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1. Lohez OD, Reynaud C, Borel F, Andreassen PR, Margolis RL: Arrest of mammalian fibroblasts in G1 in response to actin inhibition is dependent on retinoblastoma pocket proteins but not on p53. J Cell Biol; 2003 Apr 14;161(1):67-77
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  • [Title] Arrest of mammalian fibroblasts in G1 in response to actin inhibition is dependent on retinoblastoma pocket proteins but not on p53.
  • p53 and the retinoblastoma (RB) pocket proteins are central to the control of progression through the G1 phase of the cell cycle.
  • By contrast, pocket protein triple knockout mouse embryo fibroblasts and T antigen-transformed rat embryo fibroblasts lacking both p53 and RB pocket protein function do not arrest in G1.
  • Fibroblasts are very sensitive to actin inhibition in G1 and arrest at drug concentrations that do not affect cell adhesion or cell cleavage.
  • Our results thus establish that RB pocket proteins can be uniquely targeted for tumor chemotherapy.
  • [MeSH-major] Actins / biosynthesis. Cell Cycle Proteins / metabolism. Cytochalasin B / analogs & derivatives. Fibroblasts / metabolism. Retinoblastoma Protein / deficiency. Tumor Suppressor Protein p53 / deficiency
  • [MeSH-minor] Animals. Antigens, Polyomavirus Transforming. Bicyclo Compounds, Heterocyclic / pharmacology. Cell Adhesion / drug effects. Cell Adhesion / genetics. Cell Death / drug effects. Cell Death / genetics. Cell Membrane / drug effects. Cell Membrane / metabolism. Cell Size / drug effects. Cell Size / genetics. Dose-Response Relationship, Drug. Fetus. G1 Phase / drug effects. G1 Phase / genetics. HeLa Cells. Humans. Immunohistochemistry. Mice. Mice, Knockout. Neurofibromin 2 / metabolism. Protein Synthesis Inhibitors / pharmacology. Reaction Time / drug effects. Reaction Time / genetics. Thiazoles / pharmacology. Thiazolidines

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  • [Cites] J Biol Chem. 1996 Aug 23;271(34):20608-16 [8702807.001]
  • [Cites] Mol Biol Cell. 1996 Jan;7(1):101-111 [8741843.001]
  • [Cites] Genes Dev. 1996 Oct 15;10(20):2621-31 [8895663.001]
  • [Cites] Cell. 1997 Feb 7;88(3):323-31 [9039259.001]
  • [Cites] Cancer Res. 1997 Mar 15;57(6):1013-9 [9067261.001]
  • [Cites] J Biol Chem. 1997 Apr 4;272(14):8849-52 [9082999.001]
  • [Cites] EMBO J. 1997 Sep 15;16(18):5592-9 [9312018.001]
  • [Cites] Biochem J. 1997 Aug 15;326 ( Pt 1):61-8 [9337851.001]
  • [Cites] Mol Cell Biol. 1998 Feb;18(2):1055-64 [9448003.001]
  • [Cites] Curr Opin Cell Biol. 1998 Feb;10(1):123-30 [9484604.001]
  • [Cites] Mol Cell Biol. 1998 Mar;18(3):1408-15 [9488456.001]
  • [Cites] J Biol Chem. 1998 Mar 27;273(13):7757-64 [9516485.001]
  • [Cites] Curr Opin Genet Dev. 1998 Feb;8(1):21-7 [9529601.001]
  • [Cites] Curr Opin Cell Biol. 1998 Apr;10(2):220-31 [9561846.001]
  • [Cites] J Cell Biol. 1996 Nov;135(3):689-700 [8909543.001]
  • [Cites] Science. 1996 Dec 6;274(5293):1672-7 [8939849.001]
  • [Cites] J Cell Biol. 1997 Jan 13;136(1):1-4 [9026502.001]
  • [Cites] J Biol Chem. 1999 Oct 29;274(44):31223-8 [10531317.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] Curr Opin Genet Dev. 2000 Feb;10(1):94-9 [10679383.001]
  • [Cites] Exp Cell Res. 2000 Aug 25;259(1):35-53 [10942577.001]
  • [Cites] Nature. 2000 Nov 16;408(6810):307-10 [11099028.001]
  • [Cites] Genes Dev. 2000 Dec 1;14(23):3037-50 [11114892.001]
  • [Cites] Genes Dev. 2000 Dec 1;14(23):3051-64 [11114893.001]
  • [Cites] Curr Opin Genet Dev. 2001 Feb;11(1):48-53 [11163150.001]
  • [Cites] Genes Dev. 2001 Apr 15;15(8):968-80 [11316791.001]
  • [Cites] Curr Opin Cell Biol. 1997 Feb;9(1):93-8 [9013668.001]
  • [Cites] Trends Genet. 1998 Jun;14(6):223-9 [9635405.001]
  • [Cites] Genes Dev. 1998 Aug 1;12(15):2245-62 [9694791.001]
  • [Cites] Oncogene. 1998 Sep 10;17(10):1271-7 [9771970.001]
  • [Cites] Mol Biol Cell. 1998 Nov;9(11):3179-93 [9802905.001]
  • [Cites] Cell. 1999 Apr 2;97(1):53-61 [10199402.001]
  • [Cites] Genes Dev. 1999 Jun 15;13(12):1501-12 [10385618.001]
  • [Cites] Am J Physiol. 1999 Oct;277(4 Pt 1):C652-64 [10516095.001]
  • [Cites] Mol Biol Cell. 2001 May;12(5):1315-28 [11359924.001]
  • [Cites] J Biol Chem. 2001 Sep 14;276(37):34958-65 [11418594.001]
  • [Cites] Cancer Res. 2001 Oct 15;61(20):7660-8 [11606409.001]
  • [Cites] Exp Cell Res. 2001 Nov 1;270(2):277-88 [11640891.001]
  • [Cites] Curr Opin Cell Biol. 2002 Feb;14(1):104-9 [11792551.001]
  • [Cites] Mol Cell Biol. 2002 Feb;22(4):1150-7 [11809806.001]
  • [Cites] J Cell Sci. 2002 Jul 15;115(Pt 14):2829-38 [12082144.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):9819-24 [12119403.001]
  • [Cites] Int J Cancer. 1968 Sep 15;3(5):683-93 [5749478.001]
  • [Cites] Exp Cell Res. 1981 Nov;136(1):63-79 [7197632.001]
  • [Cites] Cell. 1982 Aug;30(1):253-62 [6215122.001]
  • [Cites] Cell Motil Cytoskeleton. 1989;13(3):127-44 [2776221.001]
  • [Cites] Cancer Res. 1991 Dec 1;51(23 Pt 1):6304-11 [1933891.001]
  • [Cites] Bioessays. 1991 Dec;13(12):641-8 [1789781.001]
  • [Cites] J Virol. 1992 May;66(5):2780-91 [1313902.001]
  • [Cites] J Cell Sci. 1992 Jul;102 ( Pt 3):401-16 [1506423.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Sep 1;89(17):8112-6 [1325647.001]
  • [Cites] Genes Dev. 1992 Oct;6(10):1886-98 [1398068.001]
  • [Cites] Mol Cell Biol. 1992 Dec;12(12):5581-92 [1448088.001]
  • [Cites] Cell. 1993 Nov 19;75(4):817-25 [8242752.001]
  • [Cites] Genes Dev. 1994 Jan;8(1):9-22 [8288131.001]
  • [Cites] Cell. 1994 Mar 25;76(6):1013-23 [8137420.001]
  • [Cites] Cell. 1994 Jul 15;78(1):59-66 [8033212.001]
  • [Cites] Genes Dev. 1994 Nov 1;8(21):2540-51 [7958916.001]
  • [Cites] J Cell Biol. 1994 Nov;127(3):789-802 [7962060.001]
  • [Cites] Science. 1995 Mar 3;267(5202):1353-6 [7871434.001]
  • [Cites] Cell. 1995 May 5;81(3):323-30 [7736585.001]
  • [Cites] Genes Dev. 1995 May 15;9(10):1149-63 [7758941.001]
  • [Cites] Chromosoma. 1995 Feb;103(8):517-27 [7621701.001]
  • [Cites] Eur J Cell Biol. 1995 Jun;67(2):145-57 [7545109.001]
  • [Cites] J Cell Biol. 1995 Oct;131(1):191-205 [7559776.001]
  • [Cites] Nat Med. 1996 Jan;2(1):72-9 [8564846.001]
  • [Cites] Genes Dev. 1996 Apr 15;10(8):934-47 [8608941.001]
  • (PMID = 12682090.001).
  • [ISSN] 0021-9525
  • [Journal-full-title] The Journal of cell biology
  • [ISO-abbreviation] J. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Antigens, Polyomavirus Transforming; 0 / Bicyclo Compounds, Heterocyclic; 0 / Cell Cycle Proteins; 0 / Neurofibromin 2; 0 / Protein Synthesis Inhibitors; 0 / Retinoblastoma Protein; 0 / Thiazoles; 0 / Thiazolidines; 0 / Tumor Suppressor Protein p53; 39156-67-7 / dihydrocytochalasin B; 3CHI920QS7 / Cytochalasin B; 76343-93-6 / latrunculin A
  • [Other-IDs] NLM/ PMC2172876
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2. Dalgard CL, Van Quill KR, O'Brien JM: Evaluation of the in vitro and in vivo antitumor activity of histone deacetylase inhibitors for the therapy of retinoblastoma. Clin Cancer Res; 2008 May 15;14(10):3113-23
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  • [Title] Evaluation of the in vitro and in vivo antitumor activity of histone deacetylase inhibitors for the therapy of retinoblastoma.
  • PURPOSE: To evaluate the potential utility of histone deacetylase inhibitors (HDACi) for treatment of retinoblastoma (RB).
  • Effects of TSA and MS-275 were also assessed in combination with standard therapeutic agents for RB.
  • Retinal tissue morphology was evaluated in mice after local administration of MS-275.
  • Therapeutic effects of MS-275 were determined in transgenic mouse and rat ocular xenograft models of RB after i.p. injection of 20 mg/kg every other day for 21 or 13 days, respectively.
  • Intraocular administration of 1 microL of 10 micromol/L MS-275 did not alter ocular tissue morphology.
  • Increased acetyl-histone levels confirmed MS-275 delivery to retinal tissue after systemic administration.
  • MS-275 significantly reduced tumor burden in both mouse and rat models of RB.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Animals. Annexin A5 / drug effects. Apoptosis / drug effects. Benzamides / pharmacology. Blotting, Western. Caspase 3 / drug effects. Caspase 7 / drug effects. Cell Proliferation / drug effects. Cell Survival / drug effects. Flow Cytometry. Humans. Hydroxamic Acids / pharmacology. In Vitro Techniques. Mice. Mice, Transgenic. Polymerase Chain Reaction. Pyridines / pharmacology. Rats. Reactive Oxygen Species / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 18483379.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY02162; United States / NEI NIH HHS / EY / R01 EY13812
  • [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 / Annexin A5; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Pyridines; 0 / Reactive Oxygen Species; 1ZNY4FKK9H / entinostat; 3X2S926L3Z / trichostatin A; 58IFB293JI / vorinostat; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7
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3. Davis ST, Benson BG, Bramson HN, Chapman DE, Dickerson SH, Dold KM, Eberwein DJ, Edelstein M, Frye SV, Gampe Jr RT, Griffin RJ, Harris PA, Hassell AM, Holmes WD, Hunter RN, Knick VB, Lackey K, Lovejoy B, Luzzio MJ, Murray D, Parker P, Rocque WJ, Shewchuk L, Veal JM, Walker DH, Kuyper LF: Prevention of chemotherapy-induced alopecia in rats by CDK inhibitors. Science; 2001 Jan 5;291(5501):134-7
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  • [Title] Prevention of chemotherapy-induced alopecia in rats by CDK inhibitors.
  • Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, may represent a therapeutic strategy for prevention of chemotherapy-induced alopecia (CIA) by arresting the cell cycle and reducing the sensitivity of the epithelium to many cell cycle-active antitumor agents.
  • Potent small-molecule inhibitors of CDK2 were developed using structure-based methods.
  • Topical application of these compounds in a neonatal rat model of CIA reduced hair loss at the site of application in 33 to 50% of the animals.
  • [MeSH-major] Alopecia / chemically induced. Alopecia / prevention & control. Antineoplastic Agents / toxicity. CDC2-CDC28 Kinases. Cyclin-Dependent Kinases / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. Hair Follicle / drug effects. Indoles / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Sulfonamides / pharmacology
  • [MeSH-minor] Animals. Animals, Newborn. Antineoplastic Combined Chemotherapy Protocols / toxicity. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line. Cyclin-Dependent Kinase 2. Cyclophosphamide / toxicity. Cytoprotection / drug effects. DNA / biosynthesis. Doxorubicin / toxicity. Drug Design. Epithelium / drug effects. Etoposide / toxicity. Humans. Mice. Mice, SCID. Phosphorylation. Rats. Retinoblastoma Protein / metabolism. Scalp / transplantation. Transplantation, Heterologous

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  • [CommentIn] Science. 2001 Jan 5;291(5501):25-6 [11191992.001]
  • [RetractionIn] Davis ST, Benson BG, Bramson HN, Chapman DE, Dickerson SH, Dold KM, Eberwein DJ, Edelstein M, Frye SV, Gampe RT Jr, Grifffen RJ, Harris PA, Hassell AM, Holmes WD, Hunter RN, Knick VB, Lackey K, Lovejoy B, Luzzio MJ, Murray D, Parker P, Rocque WJ, Shewchuk-Chapman L, Veal JM, Walker DH, Kuyper LF. Science. 2002 Dec 20;298(5602):2327 [12526115.001]
  • (PMID = 11141566.001).
  • [ISSN] 0036-8075
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 1FVT/ 1FVV
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Retracted Publication
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / 2-(4-((6,7-dihydro-7-oxo-5H-thiazolo(5,4-e)indol-8-ylidene)amino)phenylsulfamido)pyridine; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Indoles; 0 / Retinoblastoma Protein; 0 / Sulfonamides; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9007-49-2 / DNA; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 2.7.11.22 / CDK2 protein, human; 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
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4. Lim Y, Kim TJ, Jin YR, Kim DW, Kwon JS, Son JH, Jung JC, Avery MA, Son DJ, Hong JT, Yun YP: Epothilone B inhibits neointimal formation after rat carotid injury through the regulation of cell cycle-related proteins. J Pharmacol Exp Ther; 2007 May;321(2):648-55
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  • [Title] Epothilone B inhibits neointimal formation after rat carotid injury through the regulation of cell cycle-related proteins.
  • Therefore, we established an in vivo rat carotid injury model and examined the potential effects of epothilone B on cardiovascular disease.
  • In addition, we also showed that epothilone B significantly inhibited 5% fetal bovine serum (FBS)- and 50 ng/ml platelet-derived growth factor (PDGF)-BB-induced proliferation and cell cycle progression in rat aortic VSMCs.
  • However, epothilone B treatment caused a significant decrease in the level of cyclin-dependent protein kinase (CDK) 2, whereas it caused no change in the levels of cyclin E and down-regulated the phosphorylation of retinoblastoma, which plays a critical role in cell cycle regulation.
  • [MeSH-major] Carotid Artery Injuries / drug therapy. Cyclin-Dependent Kinase 2 / antagonists & inhibitors. Epothilones / pharmacology. Muscle, Smooth, Vascular / drug effects. Tunica Intima / drug effects
  • [MeSH-minor] Animals. Carotid Arteries / pathology. Cell Cycle / drug effects. Cell Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor p27 / biosynthesis. Extracellular Signal-Regulated MAP Kinases / metabolism. Male. Phospholipase C gamma / physiology. Phosphorylation. Rats. Rats, Sprague-Dawley. Receptor, Platelet-Derived Growth Factor beta / metabolism. Retinoblastoma Protein / metabolism

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  • (PMID = 17289837.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn1b protein, rat; 0 / Epothilones; 0 / Retinoblastoma Protein; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.11.22 / Cdk2 protein, rat; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.4.3 / Phospholipase C gamma; UEC0H0URSE / epothilone B
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5. Nassr M, Wang X, Mitra S, Freeman-Anderson NE, Patil R, Yates CR, Miller DD, Geisert EE: Treating retinoblastoma in tissue culture and in a rat model with a novel isoquinoline derivative. Invest Ophthalmol Vis Sci; 2010 Jul;51(7):3813-9
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  • [Title] Treating retinoblastoma in tissue culture and in a rat model with a novel isoquinoline derivative.
  • PURPOSE. To investigate the effectiveness of a novel isoquinoline derivative, EDL-155, in killing retinoblastoma in vitro and in vivo.
  • METHODS. Dose-response curves were generated in which Y79 retinoblastoma cells tagged with luciferase (Y79-Luc) were treated with serial concentrations of EDL-155.
  • To evaluate the efficacy of EDL-155 in vivo, Y79-Luc retinoblastoma cells were injected into the vitreous cavity of newborn rats, followed by periocular injections of EDL-155 (20 mg/kg/day) or an equivalent dosage of saline.
  • RESULTS. EDL-155 appeared to destroy the retinoblastoma cells in vitro with an EC(50) of 9.1 micriM.
  • EDL-155-treated retinoblastoma cells displayed a lack of viable mitochondria and the presence of autophagosomes wrapped in the characteristic double membranes.
  • Acridine orange staining of EDL-155-treated retinoblastoma cells demonstrated the accumulation of vacuoles, and the immunoblots displayed a shift in molecular weight of LC-3, indicative of incorporation into autophagosome vesicles.
  • In the retinoblastoma animal model, four doses of EDL-155 were delivered over 4 days, which was sufficient to see a significant decrease (P = 0.01) in viable intraocular tumors.
  • CONCLUSIONS. EDL-155 appears to eliminate retinoblastoma cells by disrupting mitochondria and inducing autophagy.
  • Local delivery of EDL-155 may be an effective therapy for some types of ocular cancers.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy. Tetrahydroisoquinolines / therapeutic use
  • [MeSH-minor] Animals. Animals, Newborn. Autophagy. Disease Models, Animal. Dose-Response Relationship, Drug. Humans. Immunoblotting. Injections. Microscopy, Confocal. Mitochondria / ultrastructure. Neoplasm Transplantation. Rats. Rats, Sprague-Dawley. Tumor Cells, Cultured

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  • (PMID = 20570997.001).
  • [ISSN] 1552-5783
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / EDL-155; 0 / Tetrahydroisoquinolines
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6. Narayanan BA, Condon MS, Bosland MC, Narayanan NK, Reddy BS: Suppression of N-methyl-N-nitrosourea/testosterone-induced rat prostate cancer growth by celecoxib: effects on cyclooxygenase-2, cell cycle regulation, and apoptosis mechanism(s). Clin Cancer Res; 2003 Aug 15;9(9):3503-13
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  • [Title] Suppression of N-methyl-N-nitrosourea/testosterone-induced rat prostate cancer growth by celecoxib: effects on cyclooxygenase-2, cell cycle regulation, and apoptosis mechanism(s).
  • EXPERIMENTAL DESIGN: To determine the level of COX-2 expression, we used paraffin-embedded tumor tissue sections and cancer cells (I-26) derived from N-methyl-N-nitroso-urea/testosterone-induced rat dorsolateral prostate, and we used immunofluorescence detection and Western blot analyses with anti-COX-2 monoclonal antibodies.
  • these cells from chemically induced rat prostate tumors express COX-2 at both the mRNA and the protein level; (b).
  • celecoxib induces cell cycle arrest at the G(1)-S phase transition point and modifies cell cycle regulatory proteins such as cyclin D1, retinoblastoma (Rb), and phosphorylated Rb, cyclin E, p27(KIP1), and p21(WAF1/CIP1).
  • [MeSH-major] Apoptosis. Isoenzymes / biosynthesis. Prostaglandin-Endoperoxide Synthases / biosynthesis. Prostatic Neoplasms / chemically induced. Prostatic Neoplasms / drug therapy. Sulfonamides / therapeutic use
  • [MeSH-minor] Alkylating Agents. Animals. Antineoplastic Agents / therapeutic use. Blotting, Western. Bromodeoxyuridine / pharmacology. Carcinogens. Celecoxib. Cell Cycle. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Survival. Coloring Agents / pharmacology. Cyclin D. Cyclin E / metabolism. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinase Inhibitor p27. Cyclins / metabolism. Cyclooxygenase 2. DNA / metabolism. Dose-Response Relationship, Drug. Down-Regulation. Flow Cytometry. Immunohistochemistry. Male. Methylnitrosourea. Microscopy, Fluorescence. Models, Biological. Pyrazoles. RNA, Messenger / metabolism. Rats. Retinoblastoma Protein / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tumor Suppressor Proteins / metabolism

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  • [RetractionIn] Clin Cancer Res. 2016 Jan 1;22(1):270 [26728412.001]
  • (PMID = 12960143.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / PHS HHS / / 01A015; United States / NCI NIH HHS / CA / CA-17613
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Antineoplastic Agents; 0 / Carcinogens; 0 / Cdkn1a protein, rat; 0 / Cdkn1b protein, rat; 0 / Cell Cycle Proteins; 0 / Coloring Agents; 0 / Cyclin D; 0 / Cyclin E; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Isoenzymes; 0 / Pyrazoles; 0 / RNA, Messenger; 0 / Retinoblastoma Protein; 0 / Sulfonamides; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 684-93-5 / Methylnitrosourea; 9007-49-2 / DNA; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; G34N38R2N1 / Bromodeoxyuridine; JCX84Q7J1L / Celecoxib
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7. Mendoza N, Fong S, Marsters J, Koeppen H, Schwall R, Wickramasinghe D: Selective cyclin-dependent kinase 2/cyclin A antagonists that differ from ATP site inhibitors block tumor growth. Cancer Res; 2003 Mar 1;63(5):1020-4
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  • A central function of the tumor suppressor retinoblastoma (Rb) is its ability to repress E2F transcriptional activity.
  • [MeSH-major] Antineoplastic Agents / pharmacology. CDC2-CDC28 Kinases. Cyclin A / antagonists & inhibitors. Cyclin-Dependent Kinases / antagonists & inhibitors. Neoplasms, Experimental / drug therapy. Oligopeptides / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors
  • [MeSH-minor] 3T3 Cells. Adenosine Triphosphate / antagonists & inhibitors. Adenosine Triphosphate / metabolism. Amino Acid Sequence. Animals. Apoptosis / drug effects. Apoptosis / physiology. Binding Sites. Cell Division / drug effects. Cell Division / physiology. Cell Line, Transformed. Cyclin D. Cyclin-Dependent Kinase 2. Cyclins / physiology. Female. Genes, erbB-2 / genetics. Humans. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / enzymology. Mammary Neoplasms, Experimental / pathology. Mice. Mice, Inbred BALB C. Mice, Transgenic. Rats. Retinoblastoma Protein / physiology. Signal Transduction / physiology

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  • (PMID = 12615717.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclin A; 0 / Cyclin D; 0 / Cyclins; 0 / Oligopeptides; 0 / Retinoblastoma Protein; 8L70Q75FXE / Adenosine Triphosphate; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 2.7.11.22 / CDK2 protein, human; 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
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8. Blaschke F, Leppanen O, Takata Y, Caglayan E, Liu J, Fishbein MC, Kappert K, Nakayama KI, Collins AR, Fleck E, Hsueh WA, Law RE, Bruemmer D: Liver X receptor agonists suppress vascular smooth muscle cell proliferation and inhibit neointima formation in balloon-injured rat carotid arteries. Circ Res; 2004 Dec 10;95(12):e110-23
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  • [Title] Liver X receptor agonists suppress vascular smooth muscle cell proliferation and inhibit neointima formation in balloon-injured rat carotid arteries.
  • Inhibition of G1 exit by LXR ligands was accompanied by a dose-dependent inhibition of retinoblastoma protein (Rb) phosphorylation, which functions as the key switch for G1-->S cell cycle progression.
  • Finally, neointima formation in a model of rat carotid artery balloon injury was significantly attenuated after treatment with the LXR ligand T1317 compared with vehicle-treated animals.
  • These data demonstrate that LXR ligands inhibit VSMC proliferation and neointima formation after balloon injury and suggest that LXR ligands may constitute a novel therapy for proliferative vascular diseases.
  • [MeSH-minor] Animals. Anticholesteremic Agents / pharmacology. Benzoates / pharmacology. Benzylamines / pharmacology. Cell Cycle / drug effects. Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Division / drug effects. Cells, Cultured / drug effects. Cells, Cultured / metabolism. Coronary Vessels / cytology. Cyclin-Dependent Kinase Inhibitor p27. G1 Phase / drug effects. Gene Expression Regulation / drug effects. Humans. Hydrocarbons, Fluorinated. Hyperplasia. Insulin / pharmacology. Ligands. Minichromosome Maintenance Complex Component 6. Myocytes, Smooth Muscle / drug effects. Myocytes, Smooth Muscle / metabolism. Orphan Nuclear Receptors. Phosphorylation / drug effects. Platelet-Derived Growth Factor / pharmacology. Protein Processing, Post-Translational / drug effects. Rats. Rats, Sprague-Dawley. Recombinant Fusion Proteins / physiology. Retinoblastoma Protein / metabolism. S-Phase Kinase-Associated Proteins / biosynthesis. S-Phase Kinase-Associated Proteins / genetics. S-Phase Kinase-Associated Proteins / physiology. Sulfonamides. Transfection. Tumor Suppressor Proteins / metabolism

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  • (PMID = 15539633.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL 58328
  • [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 / Anticholesteremic Agents; 0 / Benzoates; 0 / Benzylamines; 0 / Cdkn1b protein, rat; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / GW 3965; 0 / Hydrocarbons, Fluorinated; 0 / Insulin; 0 / Ligands; 0 / Orphan Nuclear Receptors; 0 / Platelet-Derived Growth Factor; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Recombinant Fusion Proteins; 0 / Retinoblastoma Protein; 0 / S-Phase Kinase-Associated Proteins; 0 / Sulfonamides; 0 / TO-901317; 0 / Tumor Suppressor Proteins; 0 / liver X receptor; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 3.6.4.12 / MCM6 protein, human; EC 3.6.4.12 / Minichromosome Maintenance Complex Component 6
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9. Chang YC, Chou FP, Huang HP, Hsu JD, Wang CJ: Inhibition of cell cycle progression by penta-acetyl geniposide in rat C6 glioma cells. Toxicol Appl Pharmacol; 2004 Jul 1;198(1):11-20
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  • [Title] Inhibition of cell cycle progression by penta-acetyl geniposide in rat C6 glioma cells.
  • Penta-acetyl geniposide, (Ac)5-GP, the acetylated compound of geniposide, is able to inhibit the growth of rat C6 glioma cells in culture and in the bearing rats.
  • Further immunoprecipitation studies found that, in response to the treatment, the formation of cyclin D1/cdk 4 complex declined, preventing the phosphorylation of retinoblastoma (Rb) and the subsequent dissociation of Rb/E2F complex.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Brain Neoplasms / drug therapy. Cell Cycle / drug effects. Drugs, Chinese Herbal / pharmacology. Glioma / drug therapy. Glucosides / pharmacology. Iridoids / pharmacology. Pyrans / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / metabolism. Cyclins / metabolism. Iridoid Glucosides. Phosphorylation. Plant Extracts / chemistry. Rats. Retinoblastoma Protein / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15207644.001).
  • [ISSN] 0041-008X
  • [Journal-full-title] Toxicology and applied pharmacology
  • [ISO-abbreviation] Toxicol. Appl. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cdkn1a protein, rat; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Drugs, Chinese Herbal; 0 / Glucosides; 0 / Iridoid Glucosides; 0 / Iridoids; 0 / Plant Extracts; 0 / Pyrans; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; 49776-64-9 / pentaacetyl geniposide; EC 2.7.11.22 / Cyclin-Dependent Kinases
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10. Ramagiri S, Ma F, Kosanam H, Wang X, Patil R, Miller DD, Geisert E, Yates CR: Fast and sensitive liquid chromatography/electrospray mass spectrometry method to study ocular penetration of EDL-155, a novel antitumor agent for retinoblastoma in rats. J Mass Spectrom; 2009 May;44(5):786-93
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  • [Title] Fast and sensitive liquid chromatography/electrospray mass spectrometry method to study ocular penetration of EDL-155, a novel antitumor agent for retinoblastoma in rats.
  • Our group has used the tetrahydroisoquinoline derivative EDL-155 to treat glioblastoma in animal models and it is currently being evaluated in the treatment of ocular cancers.
  • Animals were sacrificed at specified times (5, 60, 120, 240 and 360 min) and plasma and vitreous humor samples were obtained.
  • EDL-155 was isolated by protein precipitation and the extracts were analyzed by reversed-phase high-pressure liquid chromatography (HPLC) with MS/MS detection.
  • The chromatographic run time was 3.5 min per injection.
  • The method was validated for selectivity, linearity, accuracy and precision in rat vitreous humor and partially validated for accuracy and precision in rat plasma.
  • High local concentrations coupled with minimal systemic exposure supports further testing of EDL-155 as localized therapy for intraocular cancers.
  • [MeSH-minor] Animals. Drug Stability. Linear Models. Rats. Rats, Wistar. Reference Standards. Reproducibility of Results. Retinoblastoma / drug therapy. Sensitivity and Specificity

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  • [Copyright] 2009 John Wiley & Sons, Ltd.
  • (PMID = 19160451.001).
  • [ISSN] 1096-9888
  • [Journal-full-title] Journal of mass spectrometry : JMS
  • [ISO-abbreviation] J Mass Spectrom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / EDL-155; 0 / Tetrahydroisoquinolines
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11. Jori FP, Galderisi U, Piegari E, Cipollaro M, Cascino A, Peluso G, Cotrufo R, Giordano A, Melone MA: EGF-responsive rat neural stem cells: molecular follow-up of neuron and astrocyte differentiation in vitro. J Cell Physiol; 2003 May;195(2):220-33
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  • [Title] EGF-responsive rat neural stem cells: molecular follow-up of neuron and astrocyte differentiation in vitro.
  • Neural stem cells (NSCs) could be very useful for the "cell therapy" treatment of neurological disorders.
  • We carried out a molecular and immunocytochemical analysis of EGF-responsive NSCs obtained from rat pups.
  • [MeSH-major] Cell Culture Techniques / methods. Cell Differentiation / drug effects. Cell Lineage / drug effects. Cell Separation / methods. Epidermal Growth Factor / pharmacology. Nerve Tissue Proteins. Proteins. Stem Cell Transplantation / methods. Stem Cells / metabolism
  • [MeSH-minor] Animals. Animals, Newborn. Apoptosis / drug effects. Apoptosis / physiology. Astrocytes / cytology. Astrocytes / drug effects. Astrocytes / metabolism. Blood Proteins / drug effects. Blood Proteins / genetics. Blood Proteins / metabolism. Cell Cycle Proteins / drug effects. Cell Cycle Proteins / metabolism. Cells, Cultured. Cyclin-Dependent Kinase Inhibitor p27. Gene Expression Regulation / drug effects. Gene Expression Regulation / physiology. Glial Fibrillary Acidic Protein / drug effects. Glial Fibrillary Acidic Protein / genetics. Glial Fibrillary Acidic Protein / metabolism. Immunohistochemistry. Intermediate Filament Proteins / drug effects. Intermediate Filament Proteins / genetics. Intermediate Filament Proteins / metabolism. Nestin. Neurons / cytology. Neurons / drug effects. Neurons / metabolism. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Rats. Retinoblastoma Protein / drug effects. Retinoblastoma Protein / genetics. Retinoblastoma Protein / metabolism. Retinoblastoma-Like Protein p130. Tumor Suppressor Protein p53 / drug effects. Tumor Suppressor Protein p53 / metabolism. Tumor Suppressor Proteins / drug effects. Tumor Suppressor Proteins / metabolism

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12652649.001).
  • [ISSN] 0021-9541
  • [Journal-full-title] Journal of cellular physiology
  • [ISO-abbreviation] J. Cell. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Proteins; 0 / Cdkn1b protein, rat; 0 / Cell Cycle Proteins; 0 / Glial Fibrillary Acidic Protein; 0 / Intermediate Filament Proteins; 0 / Nerve Tissue Proteins; 0 / Nes protein, rat; 0 / Nestin; 0 / Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Retinoblastoma Protein; 0 / Retinoblastoma-Like Protein p130; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 62229-50-9 / Epidermal Growth Factor
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12. Lim HJ, Lee S, Park JH, Lee KS, Choi HE, Chung KS, Lee HH, Park HY: PPAR delta agonist L-165041 inhibits rat vascular smooth muscle cell proliferation and migration via inhibition of cell cycle. Atherosclerosis; 2009 Feb;202(2):446-54
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  • [Title] PPAR delta agonist L-165041 inhibits rat vascular smooth muscle cell proliferation and migration via inhibition of cell cycle.
  • Here, we investigated the effect of L-165041, a selective ligand for PPAR delta, on PDGF-induced rat VSMC proliferation.
  • Our data show that L-165041 inhibited rat VSMC proliferation in a dose dependent manner by blocking G(1) to S phase progression and repressing the phosphorylation of retinoblastoma protein (Rb).
  • In conclusion, our results suggest that PPAR delta ligand L-165041 can be a therapeutic agent to control pathologic cardiovascular conditions such as restenosis and atherosclerosis.
  • [MeSH-major] Carotid Artery Injuries / drug therapy. Muscle, Smooth, Vascular / cytology. Muscle, Smooth, Vascular / drug effects. PPAR delta / agonists. Phenoxyacetates / pharmacology
  • [MeSH-minor] Angioplasty, Balloon / adverse effects. Animals. Aorta, Thoracic / cytology. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Division / drug effects. Cell Division / physiology. Cell Movement / drug effects. Cell Movement / physiology. Cells, Cultured. Disease Models, Animal. Extracellular Signal-Regulated MAP Kinases / metabolism. Phosphorylation / drug effects. Rats. Rats, Sprague-Dawley. src-Family Kinases / metabolism

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  • (PMID = 18585719.001).
  • [ISSN] 1879-1484
  • [Journal-full-title] Atherosclerosis
  • [ISO-abbreviation] Atherosclerosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / 4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid; 0 / PPAR delta; 0 / Phenoxyacetates; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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13. Kim TJ, Lim Y, Kim DW, Kwon JS, Son JH, Jin YR, Son DJ, Jung JC, Avery MA, Hong JT, Yun YP: Epothilone D, a microtubule-stabilizing compound, inhibits neointimal hyperplasia after rat carotid artery injury by cell cycle arrest via regulation of G1-checkpoint proteins. Vascul Pharmacol; 2007 Oct;47(4):229-37
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  • [Title] Epothilone D, a microtubule-stabilizing compound, inhibits neointimal hyperplasia after rat carotid artery injury by cell cycle arrest via regulation of G1-checkpoint proteins.
  • The aim of the present study was to investigate the effects of Epo-D on neointimal hyperplasia using an in vivo rat carotid artery injury model.
  • We demonstrated that local Epo-D treatment significantly reduced neointimal hyperplasia after in vivo rat carotid artery injury, and Epo-D potently inhibited DNA synthesis, cell cycle progression and cell proliferation after FBS- and PDGF-BB-stimulation; PDGF-BB has been identified as the most potent growth factor for stimulating the proliferation of activated rat aortic smooth muscle cells (RASMCs).
  • To clarify the specific effects of Epo-D on cell cycle machinery, we examined its effects on cyclin-dependent kinase (CDK)2, CDK4, cyclin E, p27, and retinoblastoma (Rb) proteins as cell cycle-related proteins in cellular lysates from PDGF-BB-stimulated RASMCs.
  • Epo-D treatment significantly decreased the level of CDK2 protein, but did not change the levels of CDK4 and cyclin E proteins.
  • These findings suggest that Epo-D may regulate the cell cycle G1-checkpoint proteins as its major molecular mechanism for inhibiting neointimal hyperplasia after in vivo rat carotid artery injury.
  • [MeSH-major] Carotid Artery Injuries / drug therapy. Epothilones / pharmacology. G1 Phase / drug effects. Muscle, Smooth, Vascular / drug effects. Tunica Intima / drug effects

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  • (PMID = 17706465.001).
  • [ISSN] 1537-1891
  • [Journal-full-title] Vascular pharmacology
  • [ISO-abbreviation] Vascul. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epothilones; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / desoxyepothilone B; 0 / platelet-derived growth factor BB; EC 2.7.11.22 / Cdk2 protein, rat; EC 2.7.11.22 / Cdk4 protein, rat; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; VC2W18DGKR / Thymidine
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14. DePinto W, Chu XJ, Yin X, Smith M, Packman K, Goelzer P, Lovey A, Chen Y, Qian H, Hamid R, Xiang Q, Tovar C, Blain R, Nevins T, Higgins B, Luistro L, Kolinsky K, Felix B, Hussain S, Heimbrook D: In vitro and in vivo activity of R547: a potent and selective cyclin-dependent kinase inhibitor currently in phase I clinical trials. Mol Cancer Ther; 2006 Nov;5(11):2644-58
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  • In vitro, R547 effectively inhibited the proliferation of tumor cell lines independent of multidrug resistant status, histologic type, retinoblastoma protein, or p53 status, with IC(50)s </= 0.60 mumol/L.
  • R547 reduced phosphorylation of the cellular retinoblastoma protein at specific CDK phosphorylation sites at the same concentrations that induced cell cycle arrest, suggesting a potential pharmacodynamic marker for clinical use.
  • In vivo, R547 showed antitumor activity in all of the models tested to date, including six human tumor xenografts and an orthotopic syngeneic rat model.
  • R547 was efficacious with daily oral dosing as well as with once weekly i.v. dosing in established human tumor models and at the targeted efficacious exposures inhibited phosphorylation of the retinoblastoma protein in the tumors.
  • The selective kinase inhibition profile and the preclinical antitumor activity of R547 suggest that it may be promising for development for use in the treatment of solid tumors.
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Cell Proliferation / drug effects. Clinical Trials, Phase I as Topic. Female. G1 Phase / drug effects. G2 Phase / drug effects. Genes, MDR / drug effects. Humans. Mice. Mice, Nude. Phosphorylation / drug effects. Rats. Rats, Inbred F344. Retinoblastoma / drug therapy. Retinoblastoma / metabolism. Tumor Suppressor Protein p53 / metabolism


15. Miller M, Chen S, Woodliff J, Kansra S: Curcumin (diferuloylmethane) inhibits cell proliferation, induces apoptosis, and decreases hormone levels and secretion in pituitary tumor cells. Endocrinology; 2008 Aug;149(8):4158-67
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  • Dopamine D2 receptor (D2R) agonists, such as bromocriptine are the first line of therapy; however, drug intolerance/resistance to D2R agonists exists.
  • Apart from D2R agonists, there is no established medical therapy for prolactinomas; therefore, identifying novel therapeutics is warranted.
  • Using rat lactotroph cell lines, GH3 and MMQ cells, we report that curcumin had a robust dose and time-dependent inhibitory effect on GH3 and MMQ cell proliferation.
  • The growth-inhibitory effect of curcumin was accompanied by decreased expression of cyclin D3 and ser 780 phosphorylation of retinoblastoma protein.
  • Taken together we demonstrate that curcumin inhibits pituitary tumor cell proliferation, induces apoptosis, and decreases hormone production and release, and thus, we propose developing curcumin as a novel therapeutic tool in the management of prolactinomas.
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Curcumin / pharmacology. Pituitary Hormones / secretion. Pituitary Neoplasms / secretion. Prolactinoma / secretion
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Bromocriptine / pharmacology. Clone Cells / drug effects. Cyclin D3. Cyclins / metabolism. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Drug Synergism. Phosphorylation / drug effects. Rats. Retinoblastoma Protein / metabolism. Time Factors. Tumor Cells, Cultured

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  • [Cites] Physiol Rev. 2000 Oct;80(4):1523-631 [11015620.001]
  • [Cites] Mol Cell Biol Res Commun. 2000 Jun;3(6):352-9 [11032757.001]
  • [Cites] Mol Endocrinol. 2000 Nov;14(11):1872-81 [11075818.001]
  • [Cites] Anticancer Res. 2001 Jul-Aug;21(4B):2895-900 [11712783.001]
  • [Cites] Endocr Rev. 2001 Dec;22(6):724-63 [11739329.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14530-5 [12391292.001]
  • [Cites] Oncogene. 2002 Dec 12;21(57):8852-61 [12483537.001]
  • [Cites] Blood. 2003 Feb 1;101(3):1053-62 [12393461.001]
  • [Cites] J Bone Miner Metab. 2003;21(2):91-7 [12601573.001]
  • [Cites] Psychoneuroendocrinology. 2003 Apr;28 Suppl 2:97-108 [12650684.001]
  • [Cites] Mol Cancer Ther. 2006 Oct;5(10):2563-71 [17041101.001]
  • [Cites] Mol Endocrinol. 2006 Nov;20(11):2965-75 [16857743.001]
  • [Cites] Pituitary. 2006;9(3):203-9 [17001464.001]
  • [Cites] Biochem Pharmacol. 2007 Apr 1;73(7):1024-32 [17240359.001]
  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):1022-30 [17363495.001]
  • [Cites] J Neurooncol. 2007 Jun;83(2):153-62 [17216555.001]
  • [Cites] Cell. 2007 Sep 7;130(5):769-74 [17803898.001]
  • [Cites] Cell Cycle. 2007 Dec 1;6(23):2953-61 [18156803.001]
  • [Cites] FEBS Lett. 2003 Jul 3;546(1):59-64 [12829237.001]
  • [Cites] Pituitary. 2003;6(1):19-27 [14674720.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Aug 20;321(2):337-44 [15358181.001]
  • [Cites] Carcinogenesis. 2002 Jan;23(1):143-50 [11756235.001]
  • [Cites] Mol Cancer Ther. 2004 Sep;3(9):1101-8 [15367704.001]
  • [Cites] Indian J Med Res. 1971 Aug;59(8):1289-95 [5132235.001]
  • [Cites] J Pharm Pharmacol. 1973 Jun;25(6):447-52 [4146582.001]
  • [Cites] Semin Diagn Pathol. 1987 Aug;4(3):205-11 [2890193.001]
  • [Cites] J Cell Physiol. 1992 May;151(2):326-36 [1572907.001]
  • [Cites] Nature. 1992 Sep 24;359(6393):295-300 [1406933.001]
  • [Cites] Radiology. 1993 Apr;187(1):1-14 [8451394.001]
  • [Cites] Oncogene. 1994 Apr;9(4):1021-7 [8134105.001]
  • [Cites] Biochim Biophys Acta. 1994 Dec 30;1224(3):597-600 [7803521.001]
  • [Cites] Biochem Biophys Res Commun. 1995 Jan 17;206(2):533-40 [7530002.001]
  • [Cites] J Biol Chem. 1995 Oct 20;270(42):24995-5000 [7559628.001]
  • [Cites] Oncogene. 1996 Aug 1;13(3):609-16 [8760302.001]
  • [Cites] Eur J Endocrinol. 1996 Oct;135(4):413-20 [8921822.001]
  • [Cites] Mol Biol Cell. 1997 Feb;8(2):287-301 [9190208.001]
  • [Cites] Thromb Haemost. 1997 Apr;77(4):772-82 [9134658.001]
  • [Cites] J Biol Chem. 1997 May 9;272(19):12738-46 [9139732.001]
  • [Cites] Neuron. 1997 Jul;19(1):103-13 [9247267.001]
  • [Cites] Neuron. 1997 Jul;19(1):115-26 [9247268.001]
  • [Cites] Endocrinology. 1997 Dec;138(12):5589-96 [9389547.001]
  • [Cites] J Invest Dermatol. 1998 Oct;111(4):656-61 [9764849.001]
  • [Cites] Lancet. 1998 Oct 31;352(9138):1455-61 [9808008.001]
  • [Cites] J Endocrinol. 1998 Sep;158(3):425-33 [9846172.001]
  • [Cites] Int J Fertil Womens Med. 1999 Mar-Apr;44(2):74-7 [10338264.001]
  • [Cites] J Immunol. 1999 Sep 15;163(6):3474-83 [10477620.001]
  • [Cites] Carcinogenesis. 2004 Nov;25(11):2183-9 [15256484.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):51100-6 [15456744.001]
  • [Cites] Mol Cell Endocrinol. 2005 Jul 15;239(1-2):27-36 [15950373.001]
  • [Cites] Endocr Pathol. 2005 Spring;16(1):53-62 [16000847.001]
  • [Cites] Biochem Pharmacol. 2005 Sep 1;70(5):700-13 [16023083.001]
  • [Cites] Cancer. 2005 Aug 15;104(4):879-90 [16007726.001]
  • [Cites] Pituitary. 2005;8(1):43-52 [16411068.001]
  • [Cites] Endocr Rev. 2006 Aug;27(5):485-534 [16705142.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Oct;2(10):552-61 [17024154.001]
  • [Cites] Cancer Lett. 2006 Nov 18;243(2):160-9 [16530327.001]
  • (PMID = 18450960.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ccnd3 protein, rat; 0 / Cyclin D3; 0 / Cyclins; 0 / Pituitary Hormones; 0 / Retinoblastoma Protein; 3A64E3G5ZO / Bromocriptine; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ PMC2488238
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16. Fiaschi-Taesch N, Takane KK, Masters S, Lopez-Talavera JC, Stewart AF: Parathyroid-hormone-related protein as a regulator of pRb and the cell cycle in arterial smooth muscle. Circulation; 2004 Jul 13;110(2):177-85
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  • These effects require critical serine and threonine residues at positions Ser119, Ser130, Thr132, and Ser138 in the carboxy-terminus of PTHrP and are associated with the phosphorylation of the key cell cycle checkpoint regulator retinoblastoma protein, pRb.
  • Second, because PTHrP devoid of the NLS serves as an inhibitor of VSM proliferation, we hypothesized that local delivery of NLS-deleted PTHrP to the arterial wall at the time of angioplasty might prevent neointimal hyperplasia.
  • As hypothesized, using a rat carotid angioplasty model, adenoviral delivery of NLS-deleted PTHrP completely abolished the development of the neointima after angioplasty.
  • Moreover, NLS-deleted PTHrP delivered to the arterial wall at the time of angioplasty seems to have promise as an agent that could reduce or eliminate the neointimal response to angioplasty.
  • [MeSH-major] Parathyroid Hormone-Related Protein / physiology. Retinoblastoma Protein / physiology
  • [MeSH-minor] Adenoviridae / genetics. Angioplasty, Balloon / adverse effects. Animals. Aorta, Thoracic. Carotid Artery Injuries / therapy. Carotid Artery, Common. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Division. Cell Line / cytology. Cell Line / drug effects. DNA, Complementary / genetics. Genetic Therapy. Genetic Vectors / administration & dosage. Genetic Vectors / therapeutic use. Male. Muscle, Smooth, Vascular / pathology. Myocytes, Smooth Muscle / cytology. Myocytes, Smooth Muscle / drug effects. Peptide Fragments / physiology. Phosphorylation. Phosphoserine / analysis. Phosphothreonine / analysis. Protein Processing, Post-Translational. Protein Transport. Rats. Rats, Sprague-Dawley. Transfection

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  • (PMID = 15210588.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] eng
  • [Grant] United States / PHS HHS / / R-01-54308
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Parathyroid Hormone-Related Protein; 0 / Peptide Fragments; 0 / Retinoblastoma Protein; 1114-81-4 / Phosphothreonine; 17885-08-4 / Phosphoserine
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17. Niculescu MD, Yamamuro Y, Zeisel SH: Choline availability modulates human neuroblastoma cell proliferation and alters the methylation of the promoter region of the cyclin-dependent kinase inhibitor 3 gene. J Neurochem; 2004 Jun;89(5):1252-9
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  • The percentage of cells that accumulated bromodeoxyuridine (proportional to cell proliferation) was 1.8 times lower in the choline-deficient cells than in the control cells.
  • Phosphorylated retinoblastoma (p110) levels were 3 times lower in the choline-deficient cells than in control cells.
  • This may be a mechanism for our previously reported observation that stem cell proliferation in hippocampus neuroepithelium is decreased in choline-deficient rat and mouse fetuses.

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  • [Cites] Cell. 1985 Jan;40(1):91-9 [2981636.001]
  • [Cites] Carcinogenesis. 1983 Aug;4(8):1051-7 [6872150.001]
  • [Cites] Carcinogenesis. 1986 Aug;7(8):1309-12 [3731384.001]
  • [Cites] J Biol Chem. 1987 Apr 5;262(10):4778-86 [3558369.001]
  • [Cites] Carcinogenesis. 1988 Mar;9(3):343-8 [3345576.001]
  • [Cites] Cancer Genet Cytogenet. 1988 May;32(1):25-31 [3355998.001]
  • [Cites] Dev Psychobiol. 1988 May;21(4):339-53 [3378679.001]
  • [Cites] Biochem J. 1989 May 1;259(3):725-9 [2730584.001]
  • [Cites] Carcinogenesis. 1991 Jul;12(7):1307-12 [2070497.001]
  • [Cites] Adv Exp Med Biol. 1991;295:373-82 [1776578.001]
  • [Cites] Cancer Res. 1992 Apr 1;52(7 Suppl):2071s-2077s [1544143.001]
  • [Cites] Oncogene. 1992 Jun;7(6):1249-51 [1594250.001]
  • [Cites] Mutat Res. 1993 Jan;285(1):61-7 [7678134.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Mar 1;91(5):1731-5 [8127873.001]
  • [Cites] Annu Rev Nutr. 1994;14:269-96 [7946521.001]
  • [Cites] Cell. 1994 Nov 18;79(4):551-5 [7954821.001]
  • [Cites] Cytogenet Cell Genet. 1995;69(3-4):190-2 [7698009.001]
  • [Cites] Nature. 1986 May 15-21;321(6067):209-13 [2423876.001]
  • [Cites] Pharmacol Ther. 2002 Feb-Mar;93(2-3):125-33 [12191605.001]
  • [Cites] Pharmacol Ther. 2002 Feb-Mar;93(2-3):113-24 [12191604.001]
  • [Cites] Brain Res. 2002 Aug 23;947(1):9-16 [12144847.001]
  • [Cites] Cancer Res. 2002 Apr 15;62(8):2378-84 [11956100.001]
  • [Cites] Chembiochem. 2002 Apr 2;3(4):274-93 [11933228.001]
  • [Cites] Haematologica. 2002 Feb;87(2):196-214 [11836171.001]
  • [Cites] Neuroreport. 1997 Sep 8;8(13):2831-5 [9376513.001]
  • [Cites] Annu Rev Cell Dev Biol. 1997;13:261-91 [9442875.001]
  • [Cites] Neuroreport. 1997 Sep 29;8(14):3053-9 [9331913.001]
  • [Cites] Trends Genet. 1997 Aug;13(8):323-9 [9260519.001]
  • [Cites] Nucleic Acids Res. 1997 Jun 15;25(12):2532-4 [9171110.001]
  • [Cites] Cancer Lett. 1997 May 1;115(1):31-8 [9097976.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2103-5 [9122155.001]
  • [Cites] Science. 1995 Oct 6;270(5233):90-3 [7569954.001]
  • [Cites] J Neurophysiol. 1998 Apr;79(4):1790-6 [9535948.001]
  • [Cites] Genes Dev. 1998 Aug 1;12(15):2245-62 [9694791.001]
  • [Cites] FASEB J. 1999 Jan;13(1):135-42 [9872938.001]
  • [Cites] Brain Res Dev Brain Res. 1999 Mar 12;113(1-2):13-20 [10064869.001]
  • [Cites] J Biol Chem. 1999 Mar 26;274(13):8746-56 [10085115.001]
  • [Cites] Cancer Causes Control. 1998 Dec;9(6):615-20 [10189047.001]
  • [Cites] Brain Res Dev Brain Res. 1999 Jun 2;115(2):123-9 [10407130.001]
  • [Cites] Nucleic Acids Res. 1999 Aug 1;27(15):3229-35 [10454622.001]
  • [Cites] J Biol Chem. 1951 Nov;193(1):265-75 [14907713.001]
  • [Cites] Jpn J Cancer Res. 1999 Sep;90(9):909-13 [10551317.001]
  • [Cites] Brain Res Dev Brain Res. 1999 Dec 10;118(1-2):51-9 [10611503.001]
  • [Cites] Brain Res Dev Brain Res. 1999 Dec 10;118(1-2):159-67 [10611515.001]
  • [Cites] Nutr Cancer. 2000;37(1):99-107 [10965526.001]
  • [Cites] Semin Thromb Hemost. 2000;26(3):219-25 [11011839.001]
  • [Cites] Brain Res Dev Brain Res. 2000 Sep 30;123(1):25-32 [11020547.001]
  • [Cites] Gut. 2000 Nov;47(5):689-93 [11034586.001]
  • [Cites] Nat Rev Genet. 2000 Oct;1(1):11-9 [11262868.001]
  • [Cites] FASEB J. 2001 Aug;15(10):1704-10 [11481217.001]
  • [Cites] Biochem Soc Trans. 2001 Aug;29(Pt 4):385-91 [11497994.001]
  • [Cites] Dev Neurosci. 2001;23(2):100-6 [11509832.001]
  • [Cites] J Biol Chem. 2001 Nov 2;276(44):41197-204 [11483591.001]
  • (PMID = 15147518.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES010126; United States / NIDDK NIH HHS / DK / R01 DK055865; United States / NIDDK NIH HHS / DK / DK 56350; United States / NIA NIH HHS / AG / AG 09525; United States / NIDDK NIH HHS / DK / DK 55865; United States / NIEHS NIH HHS / ES / ES 10126; United States / NIDDK NIH HHS / DK / P30 DK056350; United States / NIA NIH HHS / AG / P01 AG009525
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor Proteins; 0 / Retinoblastoma Protein; EC 3.1.3.48 / CDKN3 protein, human; EC 3.1.3.48 / Dual-Specificity Phosphatases; EC 3.1.3.48 / Protein Tyrosine Phosphatases; N91BDP6H0X / Choline
  • [Other-IDs] NLM/ NIHMS12177; NLM/ PMC1592524
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18. Tsai NM, Lin SZ, Lee CC, Chen SP, Su HC, Chang WL, Harn HJ: The antitumor effects of Angelica sinensis on malignant brain tumors in vitro and in vivo. Clin Cancer Res; 2005 May 1;11(9):3475-84
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  • In vivo, human DBTRG-05MG and rat RG2 GBM tumor cells were injected s.c. or i.c. and were treated with AS-C.
  • In in vivo studies, AS-C not only can suppress growths of malignant brain tumors of rat and human origin but also shrink the volumes of in situ GBM, significantly prolonging survivals.
  • [MeSH-major] Angelica sinensis. Brain Neoplasms / drug therapy. Glioblastoma / drug therapy. Plant Extracts / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. BALB 3T3 Cells. Caspase 3. Caspase 8. Caspases / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Chloroform. Enzyme Activation / drug effects. HL-60 Cells. Humans. In Situ Nick-End Labeling. Ki-67 Antigen / metabolism. Male. Mice. Mice, Nude. Phosphorylation / drug effects. Phytotherapy. Rats. Rats, Inbred F344. Retinoblastoma Protein / metabolism. Time Factors. Tumor Suppressor Protein p53 / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 15867250.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Plant Extracts; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 7V31YC746X / Chloroform; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Casp8 protein, mouse; EC 3.4.22.- / Casp8 protein, rat; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
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19. Ahtiainen P, Sharp V, Rulli SB, Rivero-Müller A, Mamaeva V, Röyttä M, Huhtaniemi I: Enhanced LH action in transgenic female mice expressing hCGbeta-subunit induces pituitary prolactinomas; the role of high progesterone levels. Endocr Relat Cancer; 2010 Sep;17(3):611-21
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  • Curiously, despite normal estrogen levels, large prolactinomas developed in these mice, and we provide here several lines of evidence that the elevated P(4) levels are involved in the growth of these estrogen-dependent tumors.
  • The antiprogestin mifepristone inhibited tumor growth, and combined postgonadectomy estradiol/P(4) treatment was more effective than estrogen alone in inducing tumor growth.
  • Evidence for direct growth-promoting effect of P(4) was obtained from cultures of primary mouse pituitary cells and rat somatomammotroph GH3 cells.
  • The mouse tumors and cultured cells revealed stimulation of the cyclin D1/cyclin-dependent kinase 4/retinoblastoma protein/transcription factor E2F1 pathway in the growth response to P(4).
  • If extrapolated to humans, and given the importance of endogenous P(4) and synthetic progestins in female reproductive functions and their pharmacotherapy, it is relevant to revisit the potential role of these hormones in the origin and growth of prolactinomas.

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  • [Cites] J Clin Endocrinol Metab. 2000 Jan;85(1):168-74 [10634382.001]
  • [Cites] Endocr Relat Cancer. 2009 Mar;16(1):113-22 [18852162.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 1998 Jan;3(1):63-72 [10819505.001]
  • [Cites] J Neuroendocrinol. 2001 Mar;13(3):302-9 [11207946.001]
  • [Cites] Endocrinology. 2001 Oct;142(10):4479-85 [11564713.001]
  • [Cites] J Clin Invest. 2002 Jan;109(2):277-83 [11805140.001]
  • [Cites] Endocrinology. 2002 Oct;143(10):4084-95 [12239120.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):35819-25 [12121979.001]
  • [Cites] Endocrinology. 2002 Dec;143(12):4536-43 [12446580.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1034-9 [12552124.001]
  • [Cites] Front Horm Res. 2004;32:34-62 [15281339.001]
  • [Cites] Mol Cell Biol. 2004 Aug;24(16):7260-74 [15282324.001]
  • [Cites] Science. 1966 Oct 21;154(3747):402-3 [4288164.001]
  • [Cites] Endocrinology. 1970 Mar;86(3):503-5 [5410438.001]
  • [Cites] J Endocrinol. 1973 Feb;56(2):309-14 [4703244.001]
  • [Cites] Endocrinology. 1976 Dec;99(6):1482-9 [826392.001]
  • [Cites] J Biol Chem. 1982 Mar 10;257(5):2133-6 [7061411.001]
  • [Cites] Adv Exp Med Biol. 1981;138:151-63 [7342713.001]
  • [Cites] Arch Pathol Lab Med. 1983 Sep;107(9):488-91 [6309114.001]
  • [Cites] Cancer Res. 1985 Mar;45(3):1015-9 [2982481.001]
  • [Cites] J Endocrinol. 1989 Jun;121(3):409-17 [2547009.001]
  • [Cites] Endocrinology. 1991 Jul;129(1):270-6 [1711463.001]
  • [Cites] Nature. 1992 Sep 24;359(6393):295-300 [1406933.001]
  • [Cites] Cancer Res. 1993 Apr 1;53(7):1546-9 [8453621.001]
  • [Cites] Acta Endocrinol (Copenh). 1993 Jul;129 Suppl 1:1-5 [8396832.001]
  • [Cites] Hum Reprod. 1994 Jun;9 Suppl 1:63-8 [7962471.001]
  • [Cites] J Cell Sci Suppl. 1994;18:89-96 [7883799.001]
  • [Cites] Cancer Res. 1995 Nov 1;55(21):4892-8 [7585526.001]
  • [Cites] J Biol Chem. 1996 Aug 23;271(34):20608-16 [8702807.001]
  • [Cites] J Endocrinol. 1996 Nov;151(2):175-84 [8958777.001]
  • [Cites] Endocrinology. 1998 Apr;139(4):1602-9 [9528940.001]
  • [Cites] EMBO J. 1998 Apr 1;17(7):2008-18 [9524123.001]
  • [Cites] Nat Genet. 1998 Apr;18(4):360-4 [9537419.001]
  • [Cites] Genes Dev. 1998 Sep 15;12(18):2899-911 [9744866.001]
  • [Cites] Endocrinology. 2005 Nov;146(11):4917-25 [16123159.001]
  • [Cites] Oncogene. 2005 Nov 10;24(49):7301-9 [16007123.001]
  • [Cites] Cancer Cell. 2006 Jun;9(6):459-71 [16766265.001]
  • [Cites] J Clin Endocrinol Metab. 2006 Dec;91(12):4769-75 [16968795.001]
  • [Cites] Cell Cycle. 2008 Jan 1;7(1):71-80 [18196959.001]
  • [Cites] Horm Metab Res. 2008 Apr;40(4):245-50 [18548383.001]
  • [Cites] Eur J Endocrinol. 2008 Sep;159(3):197-202 [18567667.001]
  • [Cites] J Reprod Med. 1999 Dec;44(12 Suppl):1121-6 [10649822.001]
  • (PMID = 20453081.001).
  • [ISSN] 1479-6821
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / / 063552; United Kingdom / Wellcome Trust / / 082101
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human; 4G7DS2Q64Y / Progesterone; 9002-62-4 / Prolactin; 9002-67-9 / Luteinizing Hormone; EC 2.7.11.22 / Cyclin-Dependent Kinase 4
  • [Other-IDs] NLM/ PMC2881531
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20. Kim SY, Jeoung NH, Oh CJ, Choi YK, Lee HJ, Kim HJ, Kim JY, Hwang JH, Tadi S, Yim YH, Lee KU, Park KG, Huh S, Min KN, Jeong KH, Park MG, Kwak TH, Kweon GR, Inukai K, Shong M, Lee IK: Activation of NAD(P)H:quinone oxidoreductase 1 prevents arterial restenosis by suppressing vascular smooth muscle cell proliferation. Circ Res; 2009 Apr 10;104(7):842-50
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  • In this study, we investigated the effects of beta-lapachone (betaL) (3,4-Dihydro-2,2-dimethyl-2H-naphtho[1,2-b]pyran-5,6-dione), which is a potent antitumor agent that stimulates NAD(P)H:quinone oxidoreductase (NQO)1 activity, on neointimal formation in animals given vascular injury and on the proliferation of VSMCs cultured in vitro. betaL significantly reduced the neointimal formation induced by balloon injury. betaL also dose-dependently inhibited the FCS- or platelet-derived growth factor-induced proliferation of VSMCs by inhibiting G(1)/S phase transition. betaL increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase 1 in rat and human VSMCs.
  • These observations provide the molecular basis that pharmacological stimulation of NQO1 activity is a new therapy for the treatment of vascular restenosis and/or atherosclerosis which are caused by proliferation of VSMCs.
  • [MeSH-major] Carotid Artery Injuries / drug therapy. Carotid Stenosis / drug therapy. Cell Proliferation / drug effects. Enzyme Activators / pharmacology. Muscle, Smooth, Vascular / drug effects. Myocytes, Smooth Muscle / drug effects. NAD(P)H Dehydrogenase (Quinone) / metabolism. Naphthoquinones / pharmacology
  • [MeSH-minor] AMP-Activated Protein Kinases / antagonists & inhibitors. AMP-Activated Protein Kinases / metabolism. Acetyl-CoA Carboxylase / metabolism. Animals. Cell Cycle / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Disease Models, Animal. Dose-Response Relationship, Drug. Enzyme Activation. Enzyme Inhibitors / pharmacology. HeLa Cells. Humans. Hyperplasia. Male. Phosphorylation. Platelet-Derived Growth Factor / metabolism. Protein-Serine-Threonine Kinases / metabolism. RNA Interference. RNA, Small Interfering / metabolism. Rats. Rats, Sprague-Dawley. Retinoblastoma Protein / metabolism. Secondary Prevention. Time Factors. Tumor Suppressor Protein p53 / metabolism. Tunica Intima / drug effects. Tunica Intima / enzymology. Tunica Intima / pathology

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  • [CommentIn] Circ Res. 2009 Apr 10;104(7):823-5 [19359603.001]
  • (PMID = 19229058.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn1a protein, rat; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Activators; 0 / Enzyme Inhibitors; 0 / Naphthoquinones; 0 / Platelet-Derived Growth Factor; 0 / RNA, Small Interfering; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 4707-32-8 / beta-lapachone; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 1.6.5.2 / NQO1 protein, rat; EC 2.7.11.1 / AMP-Activated Protein Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Stk11 protein, rat; EC 6.4.1.2 / Acetyl-CoA Carboxylase
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21. Lim IK: TIS21 (/BTG2/PC3) as a link between ageing and cancer: cell cycle regulator and endogenous cell death molecule. J Cancer Res Clin Oncol; 2006 Jul;132(7):417-26
ZFIN. ZFIN .

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  • TIS21(/BTG2/PC3), orthologs of mouse, human and rat, respectively, is initially identified as one of the early growth response genes and induced by various stimulations.
  • On the other hand, it has lately been found that the expression of TIS21 is constitutive and high in thymus, lung alveolar epithelium, proximal tubule of kidney and basal cell layer of prostate acini.
  • (1) TIS21 inhibits early phase of carcinogenesis in its high expressers such as kidney, prostate, breast and thymus: Loss of constitutive and high expression of TIS21 was observed in the precancerous lesions as well as tumor tissues.
  • Based on the previous report that the expression of TIS21 is involved in the induction of senescence after chemotherapy of cancer cells, which can be a mechanism to resist carcinogenesis, TIS21(/BTG2/PC3), the endogenous cell death molecule and pan-cell cycle regulator, might be a link between cellular senescence and carcinogenesis.
  • [MeSH-minor] Animals. Cell Aging. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Humans. Retinoblastoma Protein / metabolism. Tumor Suppressor Protein p53 / metabolism. Tumor Suppressor Proteins. Up-Regulation

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  • [Cites] Cancer Res. 2003 Oct 1;63(19):6244-51 [14559810.001]
  • [Cites] FASEB J. 1993 Jul;7(10):880-5 [8344487.001]
  • [Cites] Oncogene. 1998 May;16(20):2687-93 [9632145.001]
  • [Cites] Leukemia. 1997 Mar;11(3):370-5 [9067576.001]
  • [Cites] J Biol Chem. 2000 Jan 7;275(1):147-53 [10617598.001]
  • [Cites] Gene. 2002 Jan 9;282(1-2):207-14 [11814693.001]
  • [Cites] Mol Carcinog. 2000 Feb;27(2):57-64 [10657898.001]
  • [Cites] Oncogene. 2004 Apr 12;23(16):2919-33 [15077154.001]
  • [Cites] Neuroreport. 2002 Mar 25;13(4):417-22 [11930152.001]
  • [Cites] Oncogene. 2002 Oct 3;21(44):6772-78 [12360398.001]
  • [Cites] Annu Rev Biochem. 1991;60:281-319 [1883198.001]
  • [Cites] Biochem Mol Biol Int. 1998 Aug;45(5):871-8 [9739451.001]
  • [Cites] Biochem J. 2001 Mar 15;354(Pt 3):635-43 [11237868.001]
  • [Cites] Mol Cell Biol. 2000 Mar;20(5):1797-815 [10669755.001]
  • [Cites] J Biol Chem. 1991 Aug 5;266(22):14511-8 [1713584.001]
  • [Cites] J Neurosci. 2005 Jul 13;25(28):6533-8 [16014714.001]
  • [Cites] Clin Cancer Res. 2005 Oct 15;11(20):7523-31 [16243827.001]
  • [Cites] J Cell Sci. 2005 Mar 15;118(Pt 6):1245-53 [15741235.001]
  • [Cites] J Cancer Res Clin Oncol. 1995;121(5):279-84 [7768965.001]
  • [Cites] EMBO J. 1997 Sep 1;16(17):5322-33 [9311992.001]
  • [Cites] J Biol Chem. 2003 Sep 26;278(39):37705-12 [12826667.001]
  • [Cites] J Cell Physiol. 2001 May;187(2):155-65 [11267995.001]
  • [Cites] Mol Cell Biol. 2004 Dec;24(23):10256-62 [15542835.001]
  • [Cites] Eur J Immunol. 2005 Oct;35(10):3030-42 [16163674.001]
  • [Cites] Carcinogenesis. 2005 May;26(5):867-74 [15471900.001]
  • [Cites] J Cell Sci. 2003 Jul 15;116(Pt 14):2929-36 [12771185.001]
  • [Cites] EMBO J. 2004 Jun 2;23(11):2314-24 [15141162.001]
  • [Cites] Drug Resist Updat. 2002 Oct;5(5):204-8 [12450785.001]
  • [Cites] Genes Cells. 2002 Jan;7(1):29-39 [11856371.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3196-201 [14963232.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3353-7 [1849653.001]
  • [Cites] Oncogene Res. 1987 Sep-Oct;1(4):343-55 [3130602.001]
  • [Cites] Nature. 1997 May 22;387(6631):422-6 [9163430.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):932-4 [15340427.001]
  • [Cites] J Biol Chem. 1998 Aug 28;273(35):22563-9 [9712883.001]
  • [Cites] J Cell Physiol. 1994 Jan;158(1):205-13 [8263025.001]
  • [Cites] Oncogene. 2004 Oct 28;23(50):8310-9 [15378000.001]
  • [Cites] Clin Cancer Res. 2005 Apr 1;11(7):2637-43 [15814644.001]
  • [Cites] Stem Cells. 2006 Mar;24(3):494-500 [16166251.001]
  • [Cites] Gene. 1999 Nov 15;240(1):165-73 [10564823.001]
  • [Cites] Asian J Androl. 2005 Dec;7(4):375-80 [16281084.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14236-40 [12391321.001]
  • [Cites] J Biol Chem. 1996 Jun 21;271(25):15034-44 [8663146.001]
  • [Cites] Tissue Cell. 2002 Feb;34(1):28-32 [11989967.001]
  • [Cites] Curr Mol Med. 2005 Mar;5(2):213-8 [15974875.001]
  • [Cites] FEBS Lett. 2001 May 25;497(2-3):67-72 [11377414.001]
  • [Cites] Cancer Res. 2004 Mar 1;64(5):1632-8 [14996721.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4639-44 [10200315.001]
  • [Cites] Dev Growth Differ. 2005 Sep;47(7):435-43 [16179070.001]
  • [Cites] J Neurosci. 2004 Mar 31;24(13):3355-69 [15056715.001]
  • [Cites] Mech Dev. 2001 Jun;104(1-2):113-5 [11404086.001]
  • [Cites] Carcinogenesis. 2001 Aug;22(8):1271-9 [11470758.001]
  • [Cites] Cancer Res. 2003 Jun 1;63(11):2705-15 [12782571.001]
  • [Cites] Mol Carcinog. 1998 Sep;23(1):25-35 [9766435.001]
  • [Cites] Dev Biol. 1997 Aug 15;188(2):322-36 [9268578.001]
  • [Cites] Nat Genet. 1996 Dec;14(4):482-6 [8944033.001]
  • [Cites] J Biol Chem. 2005 Jun 3;280(22):21256-63 [15788397.001]
  • [Cites] Bull Cancer. 2004 Jul-Aug;91(7-8):E242-53 [15381462.001]
  • [Cites] Exp Cell Res. 2004 Sep 10;299(1):159-70 [15302583.001]
  • [Cites] J Gen Virol. 1977 Jul;36(1):59-74 [886304.001]
  • [Cites] J Biol Chem. 2001 Mar 30;276(13):9640-8 [11136725.001]
  • [Cites] Genes Dev. 1997 Jun 1;11(11):1479-92 [9192874.001]
  • [Cites] Nature. 1996 Apr 11;380(6574):544-7 [8606777.001]
  • (PMID = 16456675.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Immediate-Early Proteins; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 141490-22-4 / BTG2 protein, human
  • [Number-of-references] 65
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22. Jori FP, Melone MA, Napolitano MA, Cipollaro M, Cascino A, Giordano A, Galderisi U: RB and RB2/p130 genes demonstrate both specific and overlapping functions during the early steps of in vitro neural differentiation of marrow stromal stem cells. Cell Death Differ; 2005 Jan;12(1):65-77
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  • Marrow stromal stem cells (MSCs) are stem-like cells that are currently being tested for their potential use in cell therapy for a number of human diseases.
  • To this end, we ectopically expressed either RB or RB2/p130 and monitored proliferation, differentiation and apoptosis in rat primary MSC cultures induced to differentiate toward the neuron-like phenotype.
  • [MeSH-major] Cell Differentiation / physiology. Mesenchymal Stromal Cells / physiology. Neurons / cytology. Proteins / physiology. Retinoblastoma Protein / physiology
  • [MeSH-minor] Acetylcholinesterase / genetics. Acetylcholinesterase / metabolism. Adenoviridae / genetics. Animals. Apoptosis / physiology. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Death / physiology. Cell Proliferation. Cells, Cultured. Cyclin-Dependent Kinase Inhibitor p27. DNA-Binding Proteins / genetics. E2F Transcription Factors. Enzyme Inhibitors / pharmacology. Gene Expression / drug effects. Gene Expression / genetics. Genetic Vectors / genetics. Histone Deacetylase Inhibitors. Histone Deacetylases / physiology. Hydroxamic Acids / pharmacology. Immunohistochemistry. Nerve Tissue Proteins / genetics. Nerve Tissue Proteins / metabolism. Neurofilament Proteins / metabolism. Rats. Retinoblastoma-Like Protein p130. Transcription Factors / genetics. Transfection. Tumor Suppressor Protein p53 / metabolism. Tumor Suppressor Proteins / metabolism

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  • (PMID = 15459751.001).
  • [ISSN] 1350-9047
  • [Journal-full-title] Cell death and differentiation
  • [ISO-abbreviation] Cell Death Differ.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cdkn1b protein, rat; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / E2F Transcription Factors; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Nerve Tissue Proteins; 0 / Neurofilament Proteins; 0 / Proteins; 0 / Rbl2 protein, rat; 0 / Retinoblastoma Protein; 0 / Retinoblastoma-Like Protein p130; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 3X2S926L3Z / trichostatin A; EC 3.1.1.7 / Acetylcholinesterase; EC 3.5.1.98 / Histone Deacetylases
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23. Janardhanan R, Butler JT, Banik NL, Ray SK: N-(4-Hydroxyphenyl) retinamide potentiated paclitaxel for cell cycle arrest and apoptosis in glioblastoma C6 and RG2 cells. Brain Res; 2009 May 1;1268:142-53
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  • The present study examines the synergistic actions of N-(4-hydroxyphenyl) retinamide (4-HPR) and paclitaxel (PTX) to control the growth of rat glioblastoma C6 and RG2 cell lines.
  • 4-HPR induced astrocytic differentiation that was accompanied by increased expression of the tight junction protein e-cadherin and sustained down regulation of Id2 (member of inhibitor of differentiation family), catalytic subunit of rat telomerase reverse transcriptase (rTERT), and proliferating cell nuclear antigen (PCNA).
  • This was further ratified by the upregulation of tumor suppressor protein retinoblastoma, which repressed the expression of the key signaling moieties to induce G1/S arrest.
  • Hence, the combination of 4-HPR and PTX can be considered as an effective therapeutic strategy for controlling the growth of heterogeneous glioblastoma cell populations.

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  • [Cites] J Biol Chem. 1981 Oct 25;256(20):10435-41 [6116707.001]
  • [Cites] Cancer Cell. 2003 Apr;3(4):311-6 [12726857.001]
  • [Cites] Exp Cell Res. 1997 Nov 25;237(1):118-26 [9417874.001]
  • [Cites] J Cell Biol. 1998 Jan 12;140(1):153-8 [9425163.001]
  • [Cites] J Natl Cancer Inst. 1998 Apr 15;90(8):597-605 [9554442.001]
  • [Cites] Cell. 1998 Aug 21;94(4):481-90 [9727491.001]
  • [Cites] J Biol Chem. 1999 Jun 18;274(25):17941-5 [10364241.001]
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3155-62 [15867207.001]
  • [Cites] J Biol Chem. 2005 Jun 10;280(23):22135-45 [15826955.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Feb 3;340(1):54-61 [16343421.001]
  • [Cites] Neuroscience. 2006 May 12;139(2):577-95 [16504408.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(11):4351-61 [16705184.001]
  • [Cites] Ann Oncol. 2006 Jul;17(7):1065-71 [16675486.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10166-73 [16801540.001]
  • [Cites] Cell. 2006 Nov 3;127(3):591-606 [17081980.001]
  • [Cites] FASEB J. 2007 Jan;21(1):8-17 [17093139.001]
  • [Cites] Nat Cell Biol. 2007 Feb;9(2):225-32 [17187060.001]
  • [Cites] Dev Cell. 2007 Feb;12(2):169-70 [17276331.001]
  • [Cites] Cancer Chemother Pharmacol. 2007 Aug;60(3):329-39 [17256134.001]
  • [Cites] J Cell Sci. 2007 Jul 1;120(Pt 13):2259-71 [17591690.001]
  • [Cites] Apoptosis. 2007 Nov;12(11):2077-87 [17701358.001]
  • [Cites] Genes Dev. 2007 Nov 1;21(21):2683-710 [17974913.001]
  • [Cites] Cancer Lett. 2008 Mar 8;261(1):26-36 [18164543.001]
  • [Cites] J Biol Chem. 2008 May 9;283(19):13252-60 [18326489.001]
  • [Cites] J Neurochem. 2004 Nov;91(3):634-47 [15485494.001]
  • [Cites] Oncogene. 1999 Oct 28;18(44):5991-9 [10557088.001]
  • [Cites] Cancer J. 2003 May-Jun;9(3):149-56 [12952300.001]
  • [Cites] Oncogene. 2003 Sep 18;22(40):6220-30 [13679861.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7891-9 [14633718.001]
  • [Cites] Oncogene. 2004 Jan 15;23(2):474-82 [14724576.001]
  • [Cites] J Biol Chem. 2004 Jan 30;279(5):3578-87 [14581476.001]
  • [Cites] Nat Rev Cancer. 2004 Apr;4(4):253-65 [15057285.001]
  • [Cites] Nature. 2000 May 18;405(6784):360-4 [10830966.001]
  • [Cites] Oncogene. 2000 Aug 17;19(35):4035-41 [10962560.001]
  • [Cites] Genes Dev. 2001 Feb 15;15(4):392-7 [11230147.001]
  • [Cites] Mol Cell Neurosci. 2001 Mar;17(3):415-25 [11273639.001]
  • [Cites] Cell Death Differ. 2001 May;8(5):477-85 [11423908.001]
  • [Cites] Mol Pharmacol. 2001 Aug;60(2):290-301 [11455016.001]
  • [Cites] J Neuropathol Exp Neurol. 2002 Mar;61(3):215-25; discussion 226-9 [11895036.001]
  • [Cites] Lancet. 2002 Mar 16;359(9310):943-5 [11918915.001]
  • [Cites] Glia. 2002 Jun;38(4):329-38 [12007145.001]
  • [Cites] J Neurosci Res. 2002 Jul 15;69(2):197-206 [12111801.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):616-26 [12154354.001]
  • [Cites] Cell. 2003 Feb 21;112(4):407-21 [12600307.001]
  • [Cites] Adv Pharmacol. 1995;33:315-47 [7495674.001]
  • (PMID = 19285047.001).
  • [ISSN] 1872-6240
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA091460-06; United States / NINDS NIH HHS / NS / R01 NS057811-04; United States / NCI NIH HHS / CA / R01 CA-91460; United States / NCI NIH HHS / CA / R01 CA091460; United States / NINDS NIH HHS / NS / R01 NS-57811; United States / NCI NIH HHS / CA / CA091460-06; United States / NINDS NIH HHS / NS / R01 NS057811
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cadherins; 0 / Id2 protein, rat; 0 / Inhibitor of Differentiation Protein 2; 0 / Proliferating Cell Nuclear Antigen; 0 / Tumor Suppressor Proteins; 187EJ7QEXL / Fenretinide; EC 2.7.7.49 / Telomerase; EC 3.4.- / Cathepsins; EC 3.4.22.- / Calpain; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ NIHMS101700; NLM/ PMC2683666
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24. Bacus SS, Gudkov AV, Lowe M, Lyass L, Yung Y, Komarov AP, Keyomarsi K, Yarden Y, Seger R: Taxol-induced apoptosis depends on MAP kinase pathways (ERK and p38) and is independent of p53. Oncogene; 2001 Jan 11;20(2):147-55
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  • We found that Taxol treatment strongly activated ERK, p38 MAP kinase and p53 in MAP kinase MCF7 cells prior to apoptosis.
  • However, cells with inactivated p53, unlike cells harboring wild type p53, failed to arrest in G2/M after treatment with Taxol and continued to divide or go into apoptosis.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. CDC2-CDC28 Kinases. MAP Kinase Kinase Kinase 1. MAP Kinase Signaling System / drug effects. Paclitaxel / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Carcinoma / drug therapy. Carcinoma / metabolism. Carcinoma / pathology. Cyclin-Dependent Kinase 2. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / drug effects. Cyclin-Dependent Kinases / metabolism. Cyclins / drug effects. Cyclins / metabolism. Enzyme Inhibitors / pharmacology. Female. Flavonoids / pharmacology. G2 Phase / drug effects. Humans. Imidazoles / pharmacology. Mitogen-Activated Protein Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinases / drug effects. Mitogen-Activated Protein Kinases / metabolism. Mitosis / drug effects. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / drug effects. Protein-Serine-Threonine Kinases / genetics. Protein-Serine-Threonine Kinases / metabolism. Pyridines / pharmacology. Rats. Receptor, ErbB-2 / drug effects. Receptor, ErbB-2 / genetics. Receptor, ErbB-2 / metabolism. Retinoblastoma Protein / drug effects. Retinoblastoma Protein / metabolism. Tumor Cells, Cultured. p38 Mitogen-Activated Protein Kinases

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  • (PMID = 11313944.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA60730; United States / NCI NIH HHS / CA / CA75179
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Antineoplastic Agents, Phytogenic; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, rat; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Imidazoles; 0 / Pyridines; 0 / Retinoblastoma Protein; 0 / SB 203580; 0 / Tumor Suppressor Protein p53; EC 2.7.10.1 / Receptor, ErbB-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, human; 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; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinase 1; EC 2.7.11.25 / MAP3K1 protein, human; P88XT4IS4D / Paclitaxel
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25. Shome D, Poddar N, Sharma V, Sheorey U, Maru GB, Ingle A, Sarin R, Banavali S, Dikshit R, Jain V, Honavar S, Bellare J: Does a nanomolecule of Carboplatin injected periocularly help in attaining higher intravitreal concentrations? Invest Ophthalmol Vis Sci; 2009 Dec;50(12):5896-900
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  • The right eye of each rat was injected with periocular CAC (1 mL) and the left eye with NMC (1 mL) by a trained ophthalmologist.
  • The main outcome measure was intravitreal concentrations CAC and NMC over time.
  • CONCLUSIONS: Nanoparticulate-bound carboplatin has greater transscleral transport than commercially available carboplatin, especially in the first week after injection and may help enhance the proven adjuvant efficacy of periocular carboplatin over and above systemic chemotherapy in treating human retinoblastoma, especially those with vitreal seeds.
  • This trial is being published to establish a proof of principle for this method of therapy.
  • [MeSH-major] Carboplatin / chemistry. Carboplatin / pharmacokinetics. Drug Carriers. Nanocapsules / chemistry. Vitreous Body / metabolism
  • [MeSH-minor] Animals. Biological Availability. Chromatography, High Pressure Liquid. Electrophoresis, Polyacrylamide Gel. Injections. Microscopy, Electron, Transmission. Rats. Rats, Sprague-Dawley. Serum Albumin, Bovine / chemistry. Spectroscopy, Fourier Transform Infrared. Tissue Distribution

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  • (PMID = 19628744.001).
  • [ISSN] 1552-5783
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Carriers; 0 / Nanocapsules; 0 / Serum Albumin, Bovine; BG3F62OND5 / Carboplatin
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26. Jaschke B, Milz S, Vogeser M, Michaelis C, Vorpahl M, Schömig A, Kastrati A, Wessely R: Local cyclin-dependent kinase inhibition by flavopiridol inhibits coronary artery smooth muscle cell proliferation and migration: Implications for the applicability on drug-eluting stents to prevent neointima formation following vascular injury. FASEB J; 2004 Aug;18(11):1285-7
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  • [Title] Local cyclin-dependent kinase inhibition by flavopiridol inhibits coronary artery smooth muscle cell proliferation and migration: Implications for the applicability on drug-eluting stents to prevent neointima formation following vascular injury.
  • In-stent restenosis is a hyperproliferative disease which can be successfully treated by drug-eluting stents releasing compounds that exhibit cell-cycle inhibitory properties to inhibit coronary smooth muscle cell (CASMC) proliferation and migration, resembling the key pathomechanisms of in-stent restenosis.
  • Therefore, CDK inhibitors are attractive drugs to be used for the local prevention of in-stent restenosis.
  • Hyperphosphorylation of retinoblastoma protein was abrogated and mitogen-mediated smooth muscle cell migration significantly reduced.
  • Flavopiridol-coated stents, implanted in rat carotid arteries, led to significant decrease of neointima formation.
  • Therefore, this new class of therapeutics may be suitable for further clinical investigations on drug-eluting stents to prevent in-stent restenosis.
  • [MeSH-major] Coronary Vessels / cytology. Cyclin-Dependent Kinases / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. Flavonoids / pharmacology. Muscle, Smooth, Vascular / drug effects. Myocytes, Smooth Muscle / drug effects. Piperidines / pharmacology. Stents
  • [MeSH-minor] Animals. Apoptosis / drug effects. Carotid Artery Injuries / drug therapy. Carotid Artery Injuries / etiology. Carotid Artery Injuries / pathology. Catheterization / adverse effects. Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / genetics. Cell Division / drug effects. Cell Movement / drug effects. Cells, Cultured / cytology. Cells, Cultured / drug effects. Cyclin A / biosynthesis. Cyclin A / genetics. Cyclin D. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinase Inhibitor p27. Cyclins / biosynthesis. Cyclins / genetics. Drug Implants. Endothelial Cells / cytology. Endothelial Cells / drug effects. Endothelium, Vascular / cytology. Endothelium, Vascular / drug effects. Gene Expression Regulation / drug effects. Genes, p53 / drug effects. Humans. Models, Animal. Rats. Tumor Suppressor Protein p53 / biosynthesis. Tumor Suppressor Proteins / biosynthesis. Tumor Suppressor Proteins / genetics. Tunica Intima / drug effects. Tunica Intima / pathology

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  • (PMID = 15180955.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cdkn1a protein, rat; 0 / Cdkn1b protein, rat; 0 / Cell Cycle Proteins; 0 / Cyclin A; 0 / Cyclin D; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Drug Implants; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Piperidines; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 45AD6X575G / alvocidib; EC 2.7.11.22 / Cyclin-Dependent Kinases
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27. Chang CC, Campoli M, Luo W, Zhao W, Zaenker KS, Ferrone S: Immunotherapy of melanoma targeting human high molecular weight melanoma-associated antigen: potential role of nonimmunological mechanisms. Ann N Y Acad Sci; 2004 Dec;1028:340-50
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  • These findings parallel the inhibition of the rat homologue of HMW-MAA NG2 function by anti-NG2 antibodies.
  • Taken together, all these results provide a mechanistic explanation not only for the therapeutic effect of anti-HMW-MAA antibodies in the treatment of melanoma, but also for the function of HMW-MAA in the biology of melanoma cells.
  • [MeSH-major] Antigens, Neoplasm / chemistry. Immunotherapy / methods. Melanoma / immunology. Melanoma / therapy
  • [MeSH-minor] Animals. Cell Movement. Crk-Associated Substrate Protein. Dose-Response Relationship, Drug. Extracellular Matrix / metabolism. Focal Adhesion Kinase 1. Focal Adhesion Protein-Tyrosine Kinases. Humans. Models, Biological. Neoplasms / metabolism. Protein-Tyrosine Kinases / metabolism. Proteins / metabolism. Retinoblastoma-Like Protein p130. Signal Transduction. Time Factors

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  • (PMID = 15650259.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA89480
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / BCAR1 protein, human; 0 / Crk-Associated Substrate Protein; 0 / HMW-MAA; 0 / Proteins; 0 / Retinoblastoma-Like Protein p130; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.10.2 / PTK2 protein, human
  • [Number-of-references] 38
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28. Adibhatla RM, Hatcher JF: Protection by D609 through cell-cycle regulation after stroke. Mol Neurobiol; 2010 Jun;41(2-3):206-17
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  • Tricyclodecan-9-yl-xanthogenate (D609)-increased ceramide levels after transient middle cerebral artery occlusion (tMCAO) in spontaneously hypertensive rat (SHR) probably by inhibiting sphingomyelin synthase (SMS).
  • D609 significantly reduced cerebral infarction and up-regulated Cdk inhibitor p21 and down-regulated phospho-retinoblastoma (pRb) expression after tMCAO in rat.
  • [MeSH-major] Antioxidants. Brain Ischemia / drug therapy. Brain Ischemia / pathology. Bridged-Ring Compounds. Stroke / drug therapy. Stroke / pathology. Thiones
  • [MeSH-minor] Animals. Biomarkers / metabolism. Cell Cycle / drug effects. Cell Cycle Proteins / metabolism. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Infarction, Middle Cerebral Artery. Lipid Metabolism / drug effects. Male. Rats. Rats, Inbred SHR. Rats, Sprague-Dawley. Signal Transduction / physiology

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  • [Cites] Brain Res. 2007 Feb 23;1134(1):199-205 [17204250.001]
  • [Cites] Nat Med. 2005 Jan;11(1):26-7 [15635442.001]
  • [Cites] Mol Cell Biol. 2006 Apr;26(7):2832-44 [16537924.001]
  • [Cites] Bioorg Med Chem Lett. 2006 Sep 15;16(18):4780-3 [16872828.001]
  • [Cites] J Pharmacol Exp Ther. 2004 Jun;309(3):1051-9 [14960662.001]
  • [Cites] Stroke. 2001 Oct;32(10):2376-81 [11588329.001]
  • [Cites] Biochim Biophys Acta. 2004 Nov 8;1686(1-2):85-99 [15522825.001]
  • [Cites] Brain Res. 1999 Feb 20;819(1-2):170-3 [10082875.001]
  • [Cites] J Neurosci. 2005 Apr 20;25(16):4099-107 [15843612.001]
  • [Cites] EMBO J. 2004 Jan 14;23(1):33-44 [14685263.001]
  • [Cites] Cancer Lett. 2003 Apr 25;193(2):149-54 [12706871.001]
  • [Cites] Biochim Biophys Acta. 2002 Dec 30;1585(2-3):114-25 [12531544.001]
  • [Cites] J Immunol. 2001 Nov 15;167(10):5977-85 [11698477.001]
  • [Cites] J Cereb Blood Flow Metab. 2005 Jan;25(1):119-35 [15678118.001]
  • [Cites] Prog Neurobiol. 2009 Sep;89(1):1-17 [19619927.001]
  • [Cites] J Biol Chem. 2006 Oct 20;281(42):31298-308 [16908526.001]
  • [Cites] J Neurochem. 1996 Feb;66(2):869-72 [8592164.001]
  • [Cites] J Neurosci Res. 2007 Apr;85(5):977-84 [17304573.001]
  • [Cites] J Biol Chem. 2001 Apr 20;276(16):12797-804 [11278937.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7748-53 [9636222.001]
  • [Cites] Neuroscience. 2009 Feb 6;158(3):1021-9 [18662748.001]
  • [Cites] J Neurosci. 2007 Mar 7;27(10):2596-605 [17344397.001]
  • [Cites] Free Radic Biol Med. 2006 Feb 1;40(3):376-87 [16443152.001]
  • [Cites] Cancer Metastasis Rev. 2005 Sep;24(3):383-93 [16258726.001]
  • [Cites] Exp Cell Res. 2000 Dec 15;261(2):303-11 [11112337.001]
  • [Cites] Nat Rev Neurosci. 2004 Jun;5(6):437-48 [15152194.001]
  • [Cites] J Mol Neurosci. 2000 Oct;15(2):85-97 [11220788.001]
  • [Cites] Biochem Pharmacol. 2002 Sep;64(5-6):889-92 [12213583.001]
  • [Cites] J Neurosci Res. 2004 May 1;76(3):390-6 [15079868.001]
  • [Cites] J Neurochem. 1995 Jul;65(1):463-6 [7790893.001]
  • [Cites] Neurol Res. 1998 Apr;20(3):265-70 [9583590.001]
  • [Cites] J Neurosci. 2004 Oct 20;24(42):9232-9 [15496657.001]
  • [Cites] Biochim Biophys Acta. 2000 Sep 27;1487(2-3):201-8 [11018472.001]
  • [Cites] Neuroscience. 2007 May 25;146(3):946-61 [17434680.001]
  • [Cites] Nat Rev Cancer. 2004 Aug;4(8):604-16 [15286740.001]
  • [Cites] Biochem J. 2003 Apr 15;371(Pt 2):621-9 [12492401.001]
  • [Cites] J Biol Chem. 2001 Mar 30;276(13):10548-55 [11136721.001]
  • [Cites] Antioxid Redox Signal. 2004 Apr;6(2):311-20 [15025932.001]
  • [Cites] J Immunol. 1999 Mar 1;162(5):3005-12 [10072552.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(1):359-69 [12482987.001]
  • [Cites] IUBMB Life. 2009 Aug;61(8):791-9 [19621353.001]
  • [Cites] J Neurochem. 2010 Jan;112(1):1-12 [19845827.001]
  • [Cites] Brain Res. 2005 Oct 5;1058(1-2):193-7 [16153613.001]
  • [Cites] J Neurosci Res. 2006 Aug 1;84(2):409-17 [16634065.001]
  • [Cites] Biochem J. 2003 Aug 1;373(Pt 3):917-24 [12691604.001]
  • [Cites] EMBO J. 1995 May 1;14(9):1961-9 [7744003.001]
  • [Cites] J Lipid Res. 2004 Jan;45(1):164-73 [13130125.001]
  • [Cites] J Neurosci. 2002 Oct 15;22(20):8922-31 [12388599.001]
  • [Cites] Genes Dev. 1998 Nov 15;12(22):3499-511 [9832503.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Feb 27;315 (1):44-50 [15013423.001]
  • [Cites] J Biol Chem. 2006 Mar 10;281(10 ):6718-25 [16380371.001]
  • [Cites] Neurol Res. 1996 Aug;18(4):337-41 [8875452.001]
  • [Cites] J Cereb Blood Flow Metab. 2001 Mar;21(3):226-32 [11295877.001]
  • [Cites] J Neurosci. 2007 Jun 6;27(23):6320-32 [17554006.001]
  • [Cites] J Biol Chem. 1998 Jun 5;273(23 ):14550-9 [9603970.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 15;97(17):9498-503 [10920185.001]
  • [Cites] J Exp Med. 2004 Dec 6;200(11):1359-70 [15583011.001]
  • [Cites] Neuroscience. 2006;138(4):1161-70 [16427207.001]
  • [Cites] FEBS Lett. 2001 Nov 30;509(1):115-8 [11734217.001]
  • [Cites] J Exp Med. 1996 Aug 1;184(2):725-33 [8760826.001]
  • [Cites] Antioxid Redox Signal. 2010 Jan;12(1):125-69 [19624272.001]
  • [Cites] Neurochem Res. 2002 Aug;27(7-8):609-17 [12374196.001]
  • [Cites] Int Immunopharmacol. 2001 Jul;1(7):1375-84 [11460317.001]
  • [Cites] PLoS One. 2009 Dec 01;4(12 ):e8101 [19956568.001]
  • [Cites] Front Biosci. 2008 Jan 01;13:1250-70 [17981627.001]
  • [Cites] J Biol Chem. 2002 Aug 23;277(34):31263-9 [12070150.001]
  • [Cites] Biol Chem. 2006 Oct-Nov;387(10-11):1321-8 [17081102.001]
  • [Cites] Nat Med. 2006 Aug;12 (8):885-7 [16892030.001]
  • [Cites] Biochim Biophys Acta. 2007 Apr;1772(4):484-93 [17241774.001]
  • [Cites] Drugs Exp Clin Res. 1996;22(6):287-94 [9034754.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10254-9 [10944192.001]
  • [Cites] Nat Rev Immunol. 2005 Aug;5(8):629-40 [16034365.001]
  • [Cites] Trends Cardiovasc Med. 2005 Feb;15(2):47-51 [15885569.001]
  • [Cites] J Neurochem. 2009 Mar;108(5):1309-21 [19183269.001]
  • [Cites] Cell. 1994 Sep 23;78(6):1005-15 [7923351.001]
  • [Cites] Glia. 1999 Aug;27(2):110-28 [10417811.001]
  • [Cites] Mol Cells. 2008 Nov 30;26(5):481-5 [18688177.001]
  • [Cites] J Neurosci. 2008 Jan 2;28(1):163-76 [18171934.001]
  • [Cites] Glia. 2009 Jun;57(8):908-20 [19115378.001]
  • [Cites] J Cereb Blood Flow Metab. 1990 Mar;10(2):290-3 [1689322.001]
  • [Cites] J Pharmacol Exp Ther. 2001 Jul;298(1):103-9 [11408530.001]
  • [Cites] J Neurochem. 2007 Sep;102(6):1831-41 [17532791.001]
  • (PMID = 20148315.001).
  • [ISSN] 1559-1182
  • [Journal-full-title] Molecular neurobiology
  • [ISO-abbreviation] Mol. Neurobiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Biomarkers; 0 / Bridged-Ring Compounds; 0 / Cell Cycle Proteins; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Thiones; 83373-60-8 / tricyclodecane-9-yl-xanthogenate
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29. Miyake JA, Benadiba M, Colquhoun A: Gamma-linolenic acid inhibits both tumour cell cycle progression and angiogenesis in the orthotopic C6 glioma model through changes in VEGF, Flt1, ERK1/2, MMP2, cyclin D1, pRb, p53 and p27 protein expression. Lipids Health Dis; 2009;8:8
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  • METHODS: Established C6 rat gliomas were treated for 14 days with 5 mM GLA in CSF or CSF alone.
  • Combination therapy using drugs with other, complementary targets and GLA could lead to gains in treatment efficacy in this notoriously difficult to treat tumour.
  • [MeSH-major] Cell Cycle / drug effects. Neovascularization, Pathologic / drug therapy. gamma-Linolenic Acid / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1. Glioma / drug therapy. Glioma / pathology. Matrix Metalloproteinase 2. Mitogen-Activated Protein Kinase 3. Proliferating Cell Nuclear Antigen. Rats. Retinoblastoma Protein. Tumor Suppressor Protein p53. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factor Receptor-1

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  • [Cites] Methods Mol Biol. 2001;151:399-410 [11217315.001]
  • [Cites] Nat Rev Cancer. 2008 Sep;8(9):671-82 [18650841.001]
  • [Cites] Biochim Biophys Acta. 2001 Oct 31;1533(3):207-19 [11731331.001]
  • [Cites] Prostaglandins Leukot Essent Fatty Acids. 2002 Jan;66(1):19-29 [12051954.001]
  • [Cites] Biochim Biophys Acta. 2002 Jun 13;1583(1):74-84 [12069851.001]
  • [Cites] Pharmacol Res. 2002 Aug;46(2):155-63 [12220955.001]
  • [Cites] Prostaglandins Leukot Essent Fatty Acids. 2002 Nov;67(5):283-92 [12445487.001]
  • [Cites] Am J Pathol. 2003 Apr;162(4):1083-93 [12651601.001]
  • [Cites] Nutrition. 2003 Apr;19(4):305-9 [12679162.001]
  • [Cites] Clin Cancer Res. 2003 Apr;9(4):1399-405 [12684411.001]
  • [Cites] Glia. 2003 Aug;43(2):149-66 [12838507.001]
  • [Cites] Neuropathol Appl Neurobiol. 2004 Apr;30(2):118-25 [15043709.001]
  • [Cites] Prostaglandins Leukot Essent Fatty Acids. 2004 May;70(5):449-53 [15062847.001]
  • [Cites] Oncologist. 2004;9 Suppl 1:2-10 [15178810.001]
  • [Cites] J Natl Cancer Inst. 1986 Nov;77(5):1053-62 [3464797.001]
  • [Cites] Cancer Lett. 1995 Aug 1;94(2):147-55 [7634242.001]
  • [Cites] Gen Pharmacol. 1998 Feb;30(2):191-4 [9502173.001]
  • [Cites] Biochem Biophys Res Commun. 1998 Mar 17;244(2):414-20 [9514943.001]
  • [Cites] Int J Oncol. 1998 Sep;13(3):611-7 [9683802.001]
  • [Cites] Eur J Clin Invest. 1999 Mar;29(3):220-31 [10202379.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Apr 29;258(1):113-8 [10222244.001]
  • [Cites] J Biol Chem. 1957 May;226(1):497-509 [13428781.001]
  • [Cites] Carcinogenesis. 2004 Dec;25(12):2303-10 [15358633.001]
  • [Cites] J Neurooncol. 2004 Nov;70(2):229-43 [15674480.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7267-75 [16103078.001]
  • [Cites] Brain Pathol. 2005 Oct;15(4):327-41 [16389945.001]
  • [Cites] Glia. 2006 Jun;53(8):799-808 [16541395.001]
  • [Cites] Apoptosis. 2006 May;11(5):659-61 [16554964.001]
  • [Cites] J Biochem Mol Biol. 2006 Sep 30;39(5):469-78 [17002866.001]
  • [Cites] J Nutr. 2007 Mar;137(3):641-6 [17311953.001]
  • [Cites] Drug Resist Updat. 2007 Feb-Apr;10(1-2):13-29 [17303468.001]
  • [Cites] Med Sci Monit. 2007 Jul;13(7):RA119-31 [17599036.001]
  • [Cites] Clin Exp Metastasis. 2007;24(5):341-51 [17505812.001]
  • [Cites] Free Radic Res. 2008 May;42(5):442-55 [18484409.001]
  • [Cites] Mol Cell Biochem. 2001 Feb;218(1-2):13-20 [11330827.001]
  • (PMID = 19292920.001).
  • [ISSN] 1476-511X
  • [Journal-full-title] Lipids in health and disease
  • [ISO-abbreviation] Lipids Health Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCND1 protein, human; 0 / Proliferating Cell Nuclear Antigen; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / p27 antigen; 136601-57-5 / Cyclin D1; 78YC2MAX4O / gamma-Linolenic Acid; EC 2.7.10.1 / FLT1 protein, human; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.24.24 / Matrix Metalloproteinase 2
  • [Other-IDs] NLM/ PMC2661078
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30. Barbie TU, Barbie DA, MacLaughlin DT, Maheswaran S, Donahoe PK: Mullerian Inhibiting Substance inhibits cervical cancer cell growth via a pathway involving p130 and p107. Proc Natl Acad Sci U S A; 2003 Dec 23;100(26):15601-6
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  • A number of cervical cancer cell lines express the MIS type II receptor, and MIS inhibits the growth of both human papilloma virus-transformed and non-human papilloma virus-transformed cervical cell lines, with a more dramatic effect seen in the latter.
  • Finally, normal cervical tissue expresses the MIS type II receptor in vivo, supporting the idea that MIS could be a targeted therapy for cervical cancer.

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  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3488-99 [10589763.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1357-61 [7877982.001]
  • [Cites] J Biol Chem. 2000 Nov 24;275(47):37101-9 [10958795.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3214-9 [11248058.001]
  • [Cites] J Biol Chem. 2001 Jul 20;276(29):26799-806 [11356848.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):239-44 [11773638.001]
  • [Cites] Front Biosci. 2002 Mar 1;7:d641-9 [11861215.001]
  • [Cites] Gynecol Oncol. 2002 Aug;86(2):184-9 [12144826.001]
  • [Cites] Clin Cancer Res. 2002 Aug;8(8):2640-6 [12171896.001]
  • [Cites] Arch Biochem Biophys. 2003 Apr 15;412(2):157-69 [12667479.001]
  • [Cites] Science. 1979 Aug 31;205(4409):913-5 [472712.001]
  • [Cites] Ann Surg. 1981 Oct;194(4):472-80 [6895157.001]
  • [Cites] J Clin Endocrinol Metab. 1982 May;54(5):1051-5 [6895900.001]
  • [Cites] Gynecol Oncol. 1984 Jan;17(1):124-32 [6546372.001]
  • [Cites] J Immunol Methods. 1986 May 22;89(2):271-7 [3486233.001]
  • [Cites] Proc Natl Sci Counc Repub China B. 1989 Oct;13(4):267-75 [2484046.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5523-7 [1648218.001]
  • [Cites] Genes Dev. 1993 Jul;7(7A):1111-25 [8319904.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3602-6 [8170954.001]
  • [Cites] EMBO J. 1995 May 1;14(9):1904-13 [7743997.001]
  • [Cites] Genes Dev. 1995 May 15;9(10):1149-63 [7758941.001]
  • [Cites] Exp Cell Res. 1995 Jun;218(2):499-507 [7796885.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):4350-4 [8633069.001]
  • [Cites] Cell. 1996 May 17;85(4):537-48 [8653789.001]
  • [Cites] Mol Cell Biol. 1996 Dec;16(12):6965-76 [8943352.001]
  • [Cites] Blood. 1997 Nov 15;90(10):4106-15 [9354681.001]
  • [Cites] J Clin Oncol. 1998 Jan;16(1):330-7 [9440761.001]
  • [Cites] Oncogene. 1998 Jan 15;16(2):265-72 [9464545.001]
  • [Cites] Int J Cancer. 1998 Jul 3;77(1):47-54 [9639393.001]
  • [Cites] Genes Dev. 1998 Jul 15;12(14):2120-30 [9679057.001]
  • [Cites] Genes Dev. 1998 Aug 1;12(15):2245-62 [9694791.001]
  • [Cites] Clin Cancer Res. 1995 Mar;1(3):343-9 [9815990.001]
  • [Cites] Science. 1998 Dec 18;282(5397):2270-2 [9856953.001]
  • [Cites] Anticancer Res. 1998 Nov-Dec;18(6A):4275-82 [9891478.001]
  • [Cites] Gynecol Oncol. 1999 Apr;73(1):27-34 [10094876.001]
  • [Cites] CA Cancer J Clin. 1999 Jan-Feb;49(1):8-31, 1 [10200775.001]
  • [Cites] Oncogene. 1999 Mar 4;18(9):1663-76 [10208428.001]
  • [Cites] Cell Growth Differ. 1999 Jun;10(6):413-22 [10392903.001]
  • [Cites] J Biol Chem. 2000 Sep 15;275(37):28371-9 [10874041.001]
  • [Cites] Mol Cell. 2000 Sep;6(3):729-35 [11030352.001]
  • [Cites] Mol Cell. 2000 Sep;6(3):737-42 [11030353.001]
  • [Cites] EMBO J. 1994 Jul 15;13(14):3329-38 [8045262.001]
  • [Cites] Tissue Cell. 1994 Jun;26(3):467-76 [8073421.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Dec 20;91(26):12823-7 [7809128.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jan 17;92(2):483-7 [7831315.001]
  • [Cites] Oncogene. 1999 Dec 20;18(55):7873-82 [10630640.001]
  • (PMID = 14671316.001).
  • [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 / NCI NIH HHS / CA / R01 CA017393; United States / NICHD NIH HHS / HD / R01 HD032112; United States / NCI NIH HHS / CA / CA 17393; United States / NICHD NIH HHS / HD / HD 32112
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Vesicular Transport; 0 / Cell Cycle Proteins; 0 / Glycoproteins; 0 / Nuclear Proteins; 0 / Phosphoproteins; 0 / Proteins; 0 / RBL1 protein, human; 0 / RBL2 protein, human; 0 / Rbl2 protein, rat; 0 / Retinoblastoma Protein; 0 / Retinoblastoma-Like Protein p107; 0 / Retinoblastoma-Like Protein p130; 0 / Testicular Hormones; 80497-65-0 / Anti-Mullerian Hormone; EC 2.7.11.22 / Cyclin-Dependent Kinases
  • [Other-IDs] NLM/ PMC307614
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31. Bromberg Z, Raj N, Goloubinoff P, Deutschman CS, Weiss YG: Enhanced expression of 70-kilodalton heat shock protein limits cell division in a sepsis-induced model of acute respiratory distress syndrome. Crit Care Med; 2008 Jan;36(1):246-55
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  • This may involve overproliferation of alveolar type II cells.
  • We hypothesized that this improvement may be modulated, in part, by an early AdHSP-induced attenuation of alveolar type II cell proliferation.
  • At the time of cecal ligation and double puncture, we injected phosphate-buffered saline, AdHSP, or AdGFP (an adenoviral vector expressing the marker green fluorescent protein) into the trachea.
  • After 48 hrs, cytosolic and nuclear proteins from rat lungs or cell cultures were isolated.
  • MEASUREMENTS AND MAIN RESULTS: Alveolar type I cells were lost within 48 hrs of inducing acute respiratory distress syndrome.
  • This was accompanied by alveolar type II cell proliferation.
  • Treatment with AdHSP preserved alveolar type I cells and limited alveolar type II cell proliferation.
  • Heat shock protein 70 prevented overexuberant cell division, in part, by inhibiting hyperphosphorylation of the regulatory retinoblastoma protein.
  • This prevented retinoblastoma protein ubiquitination and degradation and, thus, stabilized the interaction of retinoblastoma protein with E2F1, a key cell division transcription factor.
  • CONCLUSIONS: : Heat shock protein 70-induced attenuation of cell proliferation may be a useful strategy for limiting lung injury when treating acute respiratory distress syndrome if consistent in later time points.

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  • [Cites] Am J Respir Crit Care Med. 1999 Dec;160(6):1843-50 [10588595.001]
  • [Cites] Shock. 2000 Jan;13(1):19-23 [10638664.001]
  • [Cites] N Engl J Med. 2000 May 4;342(18):1301-8 [10793162.001]
  • [Cites] N Engl J Med. 2000 May 4;342(18):1334-49 [10793167.001]
  • [Cites] J Immunol. 2000 May 15;164(10):5416-23 [10799907.001]
  • [Cites] Cell Prolif. 2000 Jun;33(3):147-66 [10959624.001]
  • [Cites] Cell Prolif. 2000 Dec;33(6):341-65 [11101008.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2001 May;280(5):G968-73 [11292606.001]
  • [Cites] J Biol Chem. 2001 Jun 1;276(22):18657-64 [11279049.001]
  • [Cites] Mech Dev. 2001 Jul;105(1-2):105-14 [11429286.001]
  • [Cites] Anesthesiology. 2001 Oct;95(4):974-82 [11605941.001]
  • [Cites] Oncogene. 2002 May 23;21(23):3715-26 [12032840.001]
  • [Cites] J Clin Invest. 2002 Sep;110(6):801-6 [12235111.001]
  • [Cites] Cell Tissue Res. 2003 Jan;311(1):31-45 [12483282.001]
  • [Cites] Biol Chem. 2003 Jan;384(1):161-7 [12674510.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Aug 1;307(3):689-95 [12893279.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):899-911 [14701760.001]
  • [Cites] Swiss Med Wkly. 2003 Nov 22;133(43-44):586-90 [14745653.001]
  • [Cites] J Virol. 2004 Jun;78(11):5658-69 [15140963.001]
  • [Cites] FEBS Lett. 2004 May 21;566(1-3):147-50 [15147885.001]
  • [Cites] N Engl J Med. 2004 Jul 22;351(4):327-36 [15269312.001]
  • [Cites] Nature. 2004 Sep 23;431(7007):461-6 [15329734.001]
  • [Cites] Lab Invest. 1976 Dec;35(6):558-68 [62893.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Aug;87(15):5883-7 [2143024.001]
  • [Cites] Am Rev Respir Dis. 1993 Jan;147(1):218-33 [8420422.001]
  • [Cites] Genes Dev. 1994 Apr 15;8(8):869-84 [7523245.001]
  • [Cites] J Lab Clin Med. 1995 Aug;126(2):108-18 [7636384.001]
  • [Cites] J Biol Chem. 1995 Sep 22;270(38):22571-6 [7673249.001]
  • [Cites] Histol Histopathol. 1996 Apr;11(2):463-83 [8861769.001]
  • [Cites] Chest. 1997 Jun;111(6 Suppl):111S-113S [9184554.001]
  • [Cites] Am J Physiol. 1997 Nov;273(5 Pt 2):R1709-18 [9374814.001]
  • [Cites] Cell Stress Chaperones. 1998 Jun;3(2):94-9 [9672244.001]
  • [Cites] Nature. 1998 Dec 10;396(6711):590-4 [9859996.001]
  • [Cites] Genes Dev. 1998 Dec 15;12(24):3788-96 [9869631.001]
  • [Cites] Shock. 1999 Jan;11(1):1-12 [9921710.001]
  • [Cites] Lancet. 1999 Apr 10;353(9160):1232-7 [10217084.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8505-10 [10411905.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):298-306 [15549091.001]
  • [Cites] Mol Cell. 2005 Jan 21;17(2):225-36 [15664192.001]
  • [Cites] Oncogene. 2005 Apr 18;24(17):2810-26 [15838517.001]
  • [Cites] Am J Pathol. 2005 May;166(5):1321-32 [15855634.001]
  • [Cites] J Endotoxin Res. 2005;11(3):181-5 [15949147.001]
  • [Cites] Cell. 2005 Jun 17;121(6):823-35 [15960971.001]
  • [Cites] J Cell Physiol. 2005 Sep;204(3):725-41 [15744751.001]
  • [Cites] Am J Respir Cell Mol Biol. 2005 Oct;33(4):335-42 [15961725.001]
  • [Cites] N Engl J Med. 2005 Oct 20;353(16):1685-93 [16236739.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2005 Dec;289(6):L971-9 [16040629.001]
  • [Cites] Pharm Res. 2006 Sep;23(9):2078-93 [16952001.001]
  • [Cites] J Pediatr Surg. 2007 Feb;42(2):415-9 [17270560.001]
  • [Cites] Crit Care Med. 2007 Sep;35(9):2128-38 [17855826.001]
  • [CommentIn] Crit Care Med. 2008 Jan;36(1):360-2 [18158460.001]
  • (PMID = 17989570.001).
  • [ISSN] 1530-0293
  • [Journal-full-title] Critical care medicine
  • [ISO-abbreviation] Crit. Care Med.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM059930-05; United States / NIGMS NIH HHS / GM / R01 GM059930; United States / NIGMS NIH HHS / GM / GM059930; United States / NIGMS NIH HHS / GM / R01 GM059930-05
  • [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 / HSP70 Heat-Shock Proteins
  • [Other-IDs] NLM/ NIHMS105018; NLM/ PMC2668133
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32. Singh RP, Agarwal R: Prostate cancer and inositol hexaphosphate: efficacy and mechanisms. Anticancer Res; 2005 Jul-Aug;25(4):2891-903
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  • Several mechanisms, including overexpression of growth, survival and angiogenic factors and their receptors, together with a loss/decrease of tumor suppressor p53, retinoblastoma and cyclin-dependent kinase inhibitor, have been implicated in PCA growth and progression.
  • Therefore, phytochemicals targeting these molecular events could have a promising role in PCA prevention and/or therapy.
  • In vitro anticancer efficacy of IP6 has been observed in many human, mouse and rat prostate cancer cells.
  • [MeSH-major] Phytic Acid / pharmacology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / prevention & control
  • [MeSH-minor] Animals. Anticarcinogenic Agents / pharmacology. Anticarcinogenic Agents / therapeutic use. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Humans. Male

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  • (PMID = 16080543.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA83741
  • [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.; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antineoplastic Agents; 7IGF0S7R8I / Phytic Acid
  • [Number-of-references] 132
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33. Barbacci EG, Pustilnik LR, Rossi AM, Emerson E, Miller PE, Boscoe BP, Cox ED, Iwata KK, Jani JP, Provoncha K, Kath JC, Liu Z, Moyer JD: The biological and biochemical effects of CP-654577, a selective erbB2 kinase inhibitor, on human breast cancer cells. Cancer Res; 2003 Aug 1;63(15):4450-9
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  • Specific antibodies and low molecular-weight tyrosine kinase inhibitors of both proteins are in clinical trials for cancer treatment.
  • Treatment of SKBr3 human breast cancer cells with CP-654577 reduces the levels of the activated form of mitogen-activated protein kinase, increases the levels of cyclin-dependent kinase inhibitor p27(kip1) and reduces expression of cyclins D and E.
  • These biochemical changes result in a reduced level of phosphorylated retinoblastoma protein and an inhibition of cell-cycle progression at G(1).
  • The antitumor activity of CP-654577 was investigated in athymic mice bearing s.c. tumors from Fischer rat embryo fibroblasts transfected with erbB2.
  • CP-654577 warrants further evaluation in tumors with high expression of p185(erbB2) and may differ from selective EGFr inhibitors or nonselective dual EGFr/erbB2 inhibitors in efficacy and therapeutic index.
  • [MeSH-major] Breast Neoplasms / drug therapy. Enzyme Inhibitors / pharmacology. Protein-Serine-Threonine Kinases. Quinazolines / pharmacology. Receptor, ErbB-2 / antagonists & inhibitors
  • [MeSH-minor] 3T3 Cells. Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Division / drug effects. Enzyme Activation / drug effects. Erlotinib Hydrochloride. Female. Humans. Mice. Mice, Nude. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation / drug effects. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Tumor Cells, Cultured. Xenograft Model Antitumor Assays


34. Avantaggiati ML: Molecular horizons of cancer therapeutics: 11th Pezcoller symposium. Biochim Biophys Acta; 2000 May 17;1470(3):R49-59
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  • [Title] Molecular horizons of cancer therapeutics: 11th Pezcoller symposium.
  • [MeSH-major] CDC2-CDC28 Kinases. Carrier Proteins. DNA-Binding Proteins. Drug Design. Neoplasms / therapy. Signal Transduction
  • [MeSH-minor] Acetyltransferases / metabolism. Adenoviridae / genetics. Adenovirus E1B Proteins / deficiency. Animals. Antibodies / therapeutic use. Apoptosis. Cell Cycle Proteins / metabolism. Clinical Trials as Topic. Cyclin-Dependent Kinase 2. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / metabolism. Cyclins / metabolism. E2F Transcription Factors. Endothelial Growth Factors / immunology. Histone Acetyltransferases. Humans. Lymphokines / immunology. Mice. Oncogene Proteins / metabolism. Protein-Serine-Threonine Kinases / metabolism. Proteins / genetics. Rats. Retinoblastoma-Binding Protein 1. Transcription Factor DP1. Transcription Factors / agonists. Transcription Factors / metabolism. Tumor Cells, Cultured. Tumor Suppressor Protein p14ARF. Tumor Suppressor Protein p53 / antagonists & inhibitors. Tumor Suppressor Protein p53 / metabolism. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors. p300-CBP Transcription Factors

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  • (PMID = 10799750.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Congresses
  • [Publication-country] NETHERLANDS
  • [Chemical-registry-number] 0 / Adenovirus E1B Proteins; 0 / Antibodies; 0 / Arid4a protein, mouse; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cdkn1a protein, mouse; 0 / Cdkn1a protein, rat; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / DNA-Binding Proteins; 0 / E2F Transcription Factors; 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Oncogene Proteins; 0 / Proteins; 0 / Retinoblastoma-Binding Protein 1; 0 / Transcription Factor DP1; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p14ARF; 0 / Tumor Suppressor Protein p53; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / p300-CBP Transcription Factors; EC 2.3.1.48 / p300-CBP-associated factor; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 2.7.11.22 / CDK2 protein, human; 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
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