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1. Hassan HT: Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy. Leuk Res; 2004 Jul;28(7):667-71
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  • [Title] Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy.
  • Several garlic compounds including allicin and its corresponding sulfide inhibit the proliferation and induce apoptosis of several human non-leukaemia malignant cells including breast, bladder, colorectal, hepatic, prostate cancer, lymphoma and skin tumour cell lines.
  • Ajoene (4,5,9-trithiadodeca-1,6,11-triene-9-oxide) is a garlic-derived compound produced most efficiently from pure allicin and has the advantage of a greater chemical stability than allicin.
  • Several clinical trials and in vitro studies of ajoene have demonstrated its best-known anti-thrombosis, anti-microbial and cholesterol lowering activities.
  • Ajoene was shown to inhibit proliferation and induce apoptosis of several human leukaemia CD34-negative cells including HL-60, U937, HEL and OCIM-1.
  • Also, ajoene induces 30% apoptosis in myeloblasts from chronic myeloid leukaemia patient in blast crisis.
  • More significantly, ajoene profoundly enhanced the apoptotic effect of the two chemotherapeutic drugs: cytarabine and fludarabine in human CD34-positive resistant myeloid leukaemia cells through enhancing their bcl-2 inhibitory and caspase-3 activation activities.
  • The two key anti-leukaemia biological actions of ajoene were the inhibition of proliferation and the induction of apoptosis.
  • Studies have shown the anti-proliferation activity of ajoene to be associated with a block in the G2/M phase of cell cycle in human myeloid leukaemia cells.
  • The apoptosis inducing activity of ajoene is via the mitochondria-dependent caspase cascade through a significant reduction of the anti-apoptotic bcl-2 that results in release of cytochrome c and the activation of caspase-3.
  • Since acute myeloid leukaemia (AML) is a heterogeneous malignant disease in which disease progression at the level of CD34-positive cells has a major impact on resistance to chemotherapy and relapse and the inability to undergo apoptosis is a crucial mechanism of multi-drug resistance in AML patients.
  • The recent findings of the potent enhancing activity of ajoene on chemotherapy-induced apoptosis in CD34-positive resistant human myeloid leukaemia cells suggest a novel promising role for the treatment of refractory and/or relapsed AML patients as well as elderly AML patients.
  • Further studies are warranted to evaluate similar enhancing effect for ajoene in blast cells from AML patients in primary cultures before its introduction in pilot clinical study.
  • [MeSH-major] Disulfides / therapeutic use. Garlic. Leukemia, Myeloid / drug therapy. Plant Extracts / therapeutic use
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Drug Synergism. Humans

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  • (PMID = 15158086.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Disulfides; 0 / Plant Extracts; 99A0041VG8 / ajoene
  • [Number-of-references] 66
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2. Grimaudo S, Raimondi MV, Capone F, Chimirri A, Poretto F, Monforte AM, Simoni D, Tolomeo M: Apoptotic effects of thiazolobenzimidazole derivatives on sensitive and multidrug resistant leukaemic cells. Eur J Cancer; 2001 Jan;37(1):122-30
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  • We investigated the cytotoxic activity of eight thiazolobenzimidazole derivatives on sensitive HL60 and multidrug-resistant (MDR) (HL60R) leukaemia cell lines.
  • Only two compounds in this study proved to have interesting effects: (a) the S-enantiomer of TBZ, that was able to induce apoptosis in MDR cells in a slightly more selective manner than TBZ (racemic form); and (b) TBZ-4-OCH3 (TBZ-4-OCH3), that showed cytotoxic and apoptotic effects on sensitive and resistant leukaemia cells greater than TBZ, without cytotoxic effects on normal haemopoietic progenitor cells.
  • The inhibition of caspase-9 and caspase-3 by specific polypeptide inhibitors decreased the apoptotic effects of TBZ-4-OCH3 in HL60 cells indicating that apoptosis induced by this compound was, at least partly, caspase-mediated.
  • On the contrary, the blocking of FL-associated cell surface antigen (Fas) using a specific Fas-blocking monoclonal antibody did not affect the level of apoptosis induced by TBZ-4-OCH3 suggesting that the Fas pathway was not involved.
  • In addition, the caspase 8 inhibitor was unable to inhibit the apoptotic activity of TBZ-4-OCH3.
  • The very low toxicity shown by TBZ-4-OCH3 in normal haemopoietic progenitor cells and its high activity in sensitive and MDR neoplastic cells suggest a possible clinical use for this new compound.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzimidazoles / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Antigens, CD95 / metabolism. Apoptosis / drug effects. Caspase Inhibitors. Cell Cycle / drug effects. Drug Resistance, Multiple. Drug Resistance, Neoplasm. HL-60 Cells. Humans. Leukemia / drug therapy. Leukemia / pathology

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  • (PMID = 11165139.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antineoplastic Agents; 0 / Benzimidazoles; 0 / Caspase Inhibitors; 0 / Thiazoles; 138226-12-7 / 1-(2',6'-difluorophenyl)-1H,3H-thiazolo(3,4-a)benzimidazole
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3. Heidel F, Lipka DB, Mirea FK, Mahboobi S, Grundler R, Kancha RK, Duyster J, Naumann M, Huber C, Böhmer FD, Fischer T: Bis(1H-indol-2-yl)methanones are effective inhibitors of FLT3-ITD tyrosine kinase and partially overcome resistance to PKC412A in vitro. Br J Haematol; 2009 Mar;144(6):865-74
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  • Inhibition of the mutated fms-like tyrosine kinase 3 (FLT3) receptor tyrosine kinase is a promising therapeutic strategy in acute myeloid leukaemia (AML).
  • Herein we investigated two representatives of a novel class of FLT3-TKI: Bis(1H-indol-2-yl)methanones.
  • Both compounds effectively induced apoptosis in FLT3-internal tandem duplicate (ITD)-transfected murine myeloid cells and in primary FLT3-ITD positive blasts.
  • Combination of both compounds with chemotherapy revealed synergistic effects in apoptosis assays.
  • The compounds did not show significant toxicity in human bone marrow cells derived from healthy donors.
  • Western Blotting experiments of 32D-FLT3-ITD cells showed dose-dependent dephosphorylation of FLT3-ITD and of its downstream targets STAT5, AKT and ERK upon incubation with either compound.
  • In conclusion, bis(1H-indol-2-yl)methanones overcome resistance mediated by FLT3-ITD mutations at position N676 and show strong efficacy in FLT3-ITD-positive cells alone as well as in combination with chemotherapy.
  • We propose that further development of methanone compounds overcoming resistance to currently established FLT3-TKIs is an important step forward to an anticipated need within our future therapeutic algorithm in FLT3-ITD-positive AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Indoles / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Staurosporine / analogs & derivatives. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Apoptosis / drug effects. Cell Line. Drug Resistance, Neoplasm. Humans. Transfection / methods. Tumor Cells, Cultured


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4. Bright SA, Greene LM, Greene TF, Campiani G, Butini S, Brindisi M, Lawler M, Meegan MJ, Williams DC, Zisterer DM: The novel pyrrolo-1,5-benzoxazepine, PBOX-21, potentiates the apoptotic efficacy of STI571 (imatinib mesylate) in human chronic myeloid leukaemia cells. Biochem Pharmacol; 2009 Feb 1;77(3):310-21
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  • [Title] The novel pyrrolo-1,5-benzoxazepine, PBOX-21, potentiates the apoptotic efficacy of STI571 (imatinib mesylate) in human chronic myeloid leukaemia cells.
  • The Bcr-Abl kinase inhibitor, STI571, is the first line treatment for chronic myeloid leukaemia (CML), but the recent emergence of STI571 resistance has led to the examination of combination therapies.
  • In this report, we describe how a novel non-toxic G1-arresting compound, pyrrolo-1,5-benzoxazepine (PBOX)-21, potentiates the apoptotic ability of STI571 in Bcr-Abl-positive CML cells.
  • Co-treatment of CML cells with PBOX-21 and STI571 induced more apoptosis than either drug alone in parental (K562S and LAMA84) and STI571-resistant cells lines (K562R).
  • This potentiation of apoptosis was specific to Bcr-Abl-positive leukaemia cells with no effect observed on Bcr-Abl-negative HL-60 acute myeloid leukaemia cells.
  • The combined lack of an early change in mitochondrial membrane potential, release of cytochrome c and cleavage of pro-caspase-9 suggests that this pathway is not involved in the initiation of apoptosis by PBOX-21/STI571.
  • Apoptosis was significantly reduced following pre-treatment with either the general caspase inhibitor Boc-FMK or the chymotrypsin-like serine protease inhibitor TPCK, but was completely abrogated following pre-treatment with a combination of these inhibitors.
  • In conclusion, our data highlights the potential of PBOX-21 in combination with STI571 as an effective therapy against CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Carbamates / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Oxazepines / therapeutic use. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Blotting, Western. Cell Line, Tumor. Down-Regulation. Drug Synergism. Flow Cytometry. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. Membrane Potentials / drug effects. Up-Regulation

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  • (PMID = 19014913.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 7-((diethylcarbamoyl)oxy)-6-p-tolylpyrrolo(2,1-d)(1,5)benzoxazepine; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Carbamates; 0 / Oxazepines; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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5. Castelli M, Malagoli M, Lupo L, Riccomi TR, Casolari C, Cermelli C, Zanca A, Baggio G: Antiviral and antiproliferative activity in vitro of some new benzimidazole derivatives. Pharmacol Toxicol; 2001 Feb;88(2):67-74
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  • [Title] Antiviral and antiproliferative activity in vitro of some new benzimidazole derivatives.
  • The antiviral and antiproliferative activity of new compounds having n-benzenesulphony 1-2 (2 or 3-pyridylethyl) benzimidazole as a base structure were studied in vitro.
  • Their antitumour activity against human chronic myeloid leukaemia cells was evaluated and compared with that of equimolar doses of daunorubicin.
  • Only compound 7a, with the presence of both the pyridyl moiety bound at the ethylenic bridge in C-2 of benzimidazole and the nitro-group in the benzene ring, displays a selective antiproliferative effect against certain leukaemia cells and a good antiviral activity especially towards the Coxsackie B5 virus.
  • However, it should be noted that, in the case of hydroxybenzyl-benzimidazole, resistance also builds up to compound 7a, the Coxsackie B5 virus developing resistance to it after about ten runs.
  • Cytotoxicity tests show that many of these substances are well tolerated by the VERO cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antiviral Agents / pharmacology. Benzimidazoles / pharmacology. Tumor Cells, Cultured / drug effects. Viruses / drug effects
  • [MeSH-minor] Animals. Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / pathology. Cell Division / drug effects. Cercopithecus aethiops. Daunorubicin / pharmacology. Dose-Response Relationship, Drug. Drug Resistance, Microbial. Enterovirus B, Human / drug effects. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Vero Cells / drug effects

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  • (PMID = 11169164.001).
  • [ISSN] 0901-9928
  • [Journal-full-title] Pharmacology & toxicology
  • [ISO-abbreviation] Pharmacol. Toxicol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / Benzimidazoles; ZS7284E0ZP / Daunorubicin
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6. Azam M, Powers JT, Einhorn W, Huang WS, Shakespeare WC, Zhu X, Dalgarno D, Clackson T, Sawyer TK, Daley GQ: AP24163 inhibits the gatekeeper mutant of BCR-ABL and suppresses in vitro resistance. Chem Biol Drug Des; 2010 Feb;75(2):223-7
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  • Mutation in the ABL kinase domain is the principal mechanism of imatinib resistance in patients with chronic myelogenous leukaemia.
  • Here, we describe that the rationally designed compound AP24163 can inhibit native and gatekeeper mutants of the BCR/ABL kinase.
  • In vitro screening for drug resistance identified clones with compound mutations involving both the P-loop and T315I.
  • Our studies provide structural insights for the design of inhibitors against the gatekeeper mutant and suggest that up-front combination therapy may be required to prevent the emergence of compound-resistant mutations.
  • [MeSH-major] Adenine / analogs & derivatives. Benzamides / chemistry. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / antagonists & inhibitors. Protein Kinase Inhibitors / chemistry. Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Binding Sites. Cell Line. Computer Simulation. Dasatinib. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mice. Mutation. Piperazines / chemistry. Piperazines / pharmacology. Pyrimidines / chemistry. Pyrimidines / pharmacology. Thiazoles / chemistry. Thiazoles / pharmacology

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  • (PMID = 20028401.001).
  • [ISSN] 1747-0285
  • [Journal-full-title] Chemical biology & drug design
  • [ISO-abbreviation] Chem Biol Drug Des
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / AP 24163; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; JAC85A2161 / Adenine; RBZ1571X5H / Dasatinib
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7. Kim IS, Jin JY, Lee IH, Park SJ: Auranofin induces apoptosis and when combined with retinoic acid enhances differentiation of acute promyelocytic leukaemia cells in vitro. Br J Pharmacol; 2004 Jun;142(4):749-55
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  • [Title] Auranofin induces apoptosis and when combined with retinoic acid enhances differentiation of acute promyelocytic leukaemia cells in vitro.
  • 1. Acute promyelocytic leukaemia (APL) is characterized by a block in differentiation at the promyelocyte stage.
  • Here, we describe the effects of auranofin (AF), a coordinated gold compound, on apoptosis and differentiation of APL cells.
  • 3. The AF-treated NB4 cells also produced reactive oxygen species (ROS) and cotreatment with N-acetyl-l-cysteine protected the NB4 cells from AF-induced apoptosis.
  • 4. Expression of the CD11b cell surface marker and C/EBPepsilon was increased when the cells were treated for 4 days with 0.3 microm AF and a physiological concentration of all-trans retinoic acid (ATRA, 5 nm).
  • Treatment with AF in combination with ATRA markedly increased the number of cells with differentiated features, such as lobed or multiple nuclei and numerous granules and vacuoles.
  • 5. These findings suggest not only that AF induces caspase-3-dependent apoptosis via a mechanism involving ROS, but also that the combined treatment with AF and ATRA induces differentiation of NB4 cells.
  • Our results demonstrate a novel characteristic of AF from which an effective drug treatment of APL might be developed.
  • [MeSH-major] Apoptosis / drug effects. Auranofin / adverse effects. Drug Therapy, Combination. Leukemia, Promyelocytic, Acute / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Acetylcysteine / pharmacology. Antigens, CD11b / genetics. Antigens, CD11b / metabolism. Antigens, Surface / drug effects. Antigens, Surface / genetics. Antirheumatic Agents / adverse effects. Antirheumatic Agents / antagonists & inhibitors. Antirheumatic Agents / chemistry. Benzimidazoles. Caspase 3. Caspases / metabolism. Cell Differentiation / drug effects. DNA / chemistry. DNA / drug effects. Fluorescent Dyes. HL-60 Cells. Humans. Korea. Nucleosomes / chemistry. Nucleosomes / drug effects. Reactive Oxygen Species / metabolism. Signal Transduction / physiology. Tumor Cells, Cultured

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  • (PMID = 15159275.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Antigens, Surface; 0 / Antirheumatic Agents; 0 / Benzimidazoles; 0 / Fluorescent Dyes; 0 / Nucleosomes; 0 / Reactive Oxygen Species; 23491-52-3 / HOE 33342; 3H04W2810V / Auranofin; 5688UTC01R / Tretinoin; 9007-49-2 / DNA; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; WYQ7N0BPYC / Acetylcysteine
  • [Other-IDs] NLM/ PMC1575039
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8. Sukhanova A, Grokhovsky S, Zhuze A, Devy J, Pluot M, Oleinikov V, Nabiev I: Camptothecin conjugated with DNA minor-groove binder netropsin: enhanced lactone stability, inhibition of human DNA topoisomerase I and antiproliferative activity. Anticancer Res; 2003 May-Jun;23(3B):2609-15
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  • [Title] Camptothecin conjugated with DNA minor-groove binder netropsin: enhanced lactone stability, inhibition of human DNA topoisomerase I and antiproliferative activity.
  • BACKGROUND: The conjugates of camptothecin (CPT) with ligands possessing different DNA selectivity could be promising agents in cancer therapy affecting expression of specific genes by trapping DNA topoisomerase I (top I)-DNA complexes in a sequence-selective manner.
  • In an effort to develop a new molecule with good biological activity we have linked CPT with Nt and report here the first results of in vitro examination of the new compound.
  • MATERIALS AND METHODS: CPT-Nt conjugate linked with flexible spacer through position 7 of CPT chromophore was synthesized and analyzed for lactone stability, the ability to modulate a top I-mediated DNA cleavage and antiproliferative activity within a panel of six tumor cell lines.
  • The cytotoxicity of the conjugate against acute promyelocytic leukaemia (HL60), chronic myelogenous leukaemia (K562), breast adenocarcinoma (MCF7), colorectal adenocarcinoma (HT29), lung carcinoma(A549) and ovarian adenocarcinoma (CaOV3) tumor cell lines was evaluated.
  • The lowest IC50 value (0.08 microM) indicated its selective toxicity towards the ovarian adenocarcinoma cell line.
  • [MeSH-minor] Drug Stability. Enzyme Inhibitors / chemistry. Enzyme Inhibitors / pharmacology. Growth Inhibitors / chemistry. Growth Inhibitors / pharmacology. HT29 Cells. Humans. K562 Cells. Lactones / chemistry. Tumor Cells, Cultured

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  • (PMID = 12894548.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Growth Inhibitors; 0 / Lactones; 0 / Topoisomerase I Inhibitors; 64B3O0RD7N / Netropsin; XT3Z54Z28A / Camptothecin
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9. Keller G, Schafhausen P, Brümmendorf TH: Bosutinib. Recent Results Cancer Res; 2010;184:119-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In biochemical and proliferation assays, the compound was shown to be active against src family kinases and Bcr-Abl at IC50s of 100 and 90 nM, respectively.
  • The bcr-abl fusion gene product, a consecutively activated tyrosine kinase, which is crucial for the development of chronic myeloid leukaemia (CML), is highly sensitive to bosutinib.
  • Interestingly, distinctly lower concentrations of the dual src/abl inhibitor are required to ablate Bcr-Abl phosphorylation when compared to first-generation tyrosine kinase inhibitor imatinib (IM).
  • A randomised open label phase III clinical study to compare the efficacy of bosutinib and IM in first-line therapy of Ph+ chronic phase (CP) CML has recently been initiated.
  • In a phase I/II clinical study with subjects suffering from advanced stages of solid tumours, long-term responses have also been reported.
  • In conclusion, Bosutinib is a promising novel small molecule inhibitor for targeted therapy of CML and solid tumours.
  • [MeSH-major] Aniline Compounds / therapeutic use. Neoplasms / drug therapy. Nitriles / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Quinolines / therapeutic use
  • [MeSH-minor] Animals. Clinical Trials as Topic. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Oncogene Proteins v-abl / antagonists & inhibitors

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  • (PMID = 20072835.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer
  • [ISO-abbreviation] Recent Results Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Aniline Compounds; 0 / Nitriles; 0 / Oncogene Proteins v-abl; 0 / Protein Kinase Inhibitors; 0 / Quinolines; 5018V4AEZ0 / bosutinib; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 26
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10. Madlener S, Saiko P, Vonach C, Viola K, Huttary N, Stark N, Popescu R, Gridling M, Vo NT, Herbacek I, Davidovits A, Giessrigl B, Venkateswarlu S, Geleff S, Jäger W, Grusch M, Kerjaschki D, Mikulits W, Golakoti T, Fritzer-Szekeres M, Szekeres T, Krupitza G: Multifactorial anticancer effects of digalloyl-resveratrol encompass apoptosis, cell-cycle arrest, and inhibition of lymphendothelial gap formation in vitro. Br J Cancer; 2010 Apr 27;102(9):1361-70
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  • BACKGROUND: Digalloyl-resveratrol (di-GA) is a synthetic compound aimed to combine the biological effects of the plant polyhydroxy phenols gallic acid and resveratrol, which are both radical scavengers and cyclooxygenase inhibitors exhibiting anticancer activity.
  • Their broad spectrum of activities may probably be due to adjacent free hydroxyl groups.
  • METHODS: Protein activation and expression were analysed by western blotting, deoxyribonucleoside triphosphate levels by HPLC, ribonucleotide reductase activity by (14)C-cytidine incorporation into nascent DNA and cell-cycle distribution by FACS.
  • Apoptosis was measured by Hoechst 33258/propidium iodide double staining of nuclear chromatin and the formation of gaps into the lymphendothelial barrier in a three-dimensional co-culture model consisting of MCF-7 tumour cell spheroids and human lymphendothelial monolayers.
  • RESULTS: In HL-60 leukaemia cells, di-GA activated caspase 3 and dose-dependently induced apoptosis.
  • It further inhibited cell-cycle progression in the G1 phase by four different mechanisms: rapid downregulation of cyclin D1, induction of Chk2 with simultaneous downregulation of Cdc25A, induction of the Cdk-inhibitor p21(Cip/Waf) and inhibition of ribonucleotide reductase activity resulting in reduced dCTP and dTTP levels.
  • CONCLUSION: These data show that di-GA exhibits three distinct anticancer activities: induction of apoptosis, cell-cycle arrest and disruption of cancer cell-induced lymphendothelial disintegration.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Cell Cycle / drug effects. Gallic Acid / analogs & derivatives. HL-60 Cells / drug effects. Stilbenes / pharmacology
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cell Division / drug effects. Cell Line, Tumor. Coloring Agents. Fibroblasts / cytology. Fibroblasts / drug effects. Flow Cytometry. Gap Junctions / drug effects. Gap Junctions / physiology. Humans. Lung / cytology. Lung / drug effects. Signal Transduction / drug effects

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  • (PMID = 20424615.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / F 2801; Austria / Austrian Science Fund FWF / / F 2806; Austria / Austrian Science Fund FWF / / P 19598
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Coloring Agents; 0 / Stilbenes; 0 / digalloylresveratrol; 632XD903SP / Gallic Acid
  • [Other-IDs] NLM/ PMC2865764; NLM/ UKMS31287
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11. Nicolis I, Curis E, Deschamps P, Bénazeth S: Arsenite medicinal use, metabolism, pharmacokinetics and monitoring in human hair. Biochimie; 2009 Oct;91(10):1260-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenite medicinal use, metabolism, pharmacokinetics and monitoring in human hair.
  • Acute promyelocytic leukaemia (APL) is a distinctive subtype of acute myeloid leukaemias.
  • Even through this human disease can be treated by the intravenous administration of all-trans retinoic acid (ATRA), 25% of patients typically relapse after the first treatment.
  • In this context, the intravenous administration of APL patients with an aqueous solution of arsenic trioxide has also been demonstrated to be successful despite the established mammalian toxicity of this arsenic compound.
  • Accordingly, the administration of a therapeutic dose of arsenic trioxide has resulted in an improved patient survival in both relapsing as well newly diagnosed APL patients.
  • We present here a mini-review of the medicinal use of arsenite, its mammalian metabolism (with an emphasis on biomethylation pathways), its elimination and pharmacokinetics and the novel application of hair analysis as a biomonitoring material.
  • This mini-review also introduces our own results on the analysis of hair of patients receiving arsenic trioxide therapy.
  • In this work, instead of quantifying arsenic content in bulk hair, we performed longitudinal analysis in order to use hair as a marker of arsenic exposure correlated to a time scale.
  • Taking into account the hair growth rate, the longitudinal analysis of hair is demonstrated to provide a chronological record of the treatment of patients with arsenic trioxide.
  • In particular, the onset of arsenic trioxide therapy and interruptions during therapy were reflected by total arsenic content, which suggested rapid elimination.
  • Another type of experiment, micro-XRF cartography on thin hair slices, allowed us to obtain distribution maps of arsenic, which demonstrated that arsenic is located at the periphery of hair.
  • [MeSH-minor] Humans. Leukemia, Promyelocytic, Acute / drug therapy. Spectrometry, X-Ray Emission

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  • (PMID = 19527769.001).
  • [ISSN] 1638-6183
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Arsenites; N5509X556J / arsenite
  • [Number-of-references] 119
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12. Hopkin MD, Baxendale IR, Ley SV: A flow-based synthesis of imatinib: the API of Gleevec. Chem Commun (Camb); 2010 Apr 14;46(14):2450-2
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  • A concise, flow-based synthesis of Imatinib, a compound used for the treatment of chronic myeloid leukaemia, is described whereby all steps are conducted in tubular flow coils or cartridges packed with reagents or scavengers to effect clean product formation.
  • An in-line solvent switching procedure was developed enabling the procedure to be performed with limited manual handling of intermediates.
  • [MeSH-major] Antineoplastic Agents / chemical synthesis. Piperazines / chemical synthesis. Pyrimidines / chemical synthesis
  • [MeSH-minor] Benzamides. Dimethylamines / chemistry. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • (PMID = 20309467.001).
  • [ISSN] 1364-548X
  • [Journal-full-title] Chemical communications (Cambridge, England)
  • [ISO-abbreviation] Chem. Commun. (Camb.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Dimethylamines; 0 / Piperazines; 0 / Pyrimidines; 1RTM4PAL0V / piperazine; 8A1O1M485B / Imatinib Mesylate; ARQ8157E0Q / dimethylamine
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13. Bright SA, McElligott AM, O'Connell JW, O'Connor L, Carroll P, Campiani G, Deininger MW, Conneally E, Lawler M, Williams DC, Zisterer DM: Novel pyrrolo-1,5-benzoxazepine compounds display significant activity against resistant chronic myeloid leukaemia cells in vitro, in ex vivo patient samples and in vivo. Br J Cancer; 2010 May 11;102(10):1474-82
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  • [Title] Novel pyrrolo-1,5-benzoxazepine compounds display significant activity against resistant chronic myeloid leukaemia cells in vitro, in ex vivo patient samples and in vivo.
  • BACKGROUND: Imatinib is a direct and potent inhibitor of the constitutively active tyrosine kinase, breakpoint cluster region-Abelson (Bcr-Abl), which is central to the pathogenesis of chronic myeloid leukaemia (CML) patients.
  • As such, imatinib has become the front-line treatment for CML patients.
  • However, the recent emergence of imatinib resistance, commonly associated with point mutations within the kinase domain, has led to the search for alternative drug treatments and combination therapies for CML.
  • METHODS: In this report, we analyse the effects of representative members of the novel pro-apoptotic microtubule depolymerising pyrrolo-1,5-benzoxazepines or PBOX compounds on chemotherapy-refractory CML cells using a series of Bcr-Abl mutant cell lines, clinical ex vivo patient samples and an in vivo mouse model.
  • The PBOX compounds also induce apoptosis in primary CML samples including those resistant to imatinib.
  • We also show for the first time, the in vivo efficacy of the pro-apoptotic PBOX compound, PBOX-6, in a CML mouse model of the T315I Bcr-Abl mutant.
  • CONCLUSION: Results from this study highlight the potential of these novel series of PBOX compounds as an effective therapy against CML.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Oxazepines / pharmacology. Pyrroles / pharmacology
  • [MeSH-minor] Adult. Aged. Animals. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Separation. Cell Survival / drug effects. Female. Flow Cytometry. Genes, abl / genetics. Humans. Male. Mice. Mice, Inbred BALB C. Middle Aged. Mutation

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  • (PMID = 20407438.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oxazepines; 0 / PBOX-6; 0 / Pyrroles
  • [Other-IDs] NLM/ PMC2869169
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14. Szczepanek J, Pogorzala M, Konatkowska B, Juraszewska E, Badowska W, Olejnik I, Kuzmicz M, Stanczak E, Malinowska I, Stefaniak J, Sobol G, Szczepanski T, Czyzewski K, Wysocki M, Styczynski J: Differential ex vivo activity of bortezomib in newly diagnosed paediatric acute lymphoblastic and myeloblastic leukaemia. Anticancer Res; 2010 Jun;30(6):2119-24
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  • [Title] Differential ex vivo activity of bortezomib in newly diagnosed paediatric acute lymphoblastic and myeloblastic leukaemia.
  • The proteasome inhibitor, bortezomib, is known to be effective in the therapy of various neoplasms.
  • The objective of this study was the analysis of the ex vivo activity of bortezomib in paediatric acute lymphoblastic leukaemia (ALL), in comparison to paediatric acute myeloid leukaemia (AML).
  • The ex vivo sensitivity to bortezomib and 16 other drugs was studied by MTT assay.
  • Paediatric AML samples were more resistant than paediatric ALL samples to most of the tested drugs, except for cytarabine and thioguanine.
  • With respect to immunophenotype, ex vivo drug resistance in T-cell ALL (T-ALL) was higher for most of the drugs.
  • No differences in drug resistance between T-ALL and common/pre-B-cell-ALL were found for daunorubicin, mitoxantrone and 6-thioguanine.
  • Bortezomib was the only compound which was more active in T-ALL than in common/pre-B-ALL paediatric samples.
  • In conclusion, bortezomib had good ex vivo activity in paediatric T-ALL samples.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrazines / therapeutic use
  • [MeSH-minor] Adolescent. Bortezomib. Child. Child, Preschool. Drug Resistance, Neoplasm. Female. Humans. Infant. Male

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  • (PMID = 20651360.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [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 / Pyrazines; 69G8BD63PP / Bortezomib
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15. Bright SA, Campiani G, Deininger MW, Lawler M, Williams DC, Zisterer DM: Sequential treatment with flavopiridol synergistically enhances pyrrolo-1,5-benzoxazepine-induced apoptosis in human chronic myeloid leukaemia cells including those resistant to imatinib treatment. Biochem Pharmacol; 2010 Jul 1;80(1):31-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sequential treatment with flavopiridol synergistically enhances pyrrolo-1,5-benzoxazepine-induced apoptosis in human chronic myeloid leukaemia cells including those resistant to imatinib treatment.
  • The Bcr-Abl kinase inhibitor, imatinib mesylate, is the front line treatment for chronic myeloid leukaemia (CML), but the emergence of imatinib resistance has led to the search for alternative drug treatments and the examination of combination therapies to overcome imatinib resistance.
  • The pro-apoptotic PBOX compounds are a recently developed novel series of microtubule targeting agents (MTAs) that depolymerise tubulin.
  • Recent data demonstrating enhanced MTA-induced tumour cell apoptosis upon combination with the cyclin dependent kinase (CDK)-1 inhibitor flavopiridol prompted us to examine whether this compound could similarly enhance the effect of the PBOX compounds.
  • We thus characterised the apoptotic and cell cycle events associated with combination therapy of the PBOX compounds and flavopiridol and results showed a sequence dependent, synergistic enhancement of apoptosis in CML cells including those expressing the imatinib-resistant T315I mutant.
  • Flavopiridol reduced the number of polyploid cells formed in response to PBOX treatment but only to a small extent, suggesting that inhibition of endoreplication was unlikely to play a major role in the mechanism by which flavopiridol synergistically enhanced PBOX-induced apoptosis.
  • The addition of flavopiridol following PBOX-6 treatment did however result in an accelerated exit from the G2/M transition accompanied by an enhanced downregulation and deactivation of the CDK1/cyclin B1 complex and an enhanced degradation of the inhibitor of apoptosis protein (IAP) survivin.
  • In conclusion, results from this study highlight the potential of these novel series of PBOX compounds, alone or in sequential combination with flavopiridol, as an effective therapy against CML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Drug Resistance, Neoplasm / drug effects. Flavonoids / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Oxazepines / therapeutic use. Piperazines / therapeutic use. Piperidines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Pyrroles / therapeutic use
  • [MeSH-minor] Benzamides. Down-Regulation. Drug Synergism. Humans. Imatinib Mesylate. Inhibitor of Apoptosis Proteins. Microtubule-Associated Proteins / metabolism

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  • [Copyright] (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20206141.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / Benzamides; 0 / Flavonoids; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Oxazepines; 0 / PBOX-6; 0 / Piperazines; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Pyrroles; 45AD6X575G / alvocidib; 8A1O1M485B / Imatinib Mesylate
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16. D'Acunto CW, Carratù A, Rodriquez M, Taddei M, Parente L, Petrella A: LGP1, A histone deacetylase inhibitor analogue of FR235222, sensitizes promyelocytic leukaemia U937 cells to TRAIL-mediated apoptosis. Anticancer Res; 2010 Mar;30(3):887-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] LGP1, A histone deacetylase inhibitor analogue of FR235222, sensitizes promyelocytic leukaemia U937 cells to TRAIL-mediated apoptosis.
  • BACKGROUND: It has been shown that chemo-therapeutic agents, such as histone deacetylase inhibitors (HDACi), are able to increase TRAIL-induced apoptosis in many types of cancer.
  • In the present study, we investigated the effects of the novel HDACi LGP1, a new simplified analogue of FR235222, in human leukaemia U937 cells resistant to TRAIL-induced apoptosis.
  • Western blot analysis was also used to detect the expression of p21, p27, (NF-kappaB), Bcl-2 and the levels of H4 histone acetylation.
  • RESULTS: Treatment with LGP1 caused accumulation of acetylated histone H4 and G(1) cycle arrest accompanied by increase of p21.
  • The compound was also able to sensitize U937 cells to TRAIL-induced apoptosis through multiple mechanisms: (i) activation of caspase-3 and cleavage of PARP;.
  • CONCLUSION: These results demonstrate that U937 cells can be effectively killed by a combination treatment of subtoxic doses of LGP1 and TRAIL.
  • [MeSH-minor] Acetylation / drug effects. Apoptosis / drug effects. Caspases / metabolism. Cell Cycle / drug effects. Drug Synergism. Enzyme Activation. G1 Phase / drug effects. Histones / metabolism. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism. Leukemia, Promyelocytic, Acute / pathology. Peptides, Cyclic. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. Receptors, Tumor Necrosis Factor / metabolism. U937 Cells

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  • (PMID = 20393011.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Bicyclo Compounds, Heterocyclic; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / LGP1 compound; 0 / Peptides, Cyclic; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; EC 3.4.22.- / Caspases
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17. Glavas-Obrovac L, Piantanida I, Marczi S, Masić L, Timcheva II, Deligeorgiev TG: Minor structural differences of monomethine cyanine derivatives yield strong variation in their interactions with DNA, RNA as well as on their in vitro antiproliferative activity. Bioorg Med Chem; 2009 Jul 1;17(13):4747-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minor structural differences of monomethine cyanine derivatives yield strong variation in their interactions with DNA, RNA as well as on their in vitro antiproliferative activity.
  • Comparison of binding properties of a series of monomethine cyanine derivatives to ds-DNA and ds-RNA revealed significant impact of the properties of substituent attached to the longer axis of aromatic core.
  • Namely, it seems that only compounds 7, 8 characterised by length of longer axis not exceeding the length of longer axis of basepairs could intercalate into ds-DNA and ds-RNA, while the increased substituent length and additional possibility of hydrogen bonds formation directed binding of 1-6 into ds-DNA minor groove.
  • The interactions of 1-8 with ss-RNA were strongly dependent on both, structure of compound and base composition of RNA.
  • The cytotoxicity screening of compounds 1-8 by MTT test revealed considerable antiproliferative activity against solid tumours and especially toward haematological malignancies (IC(50)=0.001-6.6 microM), whereby normal human aortic endothelial cells (HAEC) were significantly less affected (IC(50)=1-200 microM).
  • The cells of chronic myeloid leukaemia in blast crisis (K562) were especially sensitive to all tested compounds (IC(50)=0.001-0.6 microM), while normal lymphocytes were more resistant (IC(50)=0.01-1 microM).
  • Results of uptake and intracellular distribution of compounds 1 and 2 in the living cells showed that they do not bind primarily to nuclear DNA but their fluorescence is scattered through the whole cells.
  • A detailed mechanism of antitumor activity of tested molecules remains to be investigated.
  • [MeSH-major] Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Benzothiazoles / chemistry. Benzothiazoles / pharmacology. Cell Proliferation / drug effects. DNA / metabolism. Pyrimidines / chemical synthesis. Pyrimidines / pharmacology. RNA / metabolism
  • [MeSH-minor] Animals. Binding Sites. Cattle. Cell Line, Tumor. Humans. Models, Molecular. Neoplasms / drug therapy. Nucleic Acid Denaturation / drug effects. RNA, Double-Stranded / chemistry. RNA, Double-Stranded / metabolism. Spectrometry, Fluorescence. Structure-Activity Relationship. Temperature. Titrimetry

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  • (PMID = 19477132.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzothiazoles; 0 / Pyrimidines; 0 / RNA, Double-Stranded; 63231-63-0 / RNA; 9007-49-2 / DNA
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18. Viola G, Facciolo L, Dall'Acqua S, Di Lisa F, Canton M, Vedaldi D, Fravolini A, Tabarrini O, Cecchetti V: 6-Aminoquinolones: photostability, cellular distribution and phototoxicity. Toxicol In Vitro; 2004 Oct;18(5):581-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Three selected aminoquinolones endowed with a potent antibacterial (compounds 1 and 2) and antiviral activity (compound 3) have been evaluated for their phototoxic properties in vitro.
  • Photostability studies of these compounds indicate that compound 3 is photostable whereas compound 1 and in particular, compound 2 are rapidly photodegraded upon UVA irradiation, yielding a toxic photoproduct.
  • Intracellular localization of these compounds has been evaluated by means of fluorescence microscopy using tetramethylrhodamine methyl ester and acridine orange, which are specific fluorescent probes for mitochondria and lysosomes, respectively.
  • No co-staining was observed with lysosomal stain for all the test compounds.
  • On the contrary compound 3 was found to be specifically incorporated in mitochondria.
  • The compounds exhibited remarkable phototoxicity in two cell culture lines: human promyelocytic leukaemia (HL-60) and human fibrosarcoma (HT-1080).
  • The quinolone-induced photodamage was also evaluated measuring the photosensitizing cross-linking in erythrocyte ghost membranes, the strand breaks activity and oxidative damage on plasmid DNA.
  • The results show that these derivatives are able to photoinduce crosslink of erythrocytes spectrin, whereas do not significantly photocleavage DNA directly, but single strand breaks were observed after treatment of photosensitized DNA with two base excision repair enzymes, Fpg and Endo III respectively.
  • [MeSH-minor] Cross-Linking Reagents / toxicity. DNA / drug effects. Dose-Response Relationship, Drug. Dose-Response Relationship, Radiation. Drug Stability. Erythrocyte Membrane / chemistry. Erythrocyte Membrane / drug effects. Erythrocyte Membrane / radiation effects. Fibrosarcoma / drug therapy. Fibrosarcoma / metabolism. HL-60 Cells / drug effects. HL-60 Cells / metabolism. Humans. Microscopy, Fluorescence. Photochemistry. Spectrin / drug effects. Spectrin / metabolism. Spectrin / radiation effects. Ultraviolet Rays

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  • (PMID = 15251175.001).
  • [ISSN] 0887-2333
  • [Journal-full-title] Toxicology in vitro : an international journal published in association with BIBRA
  • [ISO-abbreviation] Toxicol In Vitro
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Anti-Infective Agents; 0 / Cross-Linking Reagents; 0 / Photosensitizing Agents; 12634-43-4 / Spectrin; 580-15-4 / 6-aminoquinoline; 9007-49-2 / DNA
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19. Dawson MA, Curry JE, Barber K, Beer PA, Graham B, Lyons JF, Richardson CJ, Scott MA, Smyth T, Squires MS, Thompson NT, Green AR, Wallis NG: AT9283, a potent inhibitor of the Aurora kinases and Jak2, has therapeutic potential in myeloproliferative disorders. Br J Haematol; 2010 Jul;150(1):46-57
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AT9283, a potent inhibitor of the Aurora kinases and Jak2, has therapeutic potential in myeloproliferative disorders.
  • Constitutive activation of Janus kinase (Jak) 2 is the most prevalent pathogenic event observed in the myeloproliferative disorders (MPD), suggesting that inhibitors of Jak2 may prove valuable in their management.
  • Inhibition of the Aurora kinases has also proven to be an effective therapeutic strategy in a number of haematological malignancies.
  • AT9283 is a multi-targeted kinase inhibitor with potent activity against Jak2 and Aurora kinases A and B, and is currently being evaluated in clinical trials.
  • To investigate the therapeutic potential of AT9283 in the MPD we studied its activity in a number of Jak2-dependent systems.
  • The compound also demonstrated significant therapeutic potential in vivo in an ETV6-JAK2 (TEL-JAK2) murine leukaemia model.
  • Our results suggest that AT9283 may be a valuable therapy in patients with MPD and that the dual inhibition of Jak2 and the Aurora kinases may potentially offer combinatorial efficacy in the treatment of these diseases.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Benzimidazoles / pharmacology. Janus Kinase 2 / antagonists & inhibitors. Myeloproliferative Disorders / drug therapy. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Urea / analogs & derivatives
  • [MeSH-minor] Animals. Aurora Kinase B. Aurora Kinases. Cell Cycle / drug effects. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical / methods. Erythroid Precursor Cells / drug effects. Humans. Leukemia, Experimental / drug therapy. Leukemia, Experimental / pathology. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Mutation. Signal Transduction / drug effects. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 20507304.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)urea; 0 / Antineoplastic Agents; 0 / Benzimidazoles; 8W8T17847W / Urea; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurkb protein, mouse; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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