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1. Hu Y, Swerdlow S, Duffy TM, Weinmann R, Lee FY, Li S: Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice. Proc Natl Acad Sci U S A; 2006 Nov 7;103(45):16870-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice.
  • Imatinib is highly effective at treating human Philadelphia chromosome-positive (Ph(+)) chronic myeloid leukemia (CML) in chronic phase but not Ph(+) B cell acute lymphoblastic leukemia (B-ALL) and CML blast crisis.
  • We find that SRC kinases activated by BCR-ABL remain fully active in imatinib-treated mouse leukemic cells, suggesting that imatinib does not inactivate all BCR-ABL-activated signaling pathways.
  • This SRC pathway is essential for leukemic cells to survive imatinib treatment and for CML transition to lymphoid blast crisis.
  • Besides BCR-ABL and SRC kinases, stem cell pathways must be targeted for curative therapy of Ph(+) leukemia.

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  • (PMID = 17077147.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA114199; United States / NCI NIH HHS / CA / CA 114199
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / src-Family Kinases; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC1629087
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2. Robak T, Robak P, Smolewski P: TRU-016, a humanized anti-CD37 IgG fusion protein for the potential treatment of B-cell malignancies. Curr Opin Investig Drugs; 2009 Dec;10(12):1383-90
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  • [Title] TRU-016, a humanized anti-CD37 IgG fusion protein for the potential treatment of B-cell malignancies.
  • TRU-016, under development by Trubion Pharmaceuticals Inc and Facet Biotech Corp, is an intravenously administered anti-CD37 IgG fusion protein for the potential treatment of B-cell malignancies, including chronic lymphocytic leukemia (CLL) and non-Hodgkin's lymphoma (NHL), as well as for autoimmune and inflammatory diseases.
  • TRU-016 was created by humanizing SMIP-016, a mouse/human chimeric protein that demonstrated antitumor activity against lymphoid malignancies in preclinical studies, including in human B-cell tumor mouse xenograft models.
  • TRU-016 is a promising therapeutic agent for patients with B-cell lymphoid malignancies, especially patients refractory to standard treatment.
  • [MeSH-major] Antigens, CD / immunology. Antigens, Neoplasm / immunology. Antineoplastic Agents / therapeutic use. Immunoglobulin G / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, B-Cell / drug therapy. Recombinant Fusion Proteins / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Autoimmune Diseases / drug therapy. Autoimmune Diseases / immunology. Clinical Trials as Topic. Drug Evaluation, Preclinical. Humans. Inflammation / drug therapy. Inflammation / immunology. Mice. Tetraspanins

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  • (PMID = 19943209.001).
  • [ISSN] 2040-3429
  • [Journal-full-title] Current opinion in investigational drugs (London, England : 2000)
  • [ISO-abbreviation] Curr Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD37 protein, human; 0 / Immunoglobulin G; 0 / Recombinant Fusion Proteins; 0 / TRU 016; 0 / Tetraspanins
  • [Number-of-references] 73
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3. Pham LV, Tamayo AT, Li C, Bornmann W, Priebe W, Ford RJ: Degrasyn potentiates the antitumor effects of bortezomib in mantle cell lymphoma cells in vitro and in vivo: therapeutic implications. Mol Cancer Ther; 2010 Jul;9(7):2026-36
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  • [Title] Degrasyn potentiates the antitumor effects of bortezomib in mantle cell lymphoma cells in vitro and in vivo: therapeutic implications.
  • Mantle cell lymphoma (MCL) is an aggressive histotype of B-cell non-Hodgkin lymphoma that has increased in incidence over the past few decades and is incurable, usually poorly responsive to standard chemotherapy combinations, and associated with poor prognoses.
  • Discovering new therapeutic agents with low toxicity that produce better outcomes in patients with MCL is an ongoing challenge.
  • Recent studies showed that degrasyn, a novel small-molecule inhibitor of the Janus kinase/signal transducer and activation of transcription (JAK/STAT) pathway, exerts antitumor activity in lymphoid tumors by inhibiting key growth and survival signaling (JAK/STAT) pathways.
  • In the present study, we found that treatment of both typical and blastoid-variant MCL cells with degrasyn in combination with bortezomib resulted in synergistic growth inhibition and apoptosis induction in vitro.
  • In vivo, degrasyn and bortezomib interacted to synergistically prevent tumor development and prolong survival durations in a xenotransplant severe combined immunodeficient mouse model of MCL.
  • These findings suggest that agents such as degrasyn that can pharmacologically target constitutively expressed NF-kappaB and STAT3 in MCL cells may be useful therapeutic agents for MCL when administered together with bortezomib.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Boronic Acids / pharmacology. Lymphoma, Mantle-Cell / drug therapy. Nitriles / pharmacology. Pyrazines / pharmacology. Pyridines / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Bortezomib. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Cells, Cultured. Cyanoacrylates. Cyclin D1 / genetics. Dose-Response Relationship, Drug. Drug Synergism. Female. Gene Expression Regulation, Leukemic / drug effects. Humans. Mice. Mice, SCID. NF-kappa B / metabolism. Phosphorylation. Proto-Oncogene Proteins c-myc / genetics. Reverse Transcriptase Polymerase Chain Reaction. STAT3 Transcription Factor / metabolism. Survival Analysis. Xenograft Model Antitumor Assays

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  • [Copyright] (c)2010 AACR.
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  • (PMID = 20606045.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA100836; United States / NCI NIH HHS / CA / CA-16672-26; United States / NCI NIH HHS / CA / CA-RO1-100836
  • [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 / Boronic Acids; 0 / Cyanoacrylates; 0 / MYC protein, human; 0 / NF-kappa B; 0 / Nitriles; 0 / Proto-Oncogene Proteins c-myc; 0 / Pyrazines; 0 / Pyridines; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / degrasyn; 136601-57-5 / Cyclin D1; 69G8BD63PP / Bortezomib
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4. Gueven N, Luff J, Peng C, Hosokawa K, Bottle SE, Lavin MF: Dramatic extension of tumor latency and correction of neurobehavioral phenotype in Atm-mutant mice with a nitroxide antioxidant. Free Radic Biol Med; 2006 Sep 15;41(6):992-1000
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Mutations in the ATM gene (mutated in ataxia telangiectasia) in both humans and mice predispose to lymphoid tumors.
  • These data suggest that antioxidant therapy has considerable potential in the management of ataxia telangiectasia and possibly other neurodegenerative disorders where oxidative stress is implicated.
  • [MeSH-major] Antioxidants / therapeutic use. Ataxia Telangiectasia / genetics. Behavior, Animal / drug effects. Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Indoles / therapeutic use. Lymphoma / genetics. Mutation. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Animals. Apoptosis. Ataxia Telangiectasia Mutated Proteins. Cell Line, Tumor. Disease Models, Animal. Genotype. Humans. Mice. Mice, Knockout. Mice, Mutant Strains. Motor Activity / drug effects. Polymerase Chain Reaction. Precursor Cell Lymphoblastic Leukemia-Lymphoma


5. Williams RT, Roussel MF, Sherr CJ: Arf gene loss enhances oncogenicity and limits imatinib response in mouse models of Bcr-Abl-induced acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2006 Apr 25;103(17):6688-93
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  • [Title] Arf gene loss enhances oncogenicity and limits imatinib response in mouse models of Bcr-Abl-induced acute lymphoblastic leukemia.
  • Mouse bone marrow cells transduced with retroviral vectors encoding either of two oncogenic Bcr-Abl isoforms (p210(Bcr-Abl) and p185(Bcr-Abl)) induce B cell lympholeukemias when transplanted into lethally irradiated mice.
  • When mouse bone marrow cells expressing Bcr-Abl are placed in short-term cultures selectively designed to support the outgrowth of pre-B cells, only those lacking one or two Arf alleles can initiate lympholeukemias when inoculated into immunocompetent, syngeneic recipient mice.
  • Although the ABL kinase inhibitor imatinib mesylate (Gleevec) provides highly effective treatment for BCR-ABL-positive chronic myelogenous leukemia, it has proven far less efficacious in the treatment of BCR-ABL-positive acute lymphoblastic leukemias (ALLs), many of which sustain deletions of the INK4A-ARF (CDKN2A) tumor suppressor locus.
  • Mice receiving Arf-/- or Arf+/- p210(Bcr-Abl)-positive pre-B cells do not achieve remission when maintained on high doses of oral imatinib therapy and rapidly succumb to lympholeukemia.
  • Treatment of Arf-/-, p210(Bcr-Abl)-positive pre-B cells with imatinib together with an inhibitor of JAK kinases abrogates this resistance, suggesting that this combination may prove beneficial in the treatment of BCR-ABL-positive acute lymphoblastic leukemia.

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  • (PMID = 16618932.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA070089; United States / NCI NIH HHS / CA / P01 CA071907; United States / NCI NIH HHS / CA / T32-CA70089; United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA-71907
  • [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 / Benzamides; 0 / Cdkn2a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Interleukin-7; 0 / Piperazines; 0 / Pyrimidines; 0 / Tumor Suppressor Protein p14ARF; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC1440588
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6. Schmidt S, Rainer J, Riml S, Ploner C, Jesacher S, Achmüller C, Presul E, Skvortsov S, Crazzolara R, Fiegl M, Raivio T, Jänne OA, Geley S, Meister B, Kofler R: Identification of glucocorticoid-response genes in children with acute lymphoblastic leukemia. Blood; 2006 Mar 1;107(5):2061-9
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  • [Title] Identification of glucocorticoid-response genes in children with acute lymphoblastic leukemia.
  • The ability of glucocorticoids (GCs) to kill lymphoid cells led to their inclusion in essentially all chemotherapy protocols for lymphoid malignancies, particularly childhood acute lymphoblastic leukemia (ALL).
  • Here, we present a comparative whole-genome expression profiling approach using lymphoblasts (purified at 3 time points) from 13 GC-sensitive children undergoing therapy for ALL.
  • For comparisons, expression profiles were generated from an adult patient with ALL, peripheral blood lymphocytes from GC-exposed healthy donors, GC-sensitive and -resistant ALL cell lines, and mouse thymocytes treated with GCs in vivo and in vitro.
  • [MeSH-major] Apoptosis / drug effects. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Leukemic / drug effects. Glucocorticoids / pharmacology. Neoplasm Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [ErratumIn] Blood. 2007 Apr 15;109(8):3234
  • (PMID = 16293608.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Neoplasm Proteins
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7. Bosly A, Keating MJ, Stasi R, Bradstock K: Rituximab in B-cell disorders other than non-Hodgkin's lymphoma. Anticancer Drugs; 2002 Nov;13 Suppl 2:S25-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rituximab in B-cell disorders other than non-Hodgkin's lymphoma.
  • Rituximab is a human/mouse chimeric monoclonal antibody that binds to the CD20 antigen and is expressed at all stages of B-cell development.
  • Rituximab has demonstrated efficacy as monotherapy and in combination with chemotherapy in the treatment of both indolent and aggressive non-Hodgkin's lymphoma (NHL).
  • Rituximab treatment results in rapid depletion of B-cells and this has led to the consideration of other B-cell disorders as candidates for rituximab therapy.
  • Recent studies have demonstrated the efficacy of rituximab in a variety of such disorders, including chronic lymphocytic leukemia (CLL), post-transplant lymphoproliferative disorder (PTLD), Waldenström's macroglobulinemia (WM), multiple myeloma (MM), idiopathic thrombocytopenic purpura (ITP), hairy-cell leukemia (HCL) and cold agglutinin disease (CAD).
  • In patients with CLL, increasing the dose and/or frequency of rituximab treatment has given improved response rates compared with the standard dose schedule used in NHL, and combination immunochemotherapy has yielded an overall response rate of 92% (with a 60% complete response rate).
  • Available data thus indicate that rituximab can be an effective therapy in a wide range of CD20+ lymphoid disorders.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. B-Lymphocytes / pathology. Hematologic Diseases / drug therapy. Lymphoproliferative Disorders / drug therapy
  • [MeSH-minor] Anemia, Hemolytic, Autoimmune / drug therapy. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Organ Transplantation / adverse effects. Paraproteinemias / drug therapy. Purpura, Thrombocytopenic, Idiopathic / drug therapy. Rituximab

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  • [CommentIn] Curr Rheumatol Rep. 2003 Oct;5(5):381-2 [12967521.001]
  • (PMID = 12710588.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 43
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8. Bustuoabad OD, di Gianni PD, Franco M, Kordon EC, Vanzulli SI, Meiss RP, Grion LC, Díaz GS, Nosetto SH, Hockl P, Lombardi MG, Pasqualini CD, Ruggiero RA: Embryonal mass and hormone-associated effects of pregnancy inducing a differential growth of four murine tumors. Oncol Res; 2002;13(3):147-60
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  • Two tumors lacking receptors for progesterone and estrogen [methylcholanthrene-induced fibrosarcoma (MC-C) and spontaneous lymphoid leukemia (LB)] exhibited slow kinetics throughout the course of pregnancy, although inhibition was stronger beyond day 10.
  • The other tumor [mouse mammary tumor virus (MMTV)-induced mammary carcinoma(T2280)] behaved as a typical pregnancy-dependent tumor (i.e., it grew in pregnant but not in virgin mice, regressed soon after delivery, and reassumed its growth at the middle of a second round of pregnancy).
  • As for T2280, neither MPA nor estrogen alone could promote tumor growth and, in consequence, no tumor developed.
  • When the four tumors were implanted in mice bearing grafts of embryonal tissues (teratomas), all of them were inhibited.
  • [MeSH-major] Hormones / physiology. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / physiopathology. Pregnancy Complications, Neoplastic / physiopathology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adenocarcinoma / physiopathology. Animals. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Cell Division / drug effects. Cell Division / physiology. Estrogens / pharmacology. Female. Fibrosarcoma / drug therapy. Fibrosarcoma / pathology. Fibrosarcoma / physiopathology. Indomethacin / pharmacology. Leukemia, Lymphoid / drug therapy. Leukemia, Lymphoid / pathology. Leukemia, Lymphoid / physiopathology. Male. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / pathology. Mammary Neoplasms, Experimental / physiopathology. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Neovascularization, Pathologic. Pregnancy. Progesterone / metabolism. Progesterone / pharmacology. Receptors, Progesterone / metabolism. Teratoma / pathology. Teratoma / physiopathology

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  • (PMID = 12549624.001).
  • [ISSN] 0965-0407
  • [Journal-full-title] Oncology research
  • [ISO-abbreviation] Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Estrogens; 0 / Hormones; 0 / Receptors, Progesterone; 4G7DS2Q64Y / Progesterone; XXE1CET956 / Indomethacin
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9. Medyouf H, Ghysdael J: The calcineurin/NFAT signaling pathway: a novel therapeutic target in leukemia and solid tumors. Cell Cycle; 2008 Feb 1;7(3):297-303
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  • [Title] The calcineurin/NFAT signaling pathway: a novel therapeutic target in leukemia and solid tumors.
  • Deregulation of calcineurin/NFAT signaling and/or abnormal expression of its components have recently been reported in solid tumors of epithelial origin, lymphoma and lymphoid leukemia.
  • Our studies in mouse models of human T-ALL/lymphoma shows that persistent activation of calcineurin/NFAT signaling is pro-oncogenic in vivo and can be efficiently targeted by well-characterized calcineurin inhibitors.
  • We further discuss facts and hypotheses concerning the molecular events that may act upstream and downstream of calcineurin and/or NFAT activation in different type of cancer cells.
  • [MeSH-major] Calcineurin / metabolism. Drug Delivery Systems / methods. Leukemia / metabolism. NFATC Transcription Factors / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Calcineurin Inhibitors. Humans. Neoplasms / drug therapy. Neoplasms / genetics. Neoplasms / metabolism

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  • (PMID = 18235236.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [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 / Calcineurin Inhibitors; 0 / NFATC Transcription Factors; EC 3.1.3.16 / Calcineurin
  • [Number-of-references] 76
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10. Zhang B, Groffen J, Heisterkamp N: Resistance to farnesyltransferase inhibitors in Bcr/Abl-positive lymphoblastic leukemia by increased expression of a novel ABC transporter homolog ATP11a. Blood; 2005 Aug 15;106(4):1355-61
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  • [Title] Resistance to farnesyltransferase inhibitors in Bcr/Abl-positive lymphoblastic leukemia by increased expression of a novel ABC transporter homolog ATP11a.
  • Resistance to cytotoxic drugs frequently emerges during treatment of leukemia with conventional chemotherapy.
  • New classes of anticancer drugs, such as the farnesyltransferase inhibitors (FTIs), show therapeutic promise, but whether cells will easily develop resistance against them is not known.
  • Here, we grew breakpoint cluster region/Abelson murine leukemia (Bcr/Abl) P190 lymphoblasts on stroma and made them resistant to the FTI SCH66336/lonafarnib to model emerging drug resistance in a patient.
  • We showed that overexpression of this gene provided protection against the effects of SCH66336, whereas knockdown of endogenous ATP11a using small interfering RNA (siRNA) made cells more sensitive to this drug.
  • Our results show that elevated levels of ATP11a can protect malignant lymphoblastic leukemia cells against several novel small molecule signal transduction inhibitors.
  • A determination of the expression levels of this gene may have prognostic value when treatment with such classes of drugs is contemplated.
  • [MeSH-major] ATP-Binding Cassette Transporters / physiology. Alkyl and Aryl Transferases / antagonists & inhibitors. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Leukemia, Lymphoid / pathology
  • [MeSH-minor] Animals. Benzamides. Coculture Techniques. Enzyme Inhibitors / therapeutic use. Farnesyltranstransferase. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. Mice. Piperazines / pharmacology. Pyrimidines / pharmacology. RNA, Small Interfering / pharmacology. Tumor Cells, Cultured. Vincristine / pharmacology

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  • (PMID = 15860663.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA90321
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATP-Binding Cassette Transporters; 0 / Atp11a protein, mouse; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Small Interfering; 5J49Q6B70F / Vincristine; 8A1O1M485B / Imatinib Mesylate; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC1895195
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11. Medyouf H, Alcalde H, Berthier C, Guillemin MC, dos Santos NR, Janin A, Decaudin D, de Thé H, Ghysdael J: Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia. Nat Med; 2007 Jun;13(6):736-41
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  • [Title] Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia.
  • We observed sustained calcineurin activation in human B- and T-cell lymphomas and in all mouse models of lymphoid malignancies analyzed.
  • In intracellular NOTCH1 (ICN1)- and TEL-JAK2-induced T-cell lymphoblastic leukemia, two mouse models relevant to human malignancies, in vivo inhibition of calcineurin activity by CsA or FK506 induced apoptosis of leukemic cells and rapid tumor clearance, and substantially prolonged mouse survival.
  • In contrast, ectopic expression of a constitutively activated mutant of calcineurin favored leukemia progression.
  • Moreover, CsA treatment induced apoptosis in human lymphoma and leukemia cell lines.
  • Thus, calcineurin activation is critical for the maintenance of the leukemic phenotype in vivo, identifying this pathway as a relevant therapeutic target in lymphoid malignancies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Calcineurin / metabolism. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / enzymology
  • [MeSH-minor] Animals. Calcineurin Inhibitors. Cell Line, Tumor. Cyclosporine / pharmacology. Disease Models, Animal. Enzyme Activation / drug effects. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / enzymology. Lymphoma, B-Cell / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Oncogene Proteins, Fusion / deficiency. Oncogene Proteins, Fusion / genetics. Receptor, Notch1 / physiology. Tacrolimus / pharmacology

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  • [CommentIn] Nat Med. 2007 Jun;13(6):669-71 [17554330.001]
  • (PMID = 17515895.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Calcineurin Inhibitors; 0 / NOTCH1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; 0 / TEL-JAK2 fusion protein, mouse; 83HN0GTJ6D / Cyclosporine; EC 3.1.3.16 / Calcineurin; WM0HAQ4WNM / Tacrolimus
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12. DiJoseph JF, Armellino DC, Boghaert ER, Khandke K, Dougher MM, Sridharan L, Kunz A, Hamann PR, Gorovits B, Udata C, Moran JK, Popplewell AG, Stephens S, Frost P, Damle NK: Antibody-targeted chemotherapy with CMC-544: a CD22-targeted immunoconjugate of calicheamicin for the treatment of B-lymphoid malignancies. Blood; 2004 Mar 1;103(5):1807-14
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  • [Title] Antibody-targeted chemotherapy with CMC-544: a CD22-targeted immunoconjugate of calicheamicin for the treatment of B-lymphoid malignancies.
  • Antibody-targeted chemotherapy with gemtuzumab ozogamicin (CMA-676, a CD33-targeted immunoconjugate of N-acetyl-gamma-calicheamicin dimethyl hydrazide [CalichDMH], a potent DNA-binding cytotoxic antitumor antibiotic) is a clinically validated therapeutic option for patients with acute myeloid leukemia (AML).
  • Here, we describe the preclinical profile of another immunoconjugate of CalichDMH, CMC-544, targeted to CD22 expressed by B-lymphoid malignancies.
  • CMC-544 caused a potent inhibition of growth of small but established BCL xenografts leading to cures (therapeutic index > 10).
  • Thus, CD22-targeted delivery of CalichDMH is a potent and effective preclinical therapeutic strategy for BCLs.
  • The strong antitumor profile of CMC-544 supports its clinical evaluation as a treatment option for B-lymphoid malignancies.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD / biosynthesis. Antigens, Differentiation, B-Lymphocyte / biosynthesis. Cell Adhesion Molecules. Immunoconjugates / therapeutic use. Lectins / biosynthesis. Lymphoma, B-Cell / therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Female. Humans. Immunoglobulin G / metabolism. Immunotherapy / methods. Inhibitory Concentration 50. Lymphoma, Non-Hodgkin / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Models, Chemical. Neoplasm Transplantation. Protein Binding. Sialic Acid Binding Ig-like Lectin 2. Time Factors

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  • (PMID = 14615373.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, B-Lymphocyte; 0 / Antineoplastic Agents; 0 / CD22 protein, human; 0 / Cd22 protein, mouse; 0 / Cell Adhesion Molecules; 0 / Immunoconjugates; 0 / Immunoglobulin G; 0 / Inotuzumab Ozogamicin; 0 / Lectins; 0 / Sialic Acid Binding Ig-like Lectin 2
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13. Wei G, Twomey D, Lamb J, Schlis K, Agarwal J, Stam RW, Opferman JT, Sallan SE, den Boer ML, Pieters R, Golub TR, Armstrong SA: Gene expression-based chemical genomics identifies rapamycin as a modulator of MCL1 and glucocorticoid resistance. Cancer Cell; 2006 Oct;10(4):331-42
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  • Drug resistance remains a major obstacle to successful cancer treatment.
  • A database of drug-associated gene expression profiles was screened for molecules whose profile overlapped with a gene expression signature of glucocorticoid (GC) sensitivity/resistance in acute lymphoblastic leukemia (ALL) cells.
  • We tested the hypothesis that rapamycin would induce GC sensitivity in lymphoid malignancy cells and found that it sensitized to GC-induced apoptosis via modulation of antiapoptotic MCL1.
  • These data indicate that MCL1 is an important regulator of GC-induced apoptosis and that the combination of rapamycin and glucocorticoids has potential utility in lymphoid malignancies.
  • Furthermore, this approach represents a strategy for identification of promising combination therapies for cancer.
  • [MeSH-major] Gene Expression / drug effects. Genomics. Glucocorticoids / pharmacology. Neoplasm Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Sirolimus / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Databases, Genetic. Dexamethasone / pharmacology. Dose-Response Relationship, Drug. Drug Combinations. Drug Resistance, Neoplasm. Green Fluorescent Proteins / metabolism. Humans. Mice. Myeloid Cell Leukemia Sequence 1 Protein. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • [CommentIn] Cancer Cell. 2006 Nov;10(5):349-51 [17097556.001]
  • (PMID = 17010674.001).
  • [ISSN] 1535-6108
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE5258/ GSE5820/ GSE5821/ GSE5822
  • [Grant] United States / NCI NIH HHS / CA / K08 CA92551; United States / NCI NIH HHS / CA / P01 CA068484
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Glucocorticoids; 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 147336-22-9 / Green Fluorescent Proteins; 7S5I7G3JQL / Dexamethasone; W36ZG6FT64 / Sirolimus
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14. Plosker GL, Figgitt DP: Rituximab: a review of its use in non-Hodgkin's lymphoma and chronic lymphocytic leukaemia. Drugs; 2003;63(8):803-43
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  • [Title] Rituximab: a review of its use in non-Hodgkin's lymphoma and chronic lymphocytic leukaemia.
  • Rituximab is an anti-CD20 monoclonal antibody that has demonstrated efficacy in patients with various lymphoid malignancies, including indolent and aggressive forms of B-cell non-Hodgkin's lymphoma (NHL) and B-cell chronic lymphocytic leukaemia (CLL).
  • While the optimal use of the drug in many clinical settings has yet to be clarified, two pivotal trials have established rituximab as a viable treatment option in patients with relapsed or refractory indolent NHL, and as a standard first-line treatment option when combined with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy in elderly patients with diffuse large B-cell lymphoma (the most common type of aggressive NHL).
  • Treatment with rituximab is generally well tolerated, particularly in terms of adverse haematological effects and serious or opportunistic infections relative to standard chemotherapy.
  • CONCLUSIONS: Clinical trials with rituximab indicate that the drug has broad application to B-cell malignancies, although further clarification is needed to determine its optimal use in many of these clinical settings.
  • Importantly, rituximab in combination with CHOP chemotherapy has emerged as a new treatment standard for previously untreated diffuse large B-cell lymphoma, at least in elderly patients.
  • Compared with conventional chemotherapy, rituximab is associated with markedly reduced haematological events such as severe neutropenia, as well as associated infections.
  • Rituximab may be particularly suitable for elderly patients or those with poor performance status, and its tolerability profile facilitates its use in combination with cytotoxic drugs.
  • PHARMACODYNAMIC PROPERTIES: Rituximab is a mouse/human chimaeric IgG(1)-kappa monoclonal antibody that targets the CD20 antigen found on the surface of malignant and normal B lymphocytes.
  • Although treatment with rituximab induces lymphopenia in most patients, typically lasting about 6 months, a full recovery of B lymphocytes in the peripheral blood is usually seen 9-12 months after therapy, as CD20 is not expressed on haematopoietic stem cells.
  • CD20 is, however, expressed on >90% of B-cell non-Hodgkin's lymphomas (NHL) and to a lesser degree on B-cell chronic lymphocytic leukaemia (CLL) cells.
  • In addition, in vitro data indicate that rituximab sensitises tumour cells to the effects of conventional chemotherapeutic drugs.
  • The pharmacokinetic properties of rituximab are also characterised by wide inter-individual variability, and serum drug concentrations that are correlated with clinical response.
  • The pharmacokinetics of rituximab are also reported to be similar whether the drug is administered with or without cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy.
  • THERAPEUTIC USE: A number of studies have demonstrated efficacy of intravenous rituximab in patients with various lymphoid malignancies of B-cell origin, including indolent (e.g. follicular lymphoma) and aggressive (e.g. diffuse large B-cell lymphoma) forms of NHL, and CLL, but the drug has not yet been approved for use in CLL, and approved indications in NHL vary between countries.
  • In the US, for example, rituximab is available for the treatment of patients with low-grade or follicular, relapsed or refractory, CD20-positive B-cell NHL.
  • In Europe, the drug has similar approval for relapsed or refractory follicular NHL as in the US, but has also been approved for use in combination with CHOP chemotherapy for the most common aggressive form of NHL (CD20-positive, diffuse large B-cell lymphoma).
  • Indolent NHL: Results of several studies evaluating rituximab 375 mg/m(2) once weekly for 4 weeks in patients with indolent forms of B-cell NHL (primarily follicular and small lymphocytic lymphomas) showed objective response (OR) rates ranging from approximately 40-60% in those receiving the drug for relapsed or refractory indolent B-cell NHL, and slightly higher (50-70%) for those receiving rituximab as first-line therapy.
  • In a pivotal trial in 166 patients with relapsed or refractory low-grade or follicular B-cell NHL, intent-to-treat (ITT) analysis showed an OR rate of 48%, and a projected median time to progression of 13 months.
  • CHOP, fludarabine-containing regimens) or other drugs (e.g. interferon-alpha2a) in previously untreated patients with indolent forms of B-cell NHL (primarily follicular and small lymphocytic subtypes).
  • Follow-up data from a study in 40 patients with low-grade or follicular B-cell NHL treated with rituximab plus CHOP as first-line therapy showed that responses were durable with a progression-free survival and median duration of response >5 years.Bcl-2 gene rearrangement (t14;18) occurs in malignant cells in up to 85% of patients with follicular lymphoma, and minimal residual disease in peripheral blood and bone marrow can be monitored using polymerase chain reaction (PCR).
  • Aggressive NHL: Studies with rituximab as monotherapy in aggressive B-cell NHL, a potentially curable disorder, have generally been restricted to patients with relapsed or recurrent disease, since CHOP has traditionally been the standard first-line treatment regimen.
  • However, promising results from phase II monotherapy studies prompted further clinical investigation of rituximab in conjunction with chemotherapy.
  • Thus, most studies with rituximab in patients with aggressive forms of B-cell NHL have involved combination therapy, including a pivotal randomised trial comparing eight cycles of standard CHOP therapy plus rituximab 375 mg/m(2) (one dose per cycle) versus CHOP alone in 399 previously untreated elderly patients (60-80 years of age) with diffuse large B-cell lymphoma.
  • Other, smaller trials with rituximab in combination with CHOP or other chemotherapeutic regimens, either as first-line therapy or for patients with relapsed or refractory aggressive B-cell NHL, have also shown promising results in terms of clinical response rates.CLL: In relatively small trials (n < 40) conducted primarily in patients with relapsed or refractory B-cell CLL, rituximab monotherapy (various regimens) achieved OR rates of 23-45%, with median duration of response ranging from approximately 3-10 months. (ABSTRACT TRUNCATED)
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic. Drug Administration Schedule. Humans. Rituximab

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  • (PMID = 12662126.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 177
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15. Hoelbl A, Schuster C, Kovacic B, Zhu B, Wickre M, Hoelzl MA, Fajmann S, Grebien F, Warsch W, Stengl G, Hennighausen L, Poli V, Beug H, Moriggl R, Sexl V: Stat5 is indispensable for the maintenance of bcr/abl-positive leukaemia. EMBO Mol Med; 2010 Mar;2(3):98-110
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  • A key to successful cancer therapy is the identification of critical functional nodes in an oncogenic network required for disease maintenance.
  • However, to qualify as a potential drug target, a signalling pathway must be required for the maintenance of the leukaemic state.
  • Accordingly, Stat5-abrogation led to effective elimination of myeloid and lymphoid leukaemia maintenance in vivo.
  • Hence, we identified Stat5 as a vulnerable point in the oncogenic network downstream of Bcr/Abl representing a case of non-oncogene addiction (NOA).
  • [MeSH-major] Leukemia / physiopathology. STAT3 Transcription Factor / metabolism. STAT5 Transcription Factor / metabolism

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  • (PMID = 20201032.001).
  • [ISSN] 1757-4684
  • [Journal-full-title] EMBO molecular medicine
  • [ISO-abbreviation] EMBO Mol Med
  • [Language] eng
  • [Grant] Austria / Austrian Science Fund FWF / / F 2807; Austria / Austrian Science Fund FWF / / F 2810
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / STAT3 Transcription Factor; 0 / STAT5 Transcription Factor; EC 2.7.11.1 / Bcr protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
  • [Other-IDs] NLM/ PMC2906698; NLM/ UKMS30451
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16. Hu Y, Liu Y, Pelletier S, Buchdunger E, Warmuth M, Fabbro D, Hallek M, Van Etten RA, Li S: Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia. Nat Genet; 2004 May;36(5):453-61
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  • [Title] Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia.
  • The Abl kinase inhibitor imatinib mesylate is the preferred treatment for Philadelphia chromosome-positive (Ph(+)) chronic myeloid leukemia (CML) in chronic phase but is much less effective in CML blast crisis or Ph(+) B-cell acute lymphoblastic leukemia (B-ALL).
  • Here, we show that Bcr-Abl activated the Src kinases Lyn, Hck and Fgr in B-lymphoid cells.
  • The kinase inhibitor CGP76030 impaired the proliferation of B-lymphoid cells expressing Bcr-Abl in vitro and prolonged survival of mice with B-ALL but not CML.
  • The biochemical target of CGP76030 in leukemia cells was Src kinases, not Bcr-Abl.
  • These results implicate Src family kinases as therapeutic targets in Ph(+) B-ALL and suggest that simultaneous inhibition of Src and Bcr-Abl kinases may benefit individuals with Ph(+) acute leukemia.
  • [MeSH-major] Burkitt Lymphoma / enzymology. Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. src-Family Kinases / physiology
  • [MeSH-minor] Animals. Benzamides. Cell Division / drug effects. Drug Therapy, Combination. Enzyme Activation. Enzyme Inhibitors / pharmacology. Humans. Imatinib Mesylate. Male. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Knockout. Piperazines / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / physiology. Proto-Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins / physiology. Proto-Oncogene Proteins c-hck. Pyrimidines / pharmacology. Pyrroles / pharmacology


17. Williams RT, Sherr CJ: The ARF tumor suppressor in acute leukemias: insights from mouse models of Bcr-Abl-induced acute lymphoblastic leukemia. Adv Exp Med Biol; 2007;604:107-14
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  • [Title] The ARF tumor suppressor in acute leukemias: insights from mouse models of Bcr-Abl-induced acute lymphoblastic leukemia.
  • The constitutive tyrosine kinase transforms either hematopoietic stem cells (in CML) or committed pre-B lymphoid progenitors (in Ph+ ALL) to generate these distinct diseases.
  • In murine bone marrow transplant models and after transfer of syngeneic Bcr-Abl-transformed pre-B cells into immunocompetent recipient animals, Arf gene inactivation dramatically decreases the latency and enhances the aggressiveness of Bcr-Abl-induced lymphoblastic leukemia.
  • Targeted inhibition of the Bcr-Abl kinase with imatinib provides highly effective therapy for CML, but Ph+ ALL patients do not experience durable remissions.
  • Despite exquisite in vitro sensitivity of Arf-null, BCR-ABL+ pre-B cells to imatinib, these cells efficiently establish lethal leukemias when introduced into immunocompetent mice that receive continuous, maximal imatinib therapy.
  • Bcr-Abl confers interleukin-7 (IL-7) independence to pre-B cells, but imatinib treatment restores the requirement for this cytokine.
  • [MeSH-major] Fusion Proteins, bcr-abl / metabolism. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Tumor Suppressor Protein p14ARF / physiology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Benzamides. Disease Models, Animal. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Interleukin-7 / metabolism. Mice. Piperazines / pharmacology. Pyrimidines / pharmacology

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  • (PMID = 17695724.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32-CA70089
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interleukin-7; 0 / Piperazines; 0 / Pyrimidines; 0 / Tumor Suppressor Protein p14ARF; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 20
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18. Eguchi M, Eguchi-Ishimae M, Greaves M: The role of the MLL gene in infant leukemia. Int J Hematol; 2003 Dec;78(5):390-401
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The role of the MLL gene in infant leukemia.
  • The MLL gene is a major player in leukemia, particularly in infant leukemia and in secondary, therapy-related acute leukemia.
  • The normal MLL gene plays a key role in developmental regulation of gene expression (including HOX genes), and in leukemia this function is subverted by breakage, recombination, and chimeric fusion with one of 40 or more alternative partner genes.
  • These data raise fundamental issues of how such divergent MLL chimeric genes transform cells, why they so rapidly evolve to a malignant status, and what alternative or novel therapeutic strategies might be considered.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Proto-Oncogenes. Transcription Factors
  • [MeSH-minor] Acute Disease. Age of Onset. Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Disease Progression. Drug Design. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Mice. Mice, Knockout. Myeloid-Lymphoid Leukemia Protein. Oligonucleotide Array Sequence Analysis. Oncogene Proteins, Fusion / chemistry. Oncogene Proteins, Fusion / genetics. Structure-Activity Relationship. Translocation, Genetic

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  • (PMID = 14704031.001).
  • [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; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse
  • [Number-of-references] 125
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19. Bachmann PS, Piazza RG, Janes ME, Wong NC, Davies C, Mogavero A, Bhadri VA, Szymanska B, Geninson G, Magistroni V, Cazzaniga G, Biondi A, Miranda-Saavedra D, Göttgens B, Saffery R, Craig JM, Marshall GM, Gambacorti-Passerini C, Pimanda JE, Lock RB: Epigenetic silencing of BIM in glucocorticoid poor-responsive pediatric acute lymphoblastic leukemia, and its reversal by histone deacetylase inhibition. Blood; 2010 Oct 21;116(16):3013-22
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  • [Title] Epigenetic silencing of BIM in glucocorticoid poor-responsive pediatric acute lymphoblastic leukemia, and its reversal by histone deacetylase inhibition.
  • Glucocorticoids play a critical role in the therapy of lymphoid malignancies, including pediatric acute lymphoblastic leukemia (ALL), although the mechanisms underlying cellular resistance remain unclear.
  • We report glucocorticoid resistance attributable to epigenetic silencing of the BIM gene in pediatric ALL biopsies and xenografts established in immune-deficient mice from direct patient explants as well as a therapeutic approach to reverse resistance in vivo.
  • These findings provide a novel therapeutic strategy to reverse glucocorticoid resistance and improve outcome for high-risk pediatric ALL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis Regulatory Proteins / genetics. Drug Resistance, Neoplasm. Gene Silencing. Glucocorticoids / therapeutic use. Histone Deacetylase Inhibitors / therapeutic use. Membrane Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics
  • [MeSH-minor] Animals. Antineoplastic Agents, Hormonal / pharmacology. Antineoplastic Agents, Hormonal / therapeutic use. Bcl-2-Like Protein 11. Child. Dexamethasone / pharmacology. Dexamethasone / therapeutic use. Genetic Loci. Histone Deacetylases / metabolism. Humans. Hydroxamic Acids / pharmacology. Hydroxamic Acids / therapeutic use. Mice. Mice, SCID

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  • (PMID = 20647567.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0800784; United Kingdom / National Centre for the Replacement, Refinement and Reduction of Animals in Research / / G0900729/1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Apoptosis Regulatory Proteins; 0 / BCL2L11 protein, human; 0 / Bcl-2-Like Protein 11; 0 / Bcl2l11 protein, mouse; 0 / Glucocorticoids; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 58IFB293JI / vorinostat; 7S5I7G3JQL / Dexamethasone; EC 3.5.1.98 / Histone Deacetylases
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20. Mori M, Terui Y, Tanaka M, Tomizuka H, Mishima Y, Ikeda M, Kasahara T, Uwai M, Ueda M, Inoue R, Itoh T, Yamada M, Hayasawa H, Furukawa Y, Ishizaka Y, Ozawa K, Hatake K: Antitumor effect of beta2-microglobulin in leukemic cell-bearing mice via apoptosis-inducing activity: activation of caspase-3 and nuclear factor-kappaB. Cancer Res; 2001 Jun 1;61(11):4414-7
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  • Daily administration of 50 or 250 microg of beta2m induced apoptosis and an antitumor effect on K562 leukemia cell-bearing mice in the same manner as tumor necrosis factor-alpha.
  • In tumor tissues in beta2m-treated mice, both caspase-3 and nuclear factor-kappaB (NF-kappaB) were stained more strongly than in control mice by anti-caspase-3 and anti-NF-kappaB p65/Rel A polyclonal antibodies.
  • We also observed the in vivo immunological effects of beta2m on lymphoid and hematopoietic organs, such as thymus, bone marrow, Peyer's patches, liver, and spleen in normal mice.
  • Using antibodies against caspase-3 and NF-kappaB, immunohistochemical staining showed that no specific tissues were damaged or stained in normal mice.
  • We conclude that beta2m stimulates caspase-3 and NF-kappaB pathways to induce apoptosis, making it a useful approach to a new therapy for leukemia.
  • [MeSH-major] Apoptosis / drug effects. Caspases / metabolism. NF-kappa B / biosynthesis. beta 2-Microglobulin / pharmacology
  • [MeSH-minor] Animals. Caspase 3. Cell Division / drug effects. Enzyme Activation. HL-60 Cells / cytology. HL-60 Cells / drug effects. HL-60 Cells / metabolism. Humans. In Situ Nick-End Labeling. K562 Cells / cytology. K562 Cells / drug effects. K562 Cells / metabolism. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Recombinant Proteins / pharmacology. Xenograft Model Antitumor Assays

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  • (PMID = 11389069.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Recombinant Proteins; 0 / beta 2-Microglobulin; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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21. Mishra S, Zhang B, Cunnick JM, Heisterkamp N, Groffen J: Resistance to imatinib of bcr/abl p190 lymphoblastic leukemia cells. Cancer Res; 2006 May 15;66(10):5387-93
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  • [Title] Resistance to imatinib of bcr/abl p190 lymphoblastic leukemia cells.
  • Around 20% of patients with acute lymphoblastic leukemia are Philadelphia chromosome positive (Ph-positive acute lymphoblastic leukemia) and express the Bcr/Abl tyrosine kinase.
  • Treatment with the tyrosine kinase inhibitor Imatinib is currently standard for chronic myelogenous leukemia, which is also caused by Bcr/Abl.
  • However, Imatinib has shown limited efficacy for treating Ph-positive acute lymphoblastic leukemia.
  • In our study, we have investigated the effect of Imatinib therapy on murine P190 Bcr/Abl lymphoblastic leukemia cells.
  • Three of four cultures were very sensitive to treatment with 5 mumol/L Imatinib.
  • The Bcr/Abl tyrosine kinase present in the cells that were now able to multiply in the presence of 5 mumol/L Imatinib was still inhibited by the drug.
  • Therefore, therapy for Ph-positive acute lymphoblastic leukemia, aimed at interfering with the protective effect of stroma in combination with Imatinib, could be of benefit for the eradication of the leukemic cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Fusion Proteins, bcr-abl / biosynthesis. Leukemia, Lymphoid / drug therapy. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Benzamides. Cell Line, Tumor. Chemokine CXCL12. Chemokines, CXC / administration & dosage. Chemokines, CXC / pharmacology. Drug Resistance, Neoplasm. Female. Humans. Imatinib Mesylate. Mice. Mice, Nude. Point Mutation. Protein Structure, Tertiary. Stromal Cells / pathology

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  • (PMID = 16707466.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 90321
  • [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 / Benzamides; 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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22. Paoluzzi L, Gonen M, Bhagat G, Furman RR, Gardner JR, Scotto L, Gueorguiev VD, Heaney ML, Manova K, O'Connor OA: The BH3-only mimetic ABT-737 synergizes the antineoplastic activity of proteasome inhibitors in lymphoid malignancies. Blood; 2008 Oct 1;112(7):2906-16
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  • [Title] The BH3-only mimetic ABT-737 synergizes the antineoplastic activity of proteasome inhibitors in lymphoid malignancies.
  • Overexpression of antiapoptotic members of the Bcl-2 family is observed in approximately 80% of B-cell lymphomas, contributing to intrinsic and acquired drug resistance.
  • Nullifying the antiapoptotic influence of these proteins can potentially overcome this resistance, and may complement conventional chemotherapy.
  • ABT-737 plus bortezomib also induced significant apoptosis in primary samples of MCL, DLBCL, and chronic lymphocytic leukemia (CLL) but no significant cytotoxic effect was observed in peripheral blood mononuclear cells from healthy donors.
  • In severe combined immunodeficient beige mouse models of MCL, the addition of ABT-737 to bortezomib enhanced efficacy compared with either drug alone and with the control.
  • Collectively, these data suggest that ABT-737 alone or in combination with a proteasome inhibitor represents a novel and potentially important platform for the treatment of B-cell malignancies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Biphenyl Compounds / pharmacology. Enzyme Inhibitors / pharmacology. Lymphoma / enzymology. Lymphoma / pathology. Molecular Mimicry / drug effects. Nitrophenols / pharmacology. Proteasome Inhibitors. Sulfonamides / pharmacology
  • [MeSH-minor] Animals. Boronic Acids / pharmacology. Bortezomib. Cell Death / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm / drug effects. Drug Synergism. Health. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukocytes, Mononuclear / drug effects. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Mantle-Cell / pathology. Membrane Potential, Mitochondrial / drug effects. Mice. Microscopy, Confocal. Piperazines / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Pyrazines / pharmacology. Tissue Donors. Xenograft Model Antitumor Assays

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  • (PMID = 18591385.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABT-737; 0 / Antineoplastic Agents; 0 / Biphenyl Compounds; 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Nitrophenols; 0 / Piperazines; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Sulfonamides; 69G8BD63PP / Bortezomib
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23. Malone MH, Wang Z, Distelhorst CW: The glucocorticoid-induced gene tdag8 encodes a pro-apoptotic G protein-coupled receptor whose activation promotes glucocorticoid-induced apoptosis. J Biol Chem; 2004 Dec 17;279(51):52850-9
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  • The apoptotic action of glucocorticoids on lymphocytes makes them effective therapeutics for many lymphoid malignancies.
  • Together, these data suggest that TDAG8 is a regulator of glucocorticoid-induced apoptosis and that agonists of TDAG8 may be promising agents to improve the efficacy of glucocorticoids for the treatment of leukemia and lymphoma.
  • [MeSH-minor] Algorithms. Animals. Blotting, Northern. Cell Line, Tumor. Dexamethasone / pharmacology. Dose-Response Relationship, Drug. Green Fluorescent Proteins / metabolism. Humans. Immunoblotting. Leukemia / drug therapy. Lymphocytes / pathology. Lymphoma / drug therapy. Mice. Microscopy, Fluorescence. Models, Chemical. Oligonucleotide Array Sequence Analysis. Psychosine / pharmacology. RNA Interference. Sphingosine / chemistry

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  • (PMID = 15485889.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA43703; United States / NCI NIH HHS / CA / R01 CA042755; United States / NCI NIH HHS / CA / T32 CA059366-10
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GPCR25 protein, mouse; 0 / GPR65 protein, human; 0 / Glucocorticoids; 0 / Receptors, G-Protein-Coupled; 147336-22-9 / Green Fluorescent Proteins; 2238-90-6 / Psychosine; 7S5I7G3JQL / Dexamethasone; NGZ37HRE42 / Sphingosine
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24. D'Costa S, Hurwitz JL: Customized mitogen or antibody treatments enhance the sensitivity of lymphoid tumors to 5-fluorouracil in vitro and in vivo. Leuk Lymphoma; 2003 May;44(5):841-7
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  • [Title] Customized mitogen or antibody treatments enhance the sensitivity of lymphoid tumors to 5-fluorouracil in vitro and in vivo.
  • Despite impressive cure rates for certain leukemias and lymphomas, lymphoid tumors are responsible for thousands of deaths per year.
  • Refractory disease remains difficult to control, encouraging the development of new treatment options.
  • 5-fluorouracil (5-FU) has been successfully used to control (or cure) a variety of tumors, but has been only rarely applied to tumors of the lymphoid lineage.
  • Here we demonstrate that the effects of 5-FU on lymphoid tumors can be enhanced by the concomitant binding of cellular membrane molecules with mitogen or antibody.
  • When used in combination with 5-FU, mitogen treatments: (i) enhance the association of drug with cells, (ii) reduce cell proliferation in vitro and (iii) inhibit cell growth in a mouse B-cell tumor model.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Fluorouracil / pharmacokinetics. Fluorouracil / therapeutic use. Lymphoma / drug therapy. Mitogens / pharmacology
  • [MeSH-minor] Animals. Antigens, CD40 / immunology. Cell Division / drug effects. Cell Membrane / metabolism. Drug Synergism. Lymphoma, B-Cell / drug therapy. Lymphoma, T-Cell / drug therapy. Mice. Mice, SCID. Tumor Cells, Cultured

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  • (PMID = 12802924.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30-CA21765; United States / NCI NIH HHS / CA / R01-CA57419
  • [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 / Antibodies, Monoclonal; 0 / Antigens, CD40; 0 / Mitogens; U3P01618RT / Fluorouracil
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25. D'Costa S, Slobod KS, Hurwitz JL: Do the immunosuppressive drugs used as treatment for graft-versus-host disease directly inhibit lymphoid tumor cell growth? Leuk Lymphoma; 2003 Jan;44(1):139-42
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  • [Title] Do the immunosuppressive drugs used as treatment for graft-versus-host disease directly inhibit lymphoid tumor cell growth?
  • Hematopoietic stem cell transplantation (HSCT) is a curative treatment for certain leukemias and lymphomas that prove resistant to standard chemotherapy.
  • The immunosuppressive drugs prednisone and cyclosporin A (CsA) are routinely used during HSCT to prevent or treat graft-versus-host disease (GVHD) or to inhibit antibody-mediated inflammation.
  • However, little is known about the direct impact of prednisone and CsA on the growth of malignant lymphoid cells in the setting of HSCT.
  • To address this issue, we measured tumor cell growth in vitro and in vivo after treatment with prednisone and CsA, used separately, together, and in combination with irradiation.
  • Our results showed that: (i) combinations of CsA and prednisone inhibited the growth of a variety of lymphoid tumors in vitro, particularly in combination with irradiation, and (ii) tumor size was significantly reduced in a mouse B-lymphoid tumor model following CsA or CsA plus prednisone treatments, with or without HSCT.
  • [MeSH-major] Graft vs Host Disease / drug therapy. Immunosuppressive Agents / pharmacology. Lymphoma / pathology. Lymphoma / therapy
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Division / drug effects. Cell Division / radiation effects. Cyclosporine / pharmacology. Cyclosporine / therapeutic use. Hematopoietic Stem Cell Transplantation / adverse effects. Hematopoietic Stem Cell Transplantation / methods. Humans. Mice. Mice, SCID. Prednisone / pharmacology. Prednisone / therapeutic use. Tumor Cells, Cultured

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  • (PMID = 12691154.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30-CA21765; United States / NCI NIH HHS / CA / R01-CA57419
  • [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 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; VB0R961HZT / Prednisone
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26. Ikezoe T, Yang Y, Bandobashi K, Saito T, Takemoto S, Machida H, Togitani K, Koeffler HP, Taguchi H: Oridonin, a diterpenoid purified from Rabdosia rubescens, inhibits the proliferation of cells from lymphoid malignancies in association with blockade of the NF-kappa B signal pathways. Mol Cancer Ther; 2005 Apr;4(4):578-86
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  • [Title] Oridonin, a diterpenoid purified from Rabdosia rubescens, inhibits the proliferation of cells from lymphoid malignancies in association with blockade of the NF-kappa B signal pathways.
  • This study found that oridonin, a natural diterpenoid purified from Rabdosia rubescens, inhibited growth of multiple myeloma (MM; U266, RPMI8226), acute lymphoblastic T-cell leukemia (Jurkat), and adult T-cell leukemia (MT-1) cells with an effective dose that inhibited 50% of target cells (ED50) ranging from 0.75 to 2.7 microg/mL.
  • Terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling staining showed that oridonin caused apoptosis of MT-1 cells in a time-dependent manner.
  • Of note, oridonin decreased survival of freshly isolated adult T-cell leukemia (three samples), acute lymphoblastic leukemia (one sample), chronic lymphocytic leukemia (one sample), non-Hodgkin's lymphoma (three samples), and MM (four samples) cells from patients in association with inhibition of NF-kappa B DNA-binding activity.
  • On the other hand, oridonin did not affect survival of normal lymphoid cells from healthy volunteers.
  • Taken together, oridonin might be useful as adjunctive therapy for individuals with lymphoid malignancies, including the lethal disease adult T-cell leukemia.
  • [MeSH-major] Cell Proliferation / drug effects. Diterpenes / pharmacology. Isodon / metabolism. NF-kappa B / metabolism. Phytotherapy / methods. Plant Extracts / pharmacology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Apoptosis. Blotting, Western. Cell Line. Cell Line, Tumor. Diterpenes, Kaurane. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Female. Genes, Reporter. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / metabolism. Humans. In Situ Nick-End Labeling. Jurkat Cells. Leukemia / drug therapy. Leukemia / pathology. Lipopolysaccharides / metabolism. Male. Mice. Middle Aged. Models, Chemical. Multiple Myeloma / drug therapy. Multiple Myeloma / pathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction. T-Lymphocytes / metabolism. T-Lymphocytes / virology. Thymidine / chemistry. Thymidine / metabolism. Time Factors. Transfection. Trypan Blue / pharmacology. bcl-X Protein

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  • (PMID = 15827331.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / Diterpenes; 0 / Diterpenes, Kaurane; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein; 0APJ98UCLQ / oridonin; I2ZWO3LS3M / Trypan Blue; VC2W18DGKR / Thymidine
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27. Li LX, Tang YM, Zhang HZ, Shen HQ, Qian BQ, Luo CF: [Preparation of the immunotoxin 2E8-norcantharidin and its targeting killing effect in vitro]. Zhonghua Er Ke Za Zhi; 2008 Jul;46(7):493-7
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  • OBJECTIVE: Monoclonal antibody (mAb) conjugated with certain toxin to generate immunotoxin bears an important and promising effect as a new therapy for patients with hematopoietic malignancies.
  • It does not have the immunogenicity to human body so that it bears a promising potential for development of new targeting drug.
  • In this study, a new clone of self-made anti-CD19 mAb named ZCH-4-2E8 conjugated with NCTD was used to investigate its targeting efficacy against CD19+ lymphoid malignant Nalm-6 cells in vitro to provide the experimental data for the further development of this new targeting agent.
  • METHODS: A monoclonal antibody named 2E8 was prepared from mouse ascites and purified by gel chromatography.
  • CONCLUSIONS: The immunotoxin 2E8-NCTD was successfully synthesized by activated ester method with an excellent targeting killing effect on CD19+ Nalm-6 leukemia cells in vitro, which provides some experimental data for the further development of this new targeting agent.

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  • (PMID = 19099803.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / Bicyclo Compounds, Heterocyclic; 0 / Immunotoxins; 5442-12-6 / norcantharidin
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28. Zuber J, Radtke I, Pardee TS, Zhao Z, Rappaport AR, Luo W, McCurrach ME, Yang MM, Dolan ME, Kogan SC, Downing JR, Lowe SW: Mouse models of human AML accurately predict chemotherapy response. Genes Dev; 2009 Apr 1;23(7):877-89
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  • [Title] Mouse models of human AML accurately predict chemotherapy response.
  • The genetic heterogeneity of cancer influences the trajectory of tumor progression and may underlie clinical variation in therapy response.
  • To model such heterogeneity, we produced genetically and pathologically accurate mouse models of common forms of human acute myeloid leukemia (AML) and developed methods to mimic standard induction chemotherapy and efficiently monitor therapy response.
  • We see that murine AMLs harboring two common human AML genotypes show remarkably diverse responses to conventional therapy that mirror clinical experience.
  • Specifically, murine leukemias expressing the AML1/ETO fusion oncoprotein, associated with a favorable prognosis in patients, show a dramatic response to induction chemotherapy owing to robust activation of the p53 tumor suppressor network.
  • Conversely, murine leukemias expressing MLL fusion proteins, associated with a dismal prognosis in patients, are drug-resistant due to an attenuated p53 response.
  • Our studies highlight the importance of genetic information in guiding the treatment of human AML, functionally establish the p53 network as a central determinant of chemotherapy response in AML, and demonstrate that genetically engineered mouse models of human cancer can accurately predict therapy response in patients.

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  • (PMID = 19339691.001).
  • [ISSN] 1549-5477
  • [Journal-full-title] Genes & development
  • [ISO-abbreviation] Genes Dev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA008748; United States / Howard Hughes Medical Institute / /
  • [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 / AML1-ETO fusion protein, human; 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 0 / Tumor Suppressor Protein p53; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2666344
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29. Hamaguchi Y, Xiu Y, Komura K, Nimmerjahn F, Tedder TF: Antibody isotype-specific engagement of Fcgamma receptors regulates B lymphocyte depletion during CD20 immunotherapy. J Exp Med; 2006 Mar 20;203(3):743-53
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  • In a mouse model of immunotherapy using mouse anti-mouse CD20 mAbs, the innate monocyte network depletes B cells through immunoglobulin (Ig)G Fc receptor (FcgammaR)-dependent pathways with a hierarchy of IgG2a/c>IgG1/IgG2b>IgG3.
  • Although FcgammaR-dependent pathways regulated B cell depletion from lymphoid tissues, both FcgammaR-dependent and -independent pathways contributed to mature bone marrow and circulating B cell clearance by CD20 mAbs.
  • Thus, isotype-specific mAb interactions with distinct FcgammaRs contribute significantly to the effectiveness of CD20 mAbs in vivo, which may have important clinical implications for CD20 and other mAb-based therapies.

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  • (PMID = 16520392.001).
  • [ISSN] 0022-1007
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI56363; United States / NIAID NIH HHS / AI / U19 AI056363; United States / NCI NIH HHS / CA / R01 CA096547; United States / NCI NIH HHS / CA / R01 CA105001; United States / NCI NIH HHS / CA / CA96547; United States / NCI NIH HHS / CA / CA105001
  • [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 / Antibodies, Monoclonal; 0 / Antigens, CD20; 0 / Immunoglobulin G; 0 / Receptors, IgG
  • [Other-IDs] NLM/ PMC2118227
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30. Tobinai K: Rituximab and other emerging antibodies as molecular target-based therapy of lymphoma. Int J Clin Oncol; 2003 Aug;8(4):212-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rituximab and other emerging antibodies as molecular target-based therapy of lymphoma.
  • Among the monoclonal antibodies (mAbs) under clinical development, anti-CD20 mAbs have been most extensively investigated and have shown definitive clinical activities.
  • Rituximab is a genetically engineered, chimeric anti-CD20 mAb with mouse variable and human constant regions.
  • Consecutive clinical trials conducted in the United States, Europe, and Japan have revealed that rituximab is an effective agent, with acceptable toxicities, in the treatment of indolent and aggressive B-cell non-Hodgkin's lymphomas (B-NHLs).
  • A recent European phase III study in elderly patients with untreated diffuse large B-cell lymphoma suggested that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) chemotherapy is superior to CHOP chemotherapy alone in terms of complete response rate and event-free and overall survivals.
  • The aim of radioimmunotherapy is to use the mAb to target radiation to lymphoma tissue while minimizing toxicity to normal cells.
  • Clinical trials of (90)Y-ibritumomab tiuxetan and (131)I-tositumomab showed that they have definitive efficacy in relapsed indolent B-NHL, with acceptable toxicities.
  • In addition, BL22, a recombinant anti-CD22 immunotoxin, showed significant efficacy in patients with chemotherapy-resistant hairy cell leukemia.
  • Monoclonal antibodies will have significant roles in the treatment of lymphoid malignancies in the future.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Lymphoma, B-Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Antigens, Neoplasm / immunology. Clinical Trials as Topic. Drug Design. Humans. Rituximab

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  • (PMID = 12955576.001).
  • [ISSN] 1341-9625
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 76
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31. Lemaire M, Momparler LF, Farinha NJ, Bernstein M, Momparler RL: Enhancement of antineoplastic action of 5-aza-2'-deoxycytidine by phenylbutyrate on L1210 leukemic cells. Leuk Lymphoma; 2004 Jan;45(1):147-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Epigenetic changes, such as aberrant DNA methylation that silences tumor suppressor genes (TSGs), can play an important role in the development of leukemia.
  • The DNA methylation inhibitor, 5-aza-2'-deoxycytidine (5-AZA-CdR), can reactivate these silent TSGs and is an interesting agent to investigate for therapy of leukemia.
  • An interesting HDI is phenylbutyrate (PB), which has shown some clinical activity for the therapy of leukemia.
  • In this report we have investigated the antineoplastic activity of 5-AZA-CdR and PB alone and in combination on murine L1210 lymphoid leukemic cells.
  • The in vitro treatment of 5-AZA-CdR and PB in combination produced a greater inhibition of growth, DNA synthesis, and also a greater reduction on colony formation on both L1210 and human HL-60 leukemic cells as compared to either drug alone.
  • In mice with L1210 leukemia the combination showed enhanced antineoplastic activity.
  • We also observed an enhancement of the antineoplastic activity of this combination in mice with L1210 leukemia.
  • These data provide a rationale to investigate 5-AZA-CdR and PB in patients with advanced leukemia.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Leukemia / pathology. Phenylbutyrates / pharmacology
  • [MeSH-minor] Animals. Cell Cycle Proteins / metabolism. Cell Division / drug effects. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p15. DNA / biosynthesis. DNA Replication / drug effects. Drug Synergism. Genes, Tumor Suppressor. HL-60 Cells. Humans. Male. Mice. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Tumor Suppressor Proteins / metabolism

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  • (PMID = 15061212.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN2B protein, human; 0 / Cdkn2b protein, mouse; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Phenylbutyrates; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 776B62CQ27 / decitabine; 9007-49-2 / DNA; M801H13NRU / Azacitidine
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