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1. Huang F, Meng FY, Xue B, Liu XL, Zhang Y, Ye CX, Zhang X: [Therapeutic effects of chemotherapeutic regimen with pirarubicin for adult high-risk acute leukemia]. Di Yi Jun Yi Da Xue Xue Bao; 2004 Jul;24(7):768-70
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  • [Title] [Therapeutic effects of chemotherapeutic regimen with pirarubicin for adult high-risk acute leukemia].
  • OBJECTIVE: To evaluate the therapeutic effects of chemotherapeutic regimen with pirarubicin in the management of adult high-risk acute leukemia.
  • METHODS: Twenty-nine high-risk acute leukemia patients were selected as the treatment group and another 29 patients with similar pretreatment conditions as the control group.
  • In the treatment group, 18 patients had acute non-lymphocytic leukemia (ANLL), and 8 had acute lymphocytic leukemia (ALL) and 3 had mixed leukemia, all received treatment regimens with pirarubicin+cytarabine, vincristine+pirarubicin+prednisone, Vincristine+pirarubicin+L-asparaginase (L)+prednisone or pirarubicin+cytarabine+vincristine+prednisone.
  • Routine therapeutic regimens were adopted in the management of the control.
  • RESULTS: In ANLL patients, the overall remission rate was significantly higher in the treatment group than in the control group (77.78% vs 44.44%, P=0.031).
  • Patients in the treatment group had greater marrow suppression and higher incidence of infections than the control group (P=0.012).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Doxorubicin / administration & dosage. Doxorubicin / analogs & derivatives. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 15257898.001).
  • [ISSN] 1000-2588
  • [Journal-full-title] Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA
  • [ISO-abbreviation] Di Yi Jun Yi Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 80168379AG / Doxorubicin; D58G680W0G / pirarubicin
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2. Guzman ML, Li X, Corbett CA, Rossi RM, Bushnell T, Liesveld JL, Hébert J, Young F, Jordan CT: Rapid and selective death of leukemia stem and progenitor cells induced by the compound 4-benzyl, 2-methyl, 1,2,4-thiadiazolidine, 3,5 dione (TDZD-8). Blood; 2007 Dec 15;110(13):4436-44
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  • [Title] Rapid and selective death of leukemia stem and progenitor cells induced by the compound 4-benzyl, 2-methyl, 1,2,4-thiadiazolidine, 3,5 dione (TDZD-8).
  • Leukemia is thought to arise from malignant stem cells, which have been described for acute and chronic myeloid leukemia (AML and CML) and for acute lymphoblastic leukemia (ALL).
  • Leukemia stem cells (LSCs) are relatively resistant to current chemotherapy and likely contribute to disease relapse and progression.
  • Consequently, the identification of drugs that can efficiently eradicate LSCs is an important priority.
  • In the present study, we investigated the antileukemia activity of the compound TDZD-8.
  • Analysis of primary AML, blast crisis CML (bcCML), ALL, and chronic lymphoblastic leukemia (CLL) specimens showed rapid induction of cell death upon treatment with TDZD-8.
  • In addition, for myeloid leukemias, cytotoxicity was observed for phenotypically primitive cells, in vitro colony-forming progenitors, and LSCs as defined by xenotransplantation assays.
  • We conclude that TDZD-8 uses a unique and previously unknown mechanism to rapidly target leukemia cells, including malignant stem and progenitor populations.

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  • (PMID = 17785584.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090446; United States / NCI NIH HHS / CA / R01 CA90446
  • [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 / 4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione; 0 / Sulfhydryl Compounds; 0 / Thiadiazoles; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.13 / Protein Kinase C
  • [Other-IDs] NLM/ PMC2234782
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3. Puttini M, Redaelli S, Moretti L, Brussolo S, Gunby RH, Mologni L, Marchesi E, Cleris L, Donella-Deana A, Drueckes P, Sala E, Lucchini V, Kubbutat M, Formelli F, Zambon A, Scapozza L, Gambacorti-Passerini C: Characterization of compound 584, an Abl kinase inhibitor with lasting effects. Haematologica; 2008 May;93(5):653-61
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  • [Title] Characterization of compound 584, an Abl kinase inhibitor with lasting effects.
  • BACKGROUND: Resistance to imatinib is an important clinical issue in the treatment of Philadelphia chromosome-positive leukemias which is being tackled by the development of new, more potent drugs, such as the dual Src/Abl tyrosine kinase inhibitors dasatinib and bosutinib and the imatinib analog nilotinib.
  • In the current study we describe the design, synthesis and biological properties of an imatinib analog with a chlorine-substituted benzamide, namely compound 584 (cmp-584).
  • DESIGN AND METHODS: To increase the potency, we rationally designed cmp-584, a compound with enhanced shape complementarity with the kinase domain of Abl. cmp-584 was synthesized and characterized in vitro against a panel of 67 serine/threonine and tyrosine kinases using radioactive and enzyme-linked immunosorbent kinase assays.
  • The drug maintained inhibitory activity against platelet-derived growth factor receptors and c-KIT and was also active against Lyn (IC(50): 301 nM).
  • Wash-out experiments showed that short exposure to the drug impaired cell proliferation and Bcr-Abl phosphorylation for a substantially longer period of time than imatinib.
  • [MeSH-major] Anilides / pharmacology. Antineoplastic Agents / pharmacology. Drug Screening Assays, Antitumor. Leukemia / drug therapy. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-abl / antagonists & inhibitors. Pyrimidines / pharmacology
  • [MeSH-minor] Animals. Benzamides / chemistry. Cell Line, Tumor. Chemistry, Pharmaceutical / methods. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Mice. Neoplasm Transplantation. Piperazines / pharmacology. Protein Structure, Tertiary

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  • (PMID = 18367480.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / 3-chloro-4-(4-methylpiperazin-1-ylmethyl)-N-(4-methyl-3-(4-pyridin-3-ylpyrimidin-2-ylamino)phenyl)benzamide; 0 / Anilides; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
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4. Carella AM: Hypothesis: upfront use of ABL kinase inhibitor combination, either simultaneously or sequentially, in high-risk Ph+ leukemias? Ann Hematol; 2010 Jun;89(6):531-3
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  • [Title] Hypothesis: upfront use of ABL kinase inhibitor combination, either simultaneously or sequentially, in high-risk Ph+ leukemias?
  • A sequential treatment approach is the rule in CML and Ph(+) ALL with imatinib failure being followed by second-line tyrosine kinase inhibitors.
  • The sequential strategy may be vulnerable to compound mutations.
  • An alternative and fascinating hypothesis discussed in this paper is the upfront use, at least in very high-risk Ph(+) leukemias, of ABL kinase inhibitor combinations, either simultaneously or sequentially to target a wider range of mutations-based drug resistance.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Protein Kinase Inhibitors / administration & dosage. Proto-Oncogene Proteins c-abl / antagonists & inhibitors
  • [MeSH-minor] Drug Administration Schedule. Humans. Models, Theoretical. Neoadjuvant Therapy. Risk Factors

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  • (PMID = 20165848.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
  • [Number-of-references] 31
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5. Efferth T, Giaisi M, Merling A, Krammer PH, Li-Weber M: Artesunate induces ROS-mediated apoptosis in doxorubicin-resistant T leukemia cells. PLoS One; 2007;2(8):e693
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  • [Title] Artesunate induces ROS-mediated apoptosis in doxorubicin-resistant T leukemia cells.
  • BACKGROUND: A major obstacle for successful cancer treatment often is the development of drug resistance in cancer cells during chemotherapy.
  • Therefore, there is an urgent need for novel drugs with improved efficacy against tumor cells and with less toxicity on normal cells.
  • Artesunate (ART), a powerful anti-malarial herbal compound, has been shown to inhibit growth of various tumor cell lines in vitro and of xenografted Kaposi's sarcoma in mice in vivo.
  • METHODOLOGY AND PRINCIPAL FINDINGS: In this study, we used T-cell leukemias as a model system to study the molecular mechanisms of ART-induced apoptosis.
  • The most typical anticancer drugs are DNA intercalators such as Doxorubicin.
  • To investigate drug sensitivity and resistance, we chose a Doxorubicin-resistant leukemia cell line and investigated the killing effect of ART on these cells.
  • Therefore, ART can overcome the Doxorubicin-resistance and induce the Doxorubicin-resistant leukemia cells to undergo apoptosis.
  • CONCLUSIONS: Our studies raise the possibility to develop ART in combination with other established anticancer drugs which induce apoptosis through the pathways or mechanisms different from ART.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Antimalarials / pharmacology. Apoptosis / drug effects. Artemisinins / pharmacology. Doxorubicin / pharmacology. Drug Resistance, Neoplasm / physiology. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Acetylcysteine / pharmacology. Animals. Cell Line, Tumor / drug effects. Drug Screening Assays, Antitumor. Free Radical Scavengers / pharmacology. Humans. Leukemia / drug therapy. Leukemia / metabolism. Leukemia / pathology. Mice. Oxidation-Reduction

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  • (PMID = 17668070.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimalarials; 0 / Artemisinins; 0 / Free Radical Scavengers; 0 / Reactive Oxygen Species; 60W3249T9M / artesunate; 80168379AG / Doxorubicin; WYQ7N0BPYC / Acetylcysteine
  • [Other-IDs] NLM/ PMC1933253
  • [General-notes] NLM/ Original DateCompleted: 20070806
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6. Kisor DF: Nelarabine use in leukemias. Drugs Today (Barc); 2006 Jul;42(7):455-65
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  • [Title] Nelarabine use in leukemias.
  • Drug discovery and development over the past 60 years has played a central role in the continuous improvement in survival rates of patients undergoing treatment for acute lymphoblastic leukemia.
  • It has recently been suggested that in children and adolescents diagnosed with acute lymphoblastic leukemia, an overall cure rate of 90% may be achieved (1, 2).
  • Cure rates in adults, typically less than 40%, are considerably lower than in the younger populations, even in the face of currently prescribed optimal drug therapy and supportive care (3-5).
  • The search for more effective and safer anti-leukemia therapy continues to identify agents and combinations of agents that have activity against specific types of acute lymphoblastic leukemia (1).
  • This review presents a new compound, nelarabine, that has shown efficacy in treating patients with T-cell acute lymphoblastic leukemia or T-cell lymphoblastic lymphoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Humans. Molecular Structure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Treatment Outcome

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  • [Copyright] (c) 2006 Prous Science. All rights reserved.
  • (PMID = 16894400.001).
  • [ISSN] 1699-3993
  • [Journal-full-title] Drugs of today (Barcelona, Spain : 1998)
  • [ISO-abbreviation] Drugs Today
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 60158CV180 / nelarabine
  • [Number-of-references] 38
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7. Pratz KW, Cho E, Levis MJ, Karp JE, Gore SD, McDevitt M, Stine A, Zhao M, Baker SD, Carducci MA, Wright JJ, Rudek MA, Smith BD: A pharmacodynamic study of sorafenib in patients with relapsed and refractory acute leukemias. Leukemia; 2010 Aug;24(8):1437-44
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  • [Title] A pharmacodynamic study of sorafenib in patients with relapsed and refractory acute leukemias.
  • We report the results of a phase I dose escalation trial of the multikinase inhibitor sorafenib in relapsed and refractory acute leukemia patients using an intermittent dosing regimen.
  • Fifteen patients with advanced leukemia (12 with acute myeloid leukemia, 2 with acute lymphoblastic leukemia, 1 with biphenotypic) and a median age of 63 (range 37-85) years were enrolled and treated on a dose escalation trial.
  • The N-oxide metabolite of sorafenib seemed to be a more potent inhibitor of FLT3-ITD than the parent compound.
  • Although sorafenib showed only modest clinical activity as a single agent in this heavily treated population, robust inhibition of FLT3 and ERK suggests that there may be a potential important role in combination therapies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use

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  • (PMID = 20535150.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA128864; United States / NCI NIH HHS / CA / P30 CA006973-48; United States / NCRR NIH HHS / RR / UL1 RR025005; United States / NCI NIH HHS / CA / P30CA006973; United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCRR NIH HHS / RR / UL1 RR025005-04; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / P50 CA100632-06; United States / NCI NIH HHS / CA / R01 CA128864-04; United States / NCI NIH HHS / CA / U01 CA070095-17; United States / NCI NIH HHS / CA / U01CA70095
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ NIHMS201571; NLM/ PMC2921005
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8. Pendino F, Hillion J, Dudognon C, Delaunay J, Mourah S, Podgorniak MP, Lafon I, Chomienne C, Lanotte M, Dombret H, Rousselot P, Ségal-Bendirdjian E: Telomerase targeting by retinoids in cells from patients with myeloid leukemias of various subtypes, not only APL. Leukemia; 2006 Apr;20(4):599-603

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Telomerase targeting by retinoids in cells from patients with myeloid leukemias of various subtypes, not only APL.
  • Numerous strategies have been proposed to specifically inhibit telomerase (human telomerase reverse transcriptase (hTERT)) but to date only a few are clinically relevant in anticancer therapy.
  • Recently, we have shown that long-term treatment with all-trans retinoic acid (ATRA), a compound clinically approved for differentiation therapy of acute promyelocytic leukemia (APL), represses hTERT in differentiation-resistant APL cell lines leading to telomere shortening and death.
  • In contrast to differentiation-therapy, which is only successful in this subtype of leukemia, the telomerase-targeted pathway could also be of use in non-APL.
  • Here, we demonstrate that repression of hTERT occurs in fresh blasts cells from patients with myeloid leukemias of various subtypes exposed ex vivo to ATRA or synthetic retinoids.
  • These results support the idea that, by hTERT targeting, retinoids can induce telomere shortening and cell death and their integration in therapy protocols for myeloid leukemias refractory to maturation should be considered.
  • [MeSH-major] Antineoplastic Agents / pharmacology. DNA-Binding Proteins / antagonists & inhibitors. Leukemia, Myeloid / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Retinoids / pharmacology. Telomerase / antagonists & inhibitors
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Death / drug effects. Cell Differentiation / drug effects. Cell Line, Tumor. Female. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Leukemic / drug effects. Humans. Male. Middle Aged. RNA, Messenger / drug effects. RNA, Messenger / genetics. Structure-Activity Relationship. Telomere / drug effects. Telomere / genetics. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 16482212.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [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 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / Retinoids; EC 2.7.7.49 / Telomerase
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9. Chen Z, Chen GQ, Shen ZX, Sun GL, Tong JH, Wang ZY, Chen SJ: Expanding the use of arsenic trioxide: leukemias and beyond. Semin Hematol; 2002 Apr;39(2 Suppl 1):22-6
Hazardous Substances Data Bank. ARSENIC TRIOXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expanding the use of arsenic trioxide: leukemias and beyond.
  • The re-emergence of arsenic trioxide (ATO) in clinical use is due largely to purification of this compound from traditional mixtures, and the definition of effective, low-dose regimens for the treatment of acute promyelocytic leukemia (APL).
  • The mechanism of action of ATO suggests it may be active against other malignancies, and ATO has shown some activity in patients with accelerated phase chronic myelogenous leukemia (CML) and multiple myeloma (MM).
  • Clinical trials are ongoing and planned to define the optimal use of this compound in hematologic malignancies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Leukemia / drug therapy. Oxides / therapeutic use
  • [MeSH-minor] Apoptosis / drug effects. Humans. Leukemia, Promyelocytic, Acute / drug therapy. Multiple Myeloma / drug therapy. Neoplasms / drug therapy

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  • [Copyright] Copyright 2002, Elsevier Science (USA). All rights reserved.
  • (PMID = 12012319.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oxides; S7V92P67HO / arsenic trioxide
  • [Number-of-references] 27
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10. Asou H, Koshizuka K, Kyo T, Takata N, Kamada N, Koeffier HP: Resveratrol, a natural product derived from grapes, is a new inducer of differentiation in human myeloid leukemias. Int J Hematol; 2002 Jun;75(5):528-33
Hazardous Substances Data Bank. RESVERATROL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Resveratrol, a natural product derived from grapes, is a new inducer of differentiation in human myeloid leukemias.
  • We studied the in vitro biological activity of this compound by examining its effect on proliferation and differentiation in myeloid leukemia cell lines (HL-60, NB4, U937,THP-1, ML-1, Kasumi-1) and fresh samples from 17 patients with acute myeloid leukemia.
  • Eight of 19 samples of fresh acute leukemia cells reduced NBT after exposure to resveratrol (20 microM, 4 days).
  • Taken together, these findings show that resveratrol inhibits proliferation and induces differentiation of myeloid leukemia cells.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Leukemia, Myeloid / drug therapy. Stilbenes / pharmacology
  • [MeSH-minor] Cell Adhesion Molecules / biosynthesis. Cell Adhesion Molecules / drug effects. Cell Differentiation / drug effects. Cell Division / drug effects. Drug Synergism. Humans. NF-kappa B / drug effects. NF-kappa B / metabolism. Superoxides / metabolism. Tretinoin / pharmacology. Tumor Cells, Cultured / drug effects. Vitis / chemistry

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  • (PMID = 12095155.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Cell Adhesion Molecules; 0 / NF-kappa B; 0 / Stilbenes; 11062-77-4 / Superoxides; 5688UTC01R / Tretinoin; Q369O8926L / resveratrol
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11. Schimmer AD, O'Brien S, Kantarjian H, Brandwein J, Cheson BD, Minden MD, Yee K, Ravandi F, Giles F, Schuh A, Gupta V, Andreeff M, Koller C, Chang H, Kamel-Reid S, Berger M, Viallet J, Borthakur G: A phase I study of the pan bcl-2 family inhibitor obatoclax mesylate in patients with advanced hematologic malignancies. Clin Cancer Res; 2008 Dec 15;14(24):8295-301
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: The outcome of patients with refractory leukemia and myelodysplasia is poor, and new therapies are needed.
  • The antiapoptotic proteins of the Bcl-2 family are overexpressed in these malignancies and are potential therapeutic targets.
  • Therefore, we conducted a phase I clinical trial of the small-molecule pan-Bcl-2 inhibitor, obatoclax mesylate, in patients with refractory leukemia and myelodysplasia to assess its safety and define its optimal dose.
  • EXPERIMENTAL DESIGN: Forty-four patients with refractory leukemia or myelodysplasia were treated with obatoclax mesylate by continuous intravenous infusion at increasing doses and frequencies.
  • RESULTS: A total of 306 infusions of obatoclax mesylate were administered with a median of 5 infusions per patient.
  • The study drug was well tolerated up to the highest dose planned without dose-limiting toxicity.
  • Grade 1/2 central nervous system symptoms were the most common adverse events attributable to the study drug.
  • One patient with acute myeloid leukemia with mixed lineage leukemia t(9;11) rearrangement achieved a complete remission, which lasted 8 months.
  • CONCLUSIONS: Obatoclax mesylate is well tolerated and these results support its further investigation in patients with leukemia and myelodysplasia.
  • [MeSH-major] Leukemia / drug therapy. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Pyrroles / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Electrocardiography / drug effects. Female. Humans. Male. Middle Aged

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  • (PMID = 19088047.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrroles; 0 / obatoclax
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12. Dörrie J, Sapala K, Zunino SJ: Carnosol-induced apoptosis and downregulation of Bcl-2 in B-lineage leukemia cells. Cancer Lett; 2001 Sep 10;170(1):33-9
Hazardous Substances Data Bank. CARNOSOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carnosol-induced apoptosis and downregulation of Bcl-2 in B-lineage leukemia cells.
  • Carnosol, a phenolic compound extracted from the herb rosemary has been reported to have anti-cancer activity.
  • We investigated whether carnosol was cytotoxic against several pro-B and pre-B acute lymphoblastic leukemia (ALL) lines.
  • These results suggest that carnosol may be useful as a novel chemotherapeutic agent against B-lineage leukemias, and possibly other types of cancers that express high levels of the protective protein, Bcl-2.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Apoptosis / drug effects. Burkitt Lymphoma / drug therapy. Genes, bcl-2. Phenanthrenes / pharmacology
  • [MeSH-minor] Diterpenes, Abietane. Down-Regulation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Tumor Cells, Cultured

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  • (PMID = 11448532.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Diterpenes, Abietane; 0 / Phenanthrenes; 5957-80-2 / carnosol
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13. Duraj J, Bodo J, Sulikova M, Rauko P, Sedlak J: Diverse resveratrol sensitization to apoptosis induced by anticancer drugs in sensitive and resistant leukemia cells. Neoplasma; 2006;53(5):384-92
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] Diverse resveratrol sensitization to apoptosis induced by anticancer drugs in sensitive and resistant leukemia cells.
  • Naturally occurring dietary compound resveratrol (RES), possessing chemopreventive and cytostatic properties, has been shown as potent sensitizer for apoptosis induced by a variety of anticancer drugs.
  • Cell cycle analysis in sensitive promyelocytic leukemia HL60 cell line and its multidrug-resistant variant HL60/VCR (P-gp positive) treated with RES resulted in cell cycle arrest in S-phase in both cell variants.
  • Flow cytometry measurements showed diverse activities of RES in combination with anticancer drugs doxorubicin (DOX), cycloheximide (CHX), busulfan (BUS), gemcitabine (GEM) and paclitaxel (PTX), in some cases resulting in apoptosis induction, preferentially at the expense of S-phase.
  • Thus, RES could become a candidate to enhance the efficacy of combination anticancer therapy in a variety of human cancer cells inclusive leukemias.
  • [MeSH-major] Anticarcinogenic Agents / administration & dosage. Apoptosis / drug effects. Drug Resistance, Neoplasm. Leukemia / drug therapy. Stilbenes / administration & dosage
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols. Busulfan / administration & dosage. Cell Cycle / drug effects. Cell Line, Tumor. Cycloheximide / administration & dosage. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Doxorubicin / administration & dosage. Flow Cytometry. Humans. Paclitaxel / administration & dosage

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  • (PMID = 17013532.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Stilbenes; 0W860991D6 / Deoxycytidine; 80168379AG / Doxorubicin; 98600C0908 / Cycloheximide; B76N6SBZ8R / gemcitabine; G1LN9045DK / Busulfan; P88XT4IS4D / Paclitaxel; Q369O8926L / resveratrol
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14. Cilloni D, Messa F, Arruga F, Defilippi I, Morotti A, Messa E, Carturan S, Giugliano E, Pautasso M, Bracco E, Rosso V, Sen A, Martinelli G, Baccarani M, Saglio G: The NF-kappaB pathway blockade by the IKK inhibitor PS1145 can overcome imatinib resistance. Leukemia; 2006 Jan;20(1):61-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Imatinib represents at present the most attractive therapy for BCR-ABL positive leukemias, even though a percentage of CML patients develop resistance to this compound.
  • For these resistant patients a therapeutic approach based on a combination of drugs is more likely to be effective.
  • Furthermore, the identification of specific kinases within the NF-kappaB activation pathway offers a selective target to address tailored therapies.
  • Moreover, the addition of Imatinib increases the effects of PS1145 in resistant cell lines and BM cells from resistant patients, with a further increase of apoptosis and inhibition of proliferation and colony growth.
  • Our data provide the rational for a new therapeutic approach, which combines Imatinib and the IKK inhibitor PS1145 in CML resistant patients.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Heterocyclic Compounds, 3-Ring / pharmacology. I-kappa B Kinase / antagonists & inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. NF-kappa B / antagonists & inhibitors. Piperazines / therapeutic use. Pyridines / pharmacology. Pyrimidines / therapeutic use
  • [MeSH-minor] Apoptosis / drug effects. Benzamides. Binding Sites. Blotting, Western. Bone Marrow Cells / drug effects. Cell Proliferation / drug effects. Cell Survival / drug effects. Cells, Cultured. Combined Modality Therapy. DNA / metabolism. Enzyme-Linked Immunosorbent Assay. Humans. Imatinib Mesylate. In Vitro Techniques. K562 Cells. Tumor Stem Cell Assay / methods

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  • (PMID = 16270044.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [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 / Benzamides; 0 / Heterocyclic Compounds, 3-Ring; 0 / NF-kappa B; 0 / PS1145; 0 / Piperazines; 0 / Pyridines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; 9007-49-2 / DNA; EC 2.7.11.10 / I-kappa B Kinase
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15. Srinivasan RS, Nesbit JB, Marrero L, Erfurth F, LaRussa VF, Hemenway CS: The synthetic peptide PFWT disrupts AF4-AF9 protein complexes and induces apoptosis in t(4;11) leukemia cells. Leukemia; 2004 Aug;18(8):1364-72
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The synthetic peptide PFWT disrupts AF4-AF9 protein complexes and induces apoptosis in t(4;11) leukemia cells.
  • The MLL gene at chromosome band 11q23 is commonly involved in reciprocal translocations detected in acute leukemias.
  • Among the many known MLL fusion partners, AF4 is relatively common, particularly in acute lymphoblastic leukemia in infants.
  • The AF4 protein interacts with the product of another gene, AF9, which is also fused to MLL in acute leukemias.
  • Based on mapping studies of the AF9-binding domain of AF4, we have developed a peptide, designated PFWT, which disrupts the AF4-AF9 interaction in vitro and in vivo.
  • We provide evidence that this peptide is able to inhibit the proliferation of leukemia cells with t(4;11) chromosomal translocations expressing MLL-AF4 fusion genes.
  • Our findings indicate that the AF4-AF9 protein complex is a promising new target for leukemia therapy and that the PFWT peptide may serve as a lead compound for drug development.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Leukemia / pathology. Nuclear Proteins / metabolism. Oligopeptides / pharmacology
  • [MeSH-minor] Amino Acid Sequence. Cell Line, Tumor. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 4. Drug Delivery Systems. Humans. Myeloid-Lymphoid Leukemia Protein. Oncogene Proteins, Fusion. Protein Binding / drug effects. Transfection. Translocation, Genetic

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  • (PMID = 15269783.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 13539; United States / NCI NIH HHS / CA / CA 78318
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / MLL-AF4 fusion protein, human; 0 / MLLT3 protein, human; 0 / Nuclear Proteins; 0 / Oligopeptides; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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16. Gorre ME, Sawyers CL: Molecular mechanisms of resistance to STI571 in chronic myeloid leukemia. Curr Opin Hematol; 2002 Jul;9(4):303-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular mechanisms of resistance to STI571 in chronic myeloid leukemia.
  • Therapeutic use of the recently FDA-approved drug STI571 has been successful in the treatment of Philadelphia chromosome-positive leukemias.
  • STI571 is a small molecule inhibitor with activity against BCR-ABL, the deregulated tyrosine kinase responsible for initiation and maintenance of the disease in the chronic phase of chronic myeloid leukemia (CML).
  • Studies investigating the molecular mechanisms of resistance to this novel compound have progressed rapidly and point to the continued importance of BCR-ABL in disease maintenance even at its latest stages.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Animals. Benzamides. Clinical Trials as Topic. Drug Evaluation, Preclinical. Fusion Proteins, bcr-abl / antagonists & inhibitors. Humans. Imatinib Mesylate. In Vitro Techniques. Protein-Tyrosine Kinases / antagonists & inhibitors

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  • (PMID = 12042704.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM07185
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 31
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17. Koutsourea AI, Fousteris MA, Arsenou ES, Papageorgiou A, Pairas GN, Nikolaropoulos SS: Rational design, synthesis, and in vivo evaluation of the antileukemic activity of six new alkylating steroidal esters. Bioorg Med Chem; 2008 May 1;16(9):5207-15

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The synthesis and the in vivo evaluation against leukemias P388 and L1210 of six new alkylating steroidal esters are described.
  • Among the 17beta-acetamido-B-lactamic steroidal esters, the most potent compound afforded four out of six cures in leukemia P388 and was measured to be almost non-toxic, producing significant low levels of toxicity.
  • [MeSH-major] Antineoplastic Agents. Esters. Leukemia L1210 / drug therapy. Leukemia P388 / drug therapy. Steroids
  • [MeSH-minor] Alkylation. Animals. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Design. Drug Screening Assays, Antitumor. Female. Injections, Intraperitoneal. Male. Mice. Mice, Inbred BALB C. Mice, Inbred DBA. Molecular Structure. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy. Stereoisomerism. Structure-Activity Relationship

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  • (PMID = 18353651.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Esters; 0 / Steroids
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18. Marminon C, Anizon F, Moreau P, Léonce S, Pierré A, Pfeiffer B, Renard P, Prudhomme M: Syntheses and antiproliferative activities of new rebeccamycin derivatives with the sugar unit linked to both indole nitrogens. J Med Chem; 2002 Mar 14;45(6):1330-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The newly synthesized compounds were tested for their abilities to block the cell cycle of murine leukemia L1210 cells and their in vitro antiproliferative activities against four tumor cell lines (murine L1210 leukemia and human HT29 colon carcinoma, A549 non-small-cell lung carcinoma, K-562 leukemia).
  • Their biological activities are compared with those of the parent compound rebeccamycin.
  • Some of the new compounds exhibit potent antiproliferative activities, either against the four cell lines or mostly the two leukemias (L1210 and K-562 cell lines).
  • Nonselective compound 16 and 3,9-dinitro 13, which exhibited selectivity toward leukemia tumor cell lines, were selected for in-depth evaluation, including in vivo experiments.
  • [MeSH-minor] Animals. Anti-Bacterial Agents / chemistry. Carcinoma, Non-Small-Cell Lung / drug therapy. Cell Cycle / drug effects. Cell Division / drug effects. Drug Screening Assays, Antitumor. HT29 Cells / drug effects. Humans. K562 Cells / drug effects. Leukemia L1210 / drug therapy. Lung Neoplasms / drug therapy. Mice. Tumor Cells, Cultured

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  • (PMID = 11882002.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents; 0 / Carbazoles; 0 / Indoles; 0 / Pyrazoles; 93908-02-2 / rebeccamycin
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19. Oetzel C, Jonuleit T, Götz A, van der Kuip H, Michels H, Duyster J, Hallek M, Aulitzky WE: The tyrosine kinase inhibitor CGP 57148 (ST1 571) induces apoptosis in BCR-ABL-positive cells by down-regulating BCL-X. Clin Cancer Res; 2000 May;6(5):1958-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CGP 57148 is a potent inhibitor of the ABL protein tyrosine kinase and a promising new compound for the treatment of a variety of BCR-ABL-positive leukemias.
  • The growth of maturing chronic myeloid leukemia cells is independent of BCR-ABL in the presence of growth factors.
  • [MeSH-major] Apoptosis / drug effects. Enzyme Inhibitors / pharmacology. Fusion Proteins, bcr-abl / drug effects. Piperazines / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-bcl-2 / drug effects. Pyrimidines / pharmacology
  • [MeSH-minor] Animals. Antigens, CD95 / metabolism. Benzamides. Caspase 3. Caspases / drug effects. Caspases / metabolism. Cell Count / drug effects. Cell Division / drug effects. Chromones / pharmacology. Cytochrome c Group / drug effects. Cytochrome c Group / metabolism. Cytosol / drug effects. Cytosol / metabolism. Down-Regulation. Enzyme Activation / drug effects. Fas Ligand Protein. Flavonoids / pharmacology. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Membrane Glycoproteins / metabolism. Morpholines / pharmacology. Poly(ADP-ribose) Polymerases / metabolism. Protein Binding. Tumor Cells, Cultured. Tyrphostins / pharmacology. bcl-X Protein

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  • (PMID = 10815921.001).
  • [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 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Antigens, CD95; 0 / BCL2L1 protein, human; 0 / Benzamides; 0 / Chromones; 0 / Cytochrome c Group; 0 / Enzyme Inhibitors; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Flavonoids; 0 / Membrane Glycoproteins; 0 / Morpholines; 0 / Piperazines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrimidines; 0 / Tyrphostins; 0 / alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; 0 / bcl-X Protein; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 8A1O1M485B / Imatinib Mesylate; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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20. Health Quality Ontario: Extracorporeal photophoresis: an evidence-based analysis. Ont Health Technol Assess Ser; 2006;6(6):1-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To assess the effectiveness, safety and cost-effectiveness of extracorporeal photophoresis (ECP) for the treatment of refractory erythrodermic cutaneous T cell lymphoma (CTCL) and refractory chronic graft versus host disease (cGvHD).
  • The relative frequency and disease-specific 5-year survival of 1,905 primary cutaneous lymphomas classified according to the World Health Organization-European Organization for Research and Treatment of Cancer (WHO-EORTC) classification (Appendix 1).
  • Cutaneous T cell lymphoma has an annual incidence of approximately 0.4 per 100,000 and it mainly occurs in the 5(th) to 6(th) decade of life, with a male/female ratio of 2:1.
  • Mycosis fungoides is an indolent lymphoma with patients often having several years of eczematous or dermatitic skin lesions before the diagnosis is finally established.
  • Early in the disease biopsies are often difficult to interpret and the diagnosis may only become apparent by observing the patient over time.
  • CHRONIC GRAFT VERSUS HOST DISEASE: Allogeneic hematopoietic cell transplantation (HCT) is a treatment used for a variety of malignant and nonmalignant disease of the bone marrow and immune system.
  • The procedure is often associated with serious immunological complications, particularly graft versus host disease (GvHD).
  • Of the patients with extensive disease, approximately 60% will respond to treatment and eventually be able to discontinue immunosuppressive therapy.
  • The remaining patients will develop opportunistic infection, or require prolonged treatment with immunosuppressive agents.
  • The most commonly involved tissues are the skin, liver, mouth, and eyes.
  • TREATMENT:   CUTANEOUS T CELL LYMPHOMA: The optimal management of MF is undetermined because of its low prevalence, and its highly variable natural history, with frequent spontaneous remissions and exacerbations and often prolonged survival.
  • Nonaggressive approaches to therapy are usually warranted with treatment aimed at improving symptoms and physical appearance while limiting toxicity.
  • Given that multiple skin sites are usually involved, the initial treatment choices are usually topical or intralesional corticosteroids or phototherapy using psoralen (a compound found in plants which make the skin temporarily sensitive to ultraviolet A) (PUVA).
  • "Second line" therapy for early stage disease is often topical chemotherapy, radiotherapy or total skin electron beam radiation (TSEB).
  • Treatment of advanced stage (IIB-IV) MF usually consists of topical or systemic therapy in refractory or rapidly progressive SS.
  • Bone marrow transplantation and peripheral blood stem cell transplantation have been used to treat many malignant hematologic disorders (e.g., leukemias) that are refractory to conventional treatment.
  • Reports on the use of these procedures for the treatment of CTCL are limited and mostly consist of case reports or small case series.
  • CHRONIC GRAFT VERSUS HOST DISEASE: Patients who develop cGvHD require reinstitution of immunosuppressive medication (if already discontinued) or an increase in dosage and possibly addition of other agents.
  • The current literature regarding cGvHD therapy is less than optimal and many recommendations about therapy are based on common practices that await definitive testing.
  • Numerous salvage therapies have been considered in patients with refractory cGvHD, including ECP.
  • Due to uncertainty around salvage therapies, Bhushan and Collins suggested that ideally, patients with refractory cGvHD should be entered into clinical trials.
  • Two Ontario expert consultants jointly estimated that there may be approximately 30 new erythrodermic treatment resistant CTCL patients and 30 new treatment resistant cGvHD patients per year who are unresponsive to other forms of therapy and may be candidates for ECP.
  • Extracorporeal photopheresis is a procedure that was initially developed as a treatment for CTCL, particularly SS.
  • The lymphocyte layer is treated with methoxsalen (a drug that sensitizes the lymphocytes to light) and exposed to UVA, following which the lymphocytes are returned to the patient.
  • Photosensitization is achieved by administering methoxsalen to the patient orally 2 hours before the procedure, or by injecting methoxsalen directly ino the leucocyte rich fraction.
  • The latter approach avoids potential side effects such as nausea, and provides a more consistent drug level within the machine.
  • In general, from the time the intravenous line is inserted until the white blood cells are returned to the patient takes approximately 2.5-3.5 hours.
  • For CTCL, the treatment schedule is generally 2 consecutive days every 4 weeks for a median of 6 months.
  • For cGvHD, an expert in the field estimated that the treatment schedule would be 3 times a week for the 1(st) month, then 2 consecutive days every 2 weeks after that (i.e., 4 treatments a month) for a median of 6 to 9 months.
  • REGULATORY STATUS: The UVAR XTS Photopheresis System is licensed by Health Canada as a Class 3 medical device (license # 7703) for the "palliative treatment of skin manifestations of CTCL."
  • It is not licensed for the treatment of cGvHD.

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  • (PMID = 23074497.001).
  • [Journal-full-title] Ontario health technology assessment series
  • [ISO-abbreviation] Ont Health Technol Assess Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC3379535
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21. Erkizan HV, Kong Y, Merchant M, Schlottmann S, Barber-Rotenberg JS, Yuan L, Abaan OD, Chou TH, Dakshanamurthy S, Brown ML, Uren A, Toretsky JA: A small molecule blocking oncogenic protein EWS-FLI1 interaction with RNA helicase A inhibits growth of Ewing's sarcoma. Nat Med; 2009 Jul;15(7):750-6
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  • Many sarcomas and leukemias carry nonrandom chromosomal translocations encoding tumor-specific mutant fusion transcription factors that are essential to their molecular pathogenesis.
  • YK-4-279, a derivative of the lead compound from the screen, blocks RHA binding to EWS-FLI1, induces apoptosis in ESFT cells and reduces the growth of ESFT orthotopic xenografts.
  • [MeSH-major] Antineoplastic Agents / pharmacology. DEAD-box RNA Helicases / metabolism. Indoles / pharmacology. Neoplasm Proteins / metabolism. Oncogene Proteins, Fusion / antagonists & inhibitors. Sarcoma, Ewing / drug therapy. Transcription Factors / antagonists & inhibitors

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  • (PMID = 19584866.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA088004-08; United States / NCI NIH HHS / CA / R01CA138212; United States / NCI NIH HHS / CA / R01CA133662; United States / NCI NIH HHS / CA / R01 CA133662; United States / NCI NIH HHS / CA / P01 CA47179; United States / NCI NIH HHS / CA / R01 CA138212; United States / NCI NIH HHS / CA / P30 CA051008; United States / NCI NIH HHS / CA / R01 CA138212-01; United States / NCI NIH HHS / CA / R01 CA088004; United States / NCI NIH HHS / CA / T32 CA009686; United States / NCI NIH HHS / CA / R01 CA133662-01A2; United States / NCI NIH HHS / CA / P01 CA047179
  • [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 / EWS-FLI fusion protein; 0 / Indoles; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Protein c-fli-1; 0 / RNA-Binding Protein EWS; 0 / Transcription Factors; 0 / YK 4-279; EC 3.4.22.- / Caspase 3; EC 3.6.1.- / DHX9 protein, human; EC 3.6.4.13 / DEAD-box RNA Helicases
  • [Other-IDs] NLM/ NIHMS116382; NLM/ PMC2777681
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22. Dorr RT, Liddil JD, Sami SM, Remers W, Hersh EM, Alberts DS: Preclinical antitumor activity of the azonafide series of anthracene-based DNA intercalators. Anticancer Drugs; 2001 Mar;12(3):213-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Prior studies have described antitumor efficacy in murine tumor models including L-1210 and P-388 leukemias, and B-16 melanoma.
  • In freshly isolated human tumors tested in soft agar, there was marked activity (mean IC50 in microg/ml) for AMP-53 in four cell types: breast cancer (0.09), lung cancer (0.06), renal cell carcinomas (0.06) and multiple myeloma (0.03).
  • Compound AMP-1 was shown to be superior to amonafide in the mammary 16C breast cancer model in B6CF31 mice, but it had little activity in Colon-38 nor in M5076 ovarian sarcomas in vivo.
  • Nine azonafides were evaluated in the Lewis lung cancer model in C57/bl mice, but only AMP-53 demonstrated significant efficacy with a treated/control x 100% (T/C) value of 30%.
  • Only three tumors were sensitive (T/C<42%), including HL-60 leukemia (T/C=39%), MCF-7 breast cancer (T/C=39%) and A549 non-small cell lung cancer (T/C=37%).
  • [MeSH-major] Antineoplastic Agents / pharmacology. Imides / pharmacology. Intercalating Agents / pharmacology. Isoquinolines / pharmacology. Tumor Cells, Cultured / drug effects
  • [MeSH-minor] Animals. Colony-Forming Units Assay. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Female. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Nude. Naphthalimides. Neoplasms / drug therapy. Tumor Stem Cell Assay

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  • (PMID = 11290869.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM 49875
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Imides; 0 / Intercalating Agents; 0 / Isoquinolines; 0 / Naphthalimides; 0 / azonafide; 1Q8D39N37L / amonafide
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23. Moneypenny CG, Shao J, Song Y, Gallagher EP: MLL rearrangements are induced by low doses of etoposide in human fetal hematopoietic stem cells. Carcinogenesis; 2006 Apr;27(4):874-81
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  • Of interest is the role of genetic injury to fetal HSC in the etiology of the infant acute leukemias, which are characterized by chromosomal rearrangements in the 11q23 region involving the mixed lineage leukemia (MLL) gene.
  • These gene fusions also occur in leukemias in adults following chemotherapy with etoposide and other inhibitors of DNA topoisomerase II.
  • We used etoposide as a model compound to determine the sensitivity of human fetal HSC to DNA damage and to determine whether we could induce MLL rearrangements in cultured human fetal HSC.
  • Ultimately, such injury may have ramifications with regards to transplacental exposures to environmental chemicals linked to the etiology of infant acute leukemias.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Etoposide / pharmacology. Gene Rearrangement / drug effects. Hematopoietic Stem Cells / drug effects. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Cell Culture Techniques. Cell Cycle / drug effects. Cell Survival / drug effects. DNA Damage. Dose-Response Relationship, Drug. Female. Fetus. Histone-Lysine N-Methyltransferase. Humans. Leukemia / chemically induced. Maternal-Fetal Exchange. Pregnancy

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  • (PMID = 16377807.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P30-ES07033; United States / NIEHS NIH HHS / ES / R01-ES09427
  • [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] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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24. Carter BZ, Mak DH, Schober WD, McQueen T, Harris D, Estrov Z, Evans RL, Andreeff M: Triptolide induces caspase-dependent cell death mediated via the mitochondrial pathway in leukemic cells. Blood; 2006 Jul 15;108(2):630-7
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  • Here, we examined its effects on leukemic cells and found that, at 100 nM or less, it potently induced apoptosis in various leukemic cell lines and primary acute myeloid leukemia (AML) blasts.
  • The potent antileukemic activity of triptolide in vitro warrants further investigation of this compound for the treatment of leukemias and other malignancies.

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  • (PMID = 16556893.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA49639; United States / NCI NIH HHS / CA / P01 CA55164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Apoptosis Regulatory Proteins; 0 / Diterpenes; 0 / Epoxy Compounds; 0 / Phenanthrenes; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human; 19ALD1S53J / triptolide; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC1895484
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25. Konovalova NP, Goncharova SA, Volkova LM, Rajewskaya TA, Eremenko LT, Korolev AM: Nitric oxide donor increases the efficiency of cytostatic therapy and retards the development of drug resistance. Nitric Oxide; 2003 Feb;8(1):59-64
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  • [Title] Nitric oxide donor increases the efficiency of cytostatic therapy and retards the development of drug resistance.
  • This type of combined therapy results in significant increase in life span and number of survivors among mice bearing leukemias P388 and L-1210.
  • A similar effect was observed for intracerebral leukemia P388 transplantation.
  • In this case the life span of mice treated with cyclophosphamide and NO donor increased by three times in comparison to therapy with cyclophosphamide alone.
  • Comparative studies of NO donor (organic nitrate) and a similar compound in which ONO(2) moieties were replaced by OH groups demonstrated that the presence of NO(2) is required for adjuvant activity of compounds and confirmed that nitric oxide modifies the antitumor effects of cytostatics.
  • It is shown also that nitric oxide donor retards the development of drug resistance to cyclophosphamide.

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  • (PMID = 12586543.001).
  • [ISSN] 1089-8603
  • [Journal-full-title] Nitric oxide : biology and chemistry
  • [ISO-abbreviation] Nitric Oxide
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3,3-bis(hydroxymethyl)oxetane; 0 / 3,3-bis(nitroxymethyl)oxetane; 0 / Antineoplastic Agents; 0 / Ethers, Cyclic; 0 / Nitric Oxide Donors; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin
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26. Momekov G, Ferdinandov D, Zheleva-Dimitrova D, Nedialkov P, Girreser U, Kitanov G: Cytotoxic effects of hyperatomarin, a prenylated phloroglucinol from Hypericum annulatum Moris subsp. annulatum, in a panel of malignant cell lines. Phytomedicine; 2008 Nov;15(11):1010-5

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  • The cytotoxic effects of hyperatomarin - a prenylated phloroglucinol isolated from Hypericum annulatum Moris subsp. annulatum were assessed in a broad spectrum of tumor cell lines originating from leukemias, lymphomas and solid malignancies.
  • The tested compound exerted strong concentration-dependent cytotoxic effects (IC50 values ranging 0.14-15.7 μM), comparable to and even outclassing in some cell lines those of the established anti-cancer drug daunorubicin.
  • Exposure of different human tumor cell lines to hyperatomarin resulted in strong mono- and oligo-nucleosomal fragmentation of genomic DNA, as evidenced by 'Cell death detection' ELISA kit and by DNA-electrophoresis, which unambiguously indicates that the induction of apoptosis is implicated in the cytotoxic mode of action of the tested compound.
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Humans. Inhibitory Concentration 50. Leukemia / drug therapy. Leukemia / pathology. Lymphoma / drug therapy. Lymphoma / pathology

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  • (PMID = 18539018.001).
  • [ISSN] 1618-095X
  • [Journal-full-title] Phytomedicine : international journal of phytotherapy and phytopharmacology
  • [ISO-abbreviation] Phytomedicine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / hyperatomarin; DHD7FFG6YS / Phloroglucinol
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27. Klejman A, Rushen L, Morrione A, Slupianek A, Skorski T: Phosphatidylinositol-3 kinase inhibitors enhance the anti-leukemia effect of STI571. Oncogene; 2002 Aug 29;21(38):5868-76
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  • [Title] Phosphatidylinositol-3 kinase inhibitors enhance the anti-leukemia effect of STI571.
  • BCR/ABL fusion tyrosine kinase is responsible for the initiation and maintenance of the Philadelphia chromosome (Ph(1))-positive chronic myelogenous leukemia (CML) and a cohort of acute lymphocytic leukemias (ALL).
  • STI571 (Gleevec), a novel anti-leukemia drug targeting BCR/ABL kinase can induce remissions of the Ph(1)-positive leukemias.
  • STI571 was recently combined with the standard cytostatic drugs to achieve better therapeutic results and to overcome emerging drug resistance mechanisms.
  • We decided to search for a more specific partner compound for STI571.
  • Therefore the anti- Ph(1)-leukemia effect of the combination of BCR/ABL kinase inhibitor STI571 and PI-3k inhibitor wortmannin (WT) or LY294002 (LY) was tested.
  • Single colony RT-PCR assay showed that colonies arising from the mixture of CML cells and normal bone marrow cells after treatment with STI571+WT were selectively depleted of BCR/ABL-positive cells.
  • Biochemical analysis of the CML cells after the treatment revealed that combination of STI571+WT caused a more pronounced activation of caspase-3 and induced massive apoptosis, in comparison to STI571 and WT alone.
  • In conclusion, combination of STI571+WT or STI571+LY may represent a novel approach against the Ph(1)-positive leukemias.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Enzyme Inhibitors / pharmacology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Androstadienes / pharmacology. Benzamides. Caspase 3. Caspases / drug effects. Caspases / metabolism. Chromones / pharmacology. Drug Synergism. Flavonoids / pharmacology. Fusion Proteins, bcr-abl / drug effects. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Humans. Imatinib Mesylate. Morpholines / pharmacology. Reference Values. Tumor Cells, Cultured

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  • (PMID = 12185586.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA87300; United States / NIDDK NIH HHS / DK / K01 DK02896
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; 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 / Androstadienes; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / Morpholines; 0 / Piperazines; 0 / Pyrimidines; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 8A1O1M485B / Imatinib Mesylate; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; XVA4O219QW / wortmannin
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28. Park MJ, Kwon HY, Lee EO, Lee HJ, Ahn KS, Kim MO, Kim CH, Ahn KS, Kim SH: DMNQ-S17 inhibits constitutive NF-kappaB activation leading to induction of apoptosis through the activation of caspase-3 in human myeloid leukemia U937 cells. Life Sci; 2008 Sep 26;83(13-14):460-7
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  • [Title] DMNQ-S17 inhibits constitutive NF-kappaB activation leading to induction of apoptosis through the activation of caspase-3 in human myeloid leukemia U937 cells.
  • Through cytotoxicity screening with naphthoquinone derivatives, a novel compound 6-(1-oxoallkyl)-5,8-dimethoxy-1,4-naphthoquinone-S17 (DMNQ-S17) showed its potency against human myeloid leukemia U937 cells.
  • Thus, to elucidate the apoptotic mechanism of DMNQ-S17, this study was performed in myeloid leukemia U937 cells by 2,3-bis [2-methoxy-4-nitro-5-sulfophenyl]-2H-tetrazolium-5-carboxanilide (XTT) assay, eletrophoretic mobility shift assay (EMSA), terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) assay, 4',6-diamidino-2-phenylindole (DAPI) staining, and Western blotting.
  • Taken together, these findings suggest that DMNQ-S17 can be a potent anticancer candidate for myeloid leukemias by the suppression of NF-kappaB activation leading to the activation of caspase-3 in human myeloid leukemia U937 cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Caspase 3 / biosynthesis. Leukemia, Myeloid / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. NF-kappa B / biosynthesis. Naphthoquinones / pharmacology
  • [MeSH-minor] Caspase Inhibitors. Cytochromes c / metabolism. Drug Screening Assays, Antitumor. Enzyme Inhibitors / pharmacology. Fluorescent Dyes. Humans. In Situ Nick-End Labeling. Indoles. Male. Membrane Potential, Mitochondrial / drug effects. Poly(ADP-ribose) Polymerases / metabolism. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. U937 Cells

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  • (PMID = 18718843.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 6-(1-oxobutyl)-5,8-dimethoxy-1,4-naphthoquinone; 0 / Antineoplastic Agents; 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / Fluorescent Dyes; 0 / Indoles; 0 / NF-kappa B; 0 / Naphthoquinones; 47165-04-8 / DAPI; 9007-43-6 / Cytochromes c; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3
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29. Guzman ML, Rossi RM, Neelakantan S, Li X, Corbett CA, Hassane DC, Becker MW, Bennett JM, Sullivan E, Lachowicz JL, Vaughan A, Sweeney CJ, Matthews W, Carroll M, Liesveld JL, Crooks PA, Jordan CT: An orally bioavailable parthenolide analog selectively eradicates acute myelogenous leukemia stem and progenitor cells. Blood; 2007 Dec 15;110(13):4427-35
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  • [Title] An orally bioavailable parthenolide analog selectively eradicates acute myelogenous leukemia stem and progenitor cells.
  • Leukemia stem cells (LSCs) are thought to play a central role in the pathogenesis of acute leukemia and likely contribute to both disease initiation and relapse.
  • Therefore, identification of agents that target LSCs is an important consideration for the development of new therapies.
  • To this end, we have previously demonstrated that the naturally occurring compound parthenolide (PTL) can induce death of human LSCs in vitro while sparing normal hematopoietic cells.
  • However, PTL has relatively poor pharmacologic properties that limit its potential clinical use.
  • These studies identified an analog, dimethylamino-parthenolide (DMAPT), which induces rapid death of primary human LSCs from both myeloid and lymphoid leukemias, and is also highly cytotoxic to bulk leukemic cell populations.
  • The compound has approximately 70% oral bioavailability, and pharmacologic studies using both mouse xenograft models and spontaneous acute canine leukemias demonstrate in vivo bioactivity as determined by functional assays and multiple biomarkers.
  • Therefore, based on the collective preclinical data, we propose that the novel compound DMAPT has the potential to target human LSCs in vivo.

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  • (PMID = 17804695.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090446; United States / NCI NIH HHS / CA / R01 CA90446
  • [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 / NF-kappa B; 0 / Sesquiterpenes; 0 / Tumor Suppressor Protein p53; 2RDB26I5ZB / parthenolide
  • [Other-IDs] NLM/ PMC2234793
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30. Auclair D, Miller D, Yatsula V, Pickett W, Carter C, Chang Y, Zhang X, Wilkie D, Burd A, Shi H, Rocks S, Gedrich R, Abriola L, Vasavada H, Lynch M, Dumas J, Trail PA, Wilhelm SM: Antitumor activity of sorafenib in FLT3-driven leukemic cells. Leukemia; 2007 Mar;21(3):439-45
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  • Activating internal tandem duplication (ITD) insertions in the juxtamembrane domain of the FLT3 tyrosine kinase are found in about one fourth of patients with acute myeloid leukemia and have been shown to be an independent negative prognostic factor for survival.
  • In leukemia cell lines MV4-11 and EOL-1, sorafenib treatment resulted in decreased cell proliferation and inhibition of FLT3 signaling.
  • Cell cycle arrest and induction of apoptosis were observed upon treatment with sorafenib in MV4-11 and EOL-1 cells.
  • The antitumor efficacy of sorafenib was evaluated against the MV4-11 leukemia grown subcutaneously in NCr nu/nu mice.
  • The demonstration that sorafenib exhibits potent target inhibition and efficacy in FLT3-driven models suggests that this compound may have a therapeutic benefit for patients with FLT3-driven leukemias.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Benzenesulfonates / pharmacology. Leukemia, Myeloid / drug therapy. Mutant Proteins / physiology. Neoplasm Proteins / physiology. Protein Kinase Inhibitors / pharmacology. Pyridines / pharmacology. fms-Like Tyrosine Kinase 3 / physiology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line. Drug Screening Assays, Antitumor. Female. Humans. Kidney. Mice. Mice, Nude. Niacinamide / analogs & derivatives. Phenylurea Compounds. Recombinant Fusion Proteins / physiology. Tandem Repeat Sequences. Transfection. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors. Xenograft Model Antitumor Assays

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  • (PMID = 17205056.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Mutant Proteins; 0 / Neoplasm Proteins; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 0 / Recombinant Fusion Proteins; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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31. Zhang X, He Y, Liu S, Yu Z, Jiang ZX, Yang Z, Dong Y, Nabinger SC, Wu L, Gunawan AM, Wang L, Chan RJ, Zhang ZY: Salicylic acid based small molecule inhibitor for the oncogenic Src homology-2 domain containing protein tyrosine phosphatase-2 (SHP2). J Med Chem; 2010 Mar 25;53(6):2482-93
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  • Gain-of-function SHP2 mutations are associated with Noonan syndrome, various kinds of leukemias, and solid tumors.
  • Thus, there is considerable interest in SHP2 as a potential target for anticancer and antileukemia therapy.
  • Screening of the library led to the identification of a SHP2 inhibitor II-B08 (compound 9) with highly efficacious cellular activity.
  • Compound 9 blocks growth factor stimulated ERK1/2 activation and hematopoietic progenitor proliferation, providing supporting evidence that chemical inhibition of SHP2 may be therapeutically useful for anticancer and antileukemia treatment.

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  • (PMID = 20170098.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] ENG
  • [Databank-accession-numbers] PDB/ 3JRL
  • [Grant] United States / NHLBI NIH HHS / HL / HL82981; United States / NIA NIH HHS / AG / F31 AG031648; United States / NIA NIH HHS / AG / F31AG031648; United States / NCI NIH HHS / CA / CA126937-03; United States / NCI NIH HHS / CA / CA069202-15; United States / NCI NIH HHS / CA / CA126937; United States / NCI NIH HHS / CA / R01 CA126937-03; United States / NCI NIH HHS / CA / R01 CA069202-15; United States / NCI NIH HHS / CA / R01 CA126937; United States / NHLBI NIH HHS / HL / R01 HL082981; United States / NCI NIH HHS / CA / R01 CA069202; United States / NCI NIH HHS / CA / CA69202
  • [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 / 3-(1-(3-(biphenyl-4-ylamino)-3-oxopropyl)-1H-1,2,3-triazol-4-yl)-6-hydroxy-1-methyl-2-phenyl-1H-indole-5-carboxylic acid; 0 / Enzyme Inhibitors; 0 / Indoles; 0 / Small Molecule Libraries; 0 / Triazoles; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 11; O414PZ4LPZ / Salicylic Acid
  • [Other-IDs] NLM/ NIHMS181461; NLM/ PMC2842125
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32. Gontarewicz A, Brümmendorf TH: Danusertib (formerly PHA-739358)--a novel combined pan-Aurora kinases and third generation Bcr-Abl tyrosine kinase inhibitor. Recent Results Cancer Res; 2010;184:199-214
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  • Therefore, these proteins have become an attractive target for the development of new anticancer therapies.
  • In fact, several small-molecule inhibitors of Aurora kinases have already been developed and some of them have shown promising clinical efficacy in a number of human tumors in Phase I and II clinical trials.
  • Among those, one of the most advanced clinical compound currently is Danusertib (formerly PHA-739358), which exhibits inhibitory activity against all known Aurora kinases as well as other cancer-relevant kinases such as the Bcr-Abl tyrosine kinase, including its multidrug-resistant T315I mutant.
  • This mutation is responsible for up to 25% of all clinically observed resistances in CML patients undergoing Imatinib therapy.
  • Therefore, combined Aurora and Bcr-Abl inhibition (the latter including high-grade resistance conferring mutations) with compounds such as Danusertib represents a promising new strategy for treatment of Bcr-Abl positive leukemias, especially those in second and third line of treatment.
  • [MeSH-major] Benzamides / therapeutic use. Neoplasms / drug therapy. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Pyrazoles / therapeutic use

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  • (PMID = 20072840.001).
  • [ISSN] 0080-0015
  • [Journal-full-title] Recent results in cancer research. Fortschritte der Krebsforschung. Progrès 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 / Benzamides; 0 / Pyrazoles; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; M3X659D0FY / danusertib
  • [Number-of-references] 88
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33. Gumireddy K, Baker SJ, Cosenza SC, John P, Kang AD, Robell KA, Reddy MV, Reddy EP: A non-ATP-competitive inhibitor of BCR-ABL overrides imatinib resistance. Proc Natl Acad Sci U S A; 2005 Feb 8;102(6):1992-7
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  • Imatinib, which is an inhibitor of the BCR-ABL tyrosine kinase, has been a remarkable success for the treatment of Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemias (CMLs).
  • Here we describe the activity of one compound, ON012380, that can specifically inhibit BCR-ABL and induce cell death of Ph+ CML cells at a concentration of <10 nM.
  • Kinetic studies demonstrate that this compound is not ATP-competitive but is substrate-competitive and works synergistically with imatinib in wild-type BCR-ABL inhibition.
  • More importantly, ON012380 was found to induce apoptosis of all of the known imatinib-resistant mutants at concentrations of <10 nM concentration in vitro and cause regression of leukemias induced by i.v. injection of 32Dcl3 cells expressing the imatinib-resistant BCR-ABL isoform T315I.
  • Daily i.v. dosing for up to 3 weeks with a >100 mg/kg concentration of this agent is well tolerated in rodents, without any hematotoxicity.
  • [MeSH-major] Adenosine Triphosphate / metabolism. Antineoplastic Agents / metabolism. Benzene Derivatives / metabolism. Drug Resistance, Neoplasm. Piperazines / metabolism. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / metabolism. Pyrimidines / metabolism
  • [MeSH-minor] Animals. Benzamides. Cell Death. Female. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. K562 Cells. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mice. Mice, Nude. Molecular Structure. Mutation. Recombinant Proteins / genetics. Recombinant Proteins / metabolism

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  • (PMID = 15677719.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzene Derivatives; 0 / ON012380; 0 / Piperazines; 0 / Pyrimidines; 0 / Recombinant Proteins; 8A1O1M485B / Imatinib Mesylate; 8L70Q75FXE / Adenosine Triphosphate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC546016
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34. Beggiolin G, Crippa L, Menta E, Manzotti C, Cavalletti E, Pezzoni G, Torriani D, Randisi E, Cavagnoli R, Sala F, Giuliani FC, Spinelli S: Bbr 2778, an aza-anthracenedione endowed with preclinical anticancer activity and lack of delayed cardiotoxicity. Tumori; 2001 Nov-Dec;87(6):407-16
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  • From this screening, BBR 2778 (6,9-bis[(2-aminoethyl)amino] benzo[g]isoquinoline-5,10-dione dimaleate) emerged as the most interesting compound.
  • BBR 2778 was more cytotoxic in leukemia and lymphoma cell lines than in solid tumor cell lines.
  • In particular, BBR 2778 was curative against L1210 murine leukemia and YC-8 murine lymphoma.
  • In light of its spectrum of activity and marked efficacy against lymphomas and leukemias over a wide dose range, together with its lack of delayed cardiotoxicity, BBR 2778 has been entered in clinical studies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Enzyme Inhibitors / pharmacology. Heart / drug effects. Isoquinolines / pharmacology. Leukemia L1210 / drug therapy. Leukemia P388 / drug therapy
  • [MeSH-minor] Animals. Anthraquinones / adverse effects. Anthraquinones / chemistry. Anthraquinones / pharmacology. Doxorubicin / pharmacology. Drug Screening Assays, Antitumor. Male. Mice. Mice, Inbred DBA. Mitoxantrone / pharmacology. Myocardium / pathology. Tumor Cells, Cultured

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  • (PMID = 11989596.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthraquinones; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Isoquinolines; 80168379AG / Doxorubicin; BZ114NVM5P / Mitoxantrone; F5SXN2KNMR / pixantrone
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35. Rao SS, O'Neil J, Liberator CD, Hardwick JS, Dai X, Zhang T, Tyminski E, Yuan J, Kohl NE, Richon VM, Van der Ploeg LH, Carroll PM, Draetta GF, Look AT, Strack PR, Winter CG: Inhibition of NOTCH signaling by gamma secretase inhibitor engages the RB pathway and elicits cell cycle exit in T-cell acute lymphoblastic leukemia cells. Cancer Res; 2009 Apr 1;69(7):3060-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of NOTCH signaling by gamma secretase inhibitor engages the RB pathway and elicits cell cycle exit in T-cell acute lymphoblastic leukemia cells.
  • NOTCH signaling is deregulated in the majority of T-cell acute lymphoblastic leukemias (T-ALL) as a result of activating mutations in NOTCH1.
  • Gamma secretase inhibitors (GSI) block proteolytic activation of NOTCH receptors and may provide a targeted therapy for T-ALL.
  • Consistent with this evidence of cell cycle exit, short-term exposure of GSI resulted in sustained molecular and phenotypic effects after withdrawal of the compound.
  • Combination treatment with GSI and a small molecule inhibitor of CDK4 produced synergistic growth inhibition, providing evidence that GSI engagement of the CDK4/RB pathway is an important mechanism of GSI action and supports further investigation of this combination for improved efficacy in treating T-ALL.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Cyclic S-Oxides / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Protease Inhibitors / pharmacology. Receptor, Notch1 / antagonists & inhibitors. Retinoblastoma Protein / metabolism. Thiadiazoles / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Cyclin-Dependent Kinase 4 / antagonists & inhibitors. Cyclin-Dependent Kinase Inhibitor p19 / biosynthesis. Cyclin-Dependent Kinase Inhibitor p27. G1 Phase / drug effects. G1 Phase / genetics. Gene Expression Profiling. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Phosphorylation. S Phase / drug effects. S Phase / genetics. Signal Transduction / drug effects. Transcription, Genetic. Transfection

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  • (PMID = 19318552.001).
  • [ISSN] 1538-7445
  • [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 / CDKN1B protein, human; 0 / CDKN2D protein, human; 0 / Cyclic S-Oxides; 0 / Cyclin-Dependent Kinase Inhibitor p19; 0 / Intracellular Signaling Peptides and Proteins; 0 / MRK 003; 0 / NOTCH1 protein, human; 0 / Protease Inhibitors; 0 / Receptor, Notch1; 0 / Retinoblastoma Protein; 0 / Thiadiazoles; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.22 / CDK4 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 4; EC 3.4.- / Amyloid Precursor Protein Secretases
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