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1. 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


2. 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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3. 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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4. 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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5. 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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6. 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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7. 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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8. 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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9. 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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  • (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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10. 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


11. 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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  • (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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12. 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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13. 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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  • (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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14. 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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15. 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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16. 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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17. 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
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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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  • (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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18. 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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19. 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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20. 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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  • (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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21. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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  • (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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