
[ISSN]
0007-1188
[Journal-full-title]
British journal of pharmacology
[ISO-abbreviation]
Br. J. Pharmacol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antioxidants; 0 / Inflammation Mediators; 0 / NF-kappa B; 0 / Salicylates; 0 / Sesquiterpenes; 0 / Tumor Necrosis Factor-alpha; 0 / avarol-3'-thiosalicylate; 27YG812J1I / Arachidonic Acid
[Other-IDs]
NLM/ PMC2042954
84.
Tawfik OW, Kramer B, Shideler B, Danley M, Kimler BF, Holzbeierlein J:
Prognostic significance of CD44, platelet-derived growth factor receptor alpha, and cyclooxygenase 2 expression in renal cell carcinoma.
Arch Pathol Lab Med
; 2007 Feb;131(2):261-7
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[Title]
Prognostic significance of CD44, platelet-derived
growth
factor receptor
alpha
, and cyclooxygenase 2 expression in renal
cell
carcinoma.
CONTEXT: Pathologic stage is the main prognostic factor for predicting outcome in renal
cell
carcinoma (RCC).
Because of its unreliability in predicting
tumor
progression, other factors are needed to provide additional prognostic information.
OBJECTIVE: The expression of CD44, cyclooxygenase 2, and platelet-derived
growth
factor receptor
alpha
(PDGFR-
alpha
) was evaluated
as a
potential prognostic factor for survival in patients with RCC.
DESIGN: Sixty-two patients (42 men and 20 women; median age, 61 years), undergoing partial (10 cases) or radical (55 cases) nephrectomy for RCC were retrospectively analyzed by immunohistochemical analysis for CD44, cyclooxygenase 2, and PDGFR-
alpha
expression.
Impact of various factors on
disease
-specific and overall survival was calculated using Cox proportional hazards models.
RESULTS
: There was a gradual increase in CD44 and cyclooxygenase 2 expression with increasing RCC nuclear grade.
In contrast, PDGFR-
alpha
expression showed no consistent relationship with nuclear grade.
On univariate analysis, metastasis at time of surgery (P < .001),
tumor
size (P = .004), pathologic stage group (P = .001), and nuclear grade (P = .004) were correlated with
disease
-specific survival.
For overall survival, metastasis (P < .001),
tumor
size (P = .02), pathologic stage group (P = .01), nuclear grade (P = .003), and PDGFR-
alpha
(P = .03) were significant on univariate analysis.
Only metastasis (P = .001) and PDGFR-
alpha
(P = .03) were significant on multivariate analysis.
CONCLUSIONS: When combined with other variables, PDGFR-
alpha
expression in RCC may provide additional predictive value related to the patient's overall survival.
[MeSH-major]
Antigens, CD44 / biosynthesis. Carcinoma, Renal
Cell
/ metabolism. Cyclooxygenase 2 / biosynthesis. Kidney
Neoplasms
/ metabolism. Platelet-Derived
Growth
Factor / biosynthesis
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Biomarkers,
Tumor
/ analysis. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Analysis
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(PMID = 17284111.001).
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