[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 12 of about 12
1. Aikawa T, Segre GV, Lee K: Fibroblast growth factor inhibits chondrocytic growth through induction of p21 and subsequent inactivation of cyclin E-Cdk2. J Biol Chem; 2001 Aug 3;276(31):29347-52
PDF icon [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.
  • FGF2 dramatically inhibited proliferation of rat chondrosarcoma (RCS) cells and arrested their cell cycle at the G(1) phase.
  • Furthermore, inhibitory effects of FGF2 on chondrocytic proliferation were partially reduced in p21-null limbs, compared with those in wild-type limbs in vitro.
  • [MeSH-major] CDC2-CDC28 Kinases. Cartilage / embryology. Cell Cycle / physiology. Chondrocytes / drug effects. Cyclin E / metabolism. Cyclin-Dependent Kinases / metabolism. Cyclins / metabolism. Fibroblast Growth Factor 2 / pharmacology. Protein-Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Animals. Cell Division / drug effects. Chondrosarcoma. Cyclin-Dependent Kinase 2. Cyclin-Dependent Kinase Inhibitor p21. Enzyme Inhibitors / metabolism. Fetus. G1 Phase. Histones / genetics. Limb Buds / physiology. Mice. Mice, Knockout. Organ Culture Techniques. RNA, Messenger / genetics. Rats. S Phase. Transcription, Genetic / drug effects. Tumor Cells, Cultured

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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 = 11384971.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK53343
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn1a protein, mouse; 0 / Cdkn1a protein, rat; 0 / Cyclin E; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Enzyme Inhibitors; 0 / Histones; 0 / RNA, Messenger; 103107-01-3 / Fibroblast Growth Factor 2; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 2.7.11.22 / Cdk2 protein, mouse; EC 2.7.11.22 / Cdk2 protein, rat; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.22 / Cyclin-Dependent Kinases
  •  go-up   go-down


2. Fujimoto T, Kawashima H, Tanaka T, Hirose M, Toyama-Sorimachi N, Matsuzawa Y, Miyasaka M: CD44 binds a chondroitin sulfate proteoglycan, aggrecan. Int Immunol; 2001 Mar;13(3):359-66
PDF icon [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.
  • Soluble CD44-IgG and CD44(+) cells bound to aggrecan from rat chondrosarcoma and bovine cartilage, immobilized on microtiter plates.
  • Structural analysis showed that glycosaminoglycans of aggrecan from rat chondrosarcoma and bovine articular cartilage consist of mainly CS A and a mixture of CS A and C respectively.
  • [MeSH-major] Antigens, CD44 / metabolism. Extracellular Matrix Proteins. Proteoglycans / metabolism
  • [MeSH-minor] Aggrecans. Animals. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / pharmacology. Antigens, CD95 / genetics. Antigens, CD95 / physiology. Apoptosis. Biotinylation. Cartilage, Articular / chemistry. Cattle. Chickens. Chondroitin ABC Lyase / pharmacology. Chondroitin Sulfates / analysis. Chondrosarcoma / chemistry. Chondrosarcoma / pathology. Culture Media, Serum-Free. Disaccharides / analysis. Hyaluronic Acid / pharmacology. Hyaluronoglucosaminidase / pharmacology. Lectins, C-Type. Male. Mice. Mice, Inbred AKR. Protein Binding / drug effects. Rats. Recombinant Fusion Proteins / physiology. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. HYALURONIC ACID .
  • 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 .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11222505.001).
  • [ISSN] 0953-8178
  • [Journal-full-title] International immunology
  • [ISO-abbreviation] Int. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Agc1 protein, mouse; 0 / Agc1 protein, rat; 0 / Aggrecans; 0 / Antibodies, Monoclonal; 0 / Antigens, CD44; 0 / Antigens, CD95; 0 / Culture Media, Serum-Free; 0 / Disaccharides; 0 / Extracellular Matrix Proteins; 0 / Lectins, C-Type; 0 / Proteoglycans; 0 / Recombinant Fusion Proteins; 9004-61-9 / Hyaluronic Acid; 9007-28-7 / Chondroitin Sulfates; EC 3.2.1.35 / Hyaluronoglucosaminidase; EC 4.2.2.20 / Chondroitin ABC Lyase
  •  go-up   go-down


3. Hamm CA, Xie H, Costa FF, Vanin EF, Seftor EA, Sredni ST, Bischof J, Wang D, Bonaldo MF, Hendrix MJ, Soares MB: Global demethylation of rat chondrosarcoma cells after treatment with 5-aza-2'-deoxycytidine results in increased tumorigenicity. PLoS One; 2009;4(12):e8340
PDF icon [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] Global demethylation of rat chondrosarcoma cells after treatment with 5-aza-2'-deoxycytidine results in increased tumorigenicity.
  • To examine its effect on tumorigenesis, we induced DNA demethylation in a rat model of human chondrosarcoma using 5-aza-2-deoxycytidine.
  • Rat specific pyrosequencing assays were utilized to assess the methylation levels in both LINEs and satellite DNA sequences following 5-aza-2-deoxycytidine treatment.
  • Loss of DNA methylation was accompanied by an increase in invasiveness of the rat chondrosarcoma cells, in vitro, as well as by an increase in tumor growth in vivo.
  • Following withdrawal of 5-aza-2-deoxycytidine, the rat chondrosarcoma cells reestablished global DNA methylation levels that were comparable to that of control cells.
  • Concurrently, invasiveness of the rat chondrosarcoma cells, in vitro, decreased to a level indistinguishable to that of control cells.
  • Taken together these experiments demonstrate that global DNA hypomethylation induced by 5-aza-2-deoxycytidine may promote specific aspects of tumorigenesis in rat chondrosarcoma cells.
  • [MeSH-major] Azacitidine / analogs & derivatives. Chondrosarcoma / genetics. Chondrosarcoma / pathology. DNA Methylation / drug effects
  • [MeSH-minor] Animals. Cell Line, Tumor. Cytokines / genetics. Cytokines / metabolism. Epigenesis, Genetic / drug effects. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Long Interspersed Nucleotide Elements / genetics. Mice. Microsatellite Repeats / genetics. Neoplasm Invasiveness / pathology. Oligonucleotide Array Sequence Analysis. Rats. SOXB1 Transcription Factors / genetics. SOXB1 Transcription Factors / metabolism. Sequence Analysis, DNA. Xenograft Model Antitumor Assays

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • SciCrunch. ArrayExpress: Data: Microarray .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2004 Aug 15;64(16):5527-34 [15313885.001]
  • [Cites] J Biochem. 2004 Mar;135(3):413-20 [15113840.001]
  • [Cites] Cancer Res. 1967 Feb;27(2):362-6 [4225169.001]
  • [Cites] Proc Natl Acad Sci U S A. 1971 May;68(5):877-9 [4252539.001]
  • [Cites] J Virol. 1981 Aug;39(2):519-28 [6268840.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Nov;81(22):6993-7 [6209710.001]
  • [Cites] Cancer Lett. 1987 Dec;38(1-2):137-47 [3690504.001]
  • [Cites] Biochemistry. 1991 Nov 19;30(46):11018-25 [1932026.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 29;94(9):4681-5 [9114051.001]
  • [Cites] J Bone Joint Surg Am. 1999 Mar;81(3):326-38 [10199270.001]
  • [Cites] Biochem Cell Biol. 2005 Jun;83(3):296-321 [15959557.001]
  • [Cites] Oncogene. 2005 Jul 21;24(31):4965-74 [15897897.001]
  • [Cites] Iowa Orthop J. 2005;25:135-40 [16089086.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7086-90 [16103056.001]
  • [Cites] Cell. 2005 Sep 23;122(6):947-56 [16153702.001]
  • [Cites] Anal Biochem. 2005 Oct 1;345(1):102-9 [16139233.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Mar;165(2):135-43 [16527607.001]
  • [Cites] Oncol Rep. 2006 May;15(5):1157-61 [16596179.001]
  • [Cites] Cancer Res. 2006 May 15;66(10):5495-503 [16707479.001]
  • [Cites] J Neurochem. 2006 Dec;99(6):1470-9 [17230638.001]
  • [Cites] Development. 2007 Feb;134(4):635-46 [17215298.001]
  • [Cites] Nat Genet. 2007 Apr;39(4):457-66 [17334365.001]
  • [Cites] Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R96-105 [17613554.001]
  • [Cites] Clin Cancer Res. 2007 Jul 15;13(14):4225-32 [17634552.001]
  • [Cites] Epigenetics. 2006 Jan-Mar;1(1):7-13 [17998812.001]
  • [Cites] Nature. 2008 Jan 10;451(7175):141-6 [18157115.001]
  • [Cites] Gene. 2008 Feb 29;410(1):9-17 [18226475.001]
  • [Cites] Int J Cancer. 2008 Jul 1;123(1):8-13 [18425818.001]
  • [Cites] Stem Cells. 2008 Apr;26(4):920-6 [18203677.001]
  • [Cites] Cancer Sci. 2008 Jun;99(6):1125-30 [18422745.001]
  • [Cites] Breast Cancer Res Treat. 2008 Oct;111(3):411-7 [17968656.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 9;105(36):13556-61 [18768788.001]
  • [Cites] Int J Cancer. 2000 Mar 15;85(6):782-6 [10709095.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Aug 11;274(3):641-8 [10924331.001]
  • [Cites] Mod Pathol. 2000 Oct;13(10):1060-5 [11048798.001]
  • [Cites] Matrix Biol. 2001 Jan;19(8):717-25 [11223331.001]
  • [Cites] J Orthop Res. 2001 Jan;19(1):149-54 [11332612.001]
  • [Cites] APMIS. 2001 Apr;109(4):305-15 [11469503.001]
  • [Cites] Genome Res. 2002 Jun;12(6):996-1006 [12045153.001]
  • [Cites] Oncogene. 2002 Aug 12;21(35):5496-503 [12154410.001]
  • [Cites] Iowa Orthop J. 2002;22:28-34 [12180607.001]
  • [Cites] Virchows Arch. 2002 Sep;441(3):219-30 [12242518.001]
  • [Cites] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886.001]
  • [Cites] Genome Res. 2002 Dec;12(12):1921-8 [12466296.001]
  • [Cites] Science. 2003 Apr 18;300(5618):455 [12702868.001]
  • [Cites] Science. 2003 Apr 18;300(5618):489-92 [12702876.001]
  • [Cites] Nat Genet. 2003 Jun;34(2):157-65 [12730694.001]
  • [Cites] J Cell Biochem. 2003 Aug 1;89(5):992-1004 [12874833.001]
  • [Cites] Pathol Res Pract. 2003;199(6):437-44 [12924447.001]
  • [Cites] Breast Cancer Res. 2003;5(6):R223-30 [14580258.001]
  • [Cites] In Silico Biol. 2003;3(3):235-40 [12954087.001]
  • [Cites] Nucleic Acids Res. 2004;32(3):e38 [14973332.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1635-40 [14604977.001]
  • [Cites] Cancer Lett. 2004 Feb 20;204(2):127-43 [15013213.001]
  • [Cites] Am J Pathol. 2004 Oct;165(4):1087-95 [15466376.001]
  • (PMID = 20019818.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / SOXB1 Transcription Factors; 0 / Sox2 protein, rat; 137497-38-2 / midkine; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2790612
  •  go-up   go-down


Advertisement
4. Perkins GL, Derfoul A, Ast A, Hall DJ: An inhibitor of the stretch-activated cation receptor exerts a potent effect on chondrocyte phenotype. Differentiation; 2005 Jun;73(5):199-211
PDF icon [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.
  • Rat chondrosarcoma (RCS) cells are unusual in that they display a stable chondrocyte phenotype in monolayer culture.
  • This phenotype is reflected by a rounded cellular morphology with few actin-containing stress fibers and production of an extracellular matrix rich in sulfated proteoglycans, with high-level expression of aggrecan, COMP, Sox9, and collagens type II, IX, and XI.
  • Additionally, these cells do not express collagen type I.
  • Here it is shown that in the absence of any mechanical stimulation, treatment of RCS cells with gadolinium chloride (Gd3+), a stretch-activated cation channel blocker, caused the cells to undergo de-differentiation, adopting a flattened fibroblast phenotype with the marked appearance of actin stress fibers and vinculin-containing focal contacts.
  • This change was accompanied by a dramatic reduction in the expression of aggrecan, Sox9, collagen types II, IX, and XI, with a corresponding increase in the expression of collagen type I and fibronectin.
  • [MeSH-major] Chondrocytes / cytology. Chondrocytes / drug effects. Gadolinium / pharmacology. Potassium Channels, Calcium-Activated / antagonists & inhibitors
  • [MeSH-minor] Actins / metabolism. Animals. Biomarkers. Cell Proliferation / drug effects. Collagen Type II / biosynthesis. Collagen Type II / genetics. Growth Inhibitors / pharmacology. High Mobility Group Proteins / biosynthesis. High Mobility Group Proteins / genetics. Humans. Large-Conductance Calcium-Activated Potassium Channels. Mechanotransduction, Cellular / drug effects. Mechanotransduction, Cellular / physiology. Microtubules / drug effects. Promoter Regions, Genetic. RNA, Messenger / metabolism. Rats. SOX9 Transcription Factor. Stress Fibers / drug effects. Transcription Factors / biosynthesis. Transcription Factors / genetics. Tumor Cells, Cultured

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GADOLINIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16026542.001).
  • [ISSN] 0301-4681
  • [Journal-full-title] Differentiation; research in biological diversity
  • [ISO-abbreviation] Differentiation
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Biomarkers; 0 / Collagen Type II; 0 / Growth Inhibitors; 0 / High Mobility Group Proteins; 0 / Large-Conductance Calcium-Activated Potassium Channels; 0 / Potassium Channels, Calcium-Activated; 0 / RNA, Messenger; 0 / SOX9 Transcription Factor; 0 / SOX9 protein, human; 0 / Transcription Factors; AU0V1LM3JT / Gadolinium; P7082WY76D / gadolinium chloride
  •  go-up   go-down


5. Krejci P, Pejchalova K, Wilcox WR: Simple, mammalian cell-based assay for identification of inhibitors of the Erk MAP kinase pathway. Invest New Drugs; 2007 Aug;25(4):391-5
PDF icon [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.
  • In rat chondrosarcoma (RCS) cells, treatment with fibroblast growth factor 2 (FGF2) leads to sustained activation of the Erk pathway, resulting in growth arrest with more than an 80% cell count difference between control and FGF2-treated cells after 72 h of treatment.
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Enzyme Activation. Rats

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 1995 Nov 17;270(46):27711-9 [7499238.001]
  • [Cites] J Clin Oncol. 2004 Nov 15;22(22):4456-62 [15483017.001]
  • [Cites] Nature. 2002 Jun 27;417(6892):949-54 [12068308.001]
  • [Cites] FASEB J. 1995 Jun;9(9):726-35 [7601337.001]
  • [Cites] J Cell Sci. 2005 Nov 1;118(Pt 21):5089-100 [16234329.001]
  • [Cites] J Biomol Screen. 1999;4(2):67-73 [10838414.001]
  • [Cites] J Clin Oncol. 2006 Jun 1;24(16):2505-12 [16636341.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8319-23 [8397401.001]
  • [Cites] Cell. 1994 Jun 17;77(6):841-52 [7911739.001]
  • [Cites] J Clin Oncol. 2005 Aug 10;23 (23 ):5281-93 [16009947.001]
  • [Cites] Exp Cell Res. 2005 Apr 1;304(2):417-31 [15748888.001]
  • [Cites] Bioessays. 2000 Sep;22(9):818-26 [10944584.001]
  • [Cites] Exp Cell Res. 2004 Jul 1;297(1):152-64 [15194433.001]
  • [Cites] Ann Oncol. 2006 May;17(5):866-73 [16500908.001]
  • [Cites] J Biol Chem. 2004 Jan 16;279(3):1747-56 [14593093.001]
  • [Cites] Curr Opin Pharmacol. 2005 Aug;5(4):350-6 [15955734.001]
  • [Cites] J Biol Chem. 2007 Feb 2;282(5):2929-36 [17145761.001]
  • (PMID = 17458503.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 103107-01-3 / Fibroblast Growth Factor 2; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  •  go-up   go-down


6. Clark JC, Dass CR, Choong PF: Development of chondrosarcoma animal models for assessment of adjuvant therapy. ANZ J Surg; 2009 May;79(5):327-36
PDF icon [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] Development of chondrosarcoma animal models for assessment of adjuvant therapy.
  • Chondrosarcoma is a primary cancer of bone causing significant morbidity due to local recurrence and limited treatment options.
  • Relatively few chondrosarcoma animal models have been developed, and the only orthotopic model is technically demanding and has limited clinical relevance.
  • The aim of this review is to assess the features of current animal chondrosarcoma models for the purpose of developing new models in which to test adjuvant chondrosarcoma therapy.
  • The available literature on this topic was identified using the PubMed database, and then analysed for relevance to the human chondrosarcoma disease and feasibility in testing new therapeutic agents.
  • Animal-derived chondrosarcoma models comprise predominantly allograft tumour transplanted into the rat (Swarm rat chondrosarcoma) or the hamster.
  • These types of models are less relevant to the human disease and have been more useful for evaluation of chondrosarcoma growth and histology than in developing novel therapeutic agents.
  • A number of human chondrosarcoma cell lines have been successfully used to generate tumours in this species, including OUMS-27 and HCS-2/A.
  • Although effective in demonstrating anti-tumour effects of a number of agents, the lack of a representative orthotopic model diminishes overall clinical relevance.
  • More clinically relevant models of human chondrosarcoma progression are required either through transgenic mice or orthotopic human xenograft models.
  • [MeSH-major] Bone Neoplasms / therapy. Chondrosarcoma / therapy. Disease Models, Animal
  • [MeSH-minor] Animals. Cell Line, Tumor. Combined Modality Therapy. Cricetinae. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Neoplasms, Experimental / pathology. Neoplasms, Experimental / therapy. Rats. Xenograft Model Antitumor Assays

  • Genetic Alliance. consumer health - Chondrosarcoma.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19566512.001).
  • [ISSN] 1445-2197
  • [Journal-full-title] ANZ journal of surgery
  • [ISO-abbreviation] ANZ J Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Australia
  • [Number-of-references] 69
  •  go-up   go-down


7. Huang W, Chung UI, Kronenberg HM, de Crombrugghe B: The chondrogenic transcription factor Sox9 is a target of signaling by the parathyroid hormone-related peptide in the growth plate of endochondral bones. Proc Natl Acad Sci U S A; 2001 Jan 2;98(1):160-5
PDF icon [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.
  • PTHrP also increased the SOX9-dependent activity of chondrocyte-specific enhancers in the gene for type II collagen (Col2a1) in transient transfection experiments.
  • Consistent with these results, PTHrP also increased Col2a1 mRNA levels in rat chondrosarcoma cells as well as 10T1/2 mesenchymal cells transfected with a PTH/PTHrP receptor expressing plasmid.
  • In contrast in wild-type mouse embryos, previous immunohistochemistry experiments indicated that Sox9 phosphorylated at S(181) was detected almost exclusively in chondrocytes of the prehypertrophic zone.

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • PhosphoSitePlus. gene/protein/disease-specific - PhosphoSitePlus┬« - comprehensive post-translational modification resource .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Exp Cell Res. 2000 May 1;256(2):555-62 [10772827.001]
  • [Cites] J Cell Biol. 1999 May 17;145(4):783-94 [10330406.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jul;84(14):5048-52 [2885845.001]
  • [Cites] Science. 1987 Aug 21;237(4817):893-6 [3616618.001]
  • [Cites] J Biol Chem. 1988 Jun 25;263(18):8557-60 [2837457.001]
  • [Cites] Science. 1991 Nov 15;254(5034):1024-6 [1658941.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2732-6 [1313566.001]
  • [Cites] J Clin Endocrinol Metab. 1992 Aug;75(2):417-23 [1322424.001]
  • [Cites] Genes Dev. 1994 Feb 1;8(3):277-89 [8314082.001]
  • [Cites] J Biol Chem. 1994 Jun 24;269(25):17245-51 [8006032.001]
  • [Cites] Nature. 1994 Dec 8;372(6506):525-30 [7990924.001]
  • [Cites] Cell. 1994 Dec 16;79(6):1111-20 [8001137.001]
  • [Cites] Science. 1995 Apr 7;268(5207):98-100 [7701349.001]
  • [Cites] Nat Genet. 1995 Jan;9(1):15-20 [7704017.001]
  • [Cites] J Med Genet. 1995 Jun;32(6):415-20 [7666392.001]
  • [Cites] Am J Hum Genet. 1995 Nov;57(5):1028-36 [7485151.001]
  • [Cites] Dev Biol. 1995 Nov;172(1):126-38 [7589793.001]
  • [Cites] J Biol Chem. 1995 Nov 17;270(46):27711-9 [7499238.001]
  • [Cites] Hum Genet. 1996 Feb;97(2):186-93 [8566951.001]
  • [Cites] Science. 1996 Aug 2;273(5275):613-22 [8662546.001]
  • [Cites] Science. 1996 Aug 2;273(5275):663-6 [8662561.001]
  • [Cites] N Engl J Med. 1996 Sep 5;335(10):708-14 [8703170.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 17;93(19):10240-5 [8816783.001]
  • [Cites] J Endocrinol. 1996 Sep;150(3):359-68 [8882154.001]
  • [Cites] Endocrinology. 1996 Nov;137(11):5109-18 [8895385.001]
  • [Cites] Hum Mol Genet. 1997 Jan;6(1):91-8 [9002675.001]
  • [Cites] Mol Cell Biol. 1997 Apr;17(4):2336-46 [9121483.001]
  • [Cites] Dev Biol. 1997 Mar 1;183(1):108-21 [9119111.001]
  • [Cites] Nat Genet. 1997 Jun;16(2):174-8 [9171829.001]
  • [Cites] Dev Dyn. 1997 Aug;209(4):377-86 [9264261.001]
  • [Cites] J Bone Miner Res. 1997 Dec;12(12):1993-2004 [9421232.001]
  • [Cites] J Biol Chem. 1998 Jun 12;273(24):14998-5006 [9614107.001]
  • [Cites] EMBO J. 1998 Oct 1;17(19):5718-33 [9755172.001]
  • [Cites] Crit Rev Eukaryot Gene Expr. 1998;8(3-4):297-320 [9807698.001]
  • [Cites] Nat Genet. 1999 May;22(1):85-9 [10319868.001]
  • [Cites] J Bone Miner Res. 1999 May;14(5):757-63 [10320524.001]
  • [Cites] Mol Cell Biol. 2000 Jun;20(11):4149-58 [10805756.001]
  • (PMID = 11120880.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK47038; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIAMS NIH HHS / AR / P01 AR 42919-02; United States / NCI NIH HHS / CA / CA 16672; United States / NIAMS NIH HHS / AR / P01 AR042919; United States / NIAMS NIH HHS / AR / R01 AR42909
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / High Mobility Group Proteins; 0 / Parathyroid Hormone-Related Protein; 0 / Proteins; 0 / RNA, Messenger; 0 / Receptor, Parathyroid Hormone, Type 1; 0 / Receptors, Parathyroid Hormone; 0 / SOX9 Transcription Factor; 0 / Sox9 protein, mouse; 0 / Transcription Factors; 17885-08-4 / Phosphoserine; 9007-34-5 / Collagen; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinase Type II; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Other-IDs] NLM/ PMC14561
  •  go-up   go-down


8. Liu CJ, Prazak L, Fajardo M, Yu S, Tyagi N, Di Cesare PE: Leukemia/lymphoma-related factor, a POZ domain-containing transcriptional repressor, interacts with histone deacetylase-1 and inhibits cartilage oligomeric matrix protein gene expression and chondrogenesis. J Biol Chem; 2004 Nov 5;279(45):47081-91
PDF icon [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.
  • In this study, a yeast one-hybrid screen for proteins that associate with the NRE led to the identification of the leukemia/lymphoma-related factor (LRF), a transcriptional repressor that contains a POZ (poxvirus zinc finger) domain, as an NRE-binding protein.
  • LRF showed dose-dependent inhibition of COMP-specific reporter gene activity, and exogenous overexpression of LRF repressed COMP gene expression in both rat chondrosarcoma cells and bone morphogenetic protein-2-treated C3H10T1/2 progenitor cells.
  • [MeSH-major] Cartilage / metabolism. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Gene Expression Regulation. Histone Deacetylases / metabolism. Transcription Factors / biosynthesis. Transcription Factors / genetics
  • [MeSH-minor] Alcian Blue / pharmacology. Amino Acid Motifs. Animals. Base Sequence. Cell Differentiation. Cell Line. Cell Line, Tumor. Cell Nucleus / metabolism. Chondrosarcoma / embryology. Chondrosarcoma / metabolism. Chromatin / metabolism. Chromatin Immunoprecipitation. Cloning, Molecular. Dose-Response Relationship, Drug. Genes, Reporter. Glutathione Transferase / metabolism. Humans. Hydroxamic Acids / pharmacology. Immunoblotting. Immunoprecipitation. Magnetics. Mice. Mice, Inbred C3H. Molecular Sequence Data. Mutation. Plasmids / metabolism. Promoter Regions, Genetic. Protein Binding. Protein Structure, Tertiary. Rats. Transcription, Genetic. Two-Hybrid System Techniques. Zinc Fingers


9. Raucci A, Laplantine E, Mansukhani A, Basilico C: Activation of the ERK1/2 and p38 mitogen-activated protein kinase pathways mediates fibroblast growth factor-induced growth arrest of chondrocytes. J Biol Chem; 2004 Jan 16;279(3):1747-56
PDF icon [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.
  • Chemical inhibitors of the MEK1/2 or the p38 MAPK pathways applied to rat chondrosarcoma (RCS) chondrocytes significantly prevented FGF-induced growth arrest.
  • [MeSH-minor] Animals. Carrier Proteins / analysis. Cell Division / drug effects. Cells, Cultured. DNA-Binding Proteins / physiology. Epidermal Growth Factor / pharmacology. Membrane Proteins / analysis. Mitogen-Activated Protein Kinase 3. Nerve Growth Factor / pharmacology. Phospholipase C gamma. Rats. Receptor, Epidermal Growth Factor / analysis. STAT1 Transcription Factor. Signal Transduction. Trans-Activators / physiology. Type C Phospholipases / metabolism. p38 Mitogen-Activated Protein Kinases


10. Krejci P, Masri B, Salazar L, Farrington-Rock C, Prats H, Thompson LM, Wilcox WR: Bisindolylmaleimide I suppresses fibroblast growth factor-mediated activation of Erk MAP kinase in chondrocytes by preventing Shp2 association with the Frs2 and Gab1 adaptor proteins. J Biol Chem; 2007 Feb 2;282(5):2929-36
PDF icon [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] Bisindolylmaleimide I suppresses fibroblast growth factor-mediated activation of Erk MAP kinase in chondrocytes by preventing Shp2 association with the Frs2 and Gab1 adaptor proteins.
  • Erk activity in FGF2-treated RCS (rat chondrosarcoma) chondrocytes or human primary chondrocytes was abolished by the protein kinase C inhibitor bisindolylmaleimide I (Bis I).
  • Indeed, Bis I abolished the FGF2-mediated association of Shp2 tyrosine phosphatase with Frs2 and Gab1 adaptor proteins necessary for proper Ras activation.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Chondrocytes / physiology. Extracellular Signal-Regulated MAP Kinases / metabolism. Fibroblast Growth Factors / physiology. Indoles / pharmacology. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Maleimides / pharmacology. Membrane Proteins / metabolism. Protein Tyrosine Phosphatases / antagonists & inhibitors
  • [MeSH-minor] Animals. CHO Cells. Cell Line, Tumor. Cricetinae. Cricetulus. Enzyme Activation / drug effects. Enzyme Inhibitors / pharmacology. Humans. Protein Tyrosine Phosphatase, Non-Receptor Type 11. Rats

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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 .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17145761.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / 5P01-HD22657
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Enzyme Inhibitors; 0 / FRS2 protein, human; 0 / GAB1 protein, human; 0 / Indoles; 0 / Intracellular Signaling Peptides and Proteins; 0 / Maleimides; 0 / Membrane Proteins; 133052-90-1 / bisindolylmaleimide I; 62031-54-3 / Fibroblast Growth Factors; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.3.48 / PTPN11 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Ptpn11 protein, rat
  •  go-up   go-down


11. Miot-Noirault E, Gouin F, Vidal A, Rapp M, Maublant J, Askienazy S, Chezal JM, Heymann D, Redini F, Moins N: First preclinical imaging of primary cartilage neoplasm and its local recurrence using 99mTc-NTP 15-5 radiotracer. J Nucl Med; 2009 Sep;50(9):1541-7
PDF icon [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.
  • This study on a rat model of grade II chondrosarcoma aimed to determine whether the radiotracer N-(triethylammonium)-3-propyl-[15]ane-N5 radiolabeled with (99m)Tc ((99m)Tc-NTP 15-5), which binds to cartilage proteoglycans, has pathophysiologic validity for in vivo imaging of cartilage tumoral tissue.
  • METHODS: We used 2 experimental approaches with the Swarm chondrosarcoma rat model: that is, a primary paratibial location and local recurrence after intralesional curettage. (99m)Tc-NTP 15-5 scintigraphy and (99m)Tc-hydroxymethylenediphosphonate ((99m)Tc-HMDP) scanning were performed at regular intervals during 50 d after tumor implantation in a paratibial location (primary model; n = 12 animals) and after intralesional curettage in a femoral condyle location (recurrence model; n = 9 animals).
  • At study end, animals were sacrificed for histopathologic analysis.
  • CONCLUSION: These experimental results in 2 preclinical models of grade II chondrosarcoma bring forward data in favor of (99m)Tc-NTP 15-5 radiotracer for imaging primary growth of chondrosarcoma and its local recurrence after surgery.
  • [MeSH-major] Bone Neoplasms / radionuclide imaging. Chondrosarcoma / radionuclide imaging. Heterocyclic Compounds, 1-Ring. Neoplasm Recurrence, Local / radionuclide imaging. Quaternary Ammonium Compounds. Technetium Compounds
  • [MeSH-minor] Animals. Drug Evaluation, Preclinical. Male. Radiopharmaceuticals. Rats. Rats, Sprague-Dawley. Reproducibility of Results. Sensitivity and Specificity

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19690026.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Heterocyclic Compounds, 1-Ring; 0 / N-(triethylammonium)-3-propyl(15)ane-N5; 0 / Quaternary Ammonium Compounds; 0 / Radiopharmaceuticals; 0 / Technetium Compounds
  •  go-up   go-down


12. Gouin F, Ory B, R├ędini F, Heymann D: Zoledronic acid slows down rat primary chondrosarcoma development, recurrent tumor progression after intralesional curretage and increases overall survival. Int J Cancer; 2006 Sep 1;119(5):980-4
PDF icon [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] Zoledronic acid slows down rat primary chondrosarcoma development, recurrent tumor progression after intralesional curretage and increases overall survival.
  • Chondrosarcoma is a difficult musculoskeletal tumor to treat.
  • The aim of the present study was to determine the effects of zoledronic acid (ZOL) on chondrosarcoma tumor progression.
  • 100 microg/kg, twice a week) in a rat chondrosarcoma model and in vitro (10(-7)-10(-4) M) on cells derived from this model.
  • The present study demonstrates for the first time that in addition to surgery, the therapy of chondrosarcoma with BPs might be beneficial.
  • Because of these first results, new therapeutic approaches of chondrosarcoma must be considered, mainly for low grade chondrosarcoma when disabling operation is planned and when only intralesional resection can be undertaken.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Bone Density Conservation Agents / pharmacology. Chondrosarcoma / drug therapy. Chondrosarcoma / surgery. Curettage. Diphosphonates / therapeutic use. Imidazoles / therapeutic use. Neoplasm Recurrence, Local / prevention & control
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspase 1 / metabolism. Caspase 3. Caspases / metabolism. Cell Cycle / drug effects. Cell Proliferation / drug effects. Chemotherapy, Adjuvant. Disease Progression. Male. Rats. Rats, Sprague-Dawley. Survival Analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16570273.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; EC 3.4.22.36 / Caspase 1
  •  go-up   go-down






Advertisement