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1. Pehlivanov ND, Olyaee M, Sarosiek I, McCallum RW: Comparison of morning and evening administration of rabeprazole for gastro-oesophageal reflux and nocturnal gastric acid breakthrough in patients with reflux disease: a double-blind, cross-over study. Aliment Pharmacol Ther; 2003 Nov 1;18(9):883-90
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  • [Title] Comparison of morning and evening administration of rabeprazole for gastro-oesophageal reflux and nocturnal gastric acid breakthrough in patients with reflux disease: a double-blind, cross-over study.
  • AIM: To assess the effect of timing of rebeprazole (RB) 20 mg/d administration on oesophageal acid exposure and nocturnal gastric acid breakthrough (NGAB) in patients with GERD.
  • METHODS: 20 GERD patients received two 7-day treatments of RB in the morning (a.m.) or in the evening (p.m.) hours.
  • The regimens were randomized in a double-blind fashion and separated by a 7-day washout period.
  • The tablets were taken 30 min before standardized meals.
  • A combined (oesophageal & gastric) 24-hour pH monitoring was performed before and on day 7 of each treatment.
  • RESULTS: Total oesophageal acid exposure was normalized in 10/14 (71.4%) patients with RB p.m. and in 6/15 (42.8%) with RB a.m.
  • RB p.m. significantly decreased the nocturnal supine oesophageal acid exposure vs. RB a.m., 0.2% vs. 3.4%.
  • The mean NGAB duration was significantly shortened with RB a.m. and p.m. vs. the baseline recording, 4.1+/-1.8 and 3.4+/-1.5 hours vs. 7.8+/-1.7 hours.
  • CONCLUSIONS: Rabeprazole significantly reduced the NGAB duration and significantly increased the mean nocturnal gastric pH; RB p.m. normalized more effectively the total oesophageal exposure than RB-a.m.
  • ; RB p.m. provided significantly better control of nocturnal supine gastro-oesophageal reflux than a.m. dosing.
  • These data suggest that administration of a PPI before the evening meal maximizes acid control and would be the preferred dosing schedule in GERD patients, particularly those with nocturnal symptoms.
  • [MeSH-major] Anti-Ulcer Agents / administration & dosage. Benzimidazoles / administration & dosage. Gastric Acid / secretion. Gastroesophageal Reflux / drug therapy
  • [MeSH-minor] 2-Pyridinylmethylsulfinylbenzimidazoles. Circadian Rhythm. Cross-Over Studies. Double-Blind Method. Female. Heartburn / drug therapy. Humans. Hydrogen-Ion Concentration. Male. Omeprazole / analogs & derivatives. Rabeprazole

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  • (PMID = 14616152.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0 / Anti-Ulcer Agents; 0 / Benzimidazoles; 32828355LL / Rabeprazole; KG60484QX9 / Omeprazole
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2. Cougnon M, Benammou S, Brouillard F, Hulin P, Planelles G: Effect of reactive oxygen species on NH4+ permeation in Xenopus laevis oocytes. Am J Physiol Cell Physiol; 2002 Jun;282(6):C1445-53
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  • Under control conditions, NH4Cl exposure induced a large membrane depolarization (to V(m) = 4.0 +/- 1.5 mV; n = 21) and intracellular acidification [reaching a change in pH(i) (DeltapH(i)) of 0.59 +/- 0.06 pH units in 12 min]; the initial rate of cell acidification (dpH(i)/dt) was 0.06 +/- 0.01 pH units/min.
  • By contrast, in the presence of photoactivated rose bengal (RB), tert-butyl-hydroxyperoxide (t-BHP), or xanthine/xanthine oxidase (X/XO), the same experimental maneuver induced significantly greater DeltapH(i) and dpH(i)/dt.
  • These increases in DeltapH(i) and dpH(i)/dt were prevented by the ROS scavengers histidine and desferrioxamine, suggesting involvement of the reactive species (1)DeltagO2 and.OH.
  • Using the voltage-clamp technique to identify the mechanism underlying the ROS-measured effects, we found that RB induced a large increase in the oocyte membrane conductance (G(m)).
  • This RB-induced G(m) increase was prevented by 1 mM diphenylamine-2-carboxylate (DPC) and by a low Na+ concentration in the bath.
  • We conclude that RB, t-BHP, and X/XO enhance NH4+ influx into the oocyte via activation of a DPC-sensitive nonselective cation conductance pathway.
  • [MeSH-minor] Animals. Cations / metabolism. Free Radical Scavengers / pharmacology. Hydrogen Peroxide / pharmacology. Hydrogen-Ion Concentration / drug effects. Intracellular Fluid / metabolism. Ion-Selective Electrodes. Membrane Potentials / drug effects. Membrane Potentials / physiology. Microelectrodes. Oxidants / pharmacology. Patch-Clamp Techniques. Permeability / drug effects. Photochemistry. Rose Bengal / pharmacology. Xanthine / metabolism. Xanthine / pharmacology. Xanthine Oxidase / metabolism. Xanthine Oxidase / pharmacology. Xenopus laevis. tert-Butylhydroperoxide / pharmacology

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  • (PMID = 11997259.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cations; 0 / Free Radical Scavengers; 0 / Oxidants; 0 / Reactive Oxygen Species; 01Q9PC255D / Ammonium Chloride; 1AVZ07U9S7 / Xanthine; 1ZPG1ELY14 / Rose Bengal; 955VYL842B / tert-Butylhydroperoxide; BBX060AN9V / Hydrogen Peroxide; EC 1.17.3.2 / Xanthine Oxidase
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3. Roig JM, Molina MA, Cascante A, Calbó J, Carbó N, Wirtz U, Sreedharan S, Fillat C, Mazo A: Adenovirus-mediated retinoblastoma 94 gene transfer induces human pancreatic tumor regression in a mouse xenograft model. Clin Cancer Res; 2004 Feb 15;10(4):1454-62
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  • [Title] Adenovirus-mediated retinoblastoma 94 gene transfer induces human pancreatic tumor regression in a mouse xenograft model.
  • PURPOSE: Gene transfer of a truncated variant of the retinoblastoma (RB) gene encoding a M(r) 94000 protein that lacks the NH(2)-terminal 112 amino acid residues, termed RB94, has been shown to inhibit proliferation of several human tumor cell types.
  • We have assessed its therapeutic effectiveness on pancreatic cancer, one of the most aggressive and therapy-resistant types of cancer.
  • For this purpose, preclinical studies aimed to evaluate the therapeutic potential of RB94 gene transfer in pancreatic cancer were carried out.
  • EXPERIMENTAL DESIGN: We have compared the antiproliferative effects of adenovirus-mediated gene transfer of RBwt and RB94 at the in vitro and in vivo levels in three RB-positive human pancreatic tumor cell lines: (a). NP-9; (b).
  • RB94 transduction correlated with accumulation at the S-G(2) phase of the cell cycle in the three cell lines tested and induction of apoptosis in two of them.
  • Moreover, terminal deoxynucleotidyl transferase-mediated nick end labeling analyses of Ad-RB94-treated tumor sections revealed that only RB94 is able to significantly induce apoptosis.
  • CONCLUSIONS: RB94 gene expression has antiproliferative effects also in human pancreatic tumor cells, being more effective than wild-type RB in preventing tumor growth.
  • [MeSH-major] Adenoviridae / genetics. Gene Transfer Techniques. Pancreatic Neoplasms / therapy. Retinoblastoma Protein / genetics
  • [MeSH-minor] Animals. Annexin A5 / pharmacology. Apoptosis. Blotting, Western. Cell Cycle. Cell Division. Cell Line, Tumor. Coloring Agents / pharmacology. Dose-Response Relationship, Drug. Humans. In Situ Nick-End Labeling. Mice. Mice, Nude. Neoplasm Transplantation. Protein Structure, Tertiary. Time Factors

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  • (PMID = 14977849.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Coloring Agents; 0 / Retinoblastoma Protein
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4. Laurie NA, Gray JK, Zhang J, Leggas M, Relling M, Egorin M, Stewart C, Dyer MA: Topotecan combination chemotherapy in two new rodent models of retinoblastoma. Clin Cancer Res; 2005 Oct 15;11(20):7569-78
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  • [Title] Topotecan combination chemotherapy in two new rodent models of retinoblastoma.
  • Chemotherapy combined with laser therapy and cryotherapy has improved the ocular salvage rate for children with bilateral retinoblastoma.
  • However, children with late-stage disease often experience recurrence shortly after treatment.
  • To improve the vision salvage rate in advanced bilateral retinoblastoma, we have developed and characterized two new rodent models of retinoblastoma for screening chemotherapeutic drug combinations.
  • The first model is an orthotopic xenograft model in which green fluorescent protein- or luciferase-labeled human retinoblastoma cells are injected into the eyes of newborn rats.
  • Clonal, focal tumors arise from mouse retinal progenitor cells when LIA-E(E1A) is injected into the eyes of newborn p53-/- mice.
  • Using these two models combined with pharmacokinetic studies and cell culture experiments, we have tested the efficacy of topotecan combined with carboplatin and of topotecan combined with vincristine for the treatment of retinoblastoma.
  • The combination of topotecan and carboplatin most effectively halted retinoblastoma progression in our rodent models and was superior to the current triple drug therapy using vincristine, carboplatin, and etoposide.
  • Vincristine had the lowest LC50 in culture but did not reduce tumor growth in our preclinical retinoblastoma models.
  • Taken together, these data suggest that topotecan may be a suitable replacement for etoposide in combination chemotherapy for the treatment of retinoblastoma.
  • [MeSH-major] Disease Models, Animal. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy. Topotecan / therapeutic use
  • [MeSH-minor] Animals. Animals, Newborn. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Carboplatin / pharmacokinetics. Carboplatin / pharmacology. Carboplatin / therapeutic use. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Drug Therapy, Combination. Etoposide / pharmacokinetics. Etoposide / pharmacology. Etoposide / therapeutic use. Eye / metabolism. Humans. Mice. Mice, Knockout. Rats. Time Factors. Vincristine / pharmacokinetics. Vincristine / pharmacology. Vincristine / therapeutic use. Xenograft Model Antitumor Assays

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  • [ErratumIn] Clin Cancer Res. 2009 May 15;15(10):3643
  • (PMID = 16243833.001).
  • [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] Comparative Study; 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 / Antineoplastic Agents; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7M7YKX2N15 / Topotecan; BG3F62OND5 / Carboplatin
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5. Hu J, Xia X, Cheng A, Wang G, Luo X, Reed MF, Fojo T, Oetting A, Gong J, Yen PM: A peptide inhibitor derived from p55PIK phosphatidylinositol 3-kinase regulatory subunit: a novel cancer therapy. Mol Cancer Ther; 2008 Dec;7(12):3719-28
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  • [Title] A peptide inhibitor derived from p55PIK phosphatidylinositol 3-kinase regulatory subunit: a novel cancer therapy.
  • p55PIK, a regulatory subunit of phosphatidylinositol 3-kinase (PI3K), specifically interacts with retinoblastoma protein (Rb) through the unique NH2 terminus of p55PIK, N24.
  • To examine p55PIK as a potential target for cancer therapy, we generated an adenovirus expressing N24 (Ad-N24-GFP) and studied its effects on the proliferation of cultured cancer cells, including human colon (HT29) and thyroid (FTC236) cancer cells.
  • Ad-N24-GFP blocked cell proliferation and induced cell cycle arrest in all cancer cell lines tested.
  • N24 induced cell cycle arrest at G0-G1 phase in cell lines that expressed Rb.
  • Interestingly, N24 inhibited cell proliferation by blocking cell cycle transition at both S and G2-M phases in FTC236 cells, which did not express Rb.
  • When Rb was knocked down by short hairpin RNA in HT29 cells, N24 also inhibited cell cycle progression at S and G2-M phases, suggesting that p55PIK regulates cell cycle progression by Rb-dependent and Rb-independent mechanisms.
  • Finally, Ad-N24-GFP markedly decreased the growth of xenograft tumors derived from HT29 and FTC236 cancer cells in athymic nude mice.
  • Our data strongly suggest that N24 peptide is an effective anticancer therapy, which specifically inhibits PI3K signaling pathways mediated by p55PIK.
  • Moreover, they show that the regulatory subunit of an enzyme, in addition to its catalytic subunit, can be an important target for drug development.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Neoplasms / drug therapy. Neoplasms / metabolism. Peptide Fragments / pharmacology. Peptides / pharmacology. Phosphatidylinositol 3-Kinases / pharmacology. Phosphatidylinositol 3-Kinases / physiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Humans. Male. Mice. Mice, Nude. Neoplasm Transplantation. Retinoblastoma Protein / metabolism

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  • (PMID = 19074847.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / N24 peptide, human; 0 / Peptide Fragments; 0 / Peptides; 0 / Retinoblastoma Protein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3R3 protein, human
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6. Paramio JM, Segrelles C, Ruiz S, Jorcano JL: Inhibition of protein kinase B (PKB) and PKCzeta mediates keratin K10-induced cell cycle arrest. Mol Cell Biol; 2001 Nov;21(21):7449-59
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  • However, beyond this shared function, the functional significance of the carefully regulated tissue- and differentiation-specific expression of the large keratin family of cytoskeletal proteins remains unclear.
  • We recently demonstrated that expression of keratin K10 or K16 may regulate the phosphorylation of the retinoblastoma protein (pRb), inhibiting (K10) or stimulating (K16) cell proliferation (J. M.
  • Jorcano, Mol. Cell. Biol.
  • [MeSH-major] Cell Cycle / drug effects. Keratins / metabolism. Protein Kinase C / antagonists & inhibitors. Protein-Serine-Threonine Kinases. Proto-Oncogene Proteins / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Differentiation. Cell Division. Cyclin D1 / metabolism. Cyclin E / metabolism. Humans. Immunoblotting. Keratin-10. Mice. Microscopy, Fluorescence. Phosphorylation. Plasmids / metabolism. Precipitin Tests. Protein Binding. Protein Structure, Tertiary. Proto-Oncogene Proteins c-akt. Retinoblastoma Protein / metabolism. Signal Transduction. Temperature. Transfection. Tumor Cells, Cultured. Two-Hybrid System Techniques

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  • (PMID = 11585925.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin E; 0 / KRT10 protein, human; 0 / Krt1-10 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Retinoblastoma Protein; 136601-57-5 / Cyclin D1; 147785-83-9 / Keratin-10; 68238-35-7 / Keratins; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / protein kinase C zeta; EC 2.7.11.13 / Protein Kinase C
  • [Other-IDs] NLM/ PMC99917
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7. Wu X, Shi J, Wu Y, Tao Y, Hou J, Meng X, Hu X, Han Y, Jiang W, Tang S, Zangari M, Tricot G, Zhan F: Arsenic trioxide-mediated growth inhibition of myeloma cells is associated with an extrinsic or intrinsic signaling pathway through activation of TRAIL or TRAIL receptor 2. Cancer Biol Ther; 2010 Dec 1;10(11):1201-14
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  • [Title] Arsenic trioxide-mediated growth inhibition of myeloma cells is associated with an extrinsic or intrinsic signaling pathway through activation of TRAIL or TRAIL receptor 2.
  • In this study, the molecular mechanisms of ATO-induced myeloma apoptosis were explored on four myeloma cell lines of wild type or mutant p53 status and also on six primary myeloma cells.
  • Further investigation showed that ATO down-regulated c-Myc and phosphorylated (p)-Rb while up-regulating p53, p21Cip1, and p27Kip1 proteins, resulting in G0/G1 or G2/M cell cycle arrest.
  • ATO treatment increased mRNA levels of interferon regulatory factor-1 and TRAIL, as well as protein levels of caspase 8 and cleaved caspase 3, indicating the involvement of the extrinsic apoptotic pathway in the mutated p53 myeloma cells.
  • ATO also activated caspases 3 and 9, indicating involvement of the intrinsic apoptotic pathway in the wild type p53 myeloma cells.
  • More importantly, these molecular changes induced by ATO-treated myeloma cells are very similar to the baseline expression pattern of hyperdiploid myeloma, which has a relative good prognosis with high expression of TRAIL and interferon related genes.
  • These observations may be employed as prognostic tools and lead to novel therapies in primary myelomas.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Arsenicals / pharmacology. Multiple Myeloma / drug therapy. Oxides / pharmacology. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. TNF-Related Apoptosis-Inducing Ligand / metabolism
  • [MeSH-minor] Cell Cycle / drug effects. Cell Growth Processes / drug effects. Cell Survival / drug effects. Down-Regulation / drug effects. Humans. Interferon Regulatory Factor-1 / biosynthesis. Interferon Regulatory Factor-1 / genetics. Interferon Regulatory Factor-1 / metabolism. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Recombinant Proteins / pharmacology. Signal Transduction / drug effects

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  • (PMID = 20953137.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA115399; United States / NCI NIH HHS / CA / R01 CA152105; United States / NCI NIH HHS / CA / R21 CA143887
  • [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 / Antineoplastic Agents; 0 / Arsenicals; 0 / IRF1 protein, human; 0 / Interferon Regulatory Factor-1; 0 / Oxides; 0 / RNA, Messenger; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFSF10 protein, human; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ PMC3047108
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8. Márquez MF, Salica G, Hermosillo AG, Pastelín G, Cárdenas M: Drug therapy in Brugada syndrome. Curr Drug Targets Cardiovasc Haematol Disord; 2005 Oct;5(5):409-17
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  • [Title] Drug therapy in Brugada syndrome.
  • Sudden cardiac death in healthy individuals with structurally normal hearts and a characteristic morphology of the QRS complex resembling a right bundle branch block with elevation of the ST segment in V1 to V3 is known as Brugada syndrome (BrS).
  • Although placement of an implantable cardioverter-defibrillator is considered the only effective therapy for symptomatic patients, some authors have repeatedly reported a beneficial effect of quinidine and isoproterenol in patients with BrS.
  • Also, isolated case reports on the usefulness of cilostazol, sotalol, and mexiletine have been described.
  • The present article reviews the mechanisms by which these drugs may act and their role in the pharmacotherapy of BrS.
  • [MeSH-major] Bundle-Branch Block / drug therapy
  • [MeSH-minor] Electrocardiography. Humans. Isoproterenol / therapeutic use. Mexiletine / therapeutic use. Sotalol / therapeutic use. Syndrome. Tetrazoles / therapeutic use

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  • (PMID = 16248833.001).
  • [ISSN] 1568-0061
  • [Journal-full-title] Current drug targets. Cardiovascular & haematological disorders
  • [ISO-abbreviation] Curr Drug Targets Cardiovasc Haematol Disord
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Tetrazoles; 1U511HHV4Z / Mexiletine; A6D97U294I / Sotalol; L628TT009W / Isoproterenol; N7Z035406B / cilostazol
  • [Number-of-references] 76
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9. Hashiguchi Y, Tsuda H, Inoue T, Nishimura S, Suzuki T, Kawamura N: Alteration of cell cycle regulators correlates with survival in epithelial ovarian cancer patients. Hum Pathol; 2004 Feb;35(2):165-75
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  • [Title] Alteration of cell cycle regulators correlates with survival in epithelial ovarian cancer patients.
  • The p16-cyclinD1/CDK4-pRb pathway (RB pathway) and p14ARF-MDM2-p53 pathway (p53 pathway) work at the G1-S checkpoint, and the ATM-chk2-CDC25-cyclinB1/cdk1 pathway works at the G2-M checkpoint.
  • The disruption of these pathways is thought to be related to the prognosis of human cancer.
  • In this study, we analyzed the status of these pathways in 107 epithelial ovarian cancer (EOC) patients by immunohistochemistry and evaluated the relationship of these results with chemotherapy response and the prognosis.
  • Altered RB, p53, and G2 pathways were detected in 50.5% (54/107), 51.4% (55/107), and 33.6% (36/107) of cases, respectively.
  • The overall survival (OS) of 77.3% for patients with a normal RB pathway was significantly higher than the OS of 50.0% for patients with an altered RB pathway (by Kaplan-Meier analysis, P = 0.0021).
  • The OS of 66.2% for patients with a normal G2 pathway was significantly higher than the OS of 58.3% for patients with an altered G2 pathway (P = 0.0416).
  • However, the status of the p53 pathway was not related to OS.
  • By univariate and multivariate analyses, advanced stage, high histological grade, altered RB pathway, and altered G2 pathway were significant predictors of poor OS.
  • However, there was no significant relationship between pathway status and chemotherapy response.
  • The status of the RB pathway and of the G2 pathway were independent prognostic factors of EOC.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma / metabolism. Carcinoma / mortality. Cell Cycle Proteins / metabolism. Ovarian Neoplasms / metabolism. Ovarian Neoplasms / mortality
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Cyclin G2. Cyclins / metabolism. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Platinum Compounds / therapeutic use. Prognosis. Retinoblastoma Protein / metabolism. Signal Transduction. Survival Analysis. Tumor Suppressor Protein p53 / metabolism


10. Dunkel IJ, Jubran RF, Gururangan S, Chantada GL, Finlay JL, Goldman S, Khakoo Y, O'Brien JM, Orjuela M, Rodriguez-Galindo C, Souweidane MM, Abramson DH: Trilateral retinoblastoma: potentially curable with intensive chemotherapy. Pediatr Blood Cancer; 2010 Mar;54(3):384-7
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  • [Title] Trilateral retinoblastoma: potentially curable with intensive chemotherapy.
  • BACKGROUND: Trilateral retinoblastoma has been lethal in virtually all cases previously reported.
  • We describe a series of 13 patients treated with intensive chemotherapy, defined as the intention to include high-dose chemotherapy with autologous hematopoietic stem cell rescue.
  • PROCEDURE: Induction chemotherapy generally included vincristine, cisplatin or carboplatin, cyclophosphamide, and etoposide.
  • Hematopoietic stem cells typically were harvested after the first or second cycle of induction chemotherapy, usually from peripheral blood.
  • High-dose chemotherapy regimens were thiotepa-based (n = 7) or melphalan and cyclophosphamide (n = 3).
  • RESULTS: Trilateral sites were pineal (n = 11) and suprasellar (n = 2); 7 patients had localized (M-0) disease and six had leptomeningeal dissemination (M-1+).
  • Five patients had trilateral retinoblastoma at original diagnosis of intra-ocular retinoblastoma; eight later developed trilateral disease at a median of 35 months (range 3-60 months) following diagnosis of intra-ocular retinoblastoma.
  • One patient died of toxicity (septicemia and multi-organ system failure) during induction and three developed disease progression prior to high-dose chemotherapy.
  • Nine patients received high-dose chemotherapy at a median of 5 months (range 4-9) post-diagnosis of trilateral disease.
  • Five patients survive event-free at a median of 77 months (range 36-104 months) and never received external beam radiation therapy.
  • Four of seven patients with M-0 disease survive event-free versus only one of six patients with M-1+ disease.
  • CONCLUSIONS: Intensive chemotherapy is potentially curative for some patients with trilateral retinoblastoma, especially those with M-0 disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Pineal Gland / pathology. Pinealoma / drug therapy. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Carboplatin / administration & dosage. Cisplatin / administration & dosage. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Etoposide / administration & dosage. Hematopoietic Stem Cell Transplantation. Humans. Infant. Infant, Newborn. Meningeal Neoplasms / drug therapy. Meningeal Neoplasms / pathology. Retrospective Studies. Vincristine / administration & dosage

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  • [Copyright] Copyright 2009 Wiley-Liss, Inc.
  • (PMID = 19908299.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin
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11. Smits C, Swen SJ, Theo Goverts S, Moll AC, Imhof SM, Schouten-van Meeteren AY: Assessment of hearing in very young children receiving carboplatin for retinoblastoma. Eur J Cancer; 2006 Mar;42(4):492-500
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessment of hearing in very young children receiving carboplatin for retinoblastoma.
  • Children with retinoblastoma have increasingly been treated with carboplatin in the past decade.
  • Since retinoblastoma patients are very young and frequently have impaired vision, the evaluation of hearing loss is very important.
  • The hearing status of 25 children with retinoblastoma treated with carboplatin (median cumulative dose 2,240 mg/m(2)) was evaluated in detail.
  • The evaluation of hearing loss was performed by an age-appropriate measurement protocol consisting of tympanometry, otoacoustic emission measurements, auditory brainstem responses and (high-frequency) visual reinforcement audiometry (VRA) or play-audiometry.
  • The median follow-up time after last carboplatin dose was 25 months (range 1-94 months).
  • A measurement protocol that includes tympanometry, distortion product otoacoustic emission measurements and high-frequency VRA is recommended for young children receiving carboplatin or other ototoxic drugs.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Carboplatin / adverse effects. Hearing Loss / chemically induced. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Audiometry / methods. Evoked Potentials, Auditory, Brain Stem / physiology. Female. Hearing Tests / methods. Humans. Infant. Infant, Newborn. Male

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  • (PMID = 16376542.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; BG3F62OND5 / Carboplatin
  • [Number-of-references] 41
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12. Leal-Leal CA, Rivera-Luna R, Flores-Rojo ME, Amador-Zarco J, Juarez-Echenique C: Treatment of metastatic retinoblastoma with paclitaxel. Preliminary results of a pilot study with seven patients. J Clin Oncol; 2004 Jul 15;22(14_suppl):8569

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of metastatic retinoblastoma with paclitaxel. Preliminary results of a pilot study with seven patients.
  • : 8569 Background: Metastatic retinoblastoma has a very high mortality rate in most of the cases in spite that international efforts have been made with different chemotherapy regimens.
  • Only high doses of chemotherapy followed by steam cells rescue have proved to provide long lasting survival.
  • METHODS: In a prospective study patients with pathological diagnosis of metastatic retinoblastoma were included, regardless of having recurrent disease or metastasis at time of diagnosis.
  • Once the staging procedure with imaging was performed, the patients were treated with paclitaxel as a single agent at a dose of 150 mg/m<sup>2</sup> days 1, 4 and 7 days every 21 days from 2-6 courses. RESULTS: .
  • At the present time 7 patients were registered into the study.
  • Their age ranged from 10 to 60 months old with a mean of 36 months and SD of 15 months.
  • The time prior to develop metastasis was 11 months and a SD of 13 months.
  • All patients presented complete remission as per CAT scan and MRI studies by the second chemotherapy cycle, even intraocular dieses went to ptisis bublbi.
  • By the 20<sup>th</sup> month of follow up all children have died with tumor activity.
  • CONCLUSIONS: In this pilot study, placlitaxel showed to be an effective drug against intraocular and metastatic Retinoblastoma.
  • However, it should be tested in combination with other drugs in order to obtain long lasting survival for affected patients.

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  • (PMID = 28013865.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Schoeler D, Lindner T, Schulenburg S, Von der, Pink D, Reichardt P: Coincidence of retinoblastoma and leiomyosarcoma in father and daughter - a rare case report. J Clin Oncol; 2004 Jul 15;22(14_suppl):9059

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coincidence of retinoblastoma and leiomyosarcoma in father and daughter - a rare case report.
  • : 9059 Retinoblastoma is the most common primary ocular malignancy of childhood, which results from sporadic or heritable mutations in the retinoblastoma gene, RB1.
  • It is well recognized to occur in two patterns: a sporadic, non-heritable form and a genetic, heritable form presenting with uni- or bilateral disease, which is assaociated with a germline defect and greatly elevated risk of developing a second malignancy.
  • We here report a very rare case of familial retinoblastoma and leiomyosarcoma in a father and his daughter.
  • Father: The 54-years old male was diagnosed with unilateral retinoblastoma of his right eye in 1950 and underwent enucleation in the age of 1, he was not treated by chemotherapy or radiation in the childhood.
  • In 2000 a leiomyosarcoma of his right lower leg with pulmonary metastases was diagnosed.
  • He was treated by polychemotherapy, radiotherapy and surgery of lung and soft tissue metastases.
  • At the moment the patient is treated by a fourth line chemotherapy with ET-743.
  • Daughter: The 31-years old female was diagnosed with bilateral retinoblastoma in 1973.
  • In 1980 retinoblastoma recurred in the left orbita, she was treated by surgery and radiotherapy.
  • 17 years later she was diagnosed with a frontobasal leiomyosarcoma with local involvement of the left orbita.
  • Only 4 month later she recurred locally.
  • She underwent a chemotherapy with epirubicin/ifosfamide followed by surgery.
  • Since that time the situation remains stable.
  • CONCLUSIONS: The propensity for survivors of heritable retinoblastoma to develop second nonocular malignancies is well known, they can occur within the field of irradiation (case of the daughter) or fail previous radiation or chemotherapy (case of the father).
  • In the presented family the grandchild is also affected by retinoblastoma, fortunately it is under local control by laser therapy.
  • With this familial history systematic screening for tumor symptoms should be performed.

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  • (PMID = 28014098.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Hasegawa Y, Hanai N, Terada A, Ozawa T, Goto M: Orotate phosphoribosyl transferase and XPA expressions as predictive biomarkers for combined chemotherapy with 5-fluorouracil and cisplatin in oro- and hypopharyngeal cancers. J Clin Oncol; 2009 May 20;27(15_suppl):6084

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Orotate phosphoribosyl transferase and XPA expressions as predictive biomarkers for combined chemotherapy with 5-fluorouracil and cisplatin in oro- and hypopharyngeal cancers.
  • : 6084 Background: The main purpose of the present study was to find predictive biomarkers that can be routinely used for the response to chemotherapy in head and neck squamous cell carcinomas.
  • From this standpoint, we have investigated the gene expression profile of individual tumors as available predictive biomarkers.
  • METHODS: Sixty-four tumor specimens from patients undergoing radical treatment for squamous cell carcinomas of the oro- and hypopharynx in stage II, III, or IV, were included in the present study.
  • There were 30 primary tumors sites in the oropharynx and 34 in the hypopharynx, respectively.
  • All patients were administered induction chemotherapy (FP) with a combination of 5-FU (800 (600) mg/m<sup>2</sup> d1-5 (6)) and cisplatin (80 mg/m<sup>2</sup> d6 (7)) before definitive therapy.
  • This chemotherapy was used in order to select patients for organ preservation based on the response and decrease in late salvage surgery rate.
  • Treatment was repeated every 3 to 4 weeks.
  • Using biopsy specimens, we analyzed their gene expression profiles with the following 25 markers, which we thought were likely predictors of the response to anti-cancer agents: TS, DPD, OPRT, TP, COX2, MDR1, MRP1, VEGF, EGFR, HER2, PIK3CA, PTEN, p53, Rb1, Bcl2, BclX, BAX, GSTπ, ERCC1, XPA, E2F1, ENT1, Rev3, β-tubulin, and Survivin.
  • These mRNA expressions were quantified by real-time reverse transcription polymerase chain reaction (real-time RT-PCR) assay.
  • Clinical markers, such as T and N factor, gender and age were added, and logistic regression analysis and likelihood ratio test were conducted.
  • RESULTS: Univariately, response for chemotherapy was significantly correlated with T factor (p = 0.015), and the mRNA expression level of XPA (p = 0.018) and OPRT (p = 0.047).
  • Meanwhile, using a multivariate logistic regression analysis with these factors (clinical markers, OPRT and XPA), T factor (p = 0.048) and the expression of XPA (p = 0.035) were demonstrated to be independent predictors for chemotherapy.
  • CONCLUSIONS: XPA (Xeroderma Pigmentosum A) and OPRT (Orotate phosphoribosyl transferase) may be possible reliable predictive biomarkers for FP therapy, and might help the decision-making strategy for individual patients with head and neck cancers.

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  • (PMID = 27961950.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Serrano R, Gómez M, Farre X, Méndez M, De La Haba J, Morales R, Sanchez L, Barneto I, Aranda E: Tissue microarrays (TMAS) in colorectal cancer: Study of clinical and molecular markers. J Clin Oncol; 2004 Jul 15;22(14_suppl):9665

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tissue microarrays (TMAS) in colorectal cancer: Study of clinical and molecular markers.
  • : 9665 Background: TMAS are a powerful tool for testing a large number of molecular parameters in hundreds of tissue samples.
  • This technique can help us to improve our knowledge of molecular markers used to predict disease evolution.To study clinical factors and the expression pattern of proteins including Rb, p53, ki67, p21, p16, p27, cyclins (A, B1, D1, D3 y E), cyclin dependent kinases (cdks) 1, 2 and 6, Survivin, bcl-2 and activated caspase 3 in 71 patients diagnosed of carcinoma colorectal, of which 31 had metastasic disease at diagnosis 22 relapsed and 18 were of free disease.
  • Patients were included in multicentric clinical trials and had received chemotherapy.
  • As independent variables we studied age, gender, tumor localization, TNM, lymph node involvement, differentiation grade, liver metastases, symptoms at metastatic disease, and single or multiple metastatic localizations.
  • The univariate analysis was carried out for each one of the variables by means of the Kaplan-Meier method and the multivariate analysis was performed using the Cox regression model.
  • RESULTS: According to the univariate analysis the statistically significant variables were differentiation grade, liver metastasis, symptoms, number localization, cdk1,cdk 2,cdk6, cyclin A, D3, ki-67, p53 and survivin for OS, and differentiation grade, symtoms, number localization, activated caspase 3, cdk2, cdk6, cyclin D3, ki67, p21 and survivin for SV2.
  • In the multivariate analysis those variables that reached a significant value p≤ 0.2 were included.
  • CONCLUSIONS: In this study clinical factors such as differentiation grade, symptoms, number localization were independent prognostic factors for OS and symptoms for SV2; none of proteins analysed correlated with OS or SV2 in multivariate analysis.

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  • (PMID = 28016294.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Hentrich M, Gerl A, Lutz L, Karthaus M, Schiel X: Unexpected toxicity (UT) and opportunistic infections (OI) after rituximab-containing therapy for non-Hodgkin's lymphoma (NHL). J Clin Oncol; 2009 May 20;27(15_suppl):e19546

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unexpected toxicity (UT) and opportunistic infections (OI) after rituximab-containing therapy for non-Hodgkin's lymphoma (NHL).
  • : e19546 Background: Rituximab (R) is increasingly used for the treatment of B-NHL.
  • In rare cases, however, R may be associated with severe UT and OI.
  • METHODS: The records of consecutive pts treated at 2 institutions from 01/06 to 12/08 with R-containing chemotherapy or R-maintenance therapy (R-M) for NHL were analyzed for severe UT and OI.
  • UT was considered as related to R if it could not be explained otherwise.
  • Pts received a median of 6 cycles (range 1 - 18) of R.
  • A total of 517 cycles of R were evaluable for OI or UT.
  • 7 of 99 pts (7%) (2 females, 5 males) with a median age of 69.5 yrs (range 41-76) experienced UT (n=4) or OI (n=3).
  • UT consisted of interstitial pneumonitis (IP) in 2 pts after 8 and 6 cycles of R-CHOP for diffuse large cell lymphoma (DLCL), a case of congestive heart failure (NYHA III°) after 6x R-CHOP + 2x R-M for follicular lymphoma (FL) and a case of grade 4 pancytopenia lasting for 22 days following 2x R-FC for chronic lymphocytic leukemia.
  • IP completely resolved after initiation of prednisone (n=1) or under empiric antimicrobial therapy (n=1).
  • Congestive heart failure improved under appropriate therapy and the pt received 2 more cycles of R-M.
  • Pancytopenia slowly recovered under therapy with G-CSF, R was terminated.
  • OI consisted of pneumocystis jirovecii pneumonia after 5x R-CHOP-14 for DLCL, Epstein-Barr-virus (EBV)-associated hepatitis after 5x R-CHOP-21 for relapsed FL and generalized herpes zoster following 6x R-bendamustine (RB) + 1x R-M for recurrent BALT-lymphoma.
  • Infections resolved under antimicrobial therapy.
  • Moreover, 2 pts were transferred to us for therapy of enterovirus-induced encephalitis after 6x R-CHOP-21 + 2x R-M for FL (n=1) and cerebral toxoplasmosis in a pt heavily pretreated with R-containing therapy for relapsed mantle cell lymphoma (n=1).
  • Awareness of UT/OI, rapid diagnostic proceedings and, whenever possible, initiation of therapy are essential.
  • In selected cases reexposure of R may be feasible.

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  • (PMID = 27960975.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Beyer I, Bauerschmitz GJ, Breidenbach M, Dragoi A, Niederacher D, Janni W, Rein DT: Gene therapy for pretreated ovarian cancer via a novel fiber modified mdr1 targeting conditionally replicating adenovirus. J Clin Oncol; 2009 May 20;27(15_suppl):e16513

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene therapy for pretreated ovarian cancer via a novel fiber modified mdr1 targeting conditionally replicating adenovirus.
  • : e16513 Background: Ovarian cancer (OC) is a leading cause of death from gynecologic malignancies.
  • Oncolytic adenoviruses (CRAd) are a new approach for cancer treatment.
  • In this study, we constructed a fiber-modified CRAd containing the multi drug resistance gene (mdr) 1 promoter to control viral replication (Ad5/3MDR1).
  • METHODS: RT-PCR was performed for expression of mdr1 in cell lines and primary patient samples.
  • We constructed Ad5/3MDR1luc1 to determine relative activity in a variety of cell lines, patient samples, and normal control cells.
  • The specificity of viral replication was analyzed in co-culture of pretreated OC cell lines and human fibroid cells.
  • A mouse model of peritoneal carcinomatosis was used to evaluate the efficacy of a combined chemo- and gene therapy for OC.
  • Compared to the ubiquitous cmv promoter, mdr1 showed a high level of activity in chemoresistant OC cell lines (7.3%-11.5 %) and OC patient samples (8.8%-12.4%), whereas activity in normal fibroblasts (<1%) was low.
  • Cell killing of Ad5/3MDR1 was comparable to Ad5/3Δ24, a CRAD that replicates in cancer cells inactive in the Rb/p16 pathway, in chemotherapy naïve OC cells but displayed significantly (1.5 log; p < 0.05) higher oncolytic potency in pretreated OC cell lines and primary cells from pretreated OC patients.
  • Moreover, in a therapeutic orthotopic mouse model of peritoneal carcinomatosis, dramatically enhanced survival was noted with Ad5/3MDR1.
  • CONCLUSIONS: Ad5/3MDR1 is a promising candidate for gene therapy of metastatic chemoresistant OC with great potential for clinical testing.

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  • (PMID = 27960759.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Akel A, Wiecek A, Nowicki M, Kokot F: [The effect of treatment with enalapril versus losartan on levels of insulin resistance in patients with essential hypertension]. Pol Arch Med Wewn; 2000 Mar-Apr;103(3-4):123-31
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  • [Title] [The effect of treatment with enalapril versus losartan on levels of insulin resistance in patients with essential hypertension].
  • Participation of the renin-angiotensin system in the development of hyperinsulinaemia in EH patients has not been unanimously proven.
  • The present study aimed to asses the influence of antihypertensive therapy with angiotensin converting enzyme inhibitor (ACEI, enalapril = 10 mg/day) (9 male patients) or angiotensin II AT-1 receptor blocker (A II RB = losartan 50 mg/day) (9 male patients) respectively on insulin sensitivity in patients with EH.
  • 3-hours euglycaemic clamp test with constant infusion of insulin (50 mU/m2/min) was performed twice: before and after 8 weeks of therapy with ACEI or A II RB respectively.
  • The control group (CG) consisted of 12 healthy males (clamp test was performed once).
  • Glucose disposal rate (M-value = mg/kg/min) and tissue insulin sensitivity (M/I value = mg/kg/min per mU/l) were calculated in subjects of the CG and in patients with EH before and after antihypertensive therapy with ACEI or A II RB, respectively.
  • In CG the M-value (7.38 +/- 0.13) and tissue insulin sensitivity (M/I = = 6.76 +/- 0.19) were significantly higher than in EH before treatment with ACEI (M-value = 5.44 +/- 0.16; M/I = = 4.57 +/- 0.18) or A II RB (M-value = 5.75 +/- 0.21; M/I = 4.77 +/- 0.31), respectively.
  • ACEI therapy was followed by a significant increase of both M (6.82 +/- 0.25) and M/I (5.68 +/- 0.25) values.
  • In contrast to ACEI, treatment with A II RB did not influence neither M (5.75 +/- 0.21) nor M/I (4.79 +/- 0.21) values respectively.
  • In contrast to A II RB, ACEI shows a beneficial effect on insulin sensitivity in EH patients.
  • This effect does not seem to be mediated by an influence on the AT-1 receptor.
  • [MeSH-major] Enalapril / pharmacology. Hypertension / drug therapy. Insulin Resistance / physiology. Losartan / pharmacology
  • [MeSH-minor] Adult. Blood Glucose / metabolism. Glucose Clamp Technique. Humans. Insulin / blood. Male. Middle Aged

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  • (PMID = 11236238.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] pol
  • [Publication-type] Clinical Trial; Comparative Study; Controlled Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 69PN84IO1A / Enalapril; JMS50MPO89 / Losartan
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19. Doostzadeh-Cizeron J, Terry NH, Goodrich DW: The nuclear death domain protein p84N5 activates a G2/M cell cycle checkpoint prior to the onset of apoptosis. J Biol Chem; 2001 Jan 12;276(2):1127-32
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  • In contrast to extracellular signals, the mechanisms utilized to transduce nuclear apoptotic signals are not well understood.
  • Characterizing these mechanisms is important for predicting how tumors will respond to genotoxic radiation or chemotherapy.
  • The retinoblastoma (Rb) tumor suppressor protein can regulate apoptosis triggered by DNA damage through an unknown mechanism.
  • The nuclear death domain-containing protein p84N5 can induce apoptosis that is inhibited by association with Rb.
  • One hallmark of this response is the activation of a G(2)/M cell cycle checkpoint.
  • Expression of p84N5 induces changes in cell cycle distribution and kinetics that are consistent with the activation of a G(2)/M cell cycle checkpoint.
  • Like the radiation-induced checkpoint, caffeine blocks p84N5-induced G(2)/M arrest but not subsequent apoptotic cell death.
  • This conclusion is consistent with the hypotheses that p84N5 functions in an Rb-regulated cellular response that is similar to that triggered by DNA damage.
  • [MeSH-minor] Adenoviridae. Aphidicolin / pharmacology. Caffeine / pharmacology. Caspases / metabolism. Cell Line. Cyclin B / metabolism. DNA Replication / drug effects. G2 Phase. Genes, Reporter. Genetic Vectors. Humans. Kinetics. Mitosis. NF-kappa B / metabolism. Recombinant Proteins / metabolism. Transfection

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  • (PMID = 11050087.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-06294; United States / NCI NIH HHS / CA / CA-16672; United States / NCI NIH HHS / CA / CA-70292
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Cyclin B; 0 / NF-kappa B; 0 / Nuclear Proteins; 0 / Recombinant Proteins; 0 / THOC1 protein, human; 38966-21-1 / Aphidicolin; 3G6A5W338E / Caffeine; EC 3.4.22.- / Caspases
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20. Lane ME, Yu B, Rice A, Lipson KE, Liang C, Sun L, Tang C, McMahon G, Pestell RG, Wadler S: A novel cdk2-selective inhibitor, SU9516, induces apoptosis in colon carcinoma cells. Cancer Res; 2001 Aug 15;61(16):6170-7
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  • Recent studies have indicated that the development of cyclin-dependent kinase (cdk)2 inhibitors that deregulate E2F are a plausible pharmacological strategy for novel antineoplastic agents.
  • We show here that 3-[1-(3H-Imidazol-4-yl)-meth-(Z)-ylidene]-5-methoxy-1,3-dihydro-indol-2-one (SU9516), a novel 3-substituted indolinone compound, binds to and selectively inhibits the activity of cdk2.
  • This inhibition results in a time-dependent decrease (4-64%) in the phosphorylation of the retinoblastoma protein pRb, an increase in caspase-3 activation (5-84%), and alterations in cell cycle resulting in either a G(0)-G(1) or a G(2)-M block.
  • [MeSH-major] Apoptosis / drug effects. CDC2-CDC28 Kinases. Colonic Neoplasms / pathology. Cyclin-Dependent Kinases / antagonists & inhibitors. Enzyme Inhibitors / pharmacology. Imidazoles / pharmacology. Indoles / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Cell Division / drug effects. Cyclin-Dependent Kinase 2. Growth Inhibitors / pharmacology. Humans. Molecular Conformation. Phosphorylation / drug effects. Retinoblastoma Protein / metabolism. Substrate Specificity. Tumor Cells, Cultured


21. Hu QY, Li JN, Song DQ, Wang YL, Bekesi G, Weisz I, Jiang JD: Inhibition of human hepatocellular carcinoma by L-proline-m-bis (2-chloroethyl) amino-L-phenylalanyl-L-norvaline ethyl ester hydrochloride (MF13) in vitro and in vivo. Int J Oncol; 2004 Nov;25(5):1289-96
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  • [Title] Inhibition of human hepatocellular carcinoma by L-proline-m-bis (2-chloroethyl) amino-L-phenylalanyl-L-norvaline ethyl ester hydrochloride (MF13) in vitro and in vivo.
  • A new anticancer tripeptide, L-proline-m-bis (2-chloroethyl) amino-L-phenylalanyl-L-norvaline ethyl ester hydrochloride (MF13), was investigated for its activity and mechanism in human hepatocellular carcinoma (HCC) cell lines.
  • MF13 showed antiproliferative activities in the panel of 7 human HCC cell lines with IC50 in the range of 0.08-2.32 microM.
  • A significant blockade in the S-phase occurred in tumor cells 12 h after their exposure to MF13.
  • The inactivated Rb (phosphorylated Rb, pRb), which is present in the S-phase, was increased within 6 h of treatment.
  • Increased activity of caspase-9, -8 and -3 was detected in the MF13 treated cells, indicating an activated pathway of apoptosis by MF13.
  • Morphological examination as well as DNA gel electrophoresis demonstrated a nuclear fragmentation and DNA degradation in the form of multiple-unit DNA ladder in MF13 treated tumor cells.
  • MF13 alone at 10 mg/kg (i.p.) inhibited HepG2 tumor in nude mice by more than 94% in volume.
  • Bel-7402 tumor originated from a Chinese patient with HCC exhibited a sensitivity to MF13 similar to HepG2 in vivo.
  • Antitumor effect of MF13 in the nude mice bearing human hepatocarcinoma (Bel-7402 or HepG2) was stronger than mitomycin C as well as its precursor m-sarcolysin (p<0.01), and comparable with cyclophosphamide.
  • We believe MF13 merits consideration for further investigation as an agent against human hepatocellular carcinoma.
  • [MeSH-major] Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / pathology. Liver Neoplasms / drug therapy. Liver Neoplasms / pathology. Oligopeptides / pharmacology
  • [MeSH-minor] Animals. Apoptosis. Cell Cycle / drug effects. Cell Proliferation. DNA, Neoplasm / metabolism. Female. Humans. Mice. Mice, Nude. Neoplasms, Experimental. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 15492817.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Oligopeptides; 38232-20-1 / MF 13
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22. Jiang JD, Denner L, Ling YH, Li JN, Davis A, Wang Y, Li Y, Roboz J, Wang LG, Perez-Soler R, Marcelli M, Bekesi G, Holland JF: Double blockade of cell cycle at g(1)-s transition and m phase by 3-iodoacetamido benzoyl ethyl ester, a new type of tubulin ligand. Cancer Res; 2002 Nov 1;62(21):6080-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Double blockade of cell cycle at g(1)-s transition and m phase by 3-iodoacetamido benzoyl ethyl ester, a new type of tubulin ligand.
  • The primary action of 3-IAABE is to inhibit microtubule assembly by interacting with -SH groups on tubulin.
  • The blockade was determined by cell cycle analysis and chromosome distribution.
  • Kinase activities of cyclin E and cyclin-dependent kinase 2 responsible for the G(1)-S transition were increased, as were the activities of mitotic cyclin B and cdc2.
  • 3-IAABE treatment also increased p53 expression and dephosphorylated (or activated) retinoblastoma protein.
  • Investigation of the signal transduction pathway showed that 3-IAABE induced bcl-2 phosphorylation, followed by activation of caspase-9, -3, and -6, but not caspase-8.
  • 3-IAABE showed antitumor activities in the panel of 60 National Cancer Institute human tumor cell lines with total growth inhibition in the range of 0.22-4.3 micro M for solid tumor lines and 0.025-0.22 micro M for leukemia/lymphoma cell lines.
  • The 3-IAABU total growth inhibition of phytohemagglutinin-stimulated healthy human lymphocytes was 450-fold greater than that of leukemic cells.
  • 3-IAABE significantly inhibited the growth of human hepatocarcinoma (BEL-7402) in nude mice by 72% in tumor volume, more strongly than did vincristine (43 percent inhibition).
  • Besides being a novel lead for the design of new anticancer tubulin ligands, the activity of 3-IAABE in the cell cycle may also help us to understand the molecular pharmacology of microtubule-active drugs.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Cycle / drug effects. Iodoacetamide / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / pathology. Drug Screening Assays, Antitumor. Humans. Ligands. Liver Neoplasms / drug therapy. Liver Neoplasms / pathology. Male. Mice. Mice, Nude. Microtubules / drug effects. Phosphorylation / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tubulin / metabolism. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / biosynthesis. U937 Cells / drug effects. Vincristine / pharmacology. Xenograft Model Antitumor Assays

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  • (PMID = 12414632.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3-iodoacetamido benzoyl ethyl ester; 0 / Antineoplastic Agents; 0 / Ligands; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tubulin; 0 / Tumor Suppressor Protein p53; 5J49Q6B70F / Vincristine; ZRH8M27S79 / Iodoacetamide
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23. Schueler AO, Jurklies C, Heimann H, Wieland R, Havers W, Bornfeld N: Thermochemotherapy in hereditary retinoblastoma. Br J Ophthalmol; 2003 Jan;87(1):90-5
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  • [Title] Thermochemotherapy in hereditary retinoblastoma.
  • BACKGROUND/AIM: The combination of chemotherapy and transpupillary thermotherapy, thermochemotherapy (TCT) has become an established part of the treatment plan in advanced retinoblastoma.
  • The aim of this study was to identify safe indications, the complications as well as the limitations of this new treatment for retinoblastoma.
  • METHODS: Tumour response and side effects of TCT with an indirect laser ophthalmoscope (spot size about 400 micro m) in 55 tumours of 26 children with bilateral retinoblastoma were analysed.
  • Using the Reese-Ellsworth classification system, nine of 35 eyes were classified as type I, 13 eyes as type II, 10 eyes as type III, and three eyes as type V.
  • The mean tumour height was 3.5 (2.3) mm with a mean diameter of 6.1 (4.1) mm.
  • Treatment parameters were 4.3 (1.6) (median 5) thermochemotherapy sessions with a mean energy of 539 (211) mW and a mean duration of 13.5 (5.6) minutes.
  • Chemotherapy courses (vincristine, etoposide, and carboplatin) were repeated every 3 weeks.
  • RESULTS: Local recurrence occurred in 21 tumours (38%), with a mean onset of 3.2 (2.9) months after TCT.
  • The risk of tumour recurrence was correlated with tumour height.
  • The recurrence rate was 17% for tumours with a height less than 2 mm, 37% for tumours with a height between 2 and 4 mm, and 63% for larger retinoblastomas.
  • Multivariate analysis identified fish flesh regression after TCT (p = 0.0007) as the most important risk factor for tumour recurrence besides tumour height (p = 0.001) and the necessity of increased laser power during TCT sessions (p = 0.018).
  • Complications during therapy included transient corneal opacification in two eyes (6%), focal iris atrophy (three eyes, 8.5%), peripheral lens opacity (two eyes, 6%), circumscribed transient retinal detachment (one eye, 3%) and diffuse choroidal atrophy (one eye, 3%).
  • CONCLUSION: TCT using an indirect laser ophthalmoscope with a spot size of about 400 micro m was efficient for retinoblastoma with a tumour height less than 4 mm.
  • Fish flesh regression after TCT correlates with a higher rate of local tumour recurrence.
  • Treatment related complications occurred in less than 9% of the treated eyes.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hyperthermia, Induced / methods. Retinal Neoplasms / therapy. Retinoblastoma / therapy
  • [MeSH-minor] Carboplatin / administration & dosage. Child. Combined Modality Therapy / methods. Cyclophosphamide / administration & dosage. Etoposide / administration & dosage. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Neoplasm Recurrence, Local / etiology. Retrospective Studies. Risk Factors. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 12488270.001).
  • [ISSN] 0007-1161
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin
  • [Other-IDs] NLM/ PMC1771458
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24. Allen S, Wilson MW, Watkins A, Billups C, Qaddoumi I, Haik BH, Rodriguez-Galindo C: Comparison of two methods for carboplatin dosing in children with retinoblastoma. Pediatr Blood Cancer; 2010 Jul 15;55(1):47-54
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  • [Title] Comparison of two methods for carboplatin dosing in children with retinoblastoma.
  • BACKGROUND: Carboplatin is the most effective drug in retinoblastoma but systemic clearance is variable in young patients.
  • PATIENTS AND METHODS: We compared carboplatin doses between two groups of children with retinoblastoma that were treated using a flat dose of 560 mg/m(2) or a targeted AUC of 6.5 using a modified Calvert formula.
  • RESULTS: Ninety-eight patients with retinoblastoma received a total of 576 cycles of carboplatin (median 8 cycles).
  • Fifty patients (51%) received a fixed dose per m(2), 32 (33%) received a dose based on AUC, 1 patient received fixed dose per kilogram, and in 15 patients a combination AUC and fixed doses was used.
  • Patients receiving carboplatin based on fixed per m(2) dosing were 3.0 times more likely to have a platelet transfusion (95% confidence interval, 1.3-7.3).
  • The use of a targeted AUC provides the most accurate method; however, mg per kg of body weight dosing is a very reliable alternative method.

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  • (PMID = 20486170.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R25 CA023944; United States / NCI NIH HHS / CA / P30-CA23099; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P01 CA023099; United States / NCI NIH HHS / CA / P01 CA023099-310015; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA023099-310015
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; BG3F62OND5 / Carboplatin
  • [Other-IDs] NLM/ NIHMS218675; NLM/ PMC2921445
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25. Rawls SM, Karaca F, Madhani I, Bhojani V, Martinez RL, Abou-Gharbia M, Raffa RB: β-lactamase inhibitors display anti-seizure properties in an invertebrate assay. Neuroscience; 2010 Sep 15;169(4):1800-4
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  • Antibiotics containing a beta-lactam ring (e.g. ceftriaxone) display anti-glutamate effects that underlie their efficacy in animal models of central nervous system (CNS) diseases [Rothstein JD, Patel S, Regan MR, Haenggeli C, Huang YH, Bergles DE, Jin L, Dykes Hoberg M, Vidensky S, Chung DS, Toan SV, Bruijn LI, Su ZZ, Gupta P, Fisher PB (2005) Nature 433:73-77].
  • We hypothesized that the structurally related beta-lactamase inhibitors (clavulanic acid, tazobactam)--which also contain a beta-lactam ring--will mimic ceftriaxone efficacy in an invertebrate (planarian) assay designed to screen for anti-seizure activity [Rawls SM, Thomas T, Adeola M, Patil T, Raymondi N, Poles A, Loo M, Raffa RB (2009) Pharmacol Biochem Behav 93:363-367].
  • Glutamate or cocaine administration produced planarian seizure-like activity (pSLA).
  • Glutamate- or cocaine-induced pSLA was inhibited by ceftriaxone, clavulanic acid, or tazobactam, but not by the non-beta-lactam antibiotic vancomyocin.
  • The present findings indicate beta-lactamase inhibitors display efficacy, and mimic ceftriaxone activity, in an invertebrate anti-seizure screen.
  • These results suggest beta-lactamase inhibitors--particularly ones such as clavulanic acid that display enhanced brain penetrability, oral bioavailability, and negligible anti-bacterial activity--might offer an attractive alternative to direct antibiotic therapy for managing CNS diseases caused by increased glutamate transmission and provide a solution to the growing concern that ceftriaxone will be of only limited utility as a CNS-active therapeutic because of its intolerable side effects.

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  • [Copyright] (c) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
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  • (PMID = 20600649.001).
  • [ISSN] 1873-7544
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R15 DA025314; United States / NIDA NIH HHS / DA / RC1 DA028153; United States / NIDA NIH HHS / DA / RC1 DA028153-01; United States / NIDA NIH HHS / DA / R15DA025314
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Enzyme Inhibitors; 0 / beta-Lactamase Inhibitors; EC 3.5.2.6 / beta-Lactamases
  • [Other-IDs] NLM/ NIHMS217805; NLM/ PMC2924441
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26. Choi JK, Murillo G, Su BN, Pezzuto JM, Kinghorn AD, Mehta RG: Ixocarpalactone A isolated from the Mexican tomatillo shows potent antiproliferative and apoptotic activity in colon cancer cells. FEBS J; 2006 Dec;273(24):5714-23
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  • [Title] Ixocarpalactone A isolated from the Mexican tomatillo shows potent antiproliferative and apoptotic activity in colon cancer cells.
  • Studies conducted on Hepa-1c1c7 hepatoma cells revealed that withanolides were potent inducers of quinone reductase, suggesting possible cancer chemoprotective activity.
  • Here we evaluated the antiproliferative properties of the withanolides in SW480 human colon cancer cells.
  • SW480 cells treated with IxoA showed cell cycle arrest in the G2/M phase, up-regulation of hyper-phosphorylated retinoblastoma, and down-regulation of E2F-1 and DP-1.
  • On the basis of flow cytometry analysis, ethidium bromide/acridine orange, and 4',6-diamidino-2-phenylindole staining, it was found that IxoA induces apoptosis in SW480 cells.
  • Moreover, increased concentrations of the pro-apoptotic protein, BIM/BOD, were found by western blot analysis and immunocytochemistry.
  • IxoA) may have cancer chemopreventive properties.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Colonic Neoplasms / drug therapy. Ergosterol / analogs & derivatives. Physalis / chemistry. Phytotherapy
  • [MeSH-minor] Cell Cycle / drug effects. Cell Line, Tumor. Down-Regulation / drug effects. Drug Screening Assays, Antitumor. E2F1 Transcription Factor / metabolism. Humans. Mexico. Retinoblastoma Protein / metabolism. Transcription Factor DP1 / metabolism. Up-Regulation / drug effects

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  • (PMID = 17212786.001).
  • [ISSN] 1742-464X
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA103861; United States / NCI NIH HHS / CA / P01 CA48112
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / E2F1 Transcription Factor; 0 / E2F1 protein, human; 0 / Retinoblastoma Protein; 0 / TFDP1 protein, human; 0 / Transcription Factor DP1; 0 / ixocarpalactone A; Z30RAY509F / Ergosterol
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27. Khor TO, Yu S, Barve A, Hao X, Hong JL, Lin W, Foster B, Huang MT, Newmark HL, Kong AN: Dietary feeding of dibenzoylmethane inhibits prostate cancer in transgenic adenocarcinoma of the mouse prostate model. Cancer Res; 2009 Sep 1;69(17):7096-102
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  • [Title] Dietary feeding of dibenzoylmethane inhibits prostate cancer in transgenic adenocarcinoma of the mouse prostate model.
  • Dibenzoylmethane (DBM), a minor beta-diketone constituent of licorice, has been shown to exhibit antineoplastic effects in prostate cancer cell lines by induction of cell cycle arrest and regulation of androgen receptor expression.
  • DBM was found to arrest TRAMP-C1 cells at G(2)-M phase of cell cycle and suppressed phosphorylated retinoblastoma, cyclin D1, and cyclin A.
  • Importantly, DBM was found to be equally effective in suppression of prostate tumor progression in TRAMP mice.
  • Our results show that DBM-fed groups had a lower incidence of palpable tumor and high-grade prostatic intraepithelial neoplasia.
  • Subsequent mechanistic studies show that the expression of phosphorylated retinoblastoma, c-myc, cyclin D1, cyclin A, phosphorylated Akt, phosphorylated PDK-1, and phosphorylated S6 was significantly reduced by DBM.
  • Our findings suggest that DBM blocks the growth and progression of prostate cancer in TRAMP mice via modulation of tumor cell cycle regulation and therefore merits its consideration for future clinical intervention of human prostate cancer.


28. Owoeye JF, Afolayan EA, Ademola-Popoola DS: Retinoblastoma--a clinico-pathological study in Ilorin, Nigeria. Afr J Health Sci; 2006 Jan-Jun;13(1-2):117-23
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  • [Title] Retinoblastoma--a clinico-pathological study in Ilorin, Nigeria.
  • Retinoblastoma is the commonest childhood primary malignant intraocular neoplasm that is often characterized by spontaneous regression.
  • This study provides the clinical presentations and histological profiles of retinoblastoma in Ilorin, Kwara-State, in the North Central geo-political zone of Nigeria.
  • A retrospective study of clinically and histologically verified retinoblastoma at the University of Ilorin Teaching Hospital, Ilorin, Kwara-State, Nigeria from January 1989 to December 2000 was undertaken.
  • The clinical and histological features were analyzed using the patient's case folder and surgical pathology records.
  • There were 20 patients, 9 males and 11 females (M:F ratio 1: 1.2), age range from 5 (1/2) months to 6 years with 23 eyeball tumours histologically confirmed retinoblastoma during the study period.
  • Enucleation and Exenteration combined with chemotherapy were offered to 15 (75 %) and 5 (25 %) patients respectively.
  • A poorly differentiated type with extensive areas of tumour necrosis was the commonest histological pattern.
  • Thirteen (65 %) of the patients died before completing the course of chemotherapy.
  • [MeSH-major] Retinal Neoplasms / diagnosis. Retinoblastoma / diagnosis
  • [MeSH-minor] Child. Child, Preschool. Combined Modality Therapy. Eye Enucleation. Female. Humans. Infant. Male

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  • (PMID = 17348751.001).
  • [ISSN] 1022-9272
  • [Journal-full-title] African journal of health sciences
  • [ISO-abbreviation] Afr J Health Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Kenya
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29. Ishii T, Kaneda I, Furuta A, Shoji M, Ishibashi S, Hatsugai K, Ohara M, Sarashina H, Masuoka H, Sekine Y, Watanabe G: [A case of advanced gastric and rectal cancer (double cancer) successfully treated with mFOLFOX6 therapy]. Gan To Kagaku Ryoho; 2009 Jul;36(7):1171-4
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  • [Title] [A case of advanced gastric and rectal cancer (double cancer) successfully treated with mFOLFOX6 therapy].
  • A 75-year-old man was diagnosed with gastric cancer (UL post c0- II c (c T1N0) and M-less ctype II (cT2N0)) and rectal cancer (Rb ctype II (cT2N1) with multiple lung metastases (M1).
  • Chest and abdominal CT scan revealed that multiple lung metastases and abdominal lymph node metastases were obviously reduced in size.
  • The primary lesion of the rectum almost disappeared on endoscopic examination.
  • This case suggests that mFOLFOX6 regimen can be an option for gastric cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasms, Multiple Primary / drug therapy. Rectal Neoplasms / drug therapy. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Aged. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents / administration & dosage. Fluorouracil / administration & dosage. Humans. Leucovorin / administration & dosage. Male. Organoplatinum Compounds / administration & dosage. Vitamin B Complex / administration & dosage

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  • (PMID = 19620811.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; 12001-76-2 / Vitamin B Complex; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil
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30. Flørenes VA, Skrede M, Jørgensen K, Nesland JM: Deacetylase inhibition in malignant melanomas: impact on cell cycle regulation and survival. Melanoma Res; 2004 Jun;14(3):173-81
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  • [Title] Deacetylase inhibition in malignant melanomas: impact on cell cycle regulation and survival.
  • In the present study the deacetylase inhibitor trichostatin A (TSA) was used to elucidate the effect of protein acetylation on cell cycle progression and survival in seven human malignant melanoma cell lines.
  • It was shown that TSA treatment led to a transient G(2)/M phase delay and accumulation of unphosphorylated retinoblastoma protein (pRB) in all cases.
  • TSA significantly induced protein expression of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) in a dose-dependent manner in all cell lines including those not expressing p21(WAF1/CIP1) constitutively, whereas the levels of both wild-type and mutated p53 protein were reduced.
  • The effect on p53 was not a direct result of inhibition of extracellular signal-regulated kinase-1/2 (ERK1/2) activation by TSA, as treatment of the cells with the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase-1 (MEK1) inhibitor PD98059 did not result in decreased p53 protein level.
  • Furthermore, TSA treatment led to reduction in cyclin D1 whereas cyclin D3 accumulated, the latter due to increased protein stability.
  • In all the examined cell lines, TSA treatment resulted in a profound induction of apoptosis and cleavage of poly-(ADP-ribose)-polymerase (PARP) indicative of caspase activity.
  • Altogether, these results suggest that p21(WAF1/CIP1) in melanomas is silenced by deacetylation, and furthermore that inhibition of deacetylation may have potential in anticancer therapy of melanoma patients.
  • [MeSH-major] Cell Cycle / drug effects. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Melanoma / enzymology. Melanoma / pathology
  • [MeSH-minor] Apoptosis / drug effects. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Cyclin-Dependent Kinase Inhibitor p21. Down-Regulation / drug effects. Histone Deacetylases / metabolism. Humans. Hydroxamic Acids / pharmacology. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Tumor Suppressor Protein p53 / metabolism. Up-Regulation / drug effects


31. Poulaki V, Mitsiades CS, Kotoula V, Negri J, McMullan C, Miller JW, Marks PA, Mitsiades N: Molecular sequelae of histone deacetylase inhibition in human retinoblastoma cell lines: clinical implications. Invest Ophthalmol Vis Sci; 2009 Sep;50(9):4072-9
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  • [Title] Molecular sequelae of histone deacetylase inhibition in human retinoblastoma cell lines: clinical implications.
  • PURPOSE: To characterize the molecular sequelae induced in retinoblastoma (Rb) cells by histone deacetylase inhibitors (HDACIs).
  • Vorinostat has demonstrated significant anticancer activity against hematologic and solid tumors at doses well tolerated by patients and has been approved for the treatment of patients with cutaneous T-cell lymphoma.
  • METHODS: The authors evaluated the effects of the HDACIs vorinostat and m-carboxycinnamic acid bis-hydroxamide on the Rb cell lines Y79 and WERI-Rb1 with the use of the MTT assay, BrdU incorporation assay, flow cytometry, immunoblotting, gene-expression profiling, quantitative RT-PCR, and NF-kappaB DNA-binding assay.
  • RESULTS: Both HDACIs were effective against both Rb cell lines, inducing growth arrest and apoptosis in vitro.
  • Vorinostat increased p53 expression and activated caspases -8, -9 and -3, whereas caspase inhibition abrogated vorinostat-induced apoptosis.
  • Vorinostat downregulated baseline NF-kappaB activity and potentiated the activity of the DNA-damaging chemotherapeutic doxorubicin.
  • CONCLUSIONS: HDACIs, such as vorinostat, induce caspase-dependent apoptosis in Rb cells, downregulate baseline NF-kappaB activity, and potentiate the effectiveness of conventional chemotherapy.
  • The finding that vorinostat augments the effectiveness of doxorubicin provides a rationale for future clinical studies looking at the use of vorinostat in combination with conventional chemotherapy in Rb.
  • [MeSH-major] Apoptosis. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Retinal Neoplasms / pathology. Retinoblastoma / pathology
  • [MeSH-minor] Acetylation. Bromodeoxyuridine / metabolism. Caspases / metabolism. Cell Line, Tumor. Cell Proliferation. Cinnamates / pharmacology. Doxorubicin / pharmacology. Drug Synergism. Flow Cytometry. Gene Expression Profiling. Histones / metabolism. Humans. Hydroxamic Acids / pharmacology. Immunoblotting. NF-kappa B / metabolism. Neoplasm Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19387079.001).
  • [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 / Cinnamates; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Hydroxamic Acids; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53; 0 / carboxycinnamic acid bishydroxamide; 58IFB293JI / vorinostat; 80168379AG / Doxorubicin; EC 3.4.22.- / Caspases; G34N38R2N1 / Bromodeoxyuridine
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32. Singh RP, Agarwal R: Natural flavonoids targeting deregulated cell cycle progression in cancer cells. Curr Drug Targets; 2006 Mar;7(3):345-54
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  • [Title] Natural flavonoids targeting deregulated cell cycle progression in cancer cells.
  • The prolonged duration requiring alteration of multi-genetic and epigenetic molecular events for cancer development provides a strong rationale for cancer prevention, which is developing as a potential strategy to arrest or reverse carcinogenic changes before the appearance of the malignant disease.
  • In this regard, targeting deregulated cell cycle progression and its modulation by various natural and synthetic agents are gaining widespread attention in recent years to control the unchecked growth and proliferation in cancer cells.
  • In fact, a vast number of experimental studies convincingly show that many phytochemicals halt uncontrolled cell cycle progression in cancer cells.
  • Among these phytochemicals, natural flavonoids have been identified as a one of the major classes of natural anticancer agents exerting antineoplastic activity via cell cycle arrest as a major mechanism in various types of cancer cells.
  • This review is focused at the modulatory effects of natural flavonoids on cell cycle regulators including cyclin-dependent kinases and their inhibitors, cyclins, p53, retinoblastoma family of proteins, E2Fs, check-point kinases, ATM/ATR and survivin controlling G1/S and G2/M check-point transitions in cell cycle progression, and discusses how these molecular changes could contribute to the antineoplastic effects of natural flavonoids.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Cell Cycle / drug effects. Flavonoids / pharmacology. Neoplasms / drug therapy. Neoplasms / pathology
  • [MeSH-minor] Animals. Cell Differentiation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans

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  • (PMID = 16515531.001).
  • [ISSN] 1389-4501
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102514; United States / NCI NIH HHS / CA / R01 CA64514
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Flavonoids
  • [Number-of-references] 100
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33. Liu X, He H, Feng Y, Zhang M, Ren K, Shao R: Difference of cell cycle arrests induced by lidamycin in human breast cancer cells. Anticancer Drugs; 2006 Feb;17(2):173-9
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  • [Title] Difference of cell cycle arrests induced by lidamycin in human breast cancer cells.
  • In the present study, we investigated the mechanism by which LDM induced cell cycle arrest in human breast cancer cells.
  • The results showed that LDM induced G1 arrest in p53 wild-type MCF-7 cells at low concentrations, and caused both G1 and G2/M arrests at higher concentrations.
  • Western blotting analysis indicated that LDM-induced G1 and G2/M arrests in MCF-7 cells were associated with an increase of p53 and p21, and a decrease of phosphorylated retinoblastoma tumor suppressor protein, cyclin-dependent kinase (Cdk), Cdc2 and cyclin B1 protein levels.
  • Further study indicated that the downregulation of cyclin B1 by LDM in MCF-7 cells was associated with decreasing cyclin B1 mRNA levels and promoting protein degradation, whereas it was only due to inducing cyclin B1 protein degradation in MCF-7/DOX cells.
  • Taken together, we provide the first evidence that LDM induces different cell cycle arrests in human breast cancer cells, which are dependent on drug concentration and p53 status.
  • These findings are helpful in understanding the molecular anti-cancer mechanisms of LDM and support its clinical trials.
  • [MeSH-major] Aminoglycosides / pharmacology. Antibiotics, Antineoplastic / pharmacology. Breast Neoplasms / drug therapy. Cell Cycle / drug effects. Gene Expression Regulation, Neoplastic
  • [MeSH-minor] CDC2 Protein Kinase / metabolism. Checkpoint Kinase 2. Cyclin B / genetics. Cyclin B / metabolism. Cyclin B1. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Enediynes. Enzyme Activation / drug effects. Genes, Tumor Suppressor / physiology. Humans. Phosphorylation / drug effects. Protein Kinases / metabolism. Protein-Serine-Threonine Kinases / metabolism. Retinoblastoma Protein / metabolism. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16428935.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibiotics, Antineoplastic; 0 / CCNB1 protein, human; 0 / Cyclin B; 0 / Cyclin B1; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enediynes; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 120177-69-7 / C 1027; EC 2.7.- / Protein Kinases; EC 2.7.1.11 / Checkpoint Kinase 2; EC 2.7.11.1 / CHEK2 protein, human; EC 2.7.11.1 / Checkpoint kinase 1; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / CDC2 Protein Kinase
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34. Mauler F, Hinz V, Horváth E, Schuhmacher J, Hofmann HA, Wirtz S, Hahn MG, Urbahns K: Selective intermediate-/small-conductance calcium-activated potassium channel (KCNN4) blockers are potent and effective therapeutics in experimental brain oedema and traumatic brain injury caused by acute subdural haematoma. Eur J Neurosci; 2004 Oct;20(7):1761-8
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  • [Title] Selective intermediate-/small-conductance calcium-activated potassium channel (KCNN4) blockers are potent and effective therapeutics in experimental brain oedema and traumatic brain injury caused by acute subdural haematoma.
  • Early deterioration and death after brain injury is often the result of oedema in the injured and peri-lesional tissue.
  • So far, no pharmacotherapy is available that exhibits significant brain oedema-reducing efficacy in patients.
  • We selected two low molecular weight compounds from different chemical classes, a triazole (1-[(2-chlorophenyl)diphenylmethyl]-1,2,3-triazole) and a cyclohexadiene (methyl 4-[4-chloro-3-(trifluoromethyl)phenyl]-6-methyl-3-oxo-1,4,7-tetrahydroisobenzofuran-5-carboxylate) to characterize their pharmacological properties on KCNN4 channels (intermediate/small conductance calcium-activated potassium channel, subfamily N, member 4) in vitro as well as in vivo.
  • In vitro we replaced potassium by rubidium (Rb+) and determined Rb+ fluxes evoked by 10 micro m of the calcium ionophore A23187 on C6BU1 rat glioma cells.
  • It is concluded that blockade of KCNN4 channels is a new pharmacological approach to attenuate acute brain damage caused by traumatic brain injury.
  • [MeSH-major] Brain Edema / therapy. Brain Injuries / therapy. Clotrimazole / therapeutic use. Hematoma, Subdural / therapy. Potassium Channel Blockers / therapeutic use
  • [MeSH-minor] Animals. Brain Chemistry. Calcimycin / pharmacology. Cell Line, Tumor. Cerebral Infarction / pathology. Charybdotoxin / therapeutic use. DNA Primers. Erythrocytes / physiology. Glioma / genetics. Humans. Intermediate-Conductance Calcium-Activated Potassium Channels. Potassium Channels, Calcium-Activated. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction. Rubidium / blood. Water / analysis

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  • (PMID = 15379997.001).
  • [ISSN] 0953-816X
  • [Journal-full-title] The European journal of neuroscience
  • [ISO-abbreviation] Eur. J. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Intermediate-Conductance Calcium-Activated Potassium Channels; 0 / KCNN4 protein, human; 0 / Potassium Channel Blockers; 0 / Potassium Channels, Calcium-Activated; 059QF0KO0R / Water; 115422-61-2 / Charybdotoxin; 37H9VM9WZL / Calcimycin; G07GZ97H65 / Clotrimazole; MLT4718TJW / Rubidium
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35. Ong CS, Tran E, Nguyen TT, Ong CK, Lee SK, Lee JJ, Ng CP, Leong C, Huynh H: Quercetin-induced growth inhibition and cell death in nasopharyngeal carcinoma cells are associated with increase in Bad and hypophosphorylated retinoblastoma expressions. Oncol Rep; 2004 Mar;11(3):727-33
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  • [Title] Quercetin-induced growth inhibition and cell death in nasopharyngeal carcinoma cells are associated with increase in Bad and hypophosphorylated retinoblastoma expressions.
  • Nasopharyngeal carcinoma is a common cancer in South-East Asia, especially among people of Chinese origin.
  • In this report, we investigate the effects of quercetin on the growth of wild-type and mutant p53 nasopharyngeal carcinoma cell lines, HK1 and CNE2 respectively.
  • The wild-type p53 HK1 was more susceptible to growth inhibition by quercetin than the mutant p53 CNE2.
  • Cell growth arrest was initiated by the up-regulation of retinoblastoma gene expression, resulting in cell cycle arrest in either the G2/M or G0/G1 phase at 14.8 and 52.1 microM quercetin respectively regardless of the p53 status.
  • [MeSH-major] Carcinoma / drug therapy. Carrier Proteins / biosynthesis. Nasopharyngeal Neoplasms / drug therapy. Quercetin / pharmacology. Retinoblastoma Protein / biosynthesis
  • [MeSH-minor] Aged. Apoptosis. Blotting, Western. Caspase 3. Caspase 7. Caspases / metabolism. Cell Cycle. Cell Death. Cell Division / drug effects. Cell Line, Tumor. Coloring Agents / pharmacology. Flow Cytometry. Humans. Male. Necrosis. Phosphorylation. S Phase. Tumor Suppressor Protein p53 / metabolism. Up-Regulation. bcl-Associated Death Protein

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  • (PMID = 14767529.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / BAD protein, human; 0 / Carrier Proteins; 0 / Coloring Agents; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 0 / bcl-Associated Death Protein; 9IKM0I5T1E / Quercetin; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP7 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7; EC 3.4.22.- / Caspases
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36. Wu Q, Qin SK, Teng FM, Chen CJ, Wang R: Lobaplatin arrests cell cycle progression in human hepatocellular carcinoma cells. J Hematol Oncol; 2010;3:43
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  • [Title] Lobaplatin arrests cell cycle progression in human hepatocellular carcinoma cells.
  • In the present study, the effect of lobaplatin was assessed in five HCC cell lines and the underlying molecular mechanisms in terms of cell cycle kinetics were explored.
  • METHODS: Cytotoxicity of lobaplatin to human HCC cell lines was examined using MTT cell proliferation assay.
  • The phosphorylation status of cyclin-dependent kinases (CDKs) and retinoblastoma (Rb) protein was also examined using Western blot analysis.
  • RESULTS: Lobaplatin inhibited proliferation of human HCC cells in a dose-dependent manner.
  • For the most sensitive SMMC-7721 cells, lobaplatin arrested cell cycle progression in G1 and G2/M phases time-dependently which might be associated with the down-regulation of cyclin B, CDK1, CDC25C, phosphorylated CDK1 (pCDK1), pCDK4, Rb, E2F, and pRb, and the up-regulation of p53, p21, and p27.
  • CONCLUSION: Cytotoxicity of lobaplatin in human HCC cells might be due to its ability to arrest cell cycle progression which would contribute to the potential use of lobaplatin for the management of HCC.
  • [MeSH-major] Carcinoma, Hepatocellular / drug therapy. Cyclobutanes / pharmacology. Liver Neoplasms / drug therapy. Organoplatinum Compounds / pharmacology
  • [MeSH-minor] CDC2 Protein Kinase / biosynthesis. CDC2 Protein Kinase / genetics. Cell Culture Techniques. Cell Cycle / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Cyclin B / biosynthesis. Cyclin B / genetics. Cyclin-Dependent Kinase 4 / biosynthesis. Cyclin-Dependent Kinase 4 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / biosynthesis. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p27 / biosynthesis. Cyclin-Dependent Kinase Inhibitor p27 / genetics. Down-Regulation / drug effects. E2F Transcription Factors / biosynthesis. E2F Transcription Factors / genetics. Humans. Retinoblastoma Protein / biosynthesis. Retinoblastoma Protein / genetics. Tumor Suppressor Protein p53 / biosynthesis. Tumor Suppressor Protein p53 / genetics. Up-Regulation / drug effects. cdc25 Phosphatases / biosynthesis. cdc25 Phosphatases / genetics

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  • (PMID = 21034513.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin B; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclobutanes; 0 / E2F Transcription Factors; 0 / Organoplatinum Compounds; 0 / Retinoblastoma Protein; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.22 / CDC2 Protein Kinase; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 3.1.3.48 / CDC25C protein, human; EC 3.1.3.48 / cdc25 Phosphatases; OX5XK1JD8C / lobaplatin
  • [Other-IDs] NLM/ PMC2988698
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37. Jackson JG, Pereira-Smith OM: Primary and compensatory roles for RB family members at cell cycle gene promoters that are deacetylated and downregulated in doxorubicin-induced senescence of breast cancer cells. Mol Cell Biol; 2006 Apr;26(7):2501-10
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  • [Title] Primary and compensatory roles for RB family members at cell cycle gene promoters that are deacetylated and downregulated in doxorubicin-induced senescence of breast cancer cells.
  • When treated with DNA-damaging chemotherapy agents, many cancer cells, in vivo and in vitro, undergo a terminal growth arrest and acquire a senescence-like phenotype.
  • We investigated the molecular basis for this in breast cancer cells following a 2-hour treatment with 1 muM doxorubicin.
  • Treated cells arrested in G1 and G2 phases of the cell cycle, with concomitant reductions in S-phase and G2-M regulatory genes. p53 and p21 protein levels increased within hours after treatment and were maintained for 5 to 6 days but were reduced 8 days posttreatment, though the cells remained growth arrested.
  • Levels of p130 rose after drug treatment, and it was the primary RB family member recruited to the S-phase promoters cyclin A and PCNA and G2-M promoters cyclin B and cdc2, remaining present for the entire 8-day time period.
  • In contrast, p107 protein and promoter occupancy levels declined sharply after drug treatment.
  • RB was recruited to only the PCNA promoter.
  • These results demonstrate a mechanistic role for p130 and compensatory roles for p107 and RB in the long-term senescence-like growth arrest response of breast cancer cells to DNA damage.

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  • (PMID = 16537896.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / P01AG2752
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histones; 0 / Proteins; 0 / RNA, Messenger; 0 / Retinoblastoma Protein; 0 / Retinoblastoma-Like Protein p107; 0 / Retinoblastoma-Like Protein p130; 0 / Tumor Suppressor Protein p53; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ PMC1430319
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38. Albitar L, Carter MB, Davies S, Leslie KK: Consequences of the loss of p53, RB1, and PTEN: relationship to gefitinib resistance in endometrial cancer. Gynecol Oncol; 2007 Jul;106(1):94-104
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  • [Title] Consequences of the loss of p53, RB1, and PTEN: relationship to gefitinib resistance in endometrial cancer.
  • OBJECTIVE: These studies demonstrate how loss of function mutations or downregulation of key tumor suppressors missing from type I and type II endometrial cancer cells contributes to carcinogenesis and to resistance to the EGFR inhibitor gefitinib (ZD1839).
  • METHODS: Cell models devoid of tumor suppressors PTEN and RB1 or PTEN were studied.
  • PTEN, RB1 and p53 expression was reinstated, and the effects on cell cycle, apoptosis, and cell cycle regulators were evaluated.
  • RESULTS: In Ishikawa H cells that model type I endometrial cancer in the loss of PTEN and RB1, re-expressing PTEN and RB1 increased the apoptotic and G1 phases and decreased the S and G2-M phases, which further sensitize the cells to gefitinib.
  • Expressing p53 in Hec50co that model type II tumors by loss of this tumor suppressor arrested cells at the G1-S checkpoint, and apoptosis was also induced.
  • Yet this did not improve sensitivity to gefitinib.
  • Modulation of the cell cycle regulators responsible for these changes is explored, and a potential new therapeutic target, MDM2, is identified.
  • CONCLUSION: The downregulation of p53 expression in type II Hec50co cells is linked to gefitinib resistance.
  • MDM2 phosphorylation is only partially blocked by gefitinib, and high MDM2 expression may relate to drug resistance.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Endometrial Neoplasms / drug therapy. Endometrial Neoplasms / genetics. PTEN Phosphohydrolase / deficiency. Quinazolines / pharmacology. Retinoblastoma Protein / deficiency. Tumor Suppressor Protein p53 / deficiency
  • [MeSH-minor] Cell Cycle / drug effects. Cell Cycle / genetics. Cell Cycle Proteins / biosynthesis. Cell Line, Tumor. Drug Resistance, Neoplasm. Female. Genes, Tumor Suppressor. Humans. Transfection

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  • (PMID = 17490733.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA27469; United States / NCI NIH HHS / CA / R01CA99908-1; United States / NCI NIH HHS / CA / R24 CA88339
  • [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 / Antineoplastic Agents; 0 / Cell Cycle Proteins; 0 / Quinazolines; 0 / Retinoblastoma Protein; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; S65743JHBS / gefitinib
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39. Mitsiades CS, Poulaki V, McMullan C, Negri J, Fanourakis G, Goudopoulou A, Richon VM, Marks PA, Mitsiades N: Novel histone deacetylase inhibitors in the treatment of thyroid cancer. Clin Cancer Res; 2005 May 15;11(10):3958-65
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  • [Title] Novel histone deacetylase inhibitors in the treatment of thyroid cancer.
  • Histone deacetylases (HDAC) and histone acetyltransferases exert opposing enzymatic activities that modulate the degree of acetylation of histones and other intracellular molecular targets, thereby regulating gene expression, cellular differentiation, and survival.
  • In these models, both SAHA and m-carboxycinnamic acid bis-hydroxamide induced growth arrest and caspase-mediated apoptosis and increased p21 protein levels, retinoblastoma hypophosphorylation, BH3-interacting domain death agonist cleavage, Bax up-regulation, down-regulation of Bcl-2, A1, and Bcl-x(L) expression, and cleavage of poly(ADP-ribose) polymerase and caspase-8, -9, -3, -7, and -2.
  • SAHA down-regulated the expression of the apoptosis inhibitors FLIP and cIAP-2 and sensitized tumor cells to cytotoxic chemotherapy and death receptor activation.
  • Our studies provide insight into the tumor type-specific mechanisms of antitumor effects of HDAC inhibitors and a framework for future clinical applications of HDAC inhibitors in patients with thyroid cancer, including histologic subtypes (e.g., anaplastic and medullary thyroid carcinomas) for which limited, if any, therapeutic options are available.
  • [MeSH-minor] Apoptosis. Cell Death. Down-Regulation. Gene Expression Regulation, Neoplastic / drug effects. Humans. Tumor Cells, Cultured

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  • (PMID = 15897598.001).
  • [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 / Antineoplastic Agents; 0 / Cinnamates; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / carboxycinnamic acid bishydroxamide; 58IFB293JI / vorinostat
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40. Altintaş E, Ulu O, Sezgin O, Aydin O, Camdeviren H: Comparison of ranitidine bismuth citrate, tetracycline and metronidazole with ranitidine bismuth citrate and azithromycin for the eradication of Helicobacter pylori in patients resistant to PPI based triple therapy. Turk J Gastroenterol; 2004 Jun;15(2):90-3
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  • [Title] Comparison of ranitidine bismuth citrate, tetracycline and metronidazole with ranitidine bismuth citrate and azithromycin for the eradication of Helicobacter pylori in patients resistant to PPI based triple therapy.
  • BACKGROUND/AIMS: Helicobacter pylori is the most common infectious disease all over the world.
  • Ten to twenty percent of the patients remain infected despite treatment with proton pump inhibitors (PPIs), amoxicillin and clarithromycin.
  • We compared PPI, bismuth, tetracycline and metronidazole with ranitidine bismuth citrate, tetracycline and metronidazole in cases resistant to PPIs-based triple therapies.
  • METHODS: The study included 52 patients who underwent a triple therapy with PPI, clarithromycin and amoxicillin for 14 days between September 2001 and December 2002, and were found to be resistant to the therapy.
  • They were randomized to take ranitidine bismuth citrate (Rb) 400 mg twice a day, tetracycline (T) 1 g twice a day and metronidazole (M) 500 mg three times a day for 14 days (RbTM), or ranitidine bismuth citrate (Rb) 400 mg twice a day for 14 days and azithromycin (A) 500 mg once a day for 7 days (RbA).
  • Four weeks after the treatment, endoscopies were repeated, and patients were assessed with respect to changes in symptoms.
  • When H. pylori was negative on histological analysis and urease test, eradication was achieved.
  • RESULTS: A total of 52 patients, 32 females and 20 males with a mean age of 49+/-12 years, were included in the study.
  • There was a significant difference between RbA and RbTM groups (p=0.01).
  • In fact, H. pylori was eradicated in 3 (12%) out of 25 patients in the RbA group, whereas it was eradicated in 12 (44.4%) out of 27 patients in the RbTM group.
  • Symptom scores significantly improved in both groups after the treatment, though there was not a significant difference between the groups (p=0.705).
  • CONCLUSIONS: Triple therapy including azithromycin does not seem to be a good choice in cases resistant to the first line therapies; however, a similarly lower rate of eradication was achieved with the quadruple therapy proposed.
  • Therefore, different treatment schemes should be applied in resistant patients, and further studies are needed as well.
  • [MeSH-major] Anti-Infective Agents / therapeutic use. Anti-Ulcer Agents / therapeutic use. Bismuth / therapeutic use. Helicobacter Infections / drug therapy. Helicobacter pylori. Ranitidine / analogs & derivatives. Ranitidine / therapeutic use
  • [MeSH-minor] Adult. Azithromycin / pharmacology. Azithromycin / therapeutic use. Drug Resistance, Bacterial / drug effects. Female. Gastroscopy. Humans. Male. Metronidazole / pharmacology. Metronidazole / therapeutic use. Middle Aged. Proton Pump Inhibitors. Tetracycline / pharmacology. Tetracycline / therapeutic use. Treatment Failure. Treatment Outcome

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  • (PMID = 15334317.001).
  • [ISSN] 1300-4948
  • [Journal-full-title] The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology
  • [ISO-abbreviation] Turk J Gastroenterol
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Anti-Ulcer Agents; 0 / Proton Pump Inhibitors; 140QMO216E / Metronidazole; 7AJ51I17KG / ranitidine bismuth citrate; 83905-01-5 / Azithromycin; 884KT10YB7 / Ranitidine; F8VB5M810T / Tetracycline; U015TT5I8H / Bismuth
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41. Cartee L, Sankala H, Davis C, Smith R, Maggio S, Lin PS, Dent P, Grant S: 7-hydroxystaurosporine (UCN-01) and ionizing radiation combine to inhibit the growth of Bcl-2-overexpressing U937 leukemia cells through a non-apoptotic mechanism. Int J Oncol; 2002 Aug;21(2):351-9
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  • A clinically relevant dose (2.0 Gy) of ionizing radiation (IR) was employed to determine if subsequent exposure to the protein kinase C (PKC) and Chk 1 inhibitor UCN-01 for 24 h could abrogate IR-induced G2/M arrest and promote apoptosis in U937 leukemic cells ectopically expressing Bcl-2 (U937/Bcl-2).
  • IR (2 Gy) alone minimally induced apoptosis in both U937 transfectant cell lines (e.g., <5% at 24 h in each case).
  • Despite failing to enhance apoptosis, UCN-01 treatment abrogated IR-induced G2/M arrest in both cell lines, an event associated with enhanced activation of cyclin-dependent kinase 1 (cdk1), promotion of G0/G1 arrest, and dephosphorylation of the retinoblastoma protein (pRb).
  • [MeSH-major] Alkaloids / pharmacology. Antineoplastic Agents / pharmacology. Cell Cycle / drug effects. Cell Cycle / radiation effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. U937 Cells / drug effects. U937 Cells / radiation effects
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / radiation effects. Cell Division / drug effects. Cell Division / radiation effects. Combined Modality Therapy. Humans. Membrane Potentials / drug effects. Membrane Potentials / radiation effects. Mitochondria / drug effects. Mitochondria / radiation effects. Protein Kinase C / antagonists & inhibitors. Radiation, Ionizing. Staurosporine / analogs & derivatives. Transfection. Tumor Stem Cell Assay

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  • (PMID = 12118331.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA63753; United States / NCI NIH HHS / CA / P01 CA72955
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Antineoplastic Agents; 0 / Proto-Oncogene Proteins c-bcl-2; 7BU5H4V94A / 7-hydroxystaurosporine; EC 2.7.11.13 / Protein Kinase C; H88EPA0A3N / Staurosporine
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42. Guo JJ, Pandey S, Doyle J, Bian B, Lis Y, Raisch DW: A review of quantitative risk-benefit methodologies for assessing drug safety and efficacy-report of the ISPOR risk-benefit management working group. Value Health; 2010 Aug;13(5):657-66
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  • [Title] A review of quantitative risk-benefit methodologies for assessing drug safety and efficacy-report of the ISPOR risk-benefit management working group.
  • OBJECTIVE: Although regulatory authorities evaluate the risks and benefits of any new drug therapy during the new drug-approval process, quantitative risk-benefit assessment (RBA) is not typically performed, nor is it presented in a consistent and integrated framework when it is used.
  • Our purpose is to identify and describe published quantitative RBA methods for pharmaceuticals.
  • METHODS: Using MEDLINE and other Internet-based search engines, a systematic literature review was performed to identify quantitative methodologies for RBA.
  • These distinct RBA approaches were summarized to highlight the implications of their differences for the pharmaceutical industry and regulatory agencies.
  • RESULTS: Theoretical models, parameters, and key features were reviewed and compared for the 12 quantitative RBA methods identified in the literature, including the Quantitative Framework for Risk and Benefit Assessment, benefit-less-risk analysis, the quality-adjusted time without symptoms and toxicity, number needed to treat (NNT), and number needed to harm and their relative-value-adjusted versions, minimum clinical efficacy, incremental net health benefit, the risk-benefit plane (RBP), the probabilistic simulation method, multicriteria decision analysis (MCDA), the risk-benefit contour (RBC), and the stated preference method (SPM).
  • CONCLUSIONS: Several quantitative RBA methods are available that could be used to help lessen concern over subjective drug assessments and to help guide authorities toward more objective and transparent decision-making.
  • When evaluating a new drug therapy, we recommend the use of multiple RBA approaches across different therapeutic indications and treatment populations in order to bound the risk-benefit profile.
  • [MeSH-major] Drug Approval / methods. Drug-Related Side Effects and Adverse Reactions. Risk Assessment / methods
  • [MeSH-minor] Analysis of Variance. Decision Support Techniques. Decision Trees. Humans. Models, Theoretical. Monte Carlo Method. Probability. Product Surveillance, Postmarketing. Quality-Adjusted Life Years. Statistics, Nonparametric. Treatment Outcome. United States. United States Food and Drug Administration

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  • (PMID = 20412543.001).
  • [ISSN] 1524-4733
  • [Journal-full-title] Value in health : the journal of the International Society for Pharmacoeconomics and Outcomes Research
  • [ISO-abbreviation] Value Health
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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43. Schmidt B, Chun KR, Kuck KH, Ouyang F: [Ventricular tachycardias originating in the his-purkinje system. Bundle branch reentrant ventricular tachycardias and fascicular ventricular tachycardias]. Herz; 2009 Nov;34(7):554-60
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  • [Title] [Ventricular tachycardias originating in the his-purkinje system. Bundle branch reentrant ventricular tachycardias and fascicular ventricular tachycardias].
  • [Transliterated title] Ventrikuläre Tachykardien mit Ursprung im spezifischen Reizleitungssystem : Schenkeltachykardien und faszikuläre ventrikuläre Tachykardien.
  • Ventricular tachycardias (VT) associated with the His-Purkinje system may occur in patients with and without organic heart disease.
  • The former may encounter bundle branch reentrant VT, a macroreentrant VT utilizing the specific conduction system.
  • It frequently occurs in patients with preexisting conduction disturbance such as complete left bundle branch block and may be eliminated by catheter ablation of the right bundle branch.
  • After successful ablation, patient's prognosis depends on the presence or absence of structural heart disease.In patients without structural heart disease, VT with right bundle branch block pattern and superior axis, referred to as idiopathic left ventricular tachycardia, is observed.
  • It is a reentrant VT utilizing the posterior left fascicle and the Purkinje network.
  • The two treatment options include antiarrhythmic drug therapy with verapamil or curative catheter ablation.Another form of ventricular arrhythmia originating in the Purkinje network is idiopathic ventricular fibrillation (IVF).
  • Focal triggers from the right and left ventricular Purkinje network induce premature ventricular contractions inducing IVF.
  • [MeSH-major] Bundle of His / physiopathology. Bundle-Branch Block / physiopathology. Bundle-Branch Block / therapy. Catheter Ablation. Defibrillators, Implantable. Purkinje Fibers / physiopathology. Tachycardia, Atrioventricular Nodal Reentry / complications. Tachycardia, Atrioventricular Nodal Reentry / physiopathology

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  • (PMID = 20091255.001).
  • [ISSN] 1615-6692
  • [Journal-full-title] Herz
  • [ISO-abbreviation] Herz
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 33
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44. Braig M, Lee S, Loddenkemper C, Rudolph C, Peters AH, Schlegelberger B, Stein H, Dörken B, Jenuwein T, Schmitt CA: Oncogene-induced senescence as an initial barrier in lymphoma development. Nature; 2005 Aug 4;436(7051):660-5
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  • [Title] Oncogene-induced senescence as an initial barrier in lymphoma development.
  • Acute induction of oncogenic Ras provokes cellular senescence involving the retinoblastoma (Rb) pathway, but the tumour suppressive potential of senescence in vivo remains elusive.
  • Recently, Rb-mediated silencing of growth-promoting genes by heterochromatin formation associated with methylation of histone H3 lysine 9 (H3K9me) was identified as a critical feature of cellular senescence, which may depend on the histone methyltransferase Suv39h1.
  • By contrast, most N-Ras-transgenic wild-type ('control') animals develop a non-lymphoid neoplasia significantly later.
  • Proliferation of primary lymphocytes is directly stalled by a Suv39h1-dependent, H3K9me-related senescent growth arrest in response to oncogenic Ras, thereby cancelling lymphomagenesis at an initial step.
  • In contrast, only control, but not Suv39h1-deficient or p53-deficient, lymphomas senesce after drug therapy when apoptosis is blocked.
  • These results identify H3K9me-mediated senescence as a novel Suv39h1-dependent tumour suppressor mechanism whose inactivation permits the formation of aggressive but apoptosis-competent lymphomas in response to oncogenic Ras.
  • [MeSH-major] Cell Aging. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Genes, ras / genetics. Lymphoma / genetics. Lymphoma / pathology
  • [MeSH-minor] ADP-Ribosylation Factors / metabolism. Animals. Apoptosis / drug effects. Biomarkers, Tumor / analysis. Biomarkers, Tumor / metabolism. Chromosomal Instability / genetics. Disease Models, Animal. Disease Progression. Gene Expression Regulation, Neoplastic. Heterochromatin / genetics. Heterochromatin / metabolism. Methylation. Methyltransferases / deficiency. Methyltransferases / genetics. Methyltransferases / metabolism. Mice. Mice, Transgenic. Precancerous Conditions / genetics. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Repressor Proteins / genetics. Repressor Proteins / metabolism. Transgenes / genetics. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism


45. Nagao T, Higashitsuji H, Nonoguchi K, Sakurai T, Dawson S, Mayer RJ, Itoh K, Fujita J: MAGE-A4 interacts with the liver oncoprotein gankyrin and suppresses its tumorigenic activity. J Biol Chem; 2003 Mar 21;278(12):10668-74
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  • [Title] MAGE-A4 interacts with the liver oncoprotein gankyrin and suppresses its tumorigenic activity.
  • Although there are many modalities of treatment, the recurrence and metastasis rates are high, and the prognosis is unsatisfactory.
  • Gankyrin, a recently found oncoprotein, is a promising target for drug therapy because it is overexpressed in all studied hepatocellular carcinomas.
  • Gankyrin contains six ankyrin repeats and interacts with Rb, Cdk4, and the S6 ATPase of the 26 S proteasome.
  • The interaction, mediated by the C-terminal half of MAGE-A4, was reproduced in mammalian cells.
  • MAGE-A1, MAGE-A2, and MAGE-A12, did not bind to gankyrin.
  • MAGE-A4 partially suppressed both anchorage-independent growth in vitro and tumor formation in athymic mice of gankyrin-overexpressing cells.
  • These results demonstrate that MAGE-A4 binds to gankyrin and suppresses its oncogenic activity.
  • So far, the major focus of studies on the MAGE proteins has been on their potential for cancer immunotherapy.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Neoplasm Proteins. Neoplasms, Experimental / prevention & control. Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins
  • [MeSH-minor] 3T3 Cells. Amino Acid Sequence. Animals. Cell Transformation, Neoplastic / drug effects. Cyclin-Dependent Kinase 4. Cyclin-Dependent Kinases / metabolism. Female. Mice. Mice, Inbred BALB C. Molecular Sequence Data. Proteasome Endopeptidase Complex. Retinoblastoma Protein / metabolism. Ribosomal Protein S6 Kinases / metabolism

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  • (PMID = 12525503.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ D83197/ U10687; RefSeq/ NM/ 004988/ NM/ 005361/ XM/ 010079
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / MAGEA4 protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins; 0 / PSMD10 protein, human; 0 / Proto-Oncogene Proteins; 0 / Retinoblastoma Protein; EC 2.7.11.1 / Ribosomal Protein S6 Kinases; EC 2.7.11.22 / Cdk4 protein, mouse; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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46. Rigotti P, Baldan N, Valente M, Scappin S, Furian L, Cadrobbi R, Marchini F, Ancona E: Evaluation of 84 elderly donors in renal transplantation. Clin Transplant; 2004 Aug;18(4):440-5
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  • The aim of this investigation was to assess the role of renal biopsy (RB) in the assessment of kidneys from ED.
  • In 19 cases, the kidneys were not used, mainly because of atherosclerotic vascular lesions.
  • All recipients received triple-drug therapy based on calcineurin inhibitors, mycophenolate mofetil and steroids.
  • RESULTS: Primary non-function was observed in three of 40 ST and one of 21 DKT.
  • Renal function was satisfactory in both groups, with 1-yr S-Cr = 171 micromol/L and 137 micromol/L, respectively in the ST and DKT groups.
  • One-year patient survival was 92% in ST and 100% in DKT; 1-yr graft function was 87% in ST and 95% in DKT.
  • [MeSH-major] Kidney Transplantation. Tissue Donors
  • [MeSH-minor] Age Factors. Aged. Biopsy. Female. Humans. Kidney / pathology. Male. Middle Aged. Patient Selection


47. Tomoda C, Moatamed F, Naeim F, Hershman JM, Sugawara M: Indomethacin inhibits cell growth of medullary thyroid carcinoma by reducing cell cycle progression into S phase. Exp Biol Med (Maywood); 2008 Nov;233(11):1433-40
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  • Indomethacin, a non-steroidal anti-inflammatory drug (NSAID), has been reported to inhibit the growth of medullary thyroid carcinoma (MTC) cells in vitro.
  • However, the mechanism of inhibition of MTC cell growth by indomethacin and its potency have yet to be revealed.
  • Indomethacin inhibited cell growth of all three MTC cell lines but not normal thyroid cells or anaplastic thyroid carcinoma cells.
  • Indomethacin at 10 microM or greater showed a dose response inhibition of cell growth.
  • Indomethacin at 25 muM, a putative therapeutic serum indomethacin level, showed potency similar to 100 to 200 nM sunitinib, a receptor tyrosine kinase inhibitor.
  • Indomethacin did not increase apoptosis of TT cells.
  • Indomethacin, but not naproxen or indomethacin-ester, reduced cell cycle progression into S phase; this was unrelated to the degree of PGE2 depletion.
  • The expression of phosphorylated retinoblastoma (pRb) protein that shifts cells from G(1) to S phase was reduced after exposure to indomethacin.
  • In conclusion, indomethacin has specific anti-tumor effect on MTC cells, probably by reducing cell cycle progression into S phase rather than by prostaglandin depletion.
  • Since no drug therapy is currently available for MTC, indomethacin may be one of the therapeutic candidates.
  • [MeSH-major] Carcinoma, Medullary / pathology. Cell Cycle / drug effects. Cell Proliferation / drug effects. Cyclooxygenase Inhibitors / pharmacology. Indomethacin / pharmacology. Thyroid Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Calcitonin / genetics. Carcinoembryonic Antigen / genetics. Cell Line. Dinoprostone / metabolism. Gene Expression / drug effects. Humans. Indoles / pharmacology. Phosphorylation. Pyrroles / pharmacology. Retinoblastoma Protein / metabolism. S Phase / drug effects

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  • (PMID = 18791128.001).
  • [ISSN] 1535-3702
  • [Journal-full-title] Experimental biology and medicine (Maywood, N.J.)
  • [ISO-abbreviation] Exp. Biol. Med. (Maywood)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carcinoembryonic Antigen; 0 / Cyclooxygenase Inhibitors; 0 / Indoles; 0 / Pyrroles; 0 / Retinoblastoma Protein; 0 / sunitinib; 9007-12-9 / Calcitonin; K7Q1JQR04M / Dinoprostone; XXE1CET956 / Indomethacin
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48. Chung J, Turaka K, Shields CL: Retinocytoma shows lack of response to chemoreduction. J Pediatr Ophthalmol Strabismus; 2010;47 Online:e1-3
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  • The authors report a case of retinocytoma showing no response to chemoreduction.
  • A 30-month-old girl presented with Group B multifocal retinoblastoma in the right eye and Group E retinoblastoma in the left eye.
  • After the first cycle of chemotherapy (vincristine [0.9 mg/m(2)], carboplatin [336 mg/m(2)], and etoposide [90 mg/m(2)]), there was remarkable reduction in the tumor size in the left eye, whereas the right eye tumors did not regress and were diagnosed as retinocytomas/retinomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasm Seeding. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Carboplatin / therapeutic use. Child, Preschool. Combined Modality Therapy. Cryotherapy. Esotropia / diagnosis. Etoposide / therapeutic use. Female. Humans. Magnetic Resonance Imaging. Treatment Outcome. Vincristine / therapeutic use. Visual Acuity / physiology. Vitreous Body / pathology

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  • [Copyright] Copyright 2010, SLACK Incorporated.
  • (PMID = 21175116.001).
  • [ISSN] 1938-2405
  • [Journal-full-title] Journal of pediatric ophthalmology and strabismus
  • [ISO-abbreviation] J Pediatr Ophthalmol Strabismus
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin; CEV regimen
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49. Toral-Martinñon R, Collado-Corona MA, Mora-Magaña I, Leal-Leal C, Gutiérrez-Castrellón P, González-de Leo S: [Evaluation of cisplatin ototoxicity by the audiometric curve in retinoblastoma]. Cir Cir; 2006 Mar-Apr;74(2):79-82
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  • [Title] [Evaluation of cisplatin ototoxicity by the audiometric curve in retinoblastoma].
  • [Transliterated title] Evaluación de la ototoxicidad del cisplatino por el área bajo la curva audiométrica en retinoblastoma.
  • BACKGROUND: To evaluate hearing loss severity according to Brock's gradient and to compare it with the audiometric curve during cisplatin treatment in children with retinoblastoma.
  • Twenty children with the diagnosis of retinoblastoma under cisplatin treatment were included.
  • Audiometric testing was performed before treatment, after the second and fourth doses, and after the final dose.
  • This level was observed in 95% of the cases at the end of treatment.
  • Two years after completion of therapy, no patient showed auditory recovery.
  • Area below the curve showed higher sensitivity to identify initial auditory loss.
  • The area under the curve is a useful method to identify minor changes in serial conventional audiometry.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Cisplatin / adverse effects. Hearing Loss / chemically induced. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Audiometry. Child. Child, Preschool. Evaluation Studies as Topic. Female. Humans. Infant. Male. Retrospective Studies

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  • (PMID = 16887078.001).
  • [ISSN] 0009-7411
  • [Journal-full-title] Cirugía y cirujanos
  • [ISO-abbreviation] Cir Cir
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Antineoplastic Agents; Q20Q21Q62J / Cisplatin
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50. Patel J, Turaka K, Shields CL: Resolution of iris neovascularization following chemoreduction of retinoblastoma. J Pediatr Ophthalmol Strabismus; 2010;47 Online:e1-3
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  • [Title] Resolution of iris neovascularization following chemoreduction of retinoblastoma.
  • The authors report a case of advanced retinoblastoma (group E) with iris neovascularization.
  • A 30-month-old girl was diagnosed as having group B retinoblastoma in the right eye and group E retinoblastoma and iris neovascularization with an intraocular pressure of 13 mm Hg in the left eye.
  • The tumors were treated with six cycles of chemotherapy using vincristine (0.9 mg/m(2)), carboplatin (336 mg/m(2)), and etoposide (90 mg/m(2)).
  • At 1 month of follow-up, there was dramatic regression of the retinoblastoma in the left eye and complete resolution of the iris neovascularization, which remained stable at 3 months of follow-up.
  • Chemotherapy is an effective conservative treatment for advanced retinoblastoma and can successfully salvage eyes with neovascularization, particularly before the onset of glaucoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Iris / blood supply. Neovascularization, Pathologic / physiopathology. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Carboplatin / therapeutic use. Child, Preschool. Etoposide / therapeutic use. Female. Humans. Treatment Outcome. Vincristine / therapeutic use. Visual Acuity / physiology

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  • [Copyright] Copyright 2010, SLACK Incorporated.
  • (PMID = 21162463.001).
  • [ISSN] 1938-2405
  • [Journal-full-title] Journal of pediatric ophthalmology and strabismus
  • [ISO-abbreviation] J Pediatr Ophthalmol Strabismus
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; BG3F62OND5 / Carboplatin; CEV regimen
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51. Kremens B, Wieland R, Reinhard H, Neubert D, Beck JD, Klingebiel T, Bornfeld N, Havers W: High-dose chemotherapy with autologous stem cell rescue in children with retinoblastoma. Bone Marrow Transplant; 2003 Feb;31(4):281-4
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  • [Title] High-dose chemotherapy with autologous stem cell rescue in children with retinoblastoma.
  • Children with metastatic retinoblastoma are considered to have a poor prognosis after conventional chemotherapy.
  • We used high-dose chemotherapy (HDC) with peripheral hematopoietic stem cell transplantation in such patients in an attempt to improve their survival.
  • Four patients with bone marrow metastases and one child with extraorbital disease were treated with HDC after achieving complete remission by enucleation and conventional chemotherapy.
  • The child with extraorbital tumor was the only one to receive local irradiation.
  • The conditioning regimen included thiotepa (900 mg/m(2)), etoposide (40 mg/kg) and carboplatin (1.5 g/m(2)) in four patients, and BCNU (300 mg/m(2)), cyclophosphamide (6.8 g/m(2)) and etoposide (1.6 g/m(2)) in one child.
  • The child treated with the BCNU regimen developed a meningeal relapse 10 months after HDC, which was partially resected and treated with conventional chemotherapy, but not with radiotherapy.
  • He is in complete remission (CR) 105 months off treatment.
  • HDC with thiotepa, etoposide and carboplatin may represent a curative option for children with extrabulbar or disseminated retinoblastoma responsive to chemotherapy.
  • It may control occult CNS disease.
  • The necessity to irradiate these children and the curative potential of this strategy for patients with bulky CNS disease remain to be determined.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Eye Neoplasms / therapy. Retinoblastoma / therapy. Stem Cell Transplantation. Transplantation, Autologous
  • [MeSH-minor] Bone Marrow / pathology. Carmustine / administration & dosage. Child. Child, Preschool. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Etoposide / administration & dosage. Eye Enucleation. Female. Humans. Male. Recurrence. Treatment Outcome

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  • [ErratumIn] Bone Marrow Transplant. 2003 Jun;31(12):1185
  • (PMID = 12621463.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; U68WG3173Y / Carmustine
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52. 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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  • The anti-cancer agent paclitaxel (Taxol) stabilizes microtubules leading to G2/M cell cycle arrest and apoptotic cell death.
  • In order to analyse the molecular mechanisms of Taxol-induced cytotoxicity, we studied the involvement of mitogen-activated protein kinases (MAPK) ERK and p38 as well as the p53 pathways in Taxol-induced apoptosis.
  • The human breast carcinoma cell line MCF7 and its derivatives, MCF7/HER-2 and MDD2, were used in the study.
  • We found that Taxol treatment strongly activated ERK, p38 MAP kinase and p53 in MAP kinase MCF7 cells prior to apoptosis.
  • PD98059 or SB203580, specific inhibitors of ERK and p38 kinase activities, significantly decreased apoptosis, leaving the surviving cells arrested in G2/M.
  • These inhibitors did not significantly affect Taxol-induced alterations in the cell cycle regulatory proteins Rb, p53, p21/Waf1 and Cdk-2.
  • In addition, inactivation of p53 did not affect cellular sensitivity to Taxol killing.
  • 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.
  • Our data show that both ERK and p38 MAP kinase cascades are essential for apoptotic response to Taxol-induced cellular killing and are independent of p53 activity.
  • [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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53. Dunkel IJ, Aledo A, Kernan NA, Kushner B, Bayer L, Gollamudi SV, Finlay JL, Abramson DH: Successful treatment of metastatic retinoblastoma. Cancer; 2000 Nov 15;89(10):2117-21
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  • [Title] Successful treatment of metastatic retinoblastoma.
  • BACKGROUND: In the past, patients with metastatic retinoblastoma have had a poor prognosis when treated with conventional modalities.
  • In the current study, the authors evaluated the use of combined intensive conventional chemotherapy, high dose chemotherapy with autologous stem cell rescue (ASCR), and radiation therapy.
  • METHODS: Four patients with metastatic retinoblastoma were treated.
  • None had central nervous system disease.
  • Patients received intensive conventional chemotherapy that included vincristine, cyclophosphamide, etoposide, and either cisplatin or carboplatin.
  • Stem cells were harvested after bone marrow disease was no longer detectable.
  • High dose chemotherapy with carboplatin (500 mg/m(2)/day x 3 days or area under the curve = 7 via the Calvert formula) and thiotepa (300 mg/m(2)/day x 3 days) with (n = 3 patients) or without (n = 1 patient) etoposide (250 mg/m(2)/day x 3 days) was administered with ASCR.
  • Sites that originally harbored bulky disease were irradiated after recovery from the high dose chemotherapy.
  • RESULTS: The therapy was associated with substantial acute hematopoietic and mucosal toxicities.
  • At last follow-up, all four patients had survived event free from 46-80 months after the diagnosis of metastatic disease.
  • CONCLUSIONS: The treatment strategy described in the current study is effective for patients with metastatic retinoblastoma that does not involve the central nervous system.
  • However, a multicenter trial should be considered to evaluate it in a larger group of patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Bone Marrow Neoplasms / therapy. Hematopoietic Stem Cell Transplantation. Retinal Neoplasms / therapy. Retinoblastoma / therapy
  • [MeSH-minor] Adolescent. Adult. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Male. Survival Analysis. Treatment Outcome

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  • [Copyright] Copyright 2000 American Cancer Society.
  • (PMID = 11066053.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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54. Drago-Ferrante R, Santulli A, Di Fiore R, Giuliano M, Calvaruso G, Tesoriere G, Vento R: Low doses of paclitaxel potently induce apoptosis in human retinoblastoma Y79 cells by up-regulating E2F1. Int J Oncol; 2008 Oct;33(4):677-87
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  • [Title] Low doses of paclitaxel potently induce apoptosis in human retinoblastoma Y79 cells by up-regulating E2F1.
  • Paclitaxel (PTX) is an anticancer drug currently in phase II clinical trials.
  • This study shows for the first time that low doses of PTX (5 nM) potently induce apoptosis in human retinoblastoma Y79 cells.
  • PTX induced a dose- and time-dependent effect, with G2/M arrest, cyclines A, E and B1 accumulation and a marked modification in the status of Cdc2-cyclin B1 complex, the major player of the G2/M checkpoint.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis. E2F1 Transcription Factor / metabolism. Gene Expression Regulation, Neoplastic. Paclitaxel / pharmacology. Retinoblastoma / drug therapy. Retinoblastoma / pathology
  • [MeSH-minor] Cell Division. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. G2 Phase. Humans. Membrane Potential, Mitochondrial. Phosphorylation. Tumor Suppressor Protein p53 / metabolism. Up-Regulation

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  • (PMID = 18813780.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / E2F1 Transcription Factor; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; P88XT4IS4D / Paclitaxel
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55. Fouty B, Moss T, Solodushko V, Kraft M: Dexamethasone can stimulate G1-S phase transition in human airway fibroblasts in asthma. Eur Respir J; 2006 Jun;27(6):1160-7
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  • [Title] Dexamethasone can stimulate G1-S phase transition in human airway fibroblasts in asthma.
  • Corticosteroids are the first line of therapy for asthma.
  • To determine whether corticosteroids could alter the fibroblast cell cycle the current authors studied the effect of dexamethasone on cultured airway fibroblasts obtained from nine mild-to-moderate, steroid-naïve asthmatics (forced expiratory volume in one second 78+/-4% predicted), and seven normal controls.
  • Cells were exposed to dexamethasone (10(-9)-10(-7) M) and studied at 72 h to determine differences in progression through the cell cycle.
  • In asthmatic fibroblasts, dexamethasone, at concentrations of 10(-8)M and 10(-7)M, nearly doubled the number of cells in the S phase (17.8+/-3.0% and 18.4+/-3.1%, respectively) compared with untreated fibroblasts (10.3+/-1.4%).
  • Dexamethasone induced hyperphosphorylation of the tumour suppressor, retinoblastoma (RB) in asthmatic fibroblasts; fibroblasts from normal controls had significantly less hyperphosphorylation of RB.
  • This study suggests that dexamethasone can stimulate G1-S phase cell cycle transition in human airway fibroblasts obtained from asthmatics.
  • [MeSH-major] Anti-Inflammatory Agents / pharmacology. Asthma / pathology. Bronchial Hyperreactivity / pathology. Dexamethasone / pharmacology. Fibroblasts / drug effects. G1 Phase / drug effects. Muscle, Smooth / drug effects. S Phase / drug effects
  • [MeSH-minor] Adult. Biopsy. Bronchi / drug effects. Bronchi / pathology. Bronchoscopy. Cell Division / drug effects. Cells, Cultured. Female. Genes, Tumor Suppressor / drug effects. Humans. In Vitro Techniques. Lung / drug effects. Lung / pathology. Male. Phosphorylation / drug effects. Retinoblastoma Protein / drug effects. Stimulation, Chemical

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  • (PMID = 16510457.001).
  • [ISSN] 0903-1936
  • [Journal-full-title] The European respiratory journal
  • [ISO-abbreviation] Eur. Respir. J.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL64619; United States / NHLBI NIH HHS / HL / R01 HL070273
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Retinoblastoma Protein; 7S5I7G3JQL / Dexamethasone
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56. Park WH, Jung CW, Park JO, Kim K, Kim WS, Im YH, Lee MH, Kang WK, Park K: Monensin inhibits the growth of renal cell carcinoma cells via cell cycle arrest or apoptosis. Int J Oncol; 2003 Apr;22(4):855-60
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  • When we examined the effects of this drug on ACHN cells, monensin decreased the levels of CDK2, CDK6, cdc2, cyclin A and cyclin B1 proteins. p21 and p27 proteins were increased by monensin.
  • Furthermore, the activities of CDK2- and CDK6-associated kinase were reduced in association with hypophosphorylation of Rb protein.
  • Apoptotic process of Caki-2 cells was associated with the changes of Bcl-2, Bcl-XL, caspase-9, caspase-3, caspase-7 proteins as well as mitochondria transmembrane potential (DeltaPsim) loss.
  • Taken together, these results demonstrate for the first time that monensin inhibits the growth of renal cell carcinoma cells via cell cycle arrest or apoptosis.
  • [MeSH-major] Apoptosis. Carcinoma, Renal Cell / drug therapy. Kidney Neoplasms / drug therapy. Monensin / pharmacology. Muscle Proteins
  • [MeSH-minor] Antifungal Agents / pharmacology. Blotting, Western. CDC2-CDC28 Kinases / metabolism. Caspases / metabolism. Cell Cycle. Cell Division. Cell Line. Cell Line, Tumor. Cyclin-Dependent Kinase 2. Cyclin-Dependent Kinase 6. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / metabolism. Cyclins / metabolism. Dose-Response Relationship, Drug. G1 Phase. G2 Phase. Humans. Inhibitory Concentration 50. Ionophores / pharmacology. Microfilament Proteins / metabolism. Microscopy, Fluorescence. Phosphorylation. Precipitin Tests. Retinoblastoma Protein / metabolism. Sodium / metabolism

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  • (PMID = 12632079.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Ionophores; 0 / Microfilament Proteins; 0 / Muscle Proteins; 0 / Retinoblastoma Protein; 0 / Tagln protein, mouse; 906O0YJ6ZP / Monensin; 9NEZ333N27 / Sodium; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 2.7.11.22 / CDK2 protein, human; EC 2.7.11.22 / CDK6 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.22 / Cyclin-Dependent Kinase 6; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 3.4.22.- / Caspases
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57. Jehanne M, Lumbroso-Le Rouic L, Savignoni A, Aerts I, Mercier G, Bours D, Desjardins L, Doz F: Analysis of ototoxicity in young children receiving carboplatin in the context of conservative management of unilateral or bilateral retinoblastoma. Pediatr Blood Cancer; 2009 May;52(5):637-43
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  • [Title] Analysis of ototoxicity in young children receiving carboplatin in the context of conservative management of unilateral or bilateral retinoblastoma.
  • BACKGROUND: Carboplatin plays an important role in the conservative management of retinoblastoma, but is associated with risk of ototoxicity in these young children whose sensory prognosis may be also compromised by their loss of vision.
  • This retrospective study analyzed the impact of carboplatin on hearing in the context of conservative management of children with retinoblastoma.
  • RESULTS: Median age at diagnosis was 8 months (0-60).
  • Carboplatin was administered on 3 days (200 mg/m(2)/day) or 5 days (160 mg/m(2)/day) with etoposide and with diode-laser therapy at the dose of 560 mg/m(2) (chemothermotherapy).
  • Ototoxicity was investigated by pure-tone audiometry and scored by Brock's grading scale before and after treatment.
  • Two children developed bilateral high frequency hearing-loss, considered to be secondary to carboplatin but with less than Brock grade 1.
  • Ototoxicity was observed for a median cumulative dose of carboplatin of 3,120 mg/m(2) (1,200-5,830).
  • Only one child developed ototoxicity during treatment.
  • All other cases were discovered after the last dose of carboplatin with a median interval of 3.7 years (0-7.6).
  • [MeSH-major] Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Carboplatin / adverse effects. Carboplatin / therapeutic use. Ear Diseases / chemically induced. Retinoblastoma / drug therapy. Retinoblastoma / pathology
  • [MeSH-minor] Child, Preschool. Female. Follow-Up Studies. Humans. Infant. Infant, Newborn. Male. Treatment Outcome

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • [CommentIn] Pediatr Blood Cancer. 2009 Sep;53(3):517 [19484758.001]
  • (PMID = 19148943.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; BG3F62OND5 / Carboplatin
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58. Tan AR, Yang X, Berman A, Zhai S, Sparreboom A, Parr AL, Chow C, Brahim JS, Steinberg SM, Figg WD, Swain SM: Phase I trial of the cyclin-dependent kinase inhibitor flavopiridol in combination with docetaxel in patients with metastatic breast cancer. Clin Cancer Res; 2004 Aug 1;10(15):5038-47
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  • [Title] Phase I trial of the cyclin-dependent kinase inhibitor flavopiridol in combination with docetaxel in patients with metastatic breast cancer.
  • PURPOSE: The purpose of this study was to determine the toxicities and characterize the pharmacokinetics of docetaxel and flavopiridol in patients with metastatic breast cancer.
  • Because dose-limiting myelosuppression occurred, the schedule was amended to docetaxel, 50 mg/m(2), followed by escalating doses of flavopiridol (starting dose, 26 mg/m(2)/d) as a 1-hour infusion daily for 3 days.
  • Ki67, p53, and phosphorylated retinoblastoma protein (phospho-Rb) in paired tumor and buccal mucosa biopsies (obtained pre- and posttreatment) were examined by immunohistochemistry.
  • Nuclear staining with p53 increased and phospho-Rb decreased in 10 pairs of buccal mucosa biopsies posttreatment (P = 0.002 and P = 0.04, respectively).
  • No significant changes in Ki67, p53, or phospho-Rb were detected in six paired tumors.
  • Two patients sustained stable disease for >3 months (72-hour flavopiridol), and one partial response was observed (1-hour flavopiridol).
  • CONCLUSIONS: Docetaxel combined with 72-hour flavopiridol was not feasible because of dose-limiting neutropenia.
  • Dose escalation of a 1-hour infusion of flavopiridol with docetaxel was also not possible.
  • The changes in p53 and phospho-Rb in buccal mucosa suggest that a biological effect with flavopiridol was achieved.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Cyclin-Dependent Kinases / antagonists & inhibitors. Enzyme Inhibitors / administration & dosage. Flavonoids / administration & dosage. Piperidines / administration & dosage. Taxoids / administration & dosage
  • [MeSH-minor] Adult. Aged. Area Under Curve. Biomarkers, Tumor / metabolism. Biopsy. Clinical Trials as Topic. Female. Humans. Immunohistochemistry. Ki-67 Antigen / biosynthesis. Middle Aged. Mouth Mucosa / pathology. Mucous Membrane / pathology. Neoplasm Metastasis. Phosphorylation. Retinoblastoma Protein / biosynthesis. Time Factors. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15297405.001).
  • [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] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Ki-67 Antigen; 0 / Piperidines; 0 / Retinoblastoma Protein; 0 / Taxoids; 0 / Tumor Suppressor Protein p53; 15H5577CQD / docetaxel; 45AD6X575G / alvocidib; EC 2.7.11.22 / Cyclin-Dependent Kinases
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59. Terao Y, Nishida J, Horiuchi S, Rong F, Ueoka Y, Matsuda T, Kato H, Furugen Y, Yoshida K, Kato K, Wake N: Sodium butyrate induces growth arrest and senescence-like phenotypes in gynecologic cancer cells. Int J Cancer; 2001 Oct 15;94(2):257-67
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  • [Title] Sodium butyrate induces growth arrest and senescence-like phenotypes in gynecologic cancer cells.
  • We demonstrated here the growth-suppressing effects of sodium butyrate (NaB) on human endometrial and ovarian cancer cells.
  • NaB-mediated p21 might arrest endometrial and ovarian cancer cells at the G0/G1 phase by eliciting pRb unphosphorylation.
  • To demonstrate the role of pRb regulation by p21, we measured the sensitivity to NaB of cervical cancer cells in which pRb had been inactivated by HPV E7.
  • The cervical cancer cells displayed a sensitivity in NaB-mediated G2/M arrest in addition to their sensitivity in G0/G1 arrest.
  • Arrest at G0/G1 and G2/M accompanied induction of senescence-like phenotypes (SLPs).
  • Most importantly, the effect of NaB on senescence induction was not coupled with the predominance of hypophosphorylated pRb forms in the cervical cancer cells.
  • The effects of NaB on gynecologic cancer cell growth indicated its potential use in cancer treatment.
  • NaB was effective even in the cancer cells with mutant p53 and/or Rb genes by eliciting cell senescence.
  • [MeSH-major] Butyrates / pharmacology. Genital Neoplasms, Female / drug therapy
  • [MeSH-minor] Animals. Cell Aging / drug effects. Cell Cycle / drug effects. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / biosynthesis. Female. Humans. Mice. Mice, Inbred BALB C. Phenotype. Tumor Cells, Cultured

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  • [Copyright] Copyright 2001 Wiley-Liss, Inc.
  • (PMID = 11668507.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Butyrates; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins
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60. Park WH, Seol JG, Kim ES, Kang WK, Im YH, Jung CW, Kim BK, Lee YY: Monensin-mediated growth inhibition in human lymphoma cells through cell cycle arrest and apoptosis. Br J Haematol; 2002 Nov;119(2):400-7
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  • [Title] Monensin-mediated growth inhibition in human lymphoma cells through cell cycle arrest and apoptosis.
  • We investigated the in vitro antiproliferative effect of monensin on nine human lymphoma cell lines.
  • Monensin significantly inhibited the proliferation of all the lymphoma cell lines examined with a 50% inhibition concentration of about 0.5 micromol/l, and induced a G1 and/or a G2-M phase arrest in these cell lines.
  • To address the antiproliferative mechanism of monensin, we examined the effect of this drug on cell-cycle-related proteins in CA46 cells (both G1 and G2 arrest) and Molt-4 cells (G2 arrest).
  • Treatment with monensin for 72 h decreased CDK4 and cyclin A levels in CA46 cells, and cdc2 levels in Molt-4 cells.
  • Furthermore, the activities of CDK2- and CDK4-associated kinases were reduced in association with Rb hypophosphorylation in monensin-treated CA46 cells.
  • The activity of cdc2-associated kinase was decreased in both cell lines, which was accompanied by induction of Wee1.
  • Also, monensin induced apoptosis in these cell lines, as evidenced by annexin V binding assay and flow cytometric detection of sub-G1 DNA content.
  • This apoptotic process was associated with loss of mitochondria transmembrane potential (Delta(psi)m).
  • Taken together, these results demonstrated for the first time that monensin potently inhibits the proliferation of human lymphoma cell lines via cell cycle arrest and apoptosis.
  • [MeSH-major] Ionophores / pharmacology. Monensin / pharmacology. Tumor Cells, Cultured / drug effects
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. CDC2-CDC28 Kinases. Cell Division / drug effects. Cyclin A / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / metabolism. Cyclins / metabolism. Humans. Interphase. Lymphoma / drug therapy. Membrane Potentials / drug effects

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  • (PMID = 12406077.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin A; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Ionophores; 906O0YJ6ZP / Monensin; EC 2.7.11.22 / CDC2-CDC28 Kinases; EC 2.7.11.22 / Cyclin-Dependent Kinases
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61. Kuroda Y, Sakai A, Tsuyama N, Katayama Y, Munemasa S, Asaoku H, Okikawa Y, Nakaju N, Mizuno M, Ogawa K, Nishisaka T, Matsui H, Tanaka H, Kimura A: Ectopic cyclin D1 overexpression increases chemosensitivity but not cell proliferation in multiple myeloma. Int J Oncol; 2008 Dec;33(6):1201-13
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  • [Title] Ectopic cyclin D1 overexpression increases chemosensitivity but not cell proliferation in multiple myeloma.
  • Cell proliferation analysis did not show any differences among RPMI8226, mock control, and D1 transfectants.
  • The number of S-phase cells increased while the number of G0/G1- and G2/M-phase cells decreased in D1 transfectants, which indicates a prolonged S-phase caused by cyclin D1 transfection.
  • Western blot analysis revealed an increase in the hyperphosphorylated form of retinoblastoma (Rb) protein in D1 transfectants; however, the expression of p53, p16, Bax, Bad, Bcl-2, and Mcl-1 did not significantly change.
  • Treatment with anti-myeloma drugs (melphalan, dexamethasone, bortezomib and immunomodulatory compounds) induced apoptosis earlier in D1 transfectants compared with RPMI8226 and mock control via the activation of both caspase-8 and -9.
  • However, we could not detect a relationship between cyclin D1 expression and the response to treatment with VAD and bortezomib.
  • Therefore, we assume that high sensitivity to anti-myeloma drugs depends on the duration of the S-phase, but a clinical response might depend on the number of myeloma cells with cyclin D1 overexpression.
  • [MeSH-major] Antineoplastic Agents. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Multiple Myeloma / drug therapy
  • [MeSH-minor] Aged. Boronic Acids / therapeutic use. Bortezomib. Cell Line, Tumor. Cyclin D2. Cyclin-Dependent Kinase Inhibitor p27. Cyclins / metabolism. Dexamethasone / pharmacology. Female. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Male. Melphalan / pharmacology. Middle Aged. Phosphorylation. Pyrazines / therapeutic use. Retinoblastoma Protein / metabolism. Thalidomide / pharmacology. Time Factors. Transfection. Up-Regulation. Vincristine / therapeutic use

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  • (PMID = 19020753.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / CCND1 protein, human; 0 / CCND2 protein, human; 0 / CDKN1B protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Pyrazines; 0 / Retinoblastoma Protein; 136601-57-5 / Cyclin D1; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 4Z8R6ORS6L / Thalidomide; 5J49Q6B70F / Vincristine; 69G8BD63PP / Bortezomib; 7S5I7G3JQL / Dexamethasone; Q41OR9510P / Melphalan
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62. 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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  • [Title] N-(4-Hydroxyphenyl) retinamide potentiated paclitaxel for cell cycle arrest and apoptosis in glioblastoma C6 and RG2 cells.
  • Glioblastoma grows aggressively due to its ability to maintain abnormally high potentials for cell proliferation.
  • 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).
  • Flow cytometric analysis showed that the microtubule stabilizer PTX caused cell cycle deregulation due to G2/M arrest.
  • 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.
  • Collectively, the combination of 4-HPR and PTX diminished the survival factors (e.g., rTERT, PCNA, and Bcl-2) to make glioblastoma cells highly prone to apoptosis with activation of cysteine proteases (e.g., calpain, cathepsins, caspase-8, caspase-3).
  • 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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  • (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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63. Gilheeney SW, Khakoo Y, Souweidane M, Wolden S, Boulad F, Dunkel IJ: Thiotepa/topotecan/carboplatin with autologous stem cell rescue in recurrent/refractory/poor prognosis pediatric malignancies of the central nervous system. Pediatr Blood Cancer; 2010 Apr;54(4):591-5
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  • Topotecan potentiates the anti-cancer effects of alkylators and crosses the blood-brain barrier.
  • We present ten patients with recurrent or progressive central nervous system malignancies treated on a myeloablative regimen using these drugs.
  • METHODS: Treatment included: Thiotepa 300 mg/m(2) on days -8, -7, and -6; topotecan 2 mg/m(2) on days -8, -7, -6, -5, and -4; and carboplatin approximately 500 mg/m(2) (Calvert formula-area under the curve = 7) on days -5, -4, and -3.
  • Stem cell rescue was on day 0.
  • Five had medulloblastoma (MB), four had high grade glioma (HGG), and one had trilateral retinoblastoma/pineoblastoma (tRB/PB).
  • Prior treatment for all patients included surgery and chemotherapy (1-7 regimens, median 2).
  • Nine patients received radiotherapy; one patient did not receive radiotherapy pre-study.
  • Three patients had residual disease at the time of transplant.
  • Four patients are event-free survivors at a median of 6 years (range 2.8-7.6 years) after treatment including 2/5 MB patients, 1/4 HGG patients, and the tRB/PB patient.
  • Four of the seven patients with no evidence of disease/minimal residual disease status at the time of stem cell rescue are long-term survivors versus 1/3 with measurable disease.
  • Diagnosis and extent of disease prior to stem cell rescue may have an impact on outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Central Nervous System Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Carboplatin / administration & dosage. Carboplatin / adverse effects. Child. Child, Preschool. Combined Modality Therapy. Female. Hematopoietic Stem Cell Transplantation. Humans. Male. Neoplasm Recurrence, Local / drug therapy. Prognosis. Thiotepa / administration & dosage. Thiotepa / adverse effects. Topotecan / administration & dosage. Topotecan / adverse effects. Young Adult

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  • (PMID = 19998470.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 7M7YKX2N15 / Topotecan; 905Z5W3GKH / Thiotepa; BG3F62OND5 / Carboplatin
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64. Park WH, Seol JG, Kim ES, Hyun JM, Jung CW, Lee CC, Kim BK, Lee YY: Arsenic trioxide-mediated growth inhibition in MC/CAR myeloma cells via cell cycle arrest in association with induction of cyclin-dependent kinase inhibitor, p21, and apoptosis. Cancer Res; 2000 Jun 1;60(11):3065-71
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  • [Title] Arsenic trioxide-mediated growth inhibition in MC/CAR myeloma cells via cell cycle arrest in association with induction of cyclin-dependent kinase inhibitor, p21, and apoptosis.
  • We investigated the in vitro effect of As2O3 on proliferation, cell cycle regulation, and apoptosis in human myeloma cell lines.
  • DNA flow cytometric analysis indicated that As2O3 (2 microM) induced a G1 and/or a G2-M phase arrest in these cell lines.
  • Western blot analysis demonstrated that treatment with As2O3 (2 microM) for 72 h did not change the steady-state levels of CDK2, CDK4, cyclin D1, cyclin E, and cyclin B1 but decreased the levels of CDK6, cdc2, and cyclin A.
  • The mRNA and protein levels of CDKI, p21 were increased by treatment with As2O3, but those of p27 were not.
  • Furthermore, the activity of CDK6-associated kinase was reduced in association with hypophosphorylation of Rb protein.
  • The activity of cdc2-associated kinase was decreased, which was accompanied by the up-regulation of cdc2 phosphorylation (cdc2-Tyr15 phosphorylation) resulting from reduction of cdc25B and cdc25C phosphatases.
  • As2O3 also induced apoptosis in MC/CAR cells as evidenced by flow cytometric detection of sub-G1 DNA content and annexin V binding assay.
  • This apoptotic process was associated with down-regulation of Bcl-2, loss of mitochondrial transmembrane potential (delta psi(m)), and an increase of caspase-3 activity.
  • These results suggest that As2O3 inhibits the proliferation of myeloma cells, especially MC/CAR cells, via cell cycle arrest in association with induction of p21 and apoptosis.
  • [MeSH-major] Arsenicals / pharmacology. Cell Cycle / drug effects. Cyclins / metabolism. Multiple Myeloma / drug therapy. Oxides / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Northern. Blotting, Western. Caspase 3. Caspases / metabolism. Cell Division / drug effects. Cyclin-Dependent Kinase Inhibitor p21. Dose-Response Relationship, Drug. Flow Cytometry. Humans. Inhibitory Concentration 50. Precipitin Tests. Time Factors. Tumor Cells, Cultured


65. Hyun Park W, Hee Cho Y, Won Jung C, Oh Park J, Kim K, Hyuck Im Y, Lee MH, Ki Kang W, Park K: Arsenic trioxide inhibits the growth of A498 renal cell carcinoma cells via cell cycle arrest or apoptosis. Biochem Biophys Res Commun; 2003 Jan 3;300(1):230-5
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  • Previously, we showed that arsenic trioxide potently inhibited the growth of myeloma cells and head and neck cancer cells.
  • Here, we demonstrate that arsenic trioxide inhibited the proliferation of all the renal cell carcinoma cell lines (ACHN, A498, Caki-2, Cos-7, and Renca) except only one cell line (Caki-1) with IC(50) of about 2.5-10 microM.
  • When we examined the effects of this drug on A498 cells, arsenic trioxide (2.5 microM) decreased the levels of CDK2, CDK6, cyclin D1, cyclin E, and cyclin A proteins.
  • Although p21 protein was not increased by arsenic trioxide, this drug markedly enhanced the binding of p21 with CDK2.
  • In addition, the activities of CDK2- and CDK6-associated kinase were reduced in association with hypophosphorylation of Rb protein.
  • Arsenic trioxide (10 microM) also induced apoptosis in A498 cells.
  • Apoptotic process of A498 cells was associated with the changes of Bcl-(XL), caspase-9, caspase-3, and caspase-7 proteins as well as mitochondria transmembrane potential (Deltapsi(m)) loss.
  • [MeSH-major] Arsenicals / pharmacology. CDC2-CDC28 Kinases. Carcinoma, Renal Cell / drug therapy. Kidney Neoplasms / drug therapy. Oxides / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspases / metabolism. Cell Cycle / drug effects. Cell Division / drug effects. Cyclin A / metabolism. Cyclin D1 / metabolism. Cyclin E / metabolism. Cyclin-Dependent Kinase 2. Cyclin-Dependent Kinase 6. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / metabolism. Cyclins / metabolism. Humans. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retinoblastoma Protein / metabolism. Tumor Cells, Cultured. bcl-X Protein

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  • (PMID = 12480548.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenicals; 0 / BCL2L1 protein, human; 0 / CDKN1A protein, human; 0 / Cyclin A; 0 / Cyclin E; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Oxides; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Retinoblastoma Protein; 0 / bcl-X Protein; 136601-57-5 / Cyclin D1; 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 / CDK6 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.22 / Cyclin-Dependent Kinase 6; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 3.4.22.- / Caspases; S7V92P67HO / arsenic trioxide
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66. Li D, Day KV, Yu S, Shi G, Liu S, Guo M, Xu Y, Sreedharan S, O'Malley BW Jr: The role of adenovirus-mediated retinoblastoma 94 in the treatment of head and neck cancer. Cancer Res; 2002 Aug 15;62(16):4637-44
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  • [Title] The role of adenovirus-mediated retinoblastoma 94 in the treatment of head and neck cancer.
  • A truncated retinoblastoma (RB) protein of approximately 94 kDa (RB94), lacking the NH2 -terminal 112 amino acid residues of the full-length RB, has been found to have great efficacy in tumor suppression.
  • This study investigated the role of adenovirus-mediated RB94 (Ad-RB94) gene therapy for human head and neck squamous cell carcinoma (HNSCC) and explored the cellular and molecular mechanism of tumor inhibition after Ad-RB94 gene transfer.
  • Randomized controlled studies in vitro and in vivo were performed to assess antitumor responses of Ad-RB94 gene transfer against human HNSCC.
  • Human HNSCC cell lines, JHU006 and JHU012, were used in this study.
  • Ad-RB94 gene transfer was performed both in vitro and in vivo with replication-defective virus (DL312) and no treatment as controls.
  • Transgene expression, cell viability, and tumor growth were evaluated in transfected cells and tumor implants.
  • To determine the mechanism behind the observed antitumor action, cell cycle analysis was performed, and telomerase activity was examined.
  • Transgene expression of RB94 was detected by Western blot analysis, real-time quantification reverse transcription-PCR, and immunohistochemistry.
  • RB94 expression led to flattening of cell growth curves and caused tumor regression.
  • Animals treated with Ad-RB94 were seen to have a significant reduction in tumor size when compared with DL312 (P = 0.02, both cell lines) and to no treatment groups (P = 0.01, both cell lines).
  • Cell cycle arrest in the G(2)-M phase and increased levels of apoptosis occurred in tumor cells treated with Ad-RB94.
  • In addition, telomerase activity decreased significantly and specifically after Ad-RB94 treatment.
  • This study demonstrates that Ad-RB94 gene transfer effectively inhibits HNSCC tumor cell growth in vitro and in vivo.
  • The unique property of Ad-RB94 gene transfer to arrest HNSCC tumor cells in the G2-M phase of the cell cycle makes it a good candidate for adjuvant therapy with radiation or chemotherapy, as tumor cells are most sensitive to radiation or cytotoxic drug in this cell cycle phase.
  • [MeSH-major] Carcinoma, Squamous Cell / therapy. Carrier Proteins / physiology. Genetic Therapy / methods. Head and Neck Neoplasms / therapy. Ubiquitin-Protein Ligases
  • [MeSH-minor] Adenoviridae / genetics. Animals. Apoptosis / genetics. Apoptosis / physiology. Cell Division / genetics. Female. G2 Phase / genetics. Humans. Immunohistochemistry. Mice. Mice, Inbred BALB C. Mice, Nude. Mitosis / genetics. Random Allocation. Reverse Transcriptase Polymerase Chain Reaction. Telomerase / antagonists & inhibitors. Telomerase / metabolism. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12183420.001).
  • [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 / Carrier Proteins; EC 2.7.7.49 / Telomerase; EC 6.3.2.19 / RNF40 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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67. Yoon JS, Kim JY, Park HK, Kim ES, Ahn KS, Yoon SS, Cho CG, Kim BK, Lee YY: Antileukemic effect of a synthetic vitamin D3 analog, HY-11, with low potential to cause hypercalcemia. Int J Oncol; 2008 Feb;32(2):387-96
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  • [Title] Antileukemic effect of a synthetic vitamin D3 analog, HY-11, with low potential to cause hypercalcemia.
  • However, toxicity of hypercalcemia has limited the use of 1,25(OH)2D3 in clinical trials.
  • Among the 11 vitamin D3 analogs, HY-11 (code name) showed the most potent antileukemic activity with 2.5x10(-6) M of IC50, however, it did not affect the cellular growth of normal peripheral blood mononuclear cells until 10(-6) M.
  • Flow cytometric analysis indicated that HY-11 induced the G1 arrest in a dose-dependent manner, which was mediated via inactivation of CDK4 and CDK6 in association with up-regulation of CDKI (cyclin-dependent kinase inhibitor), p27 and Rb protein.
  • In addition, HY-11 enhanced the expression of TGF-beta1, TGF-beta receptor type I and II and vitamin D3 receptor (VDR).
  • Serum calcium levels were within normal limit when HY-11 was given intraperitoneally (i.p.) every other day for 5 weeks to BALB/c mice at the doses of 10(-7), 10(-6)and 10(-5) M.
  • HY-11 inhibited the growth of WEHI-3BD+ mouse leukemic cells in vitro, and syngeneic BALB/c mice that received WEHI-3BD+ mouse leukemic cells and HY-11 had a significantly longer survival without producing hypercalcemia compared to control group.
  • In summary, HY-11 is a vitamin D3 analog that inhibited the proliferation of human AML cell line, HL-60, through induction of cell cycle arrest, triggering apoptosis as well as modulation of TGF-beta1 and its receptors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cholecalciferol / analogs & derivatives. Cholecalciferol / chemistry. Hypercalcemia / prevention & control. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Animals. Calcium / metabolism. Cell Line, Tumor. Cell Proliferation. HL-60 Cells. Humans. Male. Mice. Mice, Inbred BALB C. Models, Chemical. Neoplasm Transplantation

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  • (PMID = 18202761.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / HY-11; 1C6V77QF41 / Cholecalciferol; SY7Q814VUP / Calcium
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68. Yang P, Cartwright C, Chan D, Vijjeswarapu M, Ding J, Newman RA: Zyflamend-mediated inhibition of human prostate cancer PC3 cell proliferation: effects on 12-LOX and Rb protein phosphorylation. Cancer Biol Ther; 2007 Feb;6(2):228-36
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  • [Title] Zyflamend-mediated inhibition of human prostate cancer PC3 cell proliferation: effects on 12-LOX and Rb protein phosphorylation.
  • The multiherb anti-inflammatory product Zyflamend was investigated for its antiproliferative effects on PC3 human prostate cancer cells and eicosanoid metabolism in this prostate cancer cell line.
  • Zyflamend produced a concentration-dependent inhibition of cloned COX-1, COX-2, and 5-LOX enzyme activities, with inhibition of 5-HETE production being greater than that of PGE(2) formation.
  • Applied to intact PC3 cells, Zyflamend was found to be most potent against 12-LOX, followed by 5-LOX and then COX activities.
  • The concentration-dependent inhibition of PC3 cell proliferation was associated with a selective G(2)/M arrest of the cell cycle and induction of apoptosis, as evidenced by flow cytometric staining of PC3 cells with annexin V.
  • Determination of cell signal transduction proteins demonstrated that Zyflamend produced an increase in p21 phosphorylation but down-regulated phosphorylation of retinoblastoma (Rb) protein.
  • Replenishing 12-HETE in Zyflamend-treated cells overcame the ability of this multiple herb product to inhibit cell proliferation, and concordantly, 12-HETE blocked Zyflamend's ability to down-regulate phosphorylation of Rb protein.
  • We conclude that the effective control of human prostate cancer cell proliferation with Zyflamend is multi-mechanistic but, in part, involves regulation of aberrant tumor cell eicosanoid metabolism, especially on 5- and 12-LOX, as well as restoration of Rb tumor suppressor protein function through regulation of its phosphorylation status.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Arachidonate 12-Lipoxygenase / metabolism. Plant Extracts / pharmacology. Prostatic Neoplasms / drug therapy. Retinoblastoma Protein / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Down-Regulation / drug effects. Enzyme Inhibitors / pharmacology. Humans. Lipoxygenase Inhibitors. Male. Phosphorylation / drug effects. Prostaglandin-Endoperoxide Synthases / drug effects. Treatment Outcome

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  • [CommentIn] Cancer Biol Ther. 2007 Feb;6(2):237 [17387265.001]
  • (PMID = 17218785.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Lipoxygenase Inhibitors; 0 / Plant Extracts; 0 / Retinoblastoma Protein; 0 / Zyflamend; EC 1.13.11.31 / Arachidonate 12-Lipoxygenase; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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69. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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 lower limit of quantification (LLOQ) was 0.1 ng/ml in both vitreous humor and plasma.
  • The assay was rapid, sensitive and robust enough to support EDL-155 ocular penetration studies in a rodent model of intraocular cancer.
  • High local concentrations coupled with minimal systemic exposure supports further testing of EDL-155 as localized therapy for intraocular cancers.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Chromatography, High Pressure Liquid / methods. Spectrometry, Mass, Electrospray Ionization / methods. Tetrahydroisoquinolines / pharmacokinetics. Vitreous Body / metabolism
  • [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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70. Takemura M: Biochemical properties of the stimulatory activity of DNA polymerase alpha by the hyper-phosphorylated retinoblastoma protein. Biochim Biophys Acta; 2002 Jun 6;1571(2):151-6
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  • [Title] Biochemical properties of the stimulatory activity of DNA polymerase alpha by the hyper-phosphorylated retinoblastoma protein.
  • Previously, my colleagues and I have reported that the immunopurified hyper-phosphorylated retinoblastoma protein (ppRb) stimulates the activity of DNA polymerase alpha.
  • I describe here the biochemical characteristics of this stimulatory activity.
  • DNA polymerase alpha-stimulatory activity of ppRb was most remarkable when using activated DNA as a template-primer, rather than using poly(dT)-(rA)(10), poly(dA)-(dT)(12-18), and so on.
  • Kinetic analysis showed that there was no significant difference in K(m) value for deoxyribonucleotides of DNA polymerase alpha in the presence of ppRb.
  • Adding ppRb resulted in the overcoming pause site on the template, but did not affect the rate of misincorporation of incorrect deoxyribonucleotides.
  • By adding ppRb, the optimal concentration of template-primer was shifted to a higher region, but not using M13 singly primed DNA.
  • The ppRb seemed to assist the process that DNA polymerase alpha changed its conformation resulting in appropriate enzyme activity.
  • [MeSH-major] DNA Polymerase I / metabolism. Retinoblastoma Protein / metabolism
  • [MeSH-minor] DNA / drug effects. DNA / metabolism. DNA Replication / physiology. Enzyme Activation. Humans. Kinetics. Phosphorylation. Protein Binding. Templates, Genetic

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  • (PMID = 12049795.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Retinoblastoma Protein; 9007-49-2 / DNA; EC 2.7.7.- / DNA Polymerase I
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71. Park WH, Lee MS, Park K, Kim ES, Kim BK, Lee YY: Monensin-mediated growth inhibition in acute myelogenous leukemia cells via cell cycle arrest and apoptosis. Int J Cancer; 2002 Sep 20;101(3):235-42
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  • Monensin efficiently inhibited the proliferation of all of 10 AML cell lines, with IC(50) of about 0.5 microM.
  • DNA flow cytometric analysis indicated that monensin induced a G(1) and/or a G(2)-M phase arrest in these cell lines.
  • In addition, monensin not only increased the p27 level but also enhanced its binding with CDK2.
  • Furthermore, the activities of CDK2- and CDK6-associated kinases reduced by monensin were associated with hypophosphorylation of Rb protein.
  • The apoptotic process of HL-60 cells was associated with changes in Bax, caspase-3, caspase-8 and mitochondria transmembrane potential (Deltapsi(m)).
  • In particular, monensin (i.p. at a dose of 8 mg/kg thrice weekly) significantly reduced the tumor size of BALB/c mice that were inoculated s.c. with its derived cell line, WEHI-3BD cells (69% growth inhibition relative to control group; p < 0.05).
  • Tumors from monensin-treated mice exhibited increased apoptosis, and these tumor were immunohistochemically more stained with Bax, Fas and p53 antibodies than control tumors.
  • [MeSH-major] Apoptosis / drug effects. Cell Cycle / drug effects. Ionophores / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Monensin / pharmacology
  • [MeSH-minor] Animals. Blotting, Western. Caspases / metabolism. Cell Cycle Proteins / metabolism. Cell Division / drug effects. Cyclin-Dependent Kinase Inhibitor p27. Cyclin-Dependent Kinases / metabolism. Female. Humans. Immunoenzyme Techniques. Membrane Potentials / drug effects. Mice. Mice, Inbred BALB C. Mitochondria / metabolism. Mitogen-Activated Protein Kinase Kinases / metabolism. Poly(ADP-ribose) Polymerases / metabolism. Tumor Cells, Cultured / drug effects. Tumor Suppressor Proteins / metabolism

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12209973.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdkn1b protein, mouse; 0 / Cell Cycle Proteins; 0 / Ionophores; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 906O0YJ6ZP / Monensin; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 3.4.22.- / Caspases
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72. Venè R, Arena G, Poggi A, D'Arrigo C, Mormino M, Noonan DM, Albini A, Tosetti F: Novel cell death pathways induced by N-(4-hydroxyphenyl)retinamide: therapeutic implications. Mol Cancer Ther; 2007 Jan;6(1):286-98
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  • [Title] Novel cell death pathways induced by N-(4-hydroxyphenyl)retinamide: therapeutic implications.
  • We previously reported that N-(4-hydroxyphenyl)retinamide (4HPR) inhibits retinoblastoma tumor growth in a murine model in vivo and kills Y79 retinoblastoma cells in vitro.
  • However, pharmacologic inactivation of caspases by the pan-caspase inhibitor BOC-D-fmk, or specific caspase-3 inhibition by Z-DEVD-fmk, was not sufficient to prevent cell death, as assessed by loss of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction, lactate dehydrogenase release, disruption of mitochondrial transmembrane potential (Deltapsi(m)), and ATP depletion.
  • Activation of AKT, which regulates energy level in the cell, by the retinal survival facto]r insulin-like growth factor I was impaired and insulin-like growth factor I was ineffective against ATP and Deltapsi(m) loss in the presence of 4HPR.
  • Lysosomal destabilization, associated with mitochondrial dysfunction, was induced by 4HPR also in other cancer cell lines, including PC3 prostate adenocarcinoma and the vascular tumor Kaposi sarcoma KS-Imm cells.
  • The novel finding of a lysosome-mediated cell death pathway activated by 4HPR could have implications at clinical level for the development of combination chemoprevention and therapy of cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Retinoblastoma / therapy. Tretinoin / analogs & derivatives
  • [MeSH-minor] Acetylcysteine / pharmacology. Adenosine Triphosphate / deficiency. Benzyl Compounds / pharmacology. Caspase Inhibitors. Cathepsin D / secretion. Cell Death / drug effects. Cell Survival / drug effects. Cytochromes c / secretion. Cytosol / drug effects. Cytosol / ultrastructure. Enzyme Activation / drug effects. Flow Cytometry. Humans. Hydrocarbons, Fluorinated / pharmacology. Insulin-Like Growth Factor I / pharmacology. Lysosomes / drug effects. Lysosomes / ultrastructure. Membrane Potential, Mitochondrial / drug effects. Mitochondria / drug effects. Mitochondria / ultrastructure. Proto-Oncogene Proteins c-akt / metabolism. Reactive Oxygen Species / metabolism. Time Factors

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  • (PMID = 17237288.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzyl Compounds; 0 / Boc-D-FMK; 0 / Caspase Inhibitors; 0 / Hydrocarbons, Fluorinated; 0 / Reactive Oxygen Species; 20638-84-0 / retinamide; 5688UTC01R / Tretinoin; 67763-96-6 / Insulin-Like Growth Factor I; 8L70Q75FXE / Adenosine Triphosphate; 9007-43-6 / Cytochromes c; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.23.5 / Cathepsin D; WYQ7N0BPYC / Acetylcysteine
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73. Yang G, Rosen DG, Colacino JA, Mercado-Uribe I, Liu J: Disruption of the retinoblastoma pathway by small interfering RNA and ectopic expression of the catalytic subunit of telomerase lead to immortalization of human ovarian surface epithelial cells. Oncogene; 2007 Mar 1;26(10):1492-8
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  • [Title] Disruption of the retinoblastoma pathway by small interfering RNA and ectopic expression of the catalytic subunit of telomerase lead to immortalization of human ovarian surface epithelial cells.
  • The risk of developing ovarian cancer is about 1% over a lifetime, but it is the most deadly gynecologic cancer, in part due to lack of diagnostic markers for early-stage disease and cell model system for studying early neoplastic changes.
  • Most existing immortal human ovarian surface epithelial cells were achieved by using viral protein such as SV40 T/t antigen or E6/E7, which inactivate multiple cellular pathways.
  • In the current study, we used a small interfering RNA (siRNA) against the retinoblastoma gene (pRb) and ectopic expression of human telomerase reverse transcriptase (hTERT) to immortalize the primary ovarian epithelial cell line OSE137 and two additional human ovarian surface epithelial cells.
  • The immortalized OSE137 showed increased telomerase activity, lengthened telomeres, increased G2/M phase, altered cell-cycle regulatory proteins but nontumorigenic.
  • As both Rb and hTERT pathways are commonly altered in human ovarian cancer and these genetic changes are faithfully modeled in these cells without using viral protein, these immortal cells represent an authentic in vitro model system with which to study the initiation and progression of human ovarian cancer.
  • [MeSH-major] Cell Line, Transformed. Ovary. RNA, Small Interfering / pharmacology. Retinoblastoma Protein / metabolism. Telomerase / metabolism
  • [MeSH-minor] Base Sequence. Catalytic Domain. Epithelial Cells. Female. Humans. Karyotyping. Models, Biological. Molecular Sequence Data. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / metabolism

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  • (PMID = 16953228.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA016672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 0 / Retinoblastoma Protein; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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74. Park WH, Kim ES, Kim BK, Lee YY: Monensin-mediated growth inhibition in NCI-H929 myeloma cells via cell cycle arrest and apoptosis. Int J Oncol; 2003 Jul;23(1):197-204
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  • Here, we investigated the antiproliferative effect of monensin on human myeloma cell lines.
  • Cell cycle analysis indicated that monensin induced a G1 and/or a G2-M phase arrest in these cell lines.
  • To address the mechanism of the antiproliferative effect of monensin, we examined the effect of this drug on cell cycle-related proteins in NCI-H929 cells.
  • Monensin decreased the levels of CDK2, CDK6, cdc2, cyclin A, cyclin B1, cyclin D1 and cyclin E proteins but did not alter CDK4 protein.
  • While p21 was increased by monensin, p27 was not.
  • Furthermore, the activities of CDK2- and CDK6-associated kinases were reduced in association with hypophosphorylation of Rb protein.
  • The activity of cdc2-associated kinase was decreased, which was accompanied by reduction of cdc25C phosphatase.
  • Also, monensin induced apoptosis in myeloma cells, as evidenced by annexin V binding assay and flow cytometric detection of sub-G1 DNA content.
  • This apoptotic process was associated with down-regulation of Bcl-2, loss of mitochondria transmembrane potential (Deltapsim) and an increase of caspase-3 activity.
  • In addition, monensin caused the up-regulation of ERK and p38 kinase activities.
  • Taken together, these results have demonstrated for the first time that monensin potently inhibited the proliferation of human myeloma cell lines, especially NCI-H929 cells, via cell cycle arrest in association with p21 and apoptosis.
  • [MeSH-major] Antifungal Agents / pharmacology. Apoptosis. Monensin / pharmacology. Multiple Myeloma / drug therapy. Multiple Myeloma / metabolism. Muscle Proteins
  • [MeSH-minor] Blotting, Western. CDC2 Protein Kinase / metabolism. Cell Cycle. Cell Cycle Proteins / metabolism. Cell Division. Cell Line, Tumor. Cell Separation. Cyclin D1 / metabolism. Cyclin-Dependent Kinase 6. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / metabolism. Cyclins / metabolism. Dose-Response Relationship, Drug. Down-Regulation. Electrophoresis, Polyacrylamide Gel. Flow Cytometry. G2 Phase. Humans. Inhibitory Concentration 50. Membrane Potentials. Microfilament Proteins / metabolism. Mitochondria / metabolism. Mitosis. Models, Chemical. Precipitin Tests. Protein Binding. Proto-Oncogene Proteins c-bcl-2 / metabolism. Time Factors. cdc25 Phosphatases / metabolism

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  • (PMID = 12792794.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Microfilament Proteins; 0 / Muscle Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tagln protein, mouse; 136601-57-5 / Cyclin D1; 906O0YJ6ZP / Monensin; EC 2.7.11.22 / CDC2 Protein Kinase; EC 2.7.11.22 / CDK6 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 6; EC 2.7.11.22 / Cyclin-Dependent Kinases; EC 3.1.3.48 / CDC25C protein, human; EC 3.1.3.48 / Cdc25c protein, mouse; EC 3.1.3.48 / cdc25 Phosphatases
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75. Dawson DG, Gleiser J, Zimbric ML, Darjatmoko SR, Lindstrom MJ, Strugnell SA, Albert DM: Toxicity and dose-response studies of 1-alpha hydroxyvitamin D2 in LH-beta-tag transgenic mice. Ophthalmology; 2003 Apr;110(4):835-9
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  • [Title] Toxicity and dose-response studies of 1-alpha hydroxyvitamin D2 in LH-beta-tag transgenic mice.
  • PURPOSE: To determine the effectiveness of a vitamin D analog, 1alpha-hydroxyvitamin D(2) (1alpha-OH-D(2)), in inhibiting retinoblastoma in a transgenic retinoblastoma model (LHbeta-Tag mouse) and to evaluate its toxicity.
  • PARTICIPANTS AND CONTROLS: Two hundred seventeen LHbeta-Tag transgene-positive 8- to 10-week-old mice total; 179 drug-treated animals, 38 control animals.
  • METHODS: Mice were fed a vitamin D- and calcium-restricted diet and were randomized to treatment groups receiving control (vehicle), or 0.1, 0.3, 0.5, or 1.0 micro g/day of 1alpha-OH-D(2) via oral gavage 5 times weekly for 5 weeks.
  • Body weight was measured at the start of treatment and twice weekly during treatment.
  • Animals were euthanized on the last day of treatment.
  • Representative sections from the superior, middle, and inferior regions of each globe were examined microscopically and tumor areas were measured using Optimas software.
  • MAIN OUTCOME MEASURES: Mean tumor area was measured to determine drug effectiveness.
  • Toxicity was assessed by survival, weight loss over the treatment period, serum calcium, and kidney calcification.
  • RESULTS: The mean tumor size in each 1alpha-OH-D(2) group was smaller than controls (all P values < 0.02): control, 90,248 micro m(2); 0.1 micro g, 31,545 micro m(2); 0.3 micro g, 16,750 micro m(2); 0.5 micro g, 30,245 micro m(2); and 1.0 micro g, 16,049 micro m(2).
  • The survival percentage for each group was as follows: control, 97%; 0.1 micro g, 91%; 0.3 micro g, 88%; 0.5 micro g, 70%; and 1.0 micro g, 63%.
  • Mortality was higher in the 0.5- micro g and 1.0- micro g doses (P values < 0.01) compared with other treatment groups and with the control group.
  • Serum calcium levels were significant in all treatment groups compared with controls (all P values < 0.0001).
  • CONCLUSIONS: In the LHbeta-Tag mouse, 1alpha-OH-D(2) inhibits retinoblastoma with no significant increase in mortality in lower doses (0.1-0.3 micro g).
  • 1alpha-OH-D(2) has approval by the Food and Drug Administration as an investigative drug for cancer treatment, and has shown efficacy with low toxicity in adult cancer trials.
  • 1alpha-OH-D(2) meets the criteria for human clinical trials.
  • [MeSH-major] Ergocalciferols / administration & dosage. Ergocalciferols / toxicity. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Animals. Calcinosis / chemically induced. Calcium / blood. Disease Models, Animal. Dose-Response Relationship, Drug. Kidney / drug effects. Luteinizing Hormone, beta Subunit / genetics. Mice. Mice, Transgenic. Survival Rate. Transgenes

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  • (PMID = 12689912.001).
  • [ISSN] 0161-6420
  • [Journal-full-title] Ophthalmology
  • [ISO-abbreviation] Ophthalmology
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R01 EY01917
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ergocalciferols; 0 / Luteinizing Hormone, beta Subunit; 3DIZ9LF5Y9 / 1 alpha-hydroxyergocalciferol; SY7Q814VUP / Calcium
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76. Vinodhkumar R, Song YS, Devaki T: Romidepsin (depsipeptide) induced cell cycle arrest, apoptosis and histone hyperacetylation in lung carcinoma cells (A549) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression. Biomed Pharmacother; 2008 Feb;62(2):85-93
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  • [Title] Romidepsin (depsipeptide) induced cell cycle arrest, apoptosis and histone hyperacetylation in lung carcinoma cells (A549) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression.
  • Histone deacetylase inhibitor such as romidepsin (depsipeptide, FR901228, FK228) is a promising new class of antineoplastic agent with the capacity to induce growth arrest and/or apoptosis of cancer cells.
  • Expression of Cdc2/Cdk-1, cyclin B1, cyclin A, p21/Cip1, pRb, pRb2/p130, histone H4 and H3 acetylation status were studied with western blot analysis.
  • Extent of apoptosis has been assessed measuring the activity of caspase-3.
  • The pRb protein was found to be one of the targets for the romidepsin induced cell cycle arrest.
  • Flow cytometric analysis showed that romidepsin induced cell cycle arrest at G2-M transition, with significant induction of apoptosis at 25 and 50 nM concentration of romidepsin, with an increase in the number of both early and late apoptotic cells.
  • From this study it is concluded that romidepsin inhibit advanced human lung carcinoma (A549) cell proliferation by altering the expression of cell cycle regulators and apoptotic protein.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Depsipeptides / pharmacology. Lung Neoplasms / drug therapy. Retinoblastoma Protein / drug effects
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Dose-Response Relationship, Drug. Flow Cytometry. Gene Expression Regulation / drug effects. Histone Deacetylase Inhibitors. Humans. Phosphorylation / drug effects

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  • (PMID = 17644301.001).
  • [ISSN] 0753-3322
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Depsipeptides; 0 / Histone Deacetylase Inhibitors; 0 / Retinoblastoma Protein; CX3T89XQBK / romidepsin
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77. Senderowicz AM: Novel direct and indirect cyclin-dependent kinase modulators for the prevention and treatment of human neoplasms. Cancer Chemother Pharmacol; 2003 Jul;52 Suppl 1:S61-73
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  • [Title] Novel direct and indirect cyclin-dependent kinase modulators for the prevention and treatment of human neoplasms.
  • Abnormalities in the cell cycle are responsible for the majority of human neoplasias.
  • Most abnormalities occur due to hyperphosphorylation of the tumor suppressor gene Rb by the key regulators of the cell cycle, the cyclin-dependent kinases (CDKs).
  • Thus, a pharmacological CDK inhibitor may be useful in the prevention and/or treatment of human neoplasms.
  • (1) potent CDK inhibitory activity;.
  • The first phase I trial of a CDK inhibitor, flavopiridol, has been completed.
  • Antitumor activity was observed in some patients with non-Hodgkin's lymphoma and renal, colon, and prostate cancers.
  • Phase II trials with infusional flavopiridol and phase I infusional trials in combination with standard chemotherapy are being completed with encouraging results.
  • A novel phase I trial of 1-h flavopiridol administration was recently completed.
  • The maximum tolerated doses using flavopiridol daily for 5, 3, and 1 consecutive days are 37.5, 50, and 62.5 mg/m(2) per day.
  • Phase II/III trials using this 1-h schedule in several tumor types including non-small-cell lung cancer, chronic lymphocytic leukemia, mantle cell lymphoma, and head and neck cancer are being conducted worldwide.
  • (1) it inhibits protein kinase C (PKC) activity;.
  • In the initial UCN-01 clinical trial (continuous infusion for 72 h), a prolonged half-life of about 600 h (100 times longer than in preclinical models) was observed.
  • The maximum tolerated dose was 42.5 mg/m(2) per day for 3 days.
  • One patient with melanoma achieved a partial response (8 months).
  • Another patient with refractory anaplastic large-cell lymphoma had no evidence of disease at >4 years.
  • Bone marrow and tumor samples obtained from some patients revealed loss in adducin phosphorylation, a substrate of PKC.
  • " Moreover, it is still unclear which pharmacodynamic endpoint reflects loss of CDK activity in tissue samples from patients in these trials.
  • Despite these caveats, we feel that CDKs are sensible targets for cancer therapy and that there are several small-molecule CDK modulators in clinical trials with encouraging results.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclin-Dependent Kinases / antagonists & inhibitors. Enzyme Inhibitors / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Alkaloids / administration & dosage. Animals. Cell Cycle / drug effects. Clinical Trials as Topic. Flavonoids / administration & dosage. Humans. Piperidines / administration & dosage. Staurosporine / analogs & derivatives. Tumor Cells, Cultured


78. Pushkarev VM, Starenki DV, Saenko VA, Pushkarev VV, Kovzun OI, Tronko MD, Popadiuk ID, Yamashita S: Differential effects of low and high doses of Taxol in anaplastic thyroid cancer cells: possible implication of the Pin1 prolyl isomerase. Exp Oncol; 2008 Sep;30(3):190-4
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  • [Title] Differential effects of low and high doses of Taxol in anaplastic thyroid cancer cells: possible implication of the Pin1 prolyl isomerase.
  • AIM: To study the molecular mechanisms of dose-dependent effects of an anticancer drug, Taxol, on the cell cycle machinery and apoptosis-related proteins in thyroid anaplastic cancer cell lines ARO and KTC-2.
  • MATERIALS AND METHODS: Western blot analysis was used for the detection of various proteins and of their phosphorylated forms.
  • RESULTS: Low dose of Taxol that cause apoptosis (25 nM) enhanced Rb protein phosphorylation, decreased the expression of cyclin-dependent kinase inhibitors p27(KIP1) and p21(WAF1) , and potentiated the accumulation of phosphorylated p53 and of the prolyl isomerase Pin1.
  • High Taxol doses (100 and 1000 nM) that cause necrosis-like cell death drastically decreased Pin1 level in both cell lines.
  • Drug-induced Pin1 accumulation could probably facilitate this transition and in parallel contribute to apoptosis via the p53/p73-dependent mechanism.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / administration & dosage. Carcinoma / drug therapy. Paclitaxel / administration & dosage. Peptidylprolyl Isomerase / metabolism. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Dose-Response Relationship, Drug. Humans. Necrosis. Phosphorylation / drug effects. Retinoblastoma Protein / metabolism. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18806740.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / NIMA-interacting peptidylprolyl isomerase; 0 / Retinoblastoma Protein; 0 / Tumor Suppressor Protein p53; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 5.2.1.8 / Peptidylprolyl Isomerase; P88XT4IS4D / Paclitaxel
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79. Qiu P, Dong P, Guan H, Li S, Ho CT, Pan MH, McClements DJ, Xiao H: Inhibitory effects of 5-hydroxy polymethoxyflavones on colon cancer cells. Mol Nutr Food Res; 2010 Jul;54 Suppl 2:S244-52
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  • [Title] Inhibitory effects of 5-hydroxy polymethoxyflavones on colon cancer cells.
  • We studied the effects of three major 5-hydroxy PMFs, namely: 5-hydroxy-6,7,8,3',4'-pentamethoxyflavone, 5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone, and 5-hydroxy-6,7,8,4'-tetramethoxyflavone, on human colon cancer HCT116 and HT29 cells.
  • 5-Hydroxy PMFs showed much stronger inhibitory effects on the growth of the colon cancer cells in comparison with their permethoxylated counterparts, suggesting the pivotal role of hydroxyl group at 5-position in the enhanced inhibitory activity by 5-hydroxy PMFs.
  • Flow cytometry analysis demonstrated that three 5-hydroxy PMFs produced different effects on the cell cycle and apoptosis, which may suggest that three 5-hydroxy PMFs act through different mechanisms.
  • Our results further demonstrated that the inhibitory effects of 5-hydroxy PMFs were associated with their ability in modulating key signaling proteins related to cell proliferation and apoptosis, such as p21(Cip1/Waf1), CDK-2, CDK-4, phosphor-Rb, Mcl-1, caspases 3 and 8, and poly ADP ribose polymerase (PARP).
  • [MeSH-major] Antineoplastic Agents, Phytogenic / chemistry. Antineoplastic Agents, Phytogenic / pharmacology. Cell Proliferation / drug effects. Colonic Neoplasms / drug therapy. Flavones / chemistry. Flavones / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Cycle / drug effects. Cell Survival / drug effects. Drug Screening Assays, Antitumor. HCT116 Cells. HT29 Cells. Humans. Inhibitory Concentration 50. Necrosis. Protein Biosynthesis / drug effects. Structure-Activity Relationship

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  • (PMID = 20397199.001).
  • [ISSN] 1613-4133
  • [Journal-full-title] Molecular nutrition & food research
  • [ISO-abbreviation] Mol Nutr Food Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone; 0 / 5-hydroxy-6,7,8,3',4'-pentamethoxyflavone; 0 / 5-hydroxy-6,7,8,4'-tetramethoxyflavone; 0 / Antineoplastic Agents, Phytogenic; 0 / Flavones
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80. 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.
  • CDK activity may be blocked by novel compounds such as flavopiridol.
  • Therefore, CDK inhibitors are attractive drugs to be used for the local prevention of in-stent restenosis.
  • Molecular effects on cell-cycle regulatory mechanisms and distribution were evaluated by post-transcriptional assessment of distinct cyclins and cyclin-dependent kinase inhibitor (CKI) levels and flow cytometry.
  • Hyperphosphorylation of retinoblastoma protein was abrogated and mitogen-mediated smooth muscle cell migration significantly reduced.
  • 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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81. Vijayababu MR, Kanagaraj P, Arunkumar A, Ilangovan R, Aruldhas MM, Arunakaran J: Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression. J Cancer Res Clin Oncol; 2005 Nov;131(11):765-71
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  • [Title] Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression.
  • Prostate cancer is the major health problem and the leading cause of male cancer death.
  • Quercetin is a novel antitumor and antioxidant, whose molecular mechanism involved in cell cycle arrest in androgen independent prostate cancer cells remains unclear.
  • In this study, we investigated the effects of quercetin on proliferation and cell cycle arrest by modulation of Cdc2/Cdk-1 protein in prostate cancer cells (PC-3).
  • PC- 3 cells are human androgen independent cancer cells and were cultured with quercetin at concentrations of 50 and 100 microM for 24 h.
  • Expression of Cdc2/Cdk-1, cyclin B1, cyclin A, p21/Cip1, pRb, pRb2/p130, Bcl-2, Bcl-X(L), Bax and caspase-3 proteins were studied with western blot analysis.
  • Flowcytometric analysis showed that quercetin blocks G2-M transition, with significant induction of apoptosis.
  • From this study, it was concluded that quercetin inhibits prostate cancer cell proliferation by altering the expression of cell cycle regulators and apoptotic proteins.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Quercetin / pharmacology. Retinoblastoma Protein / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Blotting, Western. Cell Death / drug effects. Cell Line, Tumor. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. Male. Phosphorylation

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  • (PMID = 16049707.001).
  • [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
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Retinoblastoma Protein; 9IKM0I5T1E / Quercetin
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82. Haddad RI, Weinstein LJ, Wieczorek TJ, Bhattacharya N, Raftopoulos H, Oster MW, Zhang X, Latham VM Jr, Costello R, Faucher J, DeRosa C, Yule M, Miller LP, Loda M, Posner MR, Shapiro GI: A phase II clinical and pharmacodynamic study of E7070 in patients with metastatic, recurrent, or refractory squamous cell carcinoma of the head and neck: modulation of retinoblastoma protein phosphorylation by a novel chloroindolyl sulfonamide cell cycle inhibitor. Clin Cancer Res; 2004 Jul 15;10(14):4680-7
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  • [Title] A phase II clinical and pharmacodynamic study of E7070 in patients with metastatic, recurrent, or refractory squamous cell carcinoma of the head and neck: modulation of retinoblastoma protein phosphorylation by a novel chloroindolyl sulfonamide cell cycle inhibitor.
  • PURPOSE: E7070 is a synthetic sulfonamide cell cycle inhibitor that induces hypophosphorylation of the retinoblastoma (Rb) protein and G(1) arrest in vitro.
  • EXPERIMENTAL DESIGN: Patients with metastatic, recurrent, or refractory SCCHN, treated with no more than one prior therapy for recurrent disease, received E7070 at 700 mg/m(2) over 1 h every 3 weeks.
  • Pre- and posttreatment tumor fine needle aspirates were subjected to immunohistochemistry with a panel of phospho-specific anti-Rb antibodies.
  • End points included progression-free survival, response rate and duration, overall survival, toxicity profile, and inhibition of Rb phosphorylation.
  • Eleven patients had oropharyngeal cancer and 12 were male.
  • Median age was 59 years (range, 49-73 years).
  • Six patients had stable disease after 2 cycles and 2 patients each subsequently received 1, 2, and 3 additional cycles, respectively, before experiencing progression.
  • Immunohistochemistry of tumor cell aspirates from 3 patients demonstrated reduced Rb phosphorylation posttreatment.
  • CONCLUSIONS: At this dose and schedule, E7070 is unlikely to be superior over single-agent chemotherapy in SCCHN.
  • However, the data suggest that cdk activity can be inhibited in tumor cells, resulting in posttreatment modulation of Rb phosphorylation.
  • In the absence of cytotoxicity, more frequent administration of E7070 may be required to sustain Rb hypophosphorylation and cytostatic growth arrest.
  • [MeSH-major] Carcinoma, Squamous Cell / drug therapy. Head and Neck Neoplasms / drug therapy. Sulfonamides / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Anemia / chemically induced. Cell Cycle / drug effects. Cell Line, Tumor. Disease-Free Survival. Dose-Response Relationship, Drug. Female. Humans. Immunohistochemistry. Ki-67 Antigen / analysis. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Recurrence, Local. Neutropenia / chemically induced. Patient Dropouts. Phosphorylation / drug effects. Proliferating Cell Nuclear Antigen / analysis. Retinoblastoma Protein / metabolism. Thrombocytopenia / chemically induced. Treatment Outcome

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  • (PMID = 15269140.001).
  • [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] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / N-(3-chloro-7-indolyl)-1,4-benzenedisulphonamide; 0 / Proliferating Cell Nuclear Antigen; 0 / Retinoblastoma Protein; 0 / Sulfonamides
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83. Hori M, Suzuki K, Udono MU, Yamauchi M, Mine M, Watanabe M, Kondo S, Hozumi Y: Establishment of ponasterone A-inducible the wild-type p53 protein-expressing clones from HSC-1 cells, cell growth suppression by p53 expression and the suppression mechanism. Arch Dermatol Res; 2009 Oct;301(9):631-46
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  • [Title] Establishment of ponasterone A-inducible the wild-type p53 protein-expressing clones from HSC-1 cells, cell growth suppression by p53 expression and the suppression mechanism.
  • Gene therapy for a variety of human cancers containing the mutant p53 (mt-p53) gene has been performed by direct injection of a retroviral or adenoviral vector containing the wild-type p53 (wt-p53) gene.
  • Because many individuals with skin squamous cell carcinoma (SCC) have been shown to carry the p53 gene mutation, these patients are candidates for p53 gene therapy.
  • For this reason, we established ponasterone A-inducible the wild-type p53 (wt-p53) protein-expressing clones by transfecting a ponasterone-inducible vector containing the wt-p53 gene into HSC-1 cells, which harbor the mutated p53 (m/w) at codon 173 (GTG --> TTG in one allele).
  • Based on the results of the expression patterns of the p21, p16, RB, BAX and Bcl-2 proteins, as well as on the results of senescence-associated beta-galactosidase staining, the suppression was caused by senescence-like growth arrest of the cells.
  • Although it is generally accepted that the suppression of tumor cell growth is caused by p53-induced apoptosis, permanent G1 arrest induced by p53 is also an important part of the growth-suppression mechanism in p53 gene therapy.
  • The present results should expand the possibilities for p53 gene therapy for human skin SCCs containing the mutant p53 gene.
  • [MeSH-major] Carcinoma / therapy. Ecdysterone / analogs & derivatives. Genetic Therapy / methods. Skin Neoplasms / therapy. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Cell Aging. Cell Division / genetics. Cell Line, Tumor. Feasibility Studies. Gene Expression / drug effects. Genetic Vectors. Humans. Plasmids. Transfection

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  • (PMID = 19009304.001).
  • [ISSN] 1432-069X
  • [Journal-full-title] Archives of dermatological research
  • [ISO-abbreviation] Arch. Dermatol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Tumor Suppressor Protein p53; 5289-74-7 / Ecdysterone; 84986BG3NG / ponasterone A
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84. Zhen Y, Sørensen V, Jin Y, Suo Z, Wiedłocha A: Indirubin-3'-monoxime inhibits autophosphorylation of FGFR1 and stimulates ERK1/2 activity via p38 MAPK. Oncogene; 2007 Sep 27;26(44):6372-85
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  • [Title] Indirubin-3'-monoxime inhibits autophosphorylation of FGFR1 and stimulates ERK1/2 activity via p38 MAPK.
  • Indirubin-3'-monoxime is a derivative of the bis-indole alkaloid indirubin, an active ingredient of a traditional Chinese medical preparation that exhibits anti-inflammatory and anti-leukemic activities.
  • Indirubin-3'-monoxime inhibits the activity of FGFR1 at a concentration lower than that required for inhibition of phosphorylation of CDK2 and retinoblastoma protein and cell proliferation stimulated by fetal calf serum.
  • In addition, we found that indirubin-3'-monoxime activates long-term p38 mitogen-activated protein kinase activity, which stimulates extracellular signal-regulated kinase 1/2 in a way unrelated to the activity of FGFR1.
  • Furthermore, we show that indirubin-3'-monoxime can inhibit proliferation of the myeloid leukemia cell line KG-1a through inhibition of the activity of the FGFR1 tyrosine kinase.
  • The data presented here demonstrate previously unknown activities of indirubin-3'-monoxime that may have clinical implications.
  • [MeSH-major] Indoles / pharmacology. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Oximes / pharmacology. Receptor, Fibroblast Growth Factor, Type 1 / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Proliferation / drug effects. Cyclin-Dependent Kinase 2 / metabolism. Endocytosis. Fibroblast Growth Factor 1 / metabolism. Humans. K562 Cells / drug effects. K562 Cells / metabolism. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / pathology. Mice. NIH 3T3 Cells / drug effects. NIH 3T3 Cells / metabolism. Phosphorylation. Receptor, Epidermal Growth Factor / metabolism. Retinoblastoma Protein / metabolism. Signal Transduction / drug effects

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  • (PMID = 17533378.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Indoles; 0 / Oximes; 0 / Retinoblastoma Protein; 0 / indirubin-3'-monoxime; 104781-85-3 / Fibroblast Growth Factor 1; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.11.22 / Cyclin-Dependent Kinase 2; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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85. Smalley KS, Eisen TG: Farnesyl transferase inhibitor SCH66336 is cytostatic, pro-apoptotic and enhances chemosensitivity to cisplatin in melanoma cells. Int J Cancer; 2003 Jun 10;105(2):165-75
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  • The constitutive activity of a number of growth and cell survival pathways are thought to contribute to the inherent resistance of melanoma to chemotherapy and radiotherapy.
  • Novel drugs such as the farnesyl transferase inhibitors (FTIs) and farnesyl thiosalicylic acid (FTS) interfere with the signaling of oncogenic Ras.
  • The aim of our study was to assess the anti-tumour activity of the FTI SCH66336 in melanoma and to assess whether SCH66336 and FTS could modulate chemoresistance in melanoma cells.
  • SCH66336 had marked anti-proliferative activity in both human and mouse melanoma cell lines, but not in non-transformed NIH 3T3 cells.
  • The anti-proliferative activity of SCH66336 was due to G1-phase cell cycle arrest and retinoblastoma protein inactivation, followed by apoptosis.
  • In combination with cisplatin, both FTS and SCH66336 markedly enhanced the level of cisplatin-induced apoptosis, an effect that was associated with enhanced G2/M cell cycle arrest.
  • Pharmacological inhibitors of either ERK or PI-3 kinase/Akt did not mimic the chemosensitising activity of either SCH66336 or FTS.
  • In summary, our study demonstrates that SCH66336 has good in vitro anti-tumour activity in both human and mouse melanoma cell lines, and suggests that Ras antagonists could be useful in overcoming chemoresistance to cisplatin in melanoma.
  • [MeSH-major] Alkyl and Aryl Transferases / antagonists & inhibitors. Apoptosis / drug effects. Cisplatin / pharmacology. Enzyme Inhibitors / pharmacology. Farnesol / analogs & derivatives. Melanoma / pathology. Piperidines / pharmacology. Protein-Serine-Threonine Kinases. Pyridines / pharmacology. Skin Neoplasms / pathology
  • [MeSH-minor] 3T3 Cells. Actins / metabolism. Animals. Blotting, Western. Cell Cycle / drug effects. Cell Division / drug effects. Colony-Forming Units Assay. Drug Synergism. Farnesyltranstransferase. Humans. In Situ Nick-End Labeling. In Vitro Techniques. Mice. Microscopy, Confocal. Mitogen-Activated Protein Kinases / drug effects. Mitogen-Activated Protein Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Retinoblastoma Protein / metabolism. Salicylates / pharmacology. Tumor Cells, Cultured

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12673674.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Enzyme Inhibitors; 0 / Piperidines; 0 / Proto-Oncogene Proteins; 0 / Pyridines; 0 / Retinoblastoma Protein; 0 / Salicylates; 0 / farnesylthiosalicylic acid; 193275-84-2 / lonafarnib; 4602-84-0 / Farnesol; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; Q20Q21Q62J / Cisplatin
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86. Lumbroso L, Doz F, Levy C, Dendale R, Vedrenne J, Bours D, Zucker JM, Asselain B, Desjardins L: [Diode laser thermotherapy and chemothermotherapy in the treatment of retinoblastoma]. J Fr Ophtalmol; 2003 Feb;26(2):154-9
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  • [Title] [Diode laser thermotherapy and chemothermotherapy in the treatment of retinoblastoma].
  • [Transliterated title] Thermothérapie et thermochimiothérapie au laser diode dans le traitement du rétinoblastome.
  • INTRODUCTION: The use of transpupillary thermotherapy alone or associated with systemic chemotherapy is a therapeutic modality of ocular retinoblastoma that allows ocular preservation without external beam irradiation of the eye.
  • We present our experience with thermotherapy in the treatment of selected cases of retinoblastoma.
  • MATERIAL AND METHODS: This paper reports a retrospective case series of patients treated for retinoblastoma by thermotherapy or chemothermotherapy (carboplatin IV followed by thermotherapy) in a single institution from October 1994 to December 2000.
  • Data collected include general characteristics of the treated children, tumor characteristics, and the results of the treatments on local tumor control.
  • Transpupillar thermotherapy was delivered with a diode laser through an operating microscope.
  • Each tumor was treated separately and laser intensity, spot size, and duration were adapted to the size of the tumor and the clinical response.
  • Chemothermotherapy consisted in thermotherapy delivered shortly after an intravenous injection of carboplatin (560 mg/m(2)) at day 1, followed by thermotherapy alone at day 8 if the lesion was 6mm or more in diameter.
  • Lesions measuring more than 15 mm, or associated with substantial vitreous seeding, retinal detachment, or optic nerve head involvement are not suitable for these techniques.
  • The median tumor diameter at the moment of thermotherapy or chemothermotherapy was 2mm (range, 0.2-15.0mm).
  • One hundred and ninety-four tumors were treated by chemothermotherapy and 18 by thermotherapy alone.
  • In 75% of the cases, the treatment was administered after two courses of chemotherapy (etoposide and carboplatin).
  • After a mean follow-up of 55 months (range, 16-89 months), tumor control was obtained in 87.1% of lesions after chemothermotherapy and 77.8% after thermotherapy.
  • DISCUSSION: Diode laser delivers hyperthermia on the tumor bed and its use alone or in association with systemic administration of carboplatin makes it possible to preserve the eye without external beam irradiation, with few side effects and less cumulative doses of chemotherapy.
  • CONCLUSION: Thermotherapy and chemothermotherapy provide excellent local tumor control and eye preservation in selected cases of retinoblastoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hyperthermia, Induced. Laser Therapy. Retinal Neoplasms / therapy. Retinoblastoma / therapy
  • [MeSH-minor] Child. Child, Preschool. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Infant. Male. Retrospective Studies

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  • (PMID = 12660589.001).
  • [ISSN] 0181-5512
  • [Journal-full-title] Journal français d'ophtalmologie
  • [ISO-abbreviation] J Fr Ophtalmol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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87. 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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  • BACKGROUND: Parathyroid hormone-related protein (PTHrP), a normal product of arterial vascular smooth muscle (VSM), contains a nuclear localization signal (NLS) and at least 2 translational initiation sites, one that generates a conventional signal peptide and one that disrupts the signal peptide.
  • First, PTHrP dramatically increases the percentage of VSM cells in the S and in G2/M phases of the cell cycle.
  • 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.
  • 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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88. Albert DM, Nickells RW, Gamm DM, Zimbric ML, Schlamp CL, Lindstrom MJ, Audo I: Vitamin D analogs, a new treatment for retinoblastoma: The first Ellsworth Lecture. Ophthalmic Genet; 2002 Sep;23(3):137-56
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  • [Title] Vitamin D analogs, a new treatment for retinoblastoma: The first Ellsworth Lecture.
  • Ellsworth, an important figure in the development of current treatments of retinoblastoma (RB), and reviews our studies of vitamin D analogs as treatments for retinoblastoma in two experimental mouse models.
  • We identified vitamin D receptors in retinoblastoma and examined the effectiveness and mechanism of action of these analogs.
  • METHODS: Reverse-transcriptase polymerase chain reaction (RT-PCR) amplification was used to detect vitamin D receptor mRNAs in human and mouse retinoblastomas.
  • The effectiveness and toxicity of vitamin D(2), calcitriol, and synthetic analogs were studied in the athymic/Y-79 xenograft and transgenic mouse models of RB.
  • Dose-response studies focused on tumor inhibition; toxicity studies investigated survival and serum calcium.
  • RESULT: Vitamin D receptor mRNAs were detectable in Y-79 RB cells, LH beta-Tag tumors, and human RB specimens using RT-PCR.
  • Calcitriol and vitamin D(2) inhibited in vivo growth in xenograft and transgenic models, but therapeutic levels were toxic due to hypercalcemia.
  • Two analogs, 16,23-D(3) and 1 alpha-OH-D( 2), inhibited tumors in animal models of RB with reduced toxicity.
  • CONCLUSION: 16,23-D(3) and 1 alpha-OH-D(2) are effective in tumor reduction in two mouse models of RB with low toxicity.
  • [MeSH-major] Calcitriol / therapeutic use. Ergocalciferols / therapeutic use. Proto-Oncogene Proteins c-bcl-2. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / metabolism. DNA Primers / chemistry. Disease Models, Animal. Humans. Immunoenzyme Techniques. Ki-67 Antigen / metabolism. Mice. Mice, Nude. Mice, Transgenic. Proto-Oncogene Proteins / metabolism. RNA, Messenger / metabolism. Receptors, Calcitriol / genetics. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism. Tumor Suppressor Protein p53 / metabolism. bcl-2-Associated X Protein

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  • (PMID = 12324873.001).
  • [ISSN] 1381-6810
  • [Journal-full-title] Ophthalmic genetics
  • [ISO-abbreviation] Ophthalmic Genet.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R01-EY01917
  • [Publication-type] Lectures; Portraits; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / DNA Primers; 0 / Ergocalciferols; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Receptors, Calcitriol; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; FXC9231JVH / Calcitriol
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89. Greenberg VL, Williams JM, Cogswell JP, Mendenhall M, Zimmer SG: Histone deacetylase inhibitors promote apoptosis and differential cell cycle arrest in anaplastic thyroid cancer cells. Thyroid; 2001 Apr;11(4):315-25
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  • [Title] Histone deacetylase inhibitors promote apoptosis and differential cell cycle arrest in anaplastic thyroid cancer cells.
  • In this study, the cellular response to the histone deacetylase inhibitors, sodium butyrate and trichostatin A, was analyzed in cell lines derived from primary anaplastic thyroid carcinomas.
  • Apoptosis increases in response to drug treatment and is associated with the appearance of the cleaved form of the caspase substrate, poly-(ADP-ribose) polymerase (PARP).
  • Cell cycle arrest is associated with the reduced expression of cyclins A and B, the increased expression of the cyclin-dependent kinase inhibitors, p21(Cip1/WAF1) and p27Kip1, the reduced phosphorylation of the retinoblastoma protein (pRb), and a reduction in cdk2 and cdk1-associated kinase activities.
  • In ATC cells overexpressing cyclin E, drug treatment failed to replicate these events.
  • These results suggest that growth inhibition of ATC cells by HDAIs is due to the promotion of apoptosis through the activation of the caspase cascade and the induction of cell cycle arrest via a reduction in cdk2- and cdk1-associated kinase activities.
  • [MeSH-major] Apoptosis / drug effects. Butyrates / pharmacology. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Hydroxamic Acids / pharmacology. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Cell Cycle / drug effects. Cyclin E / physiology. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / physiology. Humans. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / physiology

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  • (PMID = 11349829.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA77614
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Butyrates; 0 / CDKN1A protein, human; 0 / Cyclin E; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Tumor Suppressor Protein p53; 3X2S926L3Z / trichostatin A
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90. Phipps JA, Wilkinson-Berka JL, Fletcher EL: Retinal dysfunction in diabetic ren-2 rats is ameliorated by treatment with valsartan but not atenolol. Invest Ophthalmol Vis Sci; 2007 Feb;48(2):927-34
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  • [Title] Retinal dysfunction in diabetic ren-2 rats is ameliorated by treatment with valsartan but not atenolol.
  • PURPOSE: To determine whether diabetes leads to retinal neuronal dysfunction in hypertensive transgenic (mRen-2)27 rats (Ren-2), and whether the effect can be prevented by treatment of hypertension with either the angiotensin-1 receptor blocker (AT1-RB) valsartan or the beta1-adrenergic receptor antagonist atenolol.
  • A subset of animals received valsartan (4 mg/kg per day) or atenolol (30 mg/kg per day) by gavage.
  • Sprague-Dawley (SD) rats served as normotensive controls for blood pressure (BP).
  • We evaluated retinal function in all groups with a paired-flash electroretinogram over high light intensities (0.5-2.0 log cd-s .
  • Treatment of both nondiabetic and diabetic Ren-2 rats with valsartan or atenolol reduced BP to within normal limits.
  • However, in treated diabetic Ren-2 rats, retinal dysfunction was ameliorated by valsartan but not by atenolol, with a significant improvement (P < 0.05) observed in all components of the electroretinogram, with the exception of the OPs.
  • CONCLUSIONS: These findings suggest that hypertension induces retinal dysfunction that is exacerbated with diabetes and ameliorated by treatment with an AT1-RB, and not just by normalizing BP.
  • [MeSH-major] Antihypertensive Agents / therapeutic use. Atenolol / therapeutic use. Diabetic Retinopathy / drug therapy. Hypertension / drug therapy. Tetrazoles / therapeutic use. Valine / analogs & derivatives
  • [MeSH-minor] Adrenergic beta-Antagonists / therapeutic use. Angiotensin II Type 1 Receptor Blockers / therapeutic use. Animals. Animals, Genetically Modified. Blood Pressure / drug effects. Diabetes Mellitus, Experimental / drug therapy. Diabetes Mellitus, Experimental / physiopathology. Electroretinography. Female. Neuroglia / physiology. Photic Stimulation. Rats. Retina / physiopathology. Valsartan

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  • (PMID = 17251496.001).
  • [ISSN] 0146-0404
  • [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 / Adrenergic beta-Antagonists; 0 / Angiotensin II Type 1 Receptor Blockers; 0 / Antihypertensive Agents; 0 / Tetrazoles; 50VV3VW0TI / Atenolol; 80M03YXJ7I / Valsartan; HG18B9YRS7 / Valine
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91. Dunkel IJ, Lee TC, Shi W, Beaverson KL, Novetsky D, Lyden D, Finlay JL, McCormick B, Abramson DH: A phase II trial of carboplatin for intraocular retinoblastoma. Pediatr Blood Cancer; 2007 Oct 15;49(5):643-8
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  • [Title] A phase II trial of carboplatin for intraocular retinoblastoma.
  • BACKGROUND: Retinoblastoma patients with RB1 germline mutations are at risk of developing second malignancies and external beam radiation therapy increases the risk.
  • Carboplatin-containing chemotherapy regimens in conjunction with local therapies have been investigated for intraocular retinoblastoma, but the lack of data regarding the efficacy of single agent intravenous carboplatin prompted this phase II study.
  • PROCEDURE: Twenty-five patients (43 eyes) were treated with intravenous carboplatin (18.7 mg/kg for patients < 12 kg, 560 mg/m(2) for patients >/= 12 kg).
  • Patients received a median of two cycles of carboplatin (range one to five cycles) beginning at a median age of 5 months (range 14 days to 22 months).
  • RESULTS: All patients were extraocular disease free during the follow-up period (median 76.3 months).
  • The 5-year overall ocular and ocular event-free survivals were 93.3% (95% CI, 84.4-100%) and 43.5% (95% CI, 25.8-61.3%) for eyes treated for Reese-Ellsworth (RE) group 1-3 disease and 25.0% (95% CI, 1.0-50.0%) and 8.3% (95% CI, 0-24.0%) for RE group 4-5 disease, respectively.
  • No non-hematopoietic serious or permanent toxicities related to the chemotherapy were observed.
  • CONCLUSION: When used as a neoadjuvant agent, carboplatin usually leads to objective responses of intraocular retinoblastoma.
  • The 5-year ocular event-free survival appears inferior to other protocols using more extensive chemotherapy, but with greater radiation therapy usage, overall ocular survival rate for RE group 1-3 eyes was excellent.
  • [MeSH-major] Carboplatin / administration & dosage. Retinoblastoma / drug therapy
  • [MeSH-minor] Antineoplastic Agents. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Infant. Infant, Newborn. Male. Neoadjuvant Therapy. Remission Induction. Survival Analysis

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17301956.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; BG3F62OND5 / Carboplatin
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92. Kim KC, Jun HJ, Kim JS, Kim IG: Enhancement of radiation response with combined Ganoderma lucidum and Duchesnea chrysantha extracts in human leukemia HL-60 cells. Int J Mol Med; 2008 Apr;21(4):489-98
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  • [Title] Enhancement of radiation response with combined Ganoderma lucidum and Duchesnea chrysantha extracts in human leukemia HL-60 cells.
  • We previously demonstrated that combined treatment with extracts of the medicinal mushroom Ganoderma lucidum and the herb Duchesnea chrysantha (GDE) significantly suppresses cell growth and selectively induces apoptosis in human leukemia HL-60 cells, but not in normal cells.
  • GDE?s mechanism of action and its activity against HL-60 cells suggest that it could be suitable for the combined-modality treatment of hematological malignancies.
  • In the present study, we examined whether treatment with a combination of GDE and ionizing radiation enhances the therapeutic effect.
  • We demonstrated that, when used in combination with radiation at a clinically relevant dose of 2 Gy, GDE further suppressed cell proliferation and induced apoptosis as well as micronuclei formation in HL-60 cells, leading to increased cell death.
  • Furthermore, GDE pretreatment not only reduced radiation-induced G2/M-phase arrest, but also induced G1-phase arrest.
  • These events are associated with the inhibition of cyclin-dependent kinase 1 (CDK1) phosphorylation and the dephosphorylation of retinoblastoma protein (pRB).
  • Collectively, these data show that combined treatment with GDE and radiation enhances radiation-induced apoptosis and overall cell death.
  • These findings may be clinically relevant and suggest a novel therapeutic strategy for increasing the efficacy of radiotherapy.
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / radiation effects. CDC2 Protein Kinase / metabolism. Caspase 3 / metabolism. Cell Proliferation / drug effects. Cell Proliferation / radiation effects. Combined Modality Therapy. Drug Synergism. Drugs, Chinese Herbal / administration & dosage. G1 Phase / drug effects. G1 Phase / radiation effects. Gamma Rays / therapeutic use. HL-60 Cells. Humans. Micronucleus Tests. Mitochondria / drug effects. Mitochondria / radiation effects. Phosphorylation. Phytotherapy. Plant Extracts / administration & dosage. Retinoblastoma Protein / metabolism

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  • (PMID = 18360695.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Plant Extracts; 0 / Radiation-Sensitizing Agents; 0 / Retinoblastoma Protein; EC 2.7.11.22 / CDC2 Protein Kinase; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3
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93. Cozzi SJ, Parsons PG, Ogbourne SM, Pedley J, Boyle GM: Induction of senescence in diterpene ester-treated melanoma cells via protein kinase C-dependent hyperactivation of the mitogen-activated protein kinase pathway. Cancer Res; 2006 Oct 15;66(20):10083-91
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  • [Title] Induction of senescence in diterpene ester-treated melanoma cells via protein kinase C-dependent hyperactivation of the mitogen-activated protein kinase pathway.
  • We now describe the in vitro cytostatic effects of PEP005 and the diterpene ester phorbol 12-myristate 13-acetate, observed in 20% of human melanoma cell lines.
  • Primary cultures of normal human neonatal fibroblasts were resistant to growth arrest, indicating a potential for tumor selectivity.
  • There was sustained expression of p21(WAF1/CIP1), irreversible dephosphorylation of the retinoblastoma protein, and transcriptional silencing of E2F-responsive genes in sensitive cell lines.
  • Activation of mitogen-activated protein (MAP)/extracellular signal-regulated kinase (ERK) kinase (MEK) 1/2 by PKC was required for diterpene ester-induced senescence.
  • We propose that activation of PKC overstimulates the RAS/RAF/MEK/ERK pathway, resulting in molecular changes leading to the senescent phenotype.
  • [MeSH-major] Diterpenes / pharmacology. Esters / pharmacology. MAP Kinase Signaling System / physiology. Melanoma / drug therapy. Melanoma / enzymology. Protein Kinase C / metabolism
  • [MeSH-minor] Cell Aging / drug effects. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. E2F1 Transcription Factor / genetics. E2F1 Transcription Factor / metabolism. Enzyme Activation / drug effects. Gene Silencing / drug effects. Humans. Isoenzymes / biosynthesis. Isoenzymes / genetics. Isoenzymes / metabolism. Phosphorylation / drug effects. Retinoblastoma Protein / metabolism. Tetradecanoylphorbol Acetate / pharmacology. Transcription, Genetic


94. Lim SJ, Gutiérrez-Puente Y, Tari AM: N-(4-hydroxyphenyl)-retinamide selectively increases All-TRANS retinoic acid inhibitory effects in HER2/NEU-overexpressing breast cancer cells. Tumour Biol; 2002 Sep-Oct;23(5):279-86
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  • [Title] N-(4-hydroxyphenyl)-retinamide selectively increases All-TRANS retinoic acid inhibitory effects in HER2/NEU-overexpressing breast cancer cells.
  • We previously reported that overexpression of the HER2/NEU oncogene induces all-TRANS retinoic acid (ATRA) resistance in breast cancer cells.
  • We investigated whether 4HPR, by suppressing HER2/neu or EGFR expression, could sensitize breast cancer cells to ATRA.
  • At 1.3 micro M concentration (a clinically pharmacologically achievable dose), 4HPR increased ATRA sensitivity synergistically in HER2/NEU-overexpressing BT-474, MDA-MB-453, and MCF-7/Her2 breast cancer cells.
  • However, 4HPR did not sensitize EGFR-overexpressing MDA-MB-468, Hs578T, and MCF-7/EGFR breast cancer cells to ATRA.
  • The increased inhibitory effects in HER2/NEU-overexpressing cells were not correlated with increases in expression levels of p21(WAF1/CIP1) or retinoblastoma protein.
  • Combining 4HPR with ATRA may lead to a novel, selective therapeutic or chemopreventive strategy against HER2/NEU-overexpressing breast tumors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Breast Neoplasms / drug therapy. Fenretinide / pharmacology. Receptor, ErbB-2 / analysis. Tretinoin / pharmacology
  • [MeSH-minor] Cyclin-Dependent Kinase Inhibitor p21. Cyclins / analysis. Drug Synergism. Female. Humans. Receptor, Epidermal Growth Factor / analysis. Retinoblastoma Protein / analysis. Tumor Cells, Cultured

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  • [Copyright] Copyright 2002 S. Karger AG, Basel
  • (PMID = 12595744.001).
  • [ISSN] 1010-4283
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Retinoblastoma Protein; 187EJ7QEXL / Fenretinide; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
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95. Emanuel S, Rugg CA, Gruninger RH, Lin R, Fuentes-Pesquera A, Connolly PJ, Wetter SK, Hollister B, Kruger WW, Napier C, Jolliffe L, Middleton SA: The in vitro and in vivo effects of JNJ-7706621: a dual inhibitor of cyclin-dependent kinases and aurora kinases. Cancer Res; 2005 Oct 1;65(19):9038-46
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  • Modulation of aberrant cell cycle regulation is a potential therapeutic strategy applicable to a wide range of tumor types.
  • JNJ-7706621 is a novel cell cycle inhibitor that showed potent inhibition of several cyclin-dependent kinases (CDK) and Aurora kinases and selectively blocked proliferation of tumor cells of various origins but was about 10-fold less effective at inhibiting normal human cell growth in vitro.
  • In human cancer cells, treatment with JNJ-7706621 inhibited cell growth independent of p53, retinoblastoma, or P-glycoprotein status; activated apoptosis; and reduced colony formation.
  • Inhibition of CDK1 kinase activity, altered CDK1 phosphorylation status, and interference with downstream substrates such as retinoblastoma were also shown in human tumor cells following drug treatment.
  • Flow cytometric analysis of DNA content showed that JNJ-7706621 delayed progression through G1 and arrested the cell cycle at the G2-M phase.
  • In a human tumor xenograft model, several intermittent dosing schedules were identified that produced significant antitumor activity.
  • These results show the therapeutic potential of this novel cell cycle inhibitor and support clinical evaluation of JNJ-7706621.
  • [MeSH-minor] Animals. Aurora Kinases. Cell Line, Tumor. Cells, Cultured. Endothelial Cells / drug effects. Endothelial Cells / enzymology. Female. HeLa Cells. Humans. Melanoma / drug therapy. Melanoma / enzymology. Mice. Mice, Nude. Xenograft Model Antitumor Assays

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  • (PMID = 16204078.001).
  • [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 / JNJ-7706621; 0 / Protein Kinase Inhibitors; 0 / Triazoles; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / Cyclin-Dependent Kinases
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96. Elangovan S, Hsieh TC, Wu JM: Growth inhibition of human MDA-mB-231 breast cancer cells by delta-tocotrienol is associated with loss of cyclin D1/CDK4 expression and accompanying changes in the state of phosphorylation of the retinoblastoma tumor suppressor gene product. Anticancer Res; 2008 Sep-Oct;28(5A):2641-7
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  • [Title] Growth inhibition of human MDA-mB-231 breast cancer cells by delta-tocotrienol is associated with loss of cyclin D1/CDK4 expression and accompanying changes in the state of phosphorylation of the retinoblastoma tumor suppressor gene product.
  • Tocotrienols, a subgroup within the vitamin E family of compounds, have shown antiproliferative and anticancer properties, however, the molecular basis of these effects remains to be elucidated.
  • In this study, the effect of 3-tocotrienol on cell cycle arrest was assessed by studying the retinoblastoma protein (Rb) levels and phosphorylation status, levels of E2F (a transcription factor critically involved in the G1/S-phase transition of the mammalian cell cycle; originally identified as a DNA-binding protein essential for early region 1A-dependent activation of the adenovirus promoter designated E2), and other cell cycle controlling proteins in estrogen receptor-negative MDA-MB-231 breast cancer cells.
  • The cell growth assay demonstrated that exposure of the MDA-MB-231 cells to 6-tocotrienol (1-20 microM) resulted in a dose- and time-dependent inhibition of cell growth as compared with vehicle treated cells and the magnitude of growth inhibition was higher at 10 and 20 microM treatment for 48 and 72 h.
  • The phosphorylation status of Rb plays a central role in the control of the cell cycle at the G0/G1-phase. delta-Tocotrienol treatment reduced the total Rb and its phosphorylation at the Ser780, Ser795, Ser 807/811 and Thr826 positions in a dose- and time-dependent fashion.
  • The site-specific inhibition of the phosphorylation of Rb by delta-tocotrienol was tightly associated with a marked reduction in the expression of cyclin D1 and its regulatory partner cyclin-dependant kinase 4 (CDK4), which is responsible for the phosphorylation of Rb at Ser780, Ser795, Ser 807/811 and Thr826.
  • In addition, delta-tocotrienol also reduced the expression of E2F that occurred simultaneously with the loss of Rb phosphorylation and inhibition of cell cycle progression.
  • To the best of our knowledge, this study was the first to reveal that the target of cell proliferative inhibitory action of delta-tocotrienol in a model estrogen receptor-negative human breast cancer cell line MDA-MB-231 is mediated by the loss of cyclin D1 and associated suppression of site-specific Rb phosphorylation, suggesting its future development and use as an anticancer agent.
  • [MeSH-major] Breast Neoplasms / drug therapy. Cyclin D1 / biosynthesis. Cyclin-Dependent Kinase 4 / biosynthesis. Retinoblastoma Protein / metabolism. Vitamin E / analogs & derivatives
  • [MeSH-minor] CDC2 Protein Kinase / biosynthesis. Cell Growth Processes / drug effects. Cell Line, Tumor. Cyclin B / biosynthesis. Cyclin B1. E2F Transcription Factors / biosynthesis. Humans. Phosphorylation / drug effects


97. Raj MH, Abd Elmageed ZY, Zhou J, Gaur RL, Nguyen L, Azam GA, Braley P, Rao PN, Fathi IM, Ouhtit A: Synergistic action of dietary phyto-antioxidants on survival and proliferation of ovarian cancer cells. Gynecol Oncol; 2008 Sep;110(3):432-8
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  • [Title] Synergistic action of dietary phyto-antioxidants on survival and proliferation of ovarian cancer cells.
  • OBJECTIVES: A number of herbal dietary antioxidant supplements containing Indole-3 Carbinol (I3C) and Resveratrol (RE) have been established as anti-proliferative agents in cancer.
  • These compounds have both similar as well as unique molecular targeting profiles.
  • The purpose of this study is to analyze their mechanism of action when used individually and in combination in ovarian cancer.
  • METHODS: SK-OV-3 ovarian cancer cells were treated with various doses of I3C, RE or I3C+RE.
  • Western blot was performed to determine the expression of the genes associated with cell cycle and apoptosis.
  • CA-125, a functional marker of ovarian cancer, and nitric oxide, were analyzed by ELISA.
  • Analysis of apoptosis-associated genes revealed an inhibition of Retinoblastoma protein (Rb) and Survivin (SVV) gene expression.
  • This was accompanied by elevation of p21, a tumor suppressor.
  • Cell cycle was inhibited at both G1 and G2/M by individual treatments, and accentuated by a combination.
  • CA125 was inhibited by either I3C or RE treatments.
  • In contrast, basal nitric oxide production was inhibited by I3C and I3C+RE but not RE alone.
  • CONCLUSIONS: This is the first evidence demonstrating the effects of I3C on ovarian cancer cells and its synergism with RE.
  • Based on this model, our data indicate that combinations of compounds with different targeting properties will be more effective in chemoprevention and/or chemotherapy of ovarian and possibly other cancers.

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  • (PMID = 18603286.001).
  • [ISSN] 1095-6859
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA091185-02; United States / NCI NIH HHS / CA / R01 CA081125; United States / NCI NIH HHS / CA / R03 CA091185-02; United States / NCI NIH HHS / CA / R25-CA47877; United States / NCI NIH HHS / CA / R03 CA091185-01A1; United States / NCI NIH HHS / CA / R03 CA091185; United States / NCI NIH HHS / CA / R03 CA091185-02S1; United States / NCI NIH HHS / CA / CA81125; United States / NCI NIH HHS / CA / R25 CA047877; United States / NCI NIH HHS / CA / CA91185; United States / NCI NIH HHS / CA / CA091185-02S1; United States / NCI NIH HHS / CA / CA091185-01A1
  • [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 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Apoptosis Regulatory Proteins; 0 / Indoles; 0 / Oxazines; 0 / Stilbenes; 0 / Xanthenes; 1FN9YD6968 / resazurin; 31C4KY9ESH / Nitric Oxide; C11E72455F / indole-3-carbinol; Q369O8926L / resveratrol
  • [Other-IDs] NLM/ NIHMS70663; NLM/ PMC2628811
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98. Jackman KM, Frye CB, Hunger SP: Flavopiridol displays preclinical activity in acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Apr;50(4):772-8
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  • [Title] Flavopiridol displays preclinical activity in acute lymphoblastic leukemia.
  • BACKGROUND: New agents are needed for treatment of children with relapsed acute lymphoblastic leukemia (ALL).
  • PROCEDURE: We evaluated the efficacy of FP in ALL cell lines using cell proliferation assays, determined the effects of FP treatment on cell growth and viability in cell lines and patient samples, examined cell cycle kinetics, and evaluated the effect of FP on endogenous cyclin-dependent kinase (CDK) activity, Mcl-1 expression, and RNA polymerase II expression and phosphorylation.
  • At lower concentrations, FP induces transient G(1)-S cell cycle arrest and modest levels of apoptosis in cell lines.
  • After treatment with FP, ALL cell lines have decreased expression of retinoblastoma protein phosphorylated at serines 795 and 807/811, indicating reduced CDK activity.
  • We also show that ALL cell lines are sensitive to clinically achievable concentrations of FP in medium supplemented with human serum and that FP reduces the expression of Mcl-1 and phosphorylated forms of the C-terminal domain of RNA polymerase II.
  • FP also increases cell death by approximately twofold over baseline in primary ALL blasts.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Flavonoids / pharmacology. Piperidines / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Humans. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / drug effects. Neoplasm Recurrence, Local / drug therapy. Proto-Oncogene Proteins c-bcl-2 / drug effects. RNA Polymerase II / drug effects. Retinoblastoma Protein / drug effects

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18000861.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Flavonoids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Piperidines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Retinoblastoma Protein; 45AD6X575G / alvocidib; EC 2.7.7.- / RNA Polymerase II
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99. Sato S, Kajiyama Y, Sugano M, Iwanuma Y, Tsurumaru M: Flavopiridol as a radio-sensitizer for esophageal cancer cell lines. Dis Esophagus; 2004;17(4):338-44
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  • [Title] Flavopiridol as a radio-sensitizer for esophageal cancer cell lines.
  • Growth inhibition was evaluated by MTT assay, cell cycle distribution was determined by flow cytometry, and cyclin D1, Bcl-2 and Rb protein expression was detected by Western blotting.
  • Exposure to 300 nmol/L flavopiridol decreased the levels of cyclin D1 and Rb protein in all three cell lines and Bcl-2 protein was also decreased in TE8 and KE4 cells.
  • Moreover, exposure to 0.05 nmol/L flavopiridol slightly decreased the levels of cyclin D1, Rb and Bcl-2 protein in KE4 cells.
  • Flavopiridol treatment (0.05 nmol/L) enhanced the radio-sensitivity in all three cell lines.
  • Administration of a low dose of flavopiridol could be a potent new therapeutic approach for improving the efficacy of radiotherapy against esophageal cancer.

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  • (PMID = 15569374.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Flavonoids; 0 / Formazans; 0 / Growth Inhibitors; 0 / Piperidines; 0 / Radiation-Sensitizing Agents; 0 / Retinoblastoma Protein; 0 / Tetrazolium Salts; 136601-57-5 / Cyclin D1; 23305-68-2 / MTT formazan; 45AD6X575G / alvocidib
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100. Myhre L, Alm K, Johansson M, Oredsson SM: Normal-like breast cells, but not breast cancer cells, recovered from treatment with N',N''-diethylnorspermine. Anticancer Drugs; 2009 Apr;20(4):230-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Normal-like breast cells, but not breast cancer cells, recovered from treatment with N',N''-diethylnorspermine.
  • A number of polyamine analogs are currently used in various clinical trials as cancer treatment and it is important to investigate their effects not only on cancer cells but also on normal cells.
  • Treatment with polyamine analogs depletes cells of polyamines and inhibits cell proliferation, but the analogs cannot take over the normal function of the natural polyamines in the cell.
  • The ability of both normal-like and breast cancer cells to recover from DENSPM treatment was also studied.
  • DENSPM treatment of MCF-10A cells resulted in a prolongation of the S and G2 +M phases, followed by a G1/S block.
  • The p53/p21/RB1 pathway was involved in the G1/S block as shown by increased levels of p53 and p21 detected by western blot.
  • We also show that MCF-10A cells rapidly recover from DENSPM-induced growth inhibition in contrast to four human breast cancer cell lines.
  • The goal of cancer treatment is to cause minimal and reversible damage to normal cells, while cancer cells should be eliminated.
  • Altogether, the data show that treatment with polyamine analogs spares normal cells, while negatively affecting the cancer cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Breast Neoplasms / drug therapy. Cell Cycle / drug effects. Spermine / analogs & derivatives
  • [MeSH-minor] Blotting, Western. Bromodeoxyuridine. Cell Line. Cell Line, Tumor. Cyclin A / drug effects. Cyclin A / metabolism. Cyclin A2. Cyclin B / drug effects. Cyclin B / metabolism. Cyclin B1. Cyclin E / drug effects. Cyclin E / metabolism. DNA. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Female. Flow Cytometry. Humans. Oncogene Proteins / drug effects. Oncogene Proteins / metabolism

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  • (PMID = 19288605.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCNA2 protein, human; 0 / CCNB1 protein, human; 0 / CCNE1 protein, human; 0 / Cyclin A; 0 / Cyclin A2; 0 / Cyclin B; 0 / Cyclin B1; 0 / Cyclin E; 0 / Oncogene Proteins; 121749-39-1 / N(1),N(11)-diethylnorspermine; 2FZ7Y3VOQX / Spermine; 9007-49-2 / DNA; G34N38R2N1 / Bromodeoxyuridine
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