BioMedLib Search Engine [ goto HOMEPAGE ]

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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 .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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) .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Clin Immunol. 2006 Dec;121(3):274-85 [16945588.001]

[Cites] Cancer Res. 2000 Jan 15;60(2):293-7 [10667579.001]

[Cites] N Engl J Med. 2006 Aug 31;355(9):873-84 [16943400.001]

[Cites] J Natl Cancer Inst. 2006 May 17;98(10):665-7 [16705118.001]

[Cites] Cancer Res. 2006 Apr 15;66(8):4542-6 [16618783.001]

[Cites] Br J Cancer. 2006 Feb 27;94(4):593-8 [16421593.001]

[Cites] Dis Colon Rectum. 2006 Jan;49(1):113-24; discussion 124-5 [16362805.001]

[Cites] Nat Clin Pract Oncol. 2005 Dec;2 Suppl 1:S4-11 [16341240.001]

[Cites] Nucleic Acids Res. 2005;33(21):6823-36 [16326863.001]

[Cites] J Natl Cancer Inst. 2005 Sep 21;97(18):1330-8 [16174854.001]

[Cites] J Natl Cancer Inst. 2005 Sep 21;97(18):1317-9 [16174847.001]

[Cites] Curr Gastroenterol Rep. 2005 Oct;7(5):389-95 [16168238.001]

[Cites] Biochem Soc Trans. 2005 Aug;33(Pt 4):709-11 [16042580.001]

[Cites] Oncol Rep. 2005 Apr;13(4):559-83 [15756426.001]

[Cites] Anal Chem. 2004 Nov 15;76(22):6829-32 [15538812.001]

[Cites] PLoS One. 2008;3(2):e1652 [18286204.001]

[Cites] Cancer Biomark. 2007;3(3):153-61 [17611306.001]

[Cites] Crit Rev Oncog. 2006 Dec;12(3-4):273-87 [17425506.001]

[Cites] PLoS One. 2007;2(3):e293 [17356702.001]

[Cites] Clin Cancer Res. 2006 Nov 15;12(22):6626-36 [17121881.001]

[Cites] Int J Colorectal Dis. 1997;12(5):267-71 [9401839.001]

[Cites] Adv Cancer Res. 1998;72:141-96 [9338076.001]

[Cites] Endoscopy. 1997 Sep;29(7):626-31 [9360872.001]

[Cites] Nat Genet. 1994 Aug;7(4):536-40 [7951326.001]

[Cites] Age Ageing. 1993 Jul;22(4):260-4 [8213330.001]

[Cites] Cancer Res. 1988 Mar 1;48(5):1159-61 [3342396.001]

[Cites] Cell. 1990 Jun 1;61(5):759-67 [2188735.001]

[Cites] Carcinogenesis. 2004 Oct;25(10):1917-23 [15205357.001]

[Cites] Semin Oncol. 2004 Apr;31(2 Suppl 7):12-21 [15252926.001]

[Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Jul;287(1):G7-17 [15194558.001]

[Cites] Clin Gastroenterol Hepatol. 2004 Jan;2(1):1-8 [15017625.001]

[Cites] N Engl J Med. 2004 Mar 4;350(10):991-1004 [14999111.001]

[Cites] Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):29-39 [15000147.001]

[Cites] Mol Carcinog. 2004 Feb;39(2):79-84 [14750212.001]

[Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]

[Cites] Cancer Res. 2003 Aug 15;63(16):4878-81 [12941809.001]

[Cites] Ann N Y Acad Sci. 2003 Mar;983:213-9 [12724226.001]

[Cites] Ann N Y Acad Sci. 2003 Mar;983:84-100 [12724214.001]

[Cites] Ann N Y Acad Sci. 2003 Mar;983:28-42 [12724210.001]

[Cites] Surg Clin North Am. 2002 Oct;82(5):891-904 [12507199.001]

[Cites] Endoscopy. 2003 Jan;35(1):27-35 [12510223.001]

[Cites] Gastroenterology. 2002 Sep;123(3):862-76 [12198712.001]

[Cites] Annu Rev Genomics Hum Genet. 2002;3:101-28 [12142355.001]

[Cites] Cell Mol Life Sci. 2002 May;59(5):821-31 [12088282.001]

[Cites] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769.001]

[Cites] Climacteric. 2002 Mar;5(1):3-14 [11974557.001]

[Cites] Ann Pharmacother. 2001 Dec;35(12):1638-43 [11793634.001]

[Cites] Genome Res. 2002 Jan;12(1):153-7 [11779840.001]

[Cites] J Pathol. 2001 Sep;195(1):111-34 [11568897.001]

[Cites] Hum Mol Genet. 2001 Apr;10(7):687-92 [11257100.001]

[Cites] Cancer Res. 2000 Sep 15;60(18):5040-4 [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

   

Advertisement

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

Genetic Alliance. consumer health - Lung Cancer.

Genetic Alliance. consumer health - Non-small cell lung cancer.

MedlinePlus Health Information. consumer health - Lung Cancer.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. PIOGLITAZONE .

Hazardous Substances Data Bank. 4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone .

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

SciCrunch. OMIM: Data: Gene Annotation .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Circ Res. 2005 Jul 22;97(2):105-14 [16037577.001]

[Cites] Thromb Haemost. 1999 Dec;82(6):1764-7 [10613667.001]

[Cites] J Bone Miner Res. 2002 Jul;17(7):1171-9 [12096831.001]

[Cites] Toxicol Appl Pharmacol. 2008 Oct 1;232(1):125-34 [18586044.001]

[Cites] Arterioscler Thromb Vasc Biol. 2009 May;29(5):761-6 [19213941.001]

[Cites] Circ Res. 2000 Sep 29;87(7):E10-7 [11009570.001]

[Cites] Connect Tissue Res. 1996;34(1):23-32 [8835845.001]

[Cites] Am J Physiol Cell Physiol. 2007 Aug;293(2):C606-20 [17494632.001]

[Cites] Br J Pharmacol. 2002 Jun;136(4):530-9 [12055131.001]

[Cites] Arterioscler Thromb Vasc Biol. 2007 May;27(5):1030-6 [17322102.001]

[Cites] Endocrinology. 2008 Apr;149(4):1646-53 [18174285.001]

[Cites] Toxicol In Vitro. 2007 Sep;21(6):1066-76 [17521863.001]

[Cites] Kidney Int. 2002 Nov;62(5):1724-31 [12371973.001]

[Cites] J Am Soc Nephrol. 2008 Feb;19(2):213-6 [18094365.001]

[Cites] Atherosclerosis. 2007 Nov;195(1):e65-75 [17412344.001]

[Cites] Ann N Y Acad Sci. 2007 Nov;1117:40-50 [18056036.001]

[Cites] Kidney Int. 2008 Feb;73(4):384-90 [18046319.001]

[Cites] Kidney Int. 2006 Apr;69(8):1464-70 [16531981.001]

[Cites] Circ Res. 2006 Apr 14;98(7):905-12 [16527991.001]

[Cites] Am J Physiol Renal Physiol. 2005 Jul;289(1):F154-65 [15769937.001]

[Cites] Atherosclerosis. 2008 Aug;199(2):271-7 [18179800.001]

[Cites] Arterioscler Thromb Vasc Biol. 2007 Dec;27(12):2589-96 [17932314.001]

[Cites] Kidney Int. 2008 Feb;73(4):456-64 [18046316.001]

[Cites] Circ Res. 2000 Nov 24;87(11):1055-62 [11090552.001]

[Cites] J Am Soc Nephrol. 2005 Feb;16(2):520-8 [15615819.001]

[Cites] Circ Res. 2004 Oct 1;95(7):671-6 [15459088.001]

[Cites] Circulation. 2005 May 10;111(18):2364-72 [15851600.001]

[Cites] Nephrol Dial Transplant. 2006 Apr;21(4):911-6 [16384827.001]

[Cites] Atherosclerosis. 2004 May;174(1):17-24 [15135246.001]

[Cites] Nephrol Dial Transplant. 2004 Sep;19(9):2387-93 [15252163.001]

[Cites] Circulation. 2000 Nov 21;102(21):2636-42 [11085968.001]

[Cites] Endocr J. 2007 Feb;54(1):103-12 [17135708.001]

[Cites] Am J Kidney Dis. 2001 Oct;38(4 Suppl 1):S34-7 [11576919.001]

[Cites] Biochem Biophys Res Commun. 2008 Sep 26;374(3):553-8 [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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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.

Genetic Alliance. consumer health - Breast Cancer.

MedlinePlus Health Information. consumer health - Breast Cancer.

COS Scholar Universe. author profiles.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

MedlinePlus Health Information. consumer health - Smoking.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. CYCLOSPORIN A .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

Genetic Alliance. consumer health - Diabetes.

MedlinePlus Health Information. consumer health - Diabetes.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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

Genetic Alliance. consumer health - Thyroid Cancer.

MedlinePlus Health Information. consumer health - Stomach Cancer.

Hazardous Substances Data Bank. LIOTHYRONINE .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Phytother Res. 2002 Dec;16(8):781-4 [12458489.001]

[Cites] Biochem Pharmacol. 2003 Jun 15;65(12):2065-71 [12787887.001]

[Cites] Int Immunopharmacol. 2005 Mar;5(3):461-83 [15683844.001]

[Cites] Am J Chin Med. 2005;33(1):87-94 [15844836.001]

[Cites] Arch Pharm Res. 1999 Dec;22(6):642-5 [10615874.001]

[Cites] Kidney Int. 1997 Feb;51(2):553-5 [9027737.001]

[Cites] J Immunol. 2002 Aug 1;169(3):1482-91 [12133975.001]

[Cites] Inflamm Res. 2000 Jul;49(7):355-60 [10959557.001]

[Cites] Agric Biol Chem. 1990 Nov;54(11):2961-6 [1368650.001]

[Cites] Mol Biotechnol. 2001 Oct;19(2):153-68 [11725485.001]

[Cites] J Pathol. 2005 Mar;205(4):530-6 [15714461.001]

[Cites] Mol Pharmacol. 2001 May;59(5):1216-24 [11306706.001]

[Cites] Ann N Y Acad Sci. 2002 Nov;973:448-53 [12485909.001]

[Cites] Planta Med. 2006 Apr;72(5):477-9 [16557465.001]

[Cites] J Agric Food Chem. 2004 Jun 2;52(11):3389-93 [15161203.001]

[Cites] J Biol Chem. 1995 Jan 20;270(3):1230-7 [7836384.001]

[Cites] Biol Reprod. 2004 Jun;70(6):1822-7 [14960485.001]

[Cites] Clin Exp Allergy. 1997 Sep;27(9):1060-6 [9678838.001]

[Cites] Am J Physiol Cell Physiol. 2001 Dec;281(6):C1971-7 [11698256.001]

[Cites] J Pharmacol Exp Ther. 2005 Jul;314(1):27-34 [15784648.001]

[Cites] Biochem J. 2000 Aug 15;350 Pt 1:307-12 [10926858.001]

[Cites] Inflammation. 2003 Jun;27(3):129-35 [12875366.001]

[Cites] Bioorg Med Chem. 2007 May 15;15(10):3381-9 [17391969.001]

[Cites] Farmaco. 1994 Nov;40(11):709-12 [7832973.001]

[Cites] Plant Foods Hum Nutr. 2006 Jun;61(2):57-65 [16816988.001]

[Cites] J Biol Chem. 2001 Oct 26;276(43):39805-11 [11514583.001]

[Cites] Immunology. 1999 Oct;98(2):253-7 [10540224.001]

[Cites] Biochem J. 2006 Jun 15;396(3):517-27 [16533170.001]

[Cites] J Nutr. 2005 Apr;135(4):870-7 [15795449.001]

[Cites] Biol Pharm Bull. 2000 Mar;23(3):356-8 [10726895.001]

[Cites] Mech Ageing Dev. 2005 Dec;126(12):1284-91 [16140359.001]

[Cites] FASEB J. 2003 Nov;17 (14 ):2115-7 [12958148.001]

[Cites] Autoimmunity. 2005 Aug;38(5):359-67 [16227151.001]

[Cites] Cancer Res. 2000 Sep 15;60(18):5059-66 [11016629.001]

[Cites] Toxicology. 2006 Sep 21;226(2-3):152-60 [16919860.001]

[Cites] Int Immunopharmacol. 2006 Feb;6(2):122-32 [16399617.001]

[Cites] Z Naturforsch C. 2003 Jul-Aug;58(7-8):580-9 [12939048.001]

[Cites] Nutr Cancer. 2005;51(1):78-82 [15749633.001]

[Cites] Planta Med. 2005 Jan;71(1):24-7 [15678369.001]

[Cites] J Biol Chem. 2001 Apr 20;276(16):12645-53 [11278891.001]

[Cites] Reproduction. 2004 Mar;127(3):379-87 [15016957.001]

[Cites] Cancer Res. 2000 Sep 1;60(17 ):4873-80 [10987301.001]

[Cites] J Biol Chem. 1993 Oct 15;268(29):21513-8 [8408001.001]

[Cites] Mol Reprod Dev. 2004 Jun;68(2):198-204 [15095341.001]

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

COS Scholar Universe. author profiles.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

MedlinePlus Health Information. consumer health - Liver Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Immunol. 1986 Dec 1;137(11):3538-43 [2946763.001]

[Cites] Clin Exp Immunol. 1989 May;76(2):262-7 [2474394.001]

[Cites] Int J Cancer. 1989 Aug 15;44(2):307-14 [2527208.001]

[Cites] Cancer Res. 1987 Feb 15;47(4):936-42 [3802100.001]

[Cites] Exp Hematol. 1990 Aug;18(7):806-11 [2143138.001]

[Cites] J Natl Cancer Inst. 1983 Apr;70(4):735-8 [6187964.001]

[Cites] J Clin Lab Immunol. 1991 Apr;34(4):183-8 [1726567.001]

[Cites] J Immunol. 1995 Jul 1;155(1):15-26 [7541413.001]

[Cites] In Vivo. 1994 May-Jun;8(3):279-83 [7803704.001]

[Cites] Immunol Invest. 1993 Jul;22(5):329-39 [7691735.001]

[Cites] Cancer Immunol Immunother. 1992;35(1):14-8 [1535284.001]

[Cites] Cell Immunol. 1992 May;141(2):398-408 [1533570.001]

[Cites] 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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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

Hazardous Substances Data Bank. FLUOROURACIL .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

Genetic Alliance. consumer health - Pulmonary Disease.

Genetic Alliance. consumer health - Chronic obstructive pulmonary disease.

MedlinePlus Health Information. consumer health - COPD.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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

MedlinePlus Health Information. consumer health - Vasculitis.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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.

COS Scholar Universe. author profiles.

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] © 2010 AACR.

[Cites] Trends Immunol. 2002 Nov;23(11):549-55 [12401408.001]

[Cites] J Immunol. 2002 Jan 15;168(2):689-95 [11777962.001]

[Cites] Cell. 2003 Mar 7;112(5):645-57 [12628185.001]

[Cites] J Immunol. 2003 May 15;170(10):5064-74 [12734351.001]

[Cites] Trends Immunol. 2003 Jun;24(6):302-6 [12810105.001]

[Cites] Am J Pathol. 2003 Nov;163(5):2113-26 [14578209.001]

[Cites] J Clin Invest. 2004 Jun;113(12):1734-42 [15199408.001]

[Cites] Cancer Res. 2004 Aug 15;64(16):5839-49 [15313928.001]

[Cites] J Exp Med. 1991 Mar 1;173(3):647-58 [1900079.001]

[Cites] J Surg Res. 1991 Apr;50(4):403-9 [2020192.001]

[Cites] Mol Cell Biol. 1992 Mar;12(3):954-61 [1312220.001]

[Cites] J Immunol. 1993 Mar 1;150(5):2072-80 [8436836.001]

[Cites] J Immunol Methods. 1994 Sep 14;174(1-2):231-5 [8083527.001]

[Cites] Int J Cancer. 1995 Mar 3;60(5):660-7 [7860141.001]

[Cites] Eur J Immunol. 1995 Apr;25(4):1101-4 [7537672.001]

[Cites] Cancer Immunol Immunother. 1995 Nov;41(5):317-24 [8536278.001]

[Cites] J Exp Med. 1996 Apr 1;183(4):1323-9 [8666890.001]

[Cites] Mol Cell Biol. 1996 Sep;16(9):4604-13 [8756616.001]

[Cites] Biochem Biophys Res Commun. 1996 Aug 14;225(2):485-8 [8753788.001]

[Cites] J Biol Chem. 1997 Feb 21;272(8):4959-63 [9030556.001]

[Cites] J Immunol. 1998 Jun 15;160(12):5729-34 [9637481.001]

[Cites] Cancer Res. 1999 Apr 1;59(7):1592-8 [10197634.001]

[Cites] Biochem J. 1999 Jun 1;340 ( Pt 2):549-53 [10333501.001]

[Cites] J Clin Invest. 2005 Jul;115(7):1806-15 [16007254.001]

[Cites] Nat Rev Immunol. 2005 Aug;5(8):641-54 [16056256.001]

[Cites] Cancer Res. 2006 Jan 15;66(2):1123-31 [16424049.001]

[Cites] Immunology. 2006 Mar;117(3):386-95 [16476058.001]

[Cites] Blood. 2006 Sep 1;108(5):1627-34 [16709924.001]

[Cites] J Clin Invest. 2006 Oct;116(10):2777-90 [17016559.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Oct 3;103(40):14895-900 [17003120.001]

[Cites] Blood. 2007 Feb 15;109(4):1568-73 [17023580.001]

[Cites] Annu Rev Immunol. 2007;25:243-65 [17129181.001]

[Cites] Eur J Immunol. 2007 Apr;37(4):935-45 [17330821.001]

[Cites] Antioxid Redox Signal. 2007 Aug;9(8):1221-35 [17536958.001]

[Cites] Cancer Metastasis Rev. 2007 Jun;26(2):225-39 [17440684.001]

[Cites] J Immunol. 2007 Sep 1;179(5):2851-9 [17709499.001]

[Cites] Clin Cancer Res. 2007 Sep 15;13(18 Pt 1):5243-8 [17875751.001]

[Cites] Nature. 2007 Dec 6;450(7171):903-7 [18026089.001]

[Cites] J Clin Invest. 2008 Jun;118(6):1991-2001 [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]

[Cites] Cancer Res. 2000 Aug 1;60(15):4010-5 [10945599.001]

[Cites] J Exp Med. 2001 Mar 19;193(6):727-40 [11257139.001]

[Cites] Nature. 2001 Apr 26;410(6832):1107-11 [11323675.001]

[Cites] J Biol Chem. 2001 May 11;276(19):15881-5 [11278602.001]

[Cites] J Exp Med. 2001 Jun 4;193(11):1261-8 [11390433.001]

[Cites] J Immunol. 2001 Oct 15;167(8):4293-302 [11591752.001]

[Cites] J Immunother. 2001 Nov-Dec;24(6):431-46 [11759067.001]

[Cites] 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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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 .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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 .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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

Genetic Alliance. consumer health - Cardiomyopathy.

Genetic Alliance. consumer health - Dilated Cardiomyopathy.

Genetic Alliance. consumer health - Idiopathic dilated cardiomyopathy.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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 .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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.

Genetic Alliance. consumer health - Lung Cancer.

MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

MedlinePlus Health Information. consumer health - Lung Cancer.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

Hazardous Substances Data Bank. 13-CIS-RETINOIC ACID .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Acta Cytol. 1982 Jan-Feb;26(1):78-85 [7039202.001]

[Cites] J Natl Cancer Inst. 1980 Dec;65(6):1307-16 [6776329.001]

[Cites] Stat Med. 1989 Apr;8(4):431-40 [2727467.001]

[Cites] N Engl J Med. 1993 Jan 7;328(1):15-20 [8416267.001]

[Cites] Invest New Drugs. 1992 Nov;10(4):239-53 [1487397.001]

[Cites] N Engl J Med. 1994 Apr 14;330(15):1029-35 [8127329.001]

[Cites] Am J Clin Nutr. 1995 Dec;62(6 Suppl):1431S-1438S [7495244.001]

[Cites] N Engl J Med. 1996 May 2;334(18):1150-5 [8602180.001]

[Cites] Cancer. 1996 Sep 1;78(5):1004-10 [8780538.001]

[Cites] Ann Oncol. 1997 Jan;8(1):85-9 [9093712.001]

[Cites] J Natl Cancer Inst. 1999 Apr 21;91(8):691-6 [10218506.001]

[Cites] J Natl Cancer Inst. 1999 Aug 4;91(15):1317-21 [10433621.001]

[Cites] Ann Intern Med. 2005 Feb 15;142(4):233-9 [15710956.001]

[Cites] J Natl Cancer Inst. 2005 Nov 16;97(22):1652-62 [16288118.001]

[Cites] Clin Cancer Res. 2006 Jan 1;12(1):314-20 [16397057.001]

[Cites] Clin Cancer Res. 2006 Apr 1;12(7 Pt 1):2281-8 [16609045.001]

[Cites] Clin Cancer Res. 2006 Jun 15;12(12):3661-97 [16778094.001]

[Cites] JAMA. 2006 Jun 21;295(23):2727-41 [16754727.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2006 Aug;15(8):1562-4 [16896051.001]

[Cites] Am J Respir Crit Care Med. 2007 May 15;175(10):1061-5 [17290039.001]

[Cites] J Natl Cancer Inst. 2007 Nov 7;99(21):1603-12 [17971525.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2007 Nov;16(11):2425-31 [18006932.001]

[Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]

[Cites] N Engl J Med. 2003 Jul 17;349(3):215-24 [12824459.001]

[Cites] J Natl Cancer Inst. 2000 Jun 21;92(12):977-86 [10861309.001]

[Cites] N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062.001]

[Cites] Clin Cancer Res. 2000 Aug;6(8):2973-9 [10955773.001]

[Cites] Histopathology. 2001 Mar;38(3):202-8 [11260299.001]

[Cites] J Natl Cancer Inst. 2001 Apr 18;93(8):605-18 [11309437.001]

[Cites] J Natl Cancer Inst. 2001 Jul 18;93(14):1042-3 [11459858.001]

[Cites] J Natl Cancer Inst. 2001 Jul 18;93(14):1081-8 [11459869.001]

[Cites] J Natl Cancer Inst. 2001 Sep 19;93(18):1385-91 [11562389.001]

[Cites] Clin Cancer Res. 2002 Feb;8(2):314-46 [11839647.001]

[Cites] N Engl J Med. 2002 Apr 4;346(14):1054-9 [11932472.001]

[Cites] J Natl Cancer Inst. 2002 Jul 3;94(13):1001-9 [12096085.001]

[Cites] J Natl Cancer Inst. 2003 Feb 5;95(3):206-14 [12569142.001]

[Cites] Stat Med. 2004 May 30;23(10):1571-8 [15122737.001]

[Cites] Clin Cancer Res. 2004 Oct 1;10(19):6502-11 [15475437.001]

[Cites] Fed Proc. 1976 May 1;35(6):1332-8 [770206.001]

[Cites] N Engl J Med. 1986 Dec 11;315(24):1501-5 [3537787.001]

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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.

MedlinePlus Health Information. consumer health - Brain Tumors.

MedlinePlus Health Information. consumer health - Childhood Brain Tumors.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .

Hazardous Substances Data Bank. ETOPOSIDE .

Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

Hazardous Substances Data Bank. VINCRISTINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] (c) 2006 Wiley-Liss, Inc.

[Cites] J Neurosurg. 1985 Aug;63(2):155-67 [2991485.001]

[Cites] Ann Oncol. 2000 Mar;11(3):263-71 [10811491.001]

[Cites] J Neurooncol. 1985;3(2):147-52 [3897472.001]

[Cites] J Neurosurg. 1986 Oct;65(4):470-5 [2428955.001]

[Cites] N Engl J Med. 1987 Jun 4;316(23):1435-40 [2437455.001]

[Cites] J Neurosurg. 1987 Jul;67(1):65-70 [2439668.001]

[Cites] Prog Exp Tumor Res. 1987;30:307-12 [2819945.001]

[Cites] J Neurosurg. 1989 May;70(5):676-81 [2540291.001]

[Cites] J Neurosurg. 1989 May;70(5):707-13 [2709111.001]

[Cites] Neuro Oncol. 2001 Jul;3(3):174-83 [11465398.001]

[Cites] J Neurooncol. 2001 Sep;54(3):311-6 [11767296.001]

[Cites] J Clin Oncol. 2002 Feb 1;20(3):857-65 [11821471.001]

[Cites] J Clin Oncol. 2004 Mar 1;22(5):846-53 [14990640.001]

[Cites] J Clin Oncol. 2004 May 15;22(10):1934-43 [15143087.001]

[Cites] J Clin Oncol. 2004 Jul 1;22(13):2691-700 [15226336.001]

[Cites] Pediatr Blood Cancer. 2004 Aug;43(2):126-33 [15236278.001]

[Cites] Int J Radiat Oncol Biol Phys. 1990 Mar;18(3):541-5 [2318686.001]

[Cites] Int J Radiat Oncol Biol Phys. 1990 Apr;18(4):773-81 [2323968.001]

[Cites] Med Pediatr Oncol. 1990;18(4):304-10 [2355890.001]

[Cites] Pediatr Hematol Oncol. 1990;7(2):183-8 [2206859.001]

[Cites] Neurosurgery. 1990 Sep;27(3):454-60 [1700327.001]

[Cites] J Neurosurg. 1991 Apr;74(4):545-51 [1848284.001]

[Cites] J Neurooncol. 1992 Jan;12(1):47-52 [1541978.001]

[Cites] Ann Neurol. 1992 Oct;32(4):551-4 [1456739.001]

[Cites] N Engl J Med. 1993 Jan 14;328(2):87-94 [8416438.001]

[Cites] Acta Neurochir (Wien). 1993;120(3-4):111-7 [7681619.001]

[Cites] Cancer. 1993 May 15;71(10):3182-4 [8490849.001]

[Cites] Int J Radiat Oncol Biol Phys. 1994 Jan 1;28(1):229-45 [8270446.001]

[Cites] Neuropediatrics. 1994 Feb;25(1):26-32 [8208347.001]

[Cites] Cancer. 1994 Aug 1;74(3):940-4 [8039122.001]

[Cites] Med Pediatr Oncol. 1995 Jun;24(6):368-72 [7536294.001]

[Cites] Neurosurgery. 1995 Mar;36(3):459-64; discussion 464-6 [7538635.001]

[Cites] J Child Neurol. 1995 May;10(3):209-12 [7642890.001]

[Cites] J Clin Oncol. 1996 Nov;14(11):2908-15 [8918487.001]

[Cites] J Neurosurg. 1997 Mar;86(3):446-55 [9046301.001]

[Cites] Int J Radiat Oncol Biol Phys. 1997 Feb 1;37(3):505-10 [9112445.001]

[Cites] Klin Padiatr. 1997 Jul-Aug;209(4):222-7 [9293454.001]

[Cites] J Neurosurg. 1998 Jan;88(1):66-72 [9420074.001]

[Cites] J Neurooncol. 1998 May;37(3):229-39 [9524081.001]

[Cites] J Clin Oncol. 1998 May;16(5):1723-8 [9586884.001]

[Cites] Eur J Cancer. 1998 Jan;34(1):104-10 [9624246.001]

[Cites] J Clin Oncol. 1999 Mar;17(3):933-40 [10071287.001]

[Cites] Br J Cancer. 1999 Mar;79(7-8):1199-204 [10098759.001]

[Cites] J Neurooncol. 1997 Mar;32(1):71-80 [9049865.001]

[Cites] J Clin Oncol. 1999 Jul;17(7):2127-36 [10561268.001]

[Cites] J Clin Oncol. 1999 Aug;17(8):2585-92 [10561326.001]

[Cites] Neurosurgery. 1999 Dec;45(6):1292-7; discussion 1297-8 [10598695.001]

[Cites] Childs Nerv Syst. 1999 Nov;15(11-12):770-3 [10603021.001]

[Cites] Int J Radiat Oncol Biol Phys. 2000 Mar 15;46(5):1171-6 [10725628.001]

[Cites] 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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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

MedlinePlus Health Information. consumer health - Dietary Fats.

MedlinePlus Health Information. consumer health - Triglycerides.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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. HYALURONIC ACID .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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. consumer health - Prostate cancer.

MedlinePlus Health Information. consumer health - Prostate Cancer.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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.

Institute for Transcriptional Informatics. gene/protein/disease-specific - Institute for Transcriptional Informatics (registration required).

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

SciCrunch. HGNC: Data: Gene Annotation .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Biol Chem. 1998 Aug 21;273(34):21594-602 [9705290.001]

[Cites] Arthritis Rheum. 1997 Dec;40(12):2207-11 [9416858.001]

[Cites] Immunity. 1999 Mar;10(3):387-98 [10204494.001]

[Cites] Circ Res. 1999 Jun 11;84(11):1258-67 [10364563.001]

[Cites] Nat Genet. 1999 Jun;22(2):145-50 [10369255.001]

[Cites] Genomics. 1999 Jun 1;58(2):146-57 [10366446.001]

[Cites] J Leukoc Biol. 1999 Oct;66(4):562-6 [10534109.001]

[Cites] Cytokine. 2000 Feb;12(2):110-9 [10671295.001]

[Cites] Mol Cell Biol. 2000 Mar;20(6):2239-47 [10688670.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):3925-9 [10760264.001]

[Cites] Mol Cell Biol. 2000 Aug;20(16):6084-94 [10913190.001]

[Cites] EMBO J. 2000 Aug 1;19(15):4154-63 [10921895.001]

[Cites] J Invest Dermatol. 2000 Oct;115(4):726-30 [10998151.001]

[Cites] Ann Rheum Dis. 2001 Jan;60(1):36-42 [11114280.001]

[Cites] Exp Hematol. 2001 Mar;29(3):330-8 [11274761.001]

[Cites] EMBO J. 2001 Jul 2;20(13):3518-25 [11432838.001]

[Cites] J Immunol. 2001 Aug 15;167(4):2202-8 [11490006.001]

[Cites] J Immunol. 2001 Dec 15;167(12):6975-82 [11739517.001]

[Cites] Nat Genet. 2003 Apr;33(4):469-75 [12627232.001]

[Cites] J Leukoc Biol. 2003 Jun;73(6):862-71 [12773519.001]

[Cites] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386.001]

[Cites] Proc Natl Acad Sci U S A. 1990 Dec;87(24):9769-73 [2263628.001]

[Cites] J Exp Med. 1991 Jul 1;174(1):73-81 [2056282.001]

[Cites] J Biol Chem. 1992 Nov 5;267(31):22102-7 [1429562.001]

[Cites] Mol Cell Biol. 1992 Dec;12(12):5355-62 [1448070.001]

[Cites] Eur J Immunol. 1994 Jan;24(1):191-5 [8020556.001]

[Cites] Clin Exp Immunol. 1994 Jul;97(1):45-7 [8033419.001]

[Cites] Dermatology. 1994;189 Suppl 1:135-7 [7914110.001]

[Cites] Biochem Mol Biol Int. 1996 Sep;40(1):43-51 [8886268.001]

[Cites] Neurosci Lett. 1996 Sep 6;215(2):75-8 [8887999.001]

[Cites] J Clin Invest. 1994 Oct;94(4):1449-55 [7929820.001]

[Cites] Nature. 1994 Oct 6;371(6497):508-10 [7935762.001]

[Cites] Clin Exp Immunol. 1995 Feb;99(2):303-10 [7851026.001]

[Cites] Cell Immunol. 1995 Mar;161(1):125-31 [7867077.001]

[Cites] Hum Immunol. 1994 Dec;41(4):259-66 [7883593.001]

[Cites] J Biol Chem. 1995 Mar 24;270(12):6577-83 [7896795.001]

[Cites] J Immunol. 1995 Jul 15;155(2):902-8 [7608567.001]

[Cites] Dis Markers. 1995 Mar;12(2):127-33 [7614782.001]

[Cites] Ann Rheum Dis. 1995 Jul;54(7):601-3 [7668906.001]

[Cites] Hum Genet. 1995 Oct;96(4):433-6 [7557966.001]

[Cites] J Exp Med. 1995 Nov 1;182(5):1259-64 [7595196.001]

[Cites] Mol Cell Biol. 1996 Feb;16(2):459-67 [8552071.001]

[Cites] J Inflamm. 1995;45(3):183-92 [8597873.001]

[Cites] Hum Genet. 1996 Jun;97(6):813-8 [8641702.001]

[Cites] N Engl J Med. 1996 Jun 27;334(26):1717-25 [8637518.001]

[Cites] Scand J Immunol. 1996 Apr;43(4):456-63 [8668926.001]

[Cites] Ann Acad Med Singapore. 1996 Jan;25(1):90-3 [8779554.001]

[Cites] Mol Cell Biol. 1996 Oct;16(10):5232-44 [8816436.001]

[Cites] J Inflamm. 1995-1996;46(1):32-41 [8832970.001]

[Cites] J Inflamm. 1995-1996;46(1):42-50 [8832971.001]

[Cites] J Rheumatol. 1996 Mar;23(3):416-8 [8832975.001]

[Cites] J Rheumatol. 1996 Oct;23(10):1725-8 [8895148.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):3195-9 [9096369.001]

[Cites] J Biol Chem. 1997 Jul 11;272(28):17795-801 [9211933.001]

[Cites] Mol Immunol. 1997 Apr;34(5):391-9 [9293772.001]

[Cites] Cytokine. 1997 Oct;9(10):787-90 [9344512.001]

[Cites] J Interferon Cytokine Res. 1997 Oct;17(10):631-5 [9355965.001]

[Cites] Tissue Antigens. 1998 Oct;52(4):359-67 [9820599.001]

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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 .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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. consumer health - Renal cell carcinoma.

MedlinePlus Health Information. consumer health - Blood Clots.

MedlinePlus Health Information. consumer health - Kidney Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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. consumer health - Glioma.

Hazardous Substances Data Bank. CALPHOSTIN C .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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. author profiles.

Hazardous Substances Data Bank. HYDROCORTISONE .

Hazardous Substances Data Bank. MITOTANE .

Hazardous Substances Data Bank. PROGESTERONE .

Hazardous Substances Data Bank. TESTOSTERONE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

MedlinePlus Health Information. consumer health - Liver Cancer.

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

[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.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. Adenosine .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Immunol. 2006 Jan 1;176(1):451-62 [16365438.001]

[Cites] J Leukoc Biol. 2005 Aug;78(2):515-23 [15894584.001]

[Cites] Nat Neurosci. 2006 Apr;9(4):501-10 [16531999.001]

[Cites] Trends Biochem Sci. 2006 Dec;31(12):680-6 [17084085.001]

[Cites] J Leukoc Biol. 2006 Dec;80(6):1542-52 [16940330.001]

[Cites] Exp Mol Med. 2007 Aug 31;39(4):421-38 [17934330.001]

[Cites] Naunyn Schmiedebergs Arch Pharmacol. 2008 Jun;377(4-6):345-57 [18176800.001]

[Cites] Nat Rev Drug Discov. 2008 Sep;7(9):759-70 [18758473.001]

[Cites] Am J Respir Cell Mol Biol. 2009 Mar;40(3):251-9 [18703794.001]

[Cites] Am J Physiol. 1999 Dec;277(6 Pt 1):C1021-8 [10600752.001]

[Cites] J Leukoc Biol. 2000 Apr;67(4):520-8 [10770285.001]

[Cites] Naunyn Schmiedebergs Arch Pharmacol. 2000 Nov;362(4-5):364-74 [11111830.001]

[Cites] Mol Pharmacol. 2001 Jan;59(1):76-82 [11125027.001]

[Cites] Mol Cell Biol. 2001 Oct;21(20):7065-77 [11564889.001]

[Cites] Cell. 2002 Apr;109 Suppl:S81-96 [11983155.001]

[Cites] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886.001]

[Cites] Nat Cell Biol. 2002 Nov;4(11):901-6 [12402047.001]

[Cites] J Leukoc Biol. 2002 Nov;72(5):1027-36 [12429726.001]

[Cites] Biochem Pharmacol. 2003 Feb 15;65(4):493-501 [12566076.001]

[Cites] Oncogene. 2003 Feb 27;22(8):1206-18 [12606947.001]

[Cites] J Pharmacol Exp Ther. 2003 Sep;306(3):1042-9 [12766259.001]

[Cites] Brain Res Mol Brain Res. 2003 Sep 10;117(1):1-7 [14499475.001]

[Cites] Trends Immunol. 2004 Jan;25(1):33-9 [14698282.001]

[Cites] Nat Rev Mol Cell Biol. 2004 May;5(5):392-401 [15122352.001]

[Cites] J Biol Chem. 2004 Jun 4;279(23):24873-80 [15140884.001]

[Cites] J Immunol. 2004 Jul 1;173(1):21-4 [15210754.001]

[Cites] Cell Signal. 2004 Oct;16(10):1113-21 [15240006.001]

[Cites] Eur J Pharmacol. 2004 Aug 16;497(1):87-95 [15321739.001]

[Cites] Virology. 2004 Oct 1;327(2):186-95 [15351206.001]

[Cites] Mol Pharmacol. 2004 Nov;66(5):1147-59 [15286208.001]

[Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]

[Cites] EMBO J. 1995 May 1;14(9):1991-2004 [7744006.001]

[Cites] J Biol Chem. 1996 Jul 19;271(29):17114-8 [8663342.001]

[Cites] Nature. 1998 Dec 3;396(6710):474-7 [9853756.001]

[Cites] Am J Physiol. 1999 May;276(5 Pt 2):H1468-81 [10330229.001]

[Cites] Eur J Immunol. 2005 Jan;35(1):31-41 [15580656.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8686-91 [15937121.001]

[Cites] J Pharmacol Exp Ther. 2006 Apr;317(1):172-80 [16339914.001]

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

COS Scholar Universe. author profiles.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

[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

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(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