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1. DeAngelo DJ, Stone RM, Heaney ML, Nimer SD, Paquette RL, Klisovic RB, Caligiuri MA, Cooper MR, Lecerf JM, Karol MD, Sheng S, Holford N, Curtin PT, Druker BJ, Heinrich MC: Phase 1 clinical results with tandutinib (MLN518), a novel FLT3 antagonist, in patients with acute myelogenous leukemia or high-risk myelodysplastic syndrome: safety, pharmacokinetics, and pharmacodynamics. Blood; 2006 Dec 1;108(12):3674-81
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  • [Title] Phase 1 clinical results with tandutinib (MLN518), a novel FLT3 antagonist, in patients with acute myelogenous leukemia or high-risk myelodysplastic syndrome: safety, pharmacokinetics, and pharmacodynamics.
  • Tandutinib (MLN518/CT53518) is a novel quinazoline-based inhibitor of the type III receptor tyrosine kinases: FMS-like tyrosine kinase 3 (FLT3), platelet-derived growth factor receptor (PDGFR), and KIT.
  • Because of the correlation between FLT3 internal tandem duplication (ITD) mutations and poor prognosis in acute myelogenous leukemia (AML), we conducted a phase 1 trial of tandutinib in 40 patients with either AML or high-risk myelodysplastic syndrome (MDS).


2. Weil SC: Minimal residual disease in acute promyelocytic leukemia. Clin Lab Med; 2000 Mar;20(1):105-17, ix
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  • [Title] Minimal residual disease in acute promyelocytic leukemia.
  • In the last decade our understanding of acute promyelocytic leukemia (APL) has advanced tremendously.
  • The recognition of all-trans retinoic acid (ATRA) as a powerful therapeutic agent paralleled the cloning of the t(15;17) breakpoint.
  • RtPCR for the PML-RARA hybrid mRNA has become the hallmark of molecular diagnosis and molecular monitoring in APL.
  • Doing this in a way so that clinically relevant minimal residual disease can be distinguished from "indolent disease" remains among the future challenges in APL.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / diagnosis

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  • (PMID = 10702899.001).
  • [ISSN] 0272-2712
  • [Journal-full-title] Clinics in laboratory medicine
  • [ISO-abbreviation] Clin. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 5688UTC01R / Tretinoin; 9008-11-1 / Interferons
  • [Number-of-references] 85
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3. Cartwright MS, Jeffery DR, Lewis ZT, Koty PP, Stewart WT, Molnár I: Mitoxantrone for multiple sclerosis causing acute lymphoblastic leukemia. Neurology; 2007 May 8;68(19):1630-1
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  • [Title] Mitoxantrone for multiple sclerosis causing acute lymphoblastic leukemia.
  • [MeSH-major] Mitoxantrone / adverse effects. Multiple Sclerosis / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology
  • [MeSH-minor] Adult. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain / drug effects. Brain / pathology. Brain / physiopathology. Female. Humans. Interferon Type I / therapeutic use. Magnetic Resonance Imaging. Oligoclonal Bands / cerebrospinal fluid. Remission Induction. Treatment Outcome


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4. Wan YF, Guo XQ, Wang ZH, Ying K, Yao MH: Effects of paclitaxel on proliferation and apoptosis in human acute myeloid leukemia HL-60 cells. Acta Pharmacol Sin; 2004 Mar;25(3):378-84
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  • [Title] Effects of paclitaxel on proliferation and apoptosis in human acute myeloid leukemia HL-60 cells.
  • AIM: To investigate the regulatory effect of paclitaxel on proliferation and apoptosis in human acute leukemia HL-60 cells.
  • METHODS: HL-60 cell growth was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tertrazolium bromide (MTT) colorimetric assay.
  • Cell cycle kinetics and apoptosis were analyzed by flow cytometry and microscopic examination.
  • RESULTS: Paclitaxel inhibited HL-60 cell growth significantly in a dose-dependent and time-dependent manner (P<0.01).
  • Marked cell accumulation in G2/M phase and multinucleated cells were also observed after treatment with paclitaxel 0.1 and 1 micromol/L.
  • Among 14400 EST elements, 277 genes were found to be markedly up- or down-expressed in the HL-60 cells treated with paclitaxel 1 micromol/L for 0.5 h, comprising 210 known genes and 67 unknown genes.
  • CONCLUSION: Paclitaxel suppresses the growth of HL-60 cells in vitro by causing cell-cycle arrest and apoptosis.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Gene Expression Profiling. Paclitaxel / pharmacology
  • [MeSH-minor] Cell Cycle / drug effects. Cell Division / drug effects. HL-60 Cells. Humans. Oligonucleotide Array Sequence Analysis

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  • (PMID = 15000894.001).
  • [ISSN] 1671-4083
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; P88XT4IS4D / Paclitaxel
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5. Crom DB, Tyc VL, Rai SN, Deng X, Hudson MM, Booth A, Rodrigues LN, Zhang L, McCammon E, Kaste SC: Retention of survivors of acute lymphoblastic leukemia in a longitudinal study of bone mineral density. J Child Health Care; 2006 Dec;10(4):337-50
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  • [Title] Retention of survivors of acute lymphoblastic leukemia in a longitudinal study of bone mineral density.
  • This study investigated the variables associated with dropout of survivors of acute lymphoblastic leukemia in a trial investigating the effect of vitamin D and calcium supplementation and nutritional counseling on bone mineral density (BMD).
  • Common reasons given for withdrawing were intolerance of the study drug, family hardship and schedule conflicts.
  • [MeSH-major] Attitude to Health. Longitudinal Studies. Motivation. Patient Dropouts / psychology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / psychology. Survivors / psychology
  • [MeSH-minor] Adaptation, Psychological. Adolescent. Bias (Epidemiology). Bone Density / drug effects. Chi-Square Distribution. Child. Child, Preschool. Humans. Nurse's Role. Nurse-Patient Relations. Nursing Methodology Research. Randomized Controlled Trials as Topic / nursing. Randomized Controlled Trials as Topic / psychology. Research Design. Social Support. Tennessee

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  • (PMID = 17101625.001).
  • [ISSN] 1367-4935
  • [Journal-full-title] Journal of child health care : for professionals working with children in the hospital and community
  • [ISO-abbreviation] J Child Health Care
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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6. Hsiao HH, Sashida G, Ito Y, Kodama A, Fukutake K, Ohyashiki JH, Ohyashiki K: Additional cytogenetic changes and previous genotoxic exposure predict unfavorable prognosis in myelodysplastic syndromes and acute myeloid leukemia with der(1;7)(q10;p10). Cancer Genet Cytogenet; 2006 Mar;165(2):161-6
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  • [Title] Additional cytogenetic changes and previous genotoxic exposure predict unfavorable prognosis in myelodysplastic syndromes and acute myeloid leukemia with der(1;7)(q10;p10).
  • We analyzed 23 patients with myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) showing a der(1;7)(q10;p10) [hereafter der(1;7)] to identify the exact predictive factor of this cytogenetic change.
  • Eight (34.8%) patients, including six with MDS and two with AML patients, had a previous history of genotoxic exposure, especially radiation and/or antimetabolites.
  • Patients with der(1;7) consisted of three groups: one third of patients had a previous history of genotoxic agents, one third had additional cytogenetic changes at the time of MDS/AML diagnosis without previous exposure history, and the remaining one third had neither a previous exposure history nor additional cytogenetic changes.
  • Identification of prognostic disadvantage might be required for applying the appropriate strategy in managing MDS/AML patients with rare der(1;7) abnormality.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 7. Leukemia, Myeloid / genetics. Mutagens / toxicity. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Prognosis


7. Hu J, Zhou GB, Wang ZY, Chen SJ, Chen Z: Mutant transcription factors and tyrosine kinases as therapeutic targets for leukemias: from acute promyelocytic leukemia to chronic myeloid leukemia and beyond. Adv Cancer Res; 2007;98:191-220
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  • [Title] Mutant transcription factors and tyrosine kinases as therapeutic targets for leukemias: from acute promyelocytic leukemia to chronic myeloid leukemia and beyond.
  • Mutations in transcription factors (TFs) and protein tyrosine kinases (PTKs), which result in inhibition of differentiation/apoptosis or enhanced proliferative/survival advantage of hematopoietic stem/progenitor cells, are two classes of the most frequently detected genetic abnormalities in leukemias.
  • The great success of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) in treating acute promyelocytic leukemia through modulation of the causative PML-RARalpha oncoprotein represents the first two paradigms of mutant TFs-targeting therapeutic strategies for leukemia.
  • More recently, tyrosine kinase inhibitor STI-571/Imatinib mesylate/Gleevec in the treatment of Breakpoint Cluster Region-Abelson (BCR-ABL) positive leukemia elicits paradigm of mutant PTKs as ideal antileukemia targets.
  • Thus to further improve clinical outcome of leukemia patients, elucidation of pathogenesis of leukemia, screening for oncoprotein-targeting small molecules, as well as rationally designed combination of drugs with potential synergy are of importance.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy. Mutation / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Transcription Factors / antagonists & inhibitors


8. Yu YB, Gau JP, You JY, Chern HH, Chau WK, Tzeng CH, Ho CH, Hsu HC: Cost-effectiveness of postremission intensive therapy in patients with acute leukemia. Ann Oncol; 2007 Mar;18(3):529-34
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  • [Title] Cost-effectiveness of postremission intensive therapy in patients with acute leukemia.
  • BACKGROUND: We assessed the cost-effectiveness of high-dose arabinoside (HiDAC)-based and allogeneic stem-cell transplantation (alloSCT)-based therapy in patients with acute leukemia.
  • PATIENTS AND METHODS: We analyzed the outcome, cost and cost-effectiveness of 106 patients treated from January 1994 to January 2002 [94 acute myelogenous leukemia (AML)/12 acute lymphoblastic leukemia (ALL)].
  • The reduced total cost for the HiDAC-based group originated from lower cost in room fees, medication, laboratory and procedure, but not in blood transfusion and professional manpower fees.

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  • (PMID = 17164232.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arabinonucleosides
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9. Liem NL, Papa RA, Milross CG, Schmid MA, Tajbakhsh M, Choi S, Ramirez CD, Rice AM, Haber M, Norris MD, MacKenzie KL, Lock RB: Characterization of childhood acute lymphoblastic leukemia xenograft models for the preclinical evaluation of new therapies. Blood; 2004 May 15;103(10):3905-14
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  • [Title] Characterization of childhood acute lymphoblastic leukemia xenograft models for the preclinical evaluation of new therapies.
  • Continuous xenografts from 10 children with acute lymphoblastic leukemia (ALL) were established in nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice.
  • Analysis of clonal antigen receptor gene rearrangements in 2 xenografts from patients at diagnosis showed that the pattern of clonal variation observed following tertiary transplantation in mice exactly reflected that in bone marrow samples at the time of clinical relapse.
  • Patients experienced diverse treatment outcomes, including 5 who died of disease (median, 13 months; range, 11-76 months, from date of diagnosis), and 5 who remain alive (median, 103 months; range, 56-131 months, following diagnosis).
  • This study shows, for the first time, that the biologic and genetic characteristics, and patterns of chemosensitivity, of childhood ALL xenografts accurately reflect the clinical disease.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Disease Models, Animal. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Transplantation, Heterologous
  • [MeSH-minor] Adolescent. Animals. Child. Child, Preschool. Dexamethasone / pharmacology. Dexamethasone / therapeutic use. Drug Evaluation, Preclinical. Female. Gene Rearrangement, T-Lymphocyte. Genes, Immunoglobulin. Humans. Immunophenotyping. Male. Methotrexate / pharmacology. Methotrexate / therapeutic use. Mice. Mice, SCID. Neoplasm Transplantation. Neoplasms, Experimental / drug therapy. Treatment Outcome. Vincristine / pharmacology. Vincristine / therapeutic use


10. VanLeeuwen JA, Keefe GP, Tremblay R, Power C, Wichtel JJ: Seroprevalence of infection with Mycobacterium avium subspecies paratuberculosis, bovine leukemia virus, and bovine viral diarrhea virus in maritime Canada dairy cattle. Can Vet J; 2001 Mar;42(3):193-8
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  • [Title] Seroprevalence of infection with Mycobacterium avium subspecies paratuberculosis, bovine leukemia virus, and bovine viral diarrhea virus in maritime Canada dairy cattle.
  • The purpose of this study was to survey the seroprevalence of infection with the agents of production-limiting diseases in dairy cattle in New Brunswick, Nova Scotia, and Prince Edward Island.
  • In 30 randomly selected herds per province, 30 cattle per herd were randomly selected and tested for antibodies to bovine leukemia virus (BLV) and Mycobacterium avium subspecies paratuberculosis (M. paratuberculosis), while 5 unvaccinated cattle over 6 months of age were tested for antibodies to bovine viral diarrhea virus (BVDV).
  • For M. paratuberculosis, 2.6% (1.8% to 3.9%) of cows were positive, and 16.7% (8.8% to 24.5%) of herds had at least 2 M. paratuberculosis-positive cows.
  • [MeSH-major] Antibodies, Bacterial / blood. Antibodies, Viral / blood. Bovine Virus Diarrhea-Mucosal Disease / epidemiology. Enzootic Bovine Leukosis / epidemiology. Paratuberculosis / epidemiology
  • [MeSH-minor] Acute Disease. Animals. Canada / epidemiology. Cattle. Cattle Diseases / epidemiology. Diarrhea Viruses, Bovine Viral / immunology. Enzyme-Linked Immunosorbent Assay. Leukemia Virus, Bovine / immunology. Mycobacterium avium subsp. paratuberculosis / immunology. Sensitivity and Specificity. Seroepidemiologic Studies

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  • [Cites] Can Vet J. 2000 Jun;41(6):464-7 [10857030.001]
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  • (PMID = 11265187.001).
  • [ISSN] 0008-5286
  • [Journal-full-title] The Canadian veterinary journal = La revue vétérinaire canadienne
  • [ISO-abbreviation] Can. Vet. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antibodies, Bacterial; 0 / Antibodies, Viral
  • [Other-IDs] NLM/ PMC1476460
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11. Chow KU, Boehrer S, Napieralski S, Nowak D, Knau A, Hoelzer D, Mitrou PS, Weidmann E: In AML cell lines Ara-C combined with purine analogues is able to exert synergistic as well as antagonistic effects on proliferation, apoptosis and disruption of mitochondrial membrane potential. Leuk Lymphoma; 2003 Jan;44(1):165-73
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  • [Title] In AML cell lines Ara-C combined with purine analogues is able to exert synergistic as well as antagonistic effects on proliferation, apoptosis and disruption of mitochondrial membrane potential.
  • The pyrimidine analogue Ara-C and the purine analogues fludarabine and cladribine (2-CdA) are essential compounds in the treatment of acute myeloid leukemia (AML).
  • Inhibition of cell proliferation and induction of apoptosis are the major mechanisms of cytotoxic agents to cause tumor cell death.
  • Therefore, we studied whether Ara-C in combination with the purine analogues exerts synergistic or antagonistic effects on cell proliferation, phosphatidylserine exposure and disruption of mitochondrial membrane potential (MMP) in the AML cell lines HL60 and HEL.
  • Furthermore, effects of the combination of Ara-C with bendamustine, a new bifunctional agent with alkylating activity and a purine nucleus, was investigated.
  • Assessment by combination index analysis showed that Ara-C combined with fludarabine or bendamustine exhibited additive to antagonistic effects on inhibition of cell proliferation, induction of apoptosis as well as on disruption of mitochondrial membrane potential, independent of a simultaneous or consecutive (purine analogues before Ara-C) incubation schedule.
  • While inducing IC50 levels of apoptosis neither the antagonistic nor the synergistic drug combinations caused a specific expression pattern of apoptosis-associated proteins such as the pro- or antiapoptotic Bcl-2 family members, executioner caspases, IAPs (inhibitor of apoptosis proteins), proapoptotic Par-4, PARP, or p53.
  • In conclusion, we here demonstrate that the in vitro efficacy of drug combinations containing Ara-C and purine analogues depends on the purine analogue applied, whereas incubation schedules or escalating dosages do not contribute to the synergistic effects.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Cytarabine / pharmacology. Leukemia, Myeloid / pathology. Purines / pharmacology
  • [MeSH-minor] Acute Disease. Apoptosis / drug effects. Cell Division / drug effects. Drug Antagonism. Drug Synergism. Humans. Intracellular Membranes / drug effects. Membrane Potentials / drug effects. Mitochondria / drug effects. Mitochondria / ultrastructure. Tumor Cells, Cultured

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  • (PMID = 12691159.001).
  • [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 / Purines; 04079A1RDZ / Cytarabine
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12. Jia PM, Pan XR, Xiao S, Li D, Wang ZY, Tong JH: [In vitro study of the effects of CDA-II combined with cAMP on apoptosis induction in retinoic acid resistant acute promyelocytic leukemia cells]. Zhonghua Xue Ye Xue Za Zhi; 2008 Sep;29(9):603-6
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  • [Title] [In vitro study of the effects of CDA-II combined with cAMP on apoptosis induction in retinoic acid resistant acute promyelocytic leukemia cells].
  • OBJECTIVE: To investigate the effects of CDA-II alone or combined with cAMP on the retinoic acid (RA)-resistant acute promyelocytic leukemia (APL) cells.
  • METHODS: The RA-resistant cell line NB4-R2 was used as an in vitro model and treated with CDA-II alone or in combination with cAMP.
  • Cell apoptosis was assessed by morphology observation, distribution of cellular DNA contents and sub-G1 cell population.
  • RESULTS: CDA-II could induce NB4-R2 cell apoptosis through decreasing the level of cellular anti-apoptotic protein Bcl-2. cAMP could significantly enhance the role of CDA-II.
  • Bcl-2 positive cell rates decreased to (15.1 +/- 4.8)% and (7.3 +/- 2.9)% in NB4-R2 cells treated with 1 mg/ml CDA-II plus 100 micromol/L cAMP for 48 h and 72 h, respectively.
  • While 100 micromol/L of cAMP could decrease Bcl-2 positive NB4-R2 cells from (92.0 +/- 0.6)% to (75.3 +/- 2.0)%.
  • [MeSH-major] Cyclic AMP / pharmacology. Leukemia, Promyelocytic, Acute / pathology. Peptides / pharmacology. Phenylacetates / pharmacology. Tretinoin / pharmacology
  • [MeSH-minor] Animals. Antigens, CD11c / metabolism. Apoptosis / drug effects. Cells, Cultured. Humans. Proto-Oncogene Proteins c-bcl-2 / metabolism

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  • (PMID = 19175987.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD11c; 0 / Peptides; 0 / Phenylacetates; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / cell differentiation agent II; 5688UTC01R / Tretinoin; E0399OZS9N / Cyclic AMP
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13. Jones D, Thomas D, Yin CC, O'Brien S, Cortes JE, Jabbour E, Breeden M, Giles FJ, Zhao W, Kantarjian HM: Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL kinase inhibitors. Cancer; 2008 Sep 1;113(5):985-94
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  • [Title] Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL kinase inhibitors.
  • BACKGROUND: BCR-ABL kinase domain (KD) mutations are detected in approximately 45% of patients with imatinib-resistant chronic myeloid leukemia.
  • Patterns of KD mutations in Philadelphia chromosome (Ph)-positive acute lympho- blastic leukemia (ALL) are less well studied.
  • Using a more sensitive pyrosequencing method, mutations were not detected at codons 315 and 253 in the diagnostic samples from those 12 patients or in 30 patients with Ph-positive ALL who never developed recurrent disease.
  • CONCLUSIONS: ABL KD mutations, especially at codons 315 and 253, emerged at the time of disease recurrence in the vast majority of patients who had Ph-positive ALL and received maintenance KI therapy.

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  • [Copyright] (c) 2008 American Cancer Society.
  • (PMID = 18615627.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P50 CA100632-010007; United States / NCI NIH HHS / CA / P50 CA100707; United States / NCI NIH HHS / CA / 1P50CA100707-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS58345; NLM/ PMC4204653
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14. Paugam A: [The latest data on posaconazole]. Med Mal Infect; 2007 Feb;37(2):71-6
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  • Posaconazole is a lipophilic triazole antifungal agent that is structurally similar to itraconazole but has an expended spectrum of activity including yeast, molds, and dimorphic fungi.
  • Posaconazole was licensed by the European Commission for the treatment of invasive aspergillosis, fusariosis, mycetoma, chromoblastomycosis, and coccidioidomycosis in adults who are refractory, or intolerant to other antifungal agents.
  • Posaconazole was recently indicated for prophylaxis of invasive fungal infections in the following patients: patients receiving remission-induction chemotherapy for acute myelogenous leukemia (AML) or myelodysplastic syndromes (MDS) expected to result in prolonged neutropenia and hematopoietic stem cell transplant (HSCT) recipients who are undergoing high-dose immunosuppressive therapy for versus host disease.
  • Posaconazole was well tolerated in clinical trials and has lower drug interaction profile compared to other available azoles.
  • [MeSH-major] Antifungal Agents / therapeutic use. Mycoses / drug therapy. Triazoles / therapeutic use
  • [MeSH-minor] Adult. Animals. Central Nervous System Fungal Infections / drug therapy. Chagas Cardiomyopathy / drug therapy. Clinical Trials as Topic. Drug Evaluation, Preclinical. Drug Resistance, Fungal. Humans. Immunocompromised Host. Mice. Premedication. Trypanocidal Agents / therapeutic use

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  • (PMID = 17267154.001).
  • [ISSN] 0399-077X
  • [Journal-full-title] Médecine et maladies infectieuses
  • [ISO-abbreviation] Med Mal Infect
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Triazoles; 0 / Trypanocidal Agents; 6TK1G07BHZ / posaconazole
  • [Number-of-references] 65
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15. Wells RJ, Adams MT, Alonzo TA, Arceci RJ, Buckley J, Buxton AB, Dusenbery K, Gamis A, Masterson M, Vik T, Warkentin P, Whitlock JA, Children's Cancer Group Study 2951: Mitoxantrone and cytarabine induction, high-dose cytarabine, and etoposide intensification for pediatric patients with relapsed or refractory acute myeloid leukemia: Children's Cancer Group Study 2951. J Clin Oncol; 2003 Aug 1;21(15):2940-7
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  • [Title] Mitoxantrone and cytarabine induction, high-dose cytarabine, and etoposide intensification for pediatric patients with relapsed or refractory acute myeloid leukemia: Children's Cancer Group Study 2951.
  • PURPOSE: To evaluate the response rate, survival, and toxicity of mitoxantrone and cytarabine induction, high-dose cytarabine and etoposide intensification, and further consolidation/maintenance therapies, including bone marrow transplantation, in children with relapsed, refractory, or secondary acute myeloid leukemia (AML).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Cytarabine / administration & dosage. Drug Administration Schedule. Etoposide / administration & dosage. Female. Humans. Male. Mitoxantrone / administration & dosage. Prognosis. Survival Rate. Treatment Outcome

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  • (PMID = 12885813.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; BZ114NVM5P / Mitoxantrone
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16. Smith BD, Karp JE: What are the endpoints of therapy for acute leukemias? Old definitions and new challenges. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S296-301
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  • [Title] What are the endpoints of therapy for acute leukemias? Old definitions and new challenges.
  • Acute leukemias are complex diseases on multiple levels, and laboratory efforts over the past 3 decades have focused on better understanding of the molecular underpinnings and their stem cell biology.
  • We now have a panoply of technologic advances that allow us to characterize individual leukemias by molecular profiles that relate directly to clinical behavior, to detect minimal residual disease, and to begin to develop "targeted" therapeutic strategies based on molecular considerations.
  • There are a number of challenges surrounding this task: first, how to combine these agents with traditional chemotherapeutics and/or with each other to maximize leukemic cell kill and increase the cure rate; second, how to use these targeted agents in the minimal residual disease with potential curative intent; third, for patients unable to tolerate or unlikely to benefit from aggressive approaches, how to use one or more of these agents to reduce tumor bulk and either permit some restoration of normal marrow function or induce morphologic and functional differentiation of the leukemic clone to overcome the leukemia-associated bone marrow failure; and lastly, how to measure the effects of these agents on the molecular and cellular biologic levels in ways that correlate with and might even predict overall clinical outcome.
  • These challenges are further complicated by the inherent heterogeneity in host biology; disease etiology and biology; and interactions among host, disease, and treatment that ultimately determine individual clinical outcomes.
  • Toward this end, we will discuss selected issues surrounding new clinical trial designs and the development of clinically relevant molecular endpoints that might facilitate the development of new treatment approaches that will improve the outlook for adults with acute leukemias.

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  • (PMID = 19778856.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973; United States / NCRR NIH HHS / RR / RR000052-466553; United States / NCI NIH HHS / CA / 2P30 CA06973-44; United States / NCI NIH HHS / CA / U01 CA70095; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCRR NIH HHS / RR / M01 RR000052; United States / NCRR NIH HHS / RR / M01 RR000052-466553
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 63
  • [Other-IDs] NLM/ NIHMS187883; NLM/ PMC2851207
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17. Sadek I, Zayed E, Hayne O, Fernandez L: Prolonged complete remission of myelodysplastic syndrome treated with danazol, retinoic acid and low-dose prednisone. Am J Hematol; 2000 Aug;64(4):306-10
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  • Different medications have been tried in MDS; however, no effective treatment has been yet established.
  • She was diagnosed as having MDS-refractory anemia and was given blood transfusions to maintain blood cell counts at acceptable levels.
  • Fourteen months later, the patient was in complete hematologic remission; she had normal peripheral blood count, and the blood smear showed normal morphology.
  • Eighty-eight months from diagnosis, she relapsed with acute myeloid leukemia.
  • This is the first reported case of MDS-RA that sustained a complete hematologic remission for a prolonged period in response to this combination treatment.
  • This report indicates that restoration of normal hematopoiesis, prolongation of disease-free survival, and delay in the transformation to acute leukemia may be achieved by this combination of treatment in a subset of patients with MDS, especially refractory anemia with severe thrombocytopenia.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Danazol / administration & dosage. Estrogen Antagonists / administration & dosage. Myelodysplastic Syndromes / drug therapy. Prednisone / administration & dosage. Tretinoin / administration & dosage
  • [MeSH-minor] Drug Therapy, Combination. Female. Humans. Middle Aged. Remission Induction


18. Cohen MH, Johnson JR, Massie T, Sridhara R, McGuinn WD Jr, Abraham S, Booth BP, Goheer MA, Morse D, Chen XH, Chidambaram N, Kenna L, Gobburu JV, Justice R, Pazdur R: Approval summary: nelarabine for the treatment of T-cell lymphoblastic leukemia/lymphoma. Clin Cancer Res; 2006 Sep 15;12(18):5329-35
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  • [Title] Approval summary: nelarabine for the treatment of T-cell lymphoblastic leukemia/lymphoma.
  • PURPOSE: To describe the clinical studies, chemistry manufacturing and controls, and clinical pharmacology and toxicology that led to Food and Drug Administration approval of nelarabine (Arranon) for the treatment of T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma.
  • CONCLUSIONS: On October 28, 2005, the Food and Drug Administration granted accelerated approval for nelarabine for treatment of patients with relapsed or refractory T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma after at least two prior regimens.
  • [MeSH-major] Arabinonucleosides / therapeutic use. Drug Approval. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Lymphoma, T-Cell / drug therapy. United States Food and Drug Administration
  • [MeSH-minor] Animals. Dogs. Drug Evaluation, Preclinical / methods. Haplorhini. Humans. Metabolic Clearance Rate. Mice. Models, Biological. Rabbits. Rats. United States

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  • (PMID = 17000665.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arabinonucleosides; 60158CV180 / nelarabine
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19. Kuendgen A, Gräf T, Zohren F, Hildebrandt B, Hünerlitürkoglu A, Gattermann N, Haas R, Kobbe G: Induction of complete remission in a patient with acute myeloid leukemia refractory to high-dose chemotherapy through treatment with 5-azacytidine. Leuk Res; 2007 Mar;31(3):407-9
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  • [Title] Induction of complete remission in a patient with acute myeloid leukemia refractory to high-dose chemotherapy through treatment with 5-azacytidine.
  • For patients with acute myeloid leukemia refractory to intensive chemotherapy prognosis is very poor and treatment options are limited.
  • 5-Azacytidine, a demethylating drug, is effective in the treatment of myelodysplastic syndromes when administered at a low-dose, subcutaneously.
  • We report a case of a patient with AML refractory to induction chemotherapy as well as to two high-dose salvage regimens.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Azacitidine / administration & dosage. Drug Resistance, Neoplasm. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Dose-Response Relationship, Drug. Fatal Outcome. Female. Follow-Up Studies. Humans. Injections, Subcutaneous. Middle Aged. Predictive Value of Tests. Prognosis. Remission Induction

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  • (PMID = 16890286.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] M801H13NRU / Azacitidine
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20. Shord SS, Faucette SR, Gillenwater HH, Pescatore SL, Hawke RL, Socinski MA, Lindley C: Gemcitabine pharmacokinetics and interaction with paclitaxel in patients with advanced non-small-cell lung cancer. Cancer Chemother Pharmacol; 2003 Apr;51(4):328-36
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  • [Title] Gemcitabine pharmacokinetics and interaction with paclitaxel in patients with advanced non-small-cell lung cancer.
  • PURPOSE: Gemcitabine administered at a fixed dose rate of 10 mg/m(2) per min has been reported to achieve plasma steady-state concentrations ranging from 10 to 20 microM in patients with acute leukemia.
  • We designed this pharmacokinetic study to assess the ability of a fixed dose rate of gemcitabine to achieve the desired steady-state concentration in the absence and presence of paclitaxel in patients with solid tumors.
  • PATIENTS AND METHODS: A group of 14 patients with advanced non-small-cell lung cancer received paclitaxel 110 mg/m(2) over 3 h on days 1 and 8 and gemcitabine 800 mg/m(2) over 80 min on days 1 and 8 every 21 days.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Carcinoma, Non-Small-Cell Lung / metabolism. Deoxycytidine / analogs & derivatives. Lung Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Drug Interactions. Female. Humans. Male. Metabolic Clearance Rate. Middle Aged. Neoplasm Staging. Paclitaxel / administration & dosage. Paclitaxel / adverse effects. Paclitaxel / pharmacokinetics

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  • (PMID = 12721761.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / RR00046
  • [Publication-type] Clinical Trial; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; P88XT4IS4D / Paclitaxel
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21. Cortes J, Thomas D, Koller C, Giles F, Estey E, Faderl S, Garcia-Manero G, McConkey D, Ruiz SL, Guerciolini R, Wright J, Kantarjian H: Phase I study of bortezomib in refractory or relapsed acute leukemias. Clin Cancer Res; 2004 May 15;10(10):3371-6
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  • [Title] Phase I study of bortezomib in refractory or relapsed acute leukemias.
  • We performed a Phase I study to investigate the maximum tolerated dose and dose-limiting toxicity of bortezomib in patients with acute leukemias refractory to or relapsing after prior therapy.
  • Incubation of blast cells with bortezomib in vitro showed induction of apoptosis in three of five patients investigated.
  • We conclude that the maximum tolerated dose of bortezomib in patients with acute leukemia is 1.25 mg/m(2), using a twice-weekly for 4 weeks every 6 weeks schedule.
  • The in vitro evidence of antileukemia and transient hematological improvements observed in some patients warrants further investigation of bortezomib in acute leukemias, probably in combination with other agents.
  • [MeSH-major] Boronic Acids / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrazines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Agents / pharmacology. Apoptosis. Bortezomib. Dose-Response Relationship, Drug. Humans. Maximum Tolerated Dose. Middle Aged. Models, Chemical. Proteasome Endopeptidase Complex / metabolism. Proteasome Inhibitors. Recurrence. Time Factors

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  • [ErratumIn] Clin Cancer Res. 2004 Nov 15;10(22):7787. Patel, Gira [removed]; Ruiz, Stacey L [added]
  • (PMID = 15161691.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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22. Ural AU, Avcu F, Zerman M, Yilmaz MI, Pekel A, Beyzadeoglu M: Differentiating effect of thalidomide and FGM-CS combination on HL-60 acute promyelocytic leukemia cells. Exp Oncol; 2006 Sep;28(3):216-9
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  • [Title] Differentiating effect of thalidomide and FGM-CS combination on HL-60 acute promyelocytic leukemia cells.
  • AIM: To investigate whether granulocyte-macrophage colony-stimulating factor (GM-CSF) with or without thalidomide can induce apoptosis and differentiation of HL-60 acute promyelocytic leukemia cell line in vitro.
  • METHODS: Effect of GM-CSF and thalidomide on proliferation of HL-60 cells was evaluated by MTT assay, cell cycle analysis was performed by propidium iodide staining approach and flow cytometry, and apoptosis rate was analyzed using FITC-conjugated annexin-V and FACScan flow cytometry.
  • RESULTS: The study revealed that thalidomide alone at high concentrations inhibited HL-60 cell growth and induced apoptosis.
  • Three days treatment of low-dose thalidomide in combination with GM-CSF induced marked terminal differentiation of HL-60 cells, as it was assessed by increased expression of differentiation antigens on cell surface.
  • CONCLUSION: Treatment of HL-60 cells by low concentration of thalidomide combined with GM-CSF induced terminal differentiation of HL60 cells in vitro, which may be advantageous for the elaboration of novel therapeutic regimens in patients with differentiation-inducible leukemias.
  • [MeSH-major] Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Leukemia, Promyelocytic, Acute / pathology. Thalidomide / pharmacology
  • [MeSH-minor] Antigens, Differentiation / analysis. Antigens, Differentiation / metabolism. Apoptosis. Cell Differentiation / drug effects. Cell Proliferation / drug effects. HL-60 Cells. Humans

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  • (PMID = 17080015.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Antigens, Differentiation; 4Z8R6ORS6L / Thalidomide; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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23. Savini V, Catavitello C, Di Marzio I, Masciarelli G, Astolfi D, Balbinot A, Bianco A, Pompilio A, Di Bonaventura G, D'Amario C, D'Antonio D: Pan-azole-resistant Candida guilliermondii from a leukemia patient's silent funguria. Mycopathologia; 2010 Jun;169(6):457-9
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  • [Title] Pan-azole-resistant Candida guilliermondii from a leukemia patient's silent funguria.
  • Isolation of Candida non-albicans yeasts as commensals or pathogens from hospitalised hosts is acquiring increasing importance, due to the frequent drug resistance expressed by such organisms.Particularly, the recover of antifungal resistant C. guilliermondii is of worrisome concern, even if recovered as a saprophyte, since commensal yeasts may behave as reservoirs for resistance elements;furthermore, they may enter the bloodstream after chemotherapy-related mucosal damage has developed,thus causing life-threatening and difficult-to-treat fungemias.
  • This communication deals with the unusual isolation of a pan-azole resistant C. guilliermondii strain from a leukaemic patient with silent candiduria and emphasizes the importance of monitoring less recurring species within the nosocomial setting to better understand fungal epidemiology within the wards and face the spread of resistance determinants.
  • [MeSH-major] Antifungal Agents / pharmacology. Azoles / pharmacology. Candida / drug effects. Candidiasis / complications. Leukemia / complications. Urine / microbiology
  • [MeSH-minor] Acute Disease. Drug Resistance, Fungal. Fatal Outcome. Humans. Microbial Sensitivity Tests

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  • [ErratumIn] Mycopathologia. 2010 Jul;170(1):77
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  • (PMID = 20135354.001).
  • [ISSN] 1573-0832
  • [Journal-full-title] Mycopathologia
  • [ISO-abbreviation] Mycopathologia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Azoles
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24. Menichetti F: How to improve the design of trials of antifungal prophylaxis among neutropenic adults with acute leukemia. Clin Infect Dis; 2004 Oct 15;39 Suppl 4:S181-4
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  • [Title] How to improve the design of trials of antifungal prophylaxis among neutropenic adults with acute leukemia.
  • The risk for invasive fungal infections in patients with acute leukemia is generally low (4%-8%), and the routine use of fungal prophylaxis is not warranted except in specific high-risk groups that should be identified among this population.
  • In a prophylactic study with a new agent, fluconazole or itraconazole oral solution represent good choices for the comparator because they are proven better than placebo or oral nonabsorbable antifungal agents in reducing the risk of invasive fungal infections in patients with acute leukemia.
  • Because prophylaxis is most valuable when the risk of infection is high, patients with well-understood risk factors (severe mucosal disruption caused by chemotherapy, impaired cell-mediated immunity caused by steroids or fludarabine, use of a central venous catheter, and colonization by Candida species) should be selected.
  • Differences in gastrointestinal toxicity of antifungal agents may limit the use of double-blind designs in some situations.
  • [MeSH-major] Antifungal Agents / therapeutic use. Leukemia / complications. Mycoses / prevention & control. Research Design
  • [MeSH-minor] Acute Disease. Adult. Clinical Trials as Topic. Fluconazole / therapeutic use. Humans. Itraconazole / therapeutic use. Neutropenia / etiology

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  • (PMID = 15546115.001).
  • [ISSN] 1537-6591
  • [Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • [ISO-abbreviation] Clin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 304NUG5GF4 / Itraconazole; 8VZV102JFY / Fluconazole
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25. Gutierrez JA, Pan YX, Koroniak L, Hiratake J, Kilberg MS, Richards NG: An inhibitor of human asparagine synthetase suppresses proliferation of an L-asparaginase-resistant leukemia cell line. Chem Biol; 2006 Dec;13(12):1339-47
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  • [Title] An inhibitor of human asparagine synthetase suppresses proliferation of an L-asparaginase-resistant leukemia cell line.
  • Drug resistance in lymphoblastic and myeloblastic leukemia cells is poorly understood, with several lines of evidence suggesting that resistance can be correlated with upregulation of human asparagine synthetase (hASNS) expression, although this hypothesis is controversial.
  • New tools are needed to investigate this clinically important question, including potent hASNS inhibitors.
  • The adenylated sulfoximine has a cytostatic effect on L-asparaginase-resistant MOLT-4 cells cultured in the presence of L-asparaginase, an enzyme that depletes L-asparagine in the growth medium.
  • These observations represent direct evidence that potent hASNS inhibitors may prove to be effective agents for the clinical treatment of acute lymphoblastic leukemia.

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  • (PMID = 17185229.001).
  • [ISSN] 1074-5521
  • [Journal-full-title] Chemistry & biology
  • [ISO-abbreviation] Chem. Biol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK052064; United States / NIDDK NIH HHS / DK / R01 DK059315; United States / NIDDK NIH HHS / DK / DK52064; United States / NIDDK NIH HHS / DK / DK59315
  • [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 / Amino Acids, Sulfur; 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase
  • [Other-IDs] NLM/ NIHMS447417; NLM/ PMC3608209
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26. McHayleh W, Foon K, Redner R, Sehgal R, Raptis A, Agha M, Luong TM, Schlesselman JJ, Boyiadzis M: Gemtuzumab ozogamicin as first-line treatment in patients aged 70 years or older with acute myeloid leukemia. Cancer; 2010 Jun 15;116(12):3001-5
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  • [Title] Gemtuzumab ozogamicin as first-line treatment in patients aged 70 years or older with acute myeloid leukemia.
  • BACKGROUND: Elderly patients with acute myeloid leukemia (AML) are generally unable to withstand the rigors of intensive induction chemotherapy and its attendant complications.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Drug Administration Schedule. Drug Evaluation. Female. Humans. Male. Retrospective Studies. Treatment Outcome

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  • (PMID = 20564405.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / gemtuzumab
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27. Banklau C, Jindadamrongwech S, Sawangpanich R, Apibal S, Hongeng S, Paisooksantivatana K, Pakakasama S: Effect of genetic alterations of cytarabine- metabolizing enzymes in childhood acute lymphoblastic leukemia. Hematol Oncol Stem Cell Ther; 2010;3(3):103-8
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  • [Title] Effect of genetic alterations of cytarabine- metabolizing enzymes in childhood acute lymphoblastic leukemia.
  • Currently, treatment of childhood acute lymphoblastic leukemia (ALL) includes cytarabine, especially in high-risk patients.
  • PATIENTS AND METHODS: We included children diagnosed with ALL and lymphoblastic lymphoma (LL) stage III and IV.
  • Minimal residual disease (MRD) at the end of the induction phase was measured using flow cytometry.
  • The median age at diagnosis was 5.8 years (range, 0.4-15 years).
  • All four SNPs showed predominant wild type alleles.
  • [MeSH-major] Cytarabine / therapeutic use. Cytidine Deaminase / genetics. Deoxycytidine Kinase / genetics. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Alleles. Antigens, CD19 / metabolism. Antigens, CD45 / metabolism. Antimetabolites, Antineoplastic / adverse effects. Antimetabolites, Antineoplastic / metabolism. Antimetabolites, Antineoplastic / therapeutic use. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Flow Cytometry. Gene Frequency. Genotype. Humans. Infant. Male. Mucositis / chemically induced. Neoplasm Staging. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Neoplasm, Residual / metabolism. Thrombocytopenia / chemically induced. Treatment Outcome

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  • (PMID = 20890066.001).
  • [ISSN] 1658-3876
  • [Journal-full-title] Hematology/oncology and stem cell therapy
  • [ISO-abbreviation] Hematol Oncol Stem Cell Ther
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.1.3.48 / Antigens, CD45; EC 3.5.4.5 / Cytidine Deaminase
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28. Menzin J, Lang K, Earle CC, Kerney D, Mallick R: The outcomes and costs of acute myeloid leukemia among the elderly. Arch Intern Med; 2002 Jul 22;162(14):1597-603
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  • [Title] The outcomes and costs of acute myeloid leukemia among the elderly.
  • BACKGROUND: The incidence of acute myeloid leukemia (AML) among the elderly can be expected to grow as the population continues to age.
  • We evaluated survival, use of health care resources, use of chemotherapy, and Medicare payments among adults 65 years and older with an initial diagnosis of AML between January 1, 1991, and December 31, 1996.
  • In the 2 years after the AML diagnosis, 790 patients (30%) underwent chemotherapy treatment.
  • Further work is needed to characterize this disease and the patient-related factors that influence treatment decisions and associated health outcomes.
  • [MeSH-major] Leukemia, Myeloid / economics
  • [MeSH-minor] Acute Disease. Age Factors. Aged. Aged, 80 and over. Cohort Studies. Delivery of Health Care / economics. Drug Therapy. Female. Humans. Incidence. Male. Multivariate Analysis. Retrospective Studies. Survival Analysis. Time Factors. United States / epidemiology

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  • (PMID = 12123403.001).
  • [ISSN] 0003-9926
  • [Journal-full-title] Archives of internal medicine
  • [ISO-abbreviation] Arch. Intern. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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29. Pavithran K, Arjun R, Aruna R, Thomas M: Scrotal ulceration during induction therapy of acute promyelocytic leukemia with ATRA. Am J Hematol; 2004 Apr;75(4):260-1
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  • [Title] Scrotal ulceration during induction therapy of acute promyelocytic leukemia with ATRA.
  • All-trans-Retinoic acid (ATRA) has been shown to improve survival in patients with acute promyelocytic leukemia (APML).
  • It is a well-tolerated drug except for the serious side effect of ATRA syndrome.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Genital Diseases, Male / chemically induced. Leukemia, Promyelocytic, Acute / drug therapy. Scrotum / pathology. Tretinoin / adverse effects. Ulcer / chemically induced
  • [MeSH-minor] Adolescent. Anti-Bacterial Agents / administration & dosage. Humans. Male. Steroids / administration & dosage

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • [CommentIn] Am J Hematol. 2004 Oct;77(2):206-7 [15389917.001]
  • (PMID = 15054825.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antineoplastic Agents; 0 / Steroids; 5688UTC01R / Tretinoin
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30. Martino R, Subirà M: Invasive fungal infections in hematology: new trends. Ann Hematol; 2002 May;81(5):233-43
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  • Invasive fungal infections (IFI) are among the most feared complications of patients being treated for a hematological malignancy.
  • Currently, most serious IFI occur in patients with acute leukemia and after allogeneic hematopoietic stem cell transplantation.
  • Although Candida albicans and Aspergillusspp. continue to be the main pathogens, the proportion of patients infected by non-albicans species of Candida and other yeasts and by other filamentous fungi is rising in most institutions.
  • Recent advances in diagnosis now allow the use of very sensitive imaging techniques with an extremely low negative predictive value.
  • Among the novel microbiologic methods, the galactomannan antigen test is now commercially available for routine use in the diagnosis of aspergillosis, while DNA fungal detection is still experimental.
  • For the first time, clinicians now have a broad range of antifungals to chose from, with special emphasis on amphotericin B preparations, novel broad-spectrum azoles, and the echinocandins.
  • However, the exact place of these agents in treating different IFI will need to be found in the near future.
  • [MeSH-minor] Antifungal Agents / therapeutic use. Humans. Incidence. Preventive Medicine / methods. Risk Factors

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  • (PMID = 12029531.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antifungal Agents
  • [Number-of-references] 80
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31. Scott LJ, Figgitt DP: Mitoxantrone: a review of its use in multiple sclerosis. CNS Drugs; 2004;18(6):379-96
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  • Mitoxantrone (Novantrone), a synthetic anthracenedione derivative, is an antineoplastic, immunomodulatory agent.
  • Intravenous mitoxantrone treatment improved neurological disability and delayed progression of MS in patients with worsening relapsing-remitting (RR) [also termed progressive-relapsing (PR) MS] or secondary-progressive (SP) disease.
  • In a pivotal randomised, double-blind, multicentre trial, mitoxantrone 12 mg/m(2) administered once every 3 months for 2 years provided significant improvements in neurological disability ratings, including Kurtzke Expanded Disability Status Scale (EDSS), Ambulatory Index (AI) and Standardised Neurological Status (SNS) scores, compared with placebo.
  • The drug also significantly reduced the mean number of corticosteroid-treated relapses and prolonged the time to the first treated relapse, with the beneficial effects on disease progression supported by magnetic resonance imaging.
  • The drug was generally well tolerated in patients with MS.
  • In conclusion, intravenous mitoxantrone reduces the relapse rate and slows progression of the disease in patients with worsening RRMS, PRMS or SPMS; thus providing a new option for the management of these patients.
  • The drug was generally well tolerated at the recommended dosage, although potential cardiotoxicity limits the total cumulative dose to 140 mg/m(2).
  • Further studies are warranted to determine which patients with worsening RRMS, PRMS or SPMS are most likely to benefit from mitoxantrone treatment and to more fully define the long-term safety and tolerability of mitoxantrone, including the use of concomitant cardioprotectants to extend the therapeutic lifespan of the drug.
  • Mitoxantrone, a synthetic anthracenedione derivative, is an established cytotoxic, antineoplastic agent.
  • In antineoplastic studies, the drug showed several immunomodulatory effects, inducing macrophage-mediated suppression of B-cell, T-helper and T-cytotoxic lymphocyte function.
  • In an animal model of the disease, mitoxantrone suppressed the development and progression of both actively and passively induced acute experimental allergic encephalomyelitis (EAE).
  • Moreover, mitoxantrone approximately doubled the mean time to onset of EAE versus control animals (279 vs 148 days after immunisation; p < 0.00005).
  • In vitro, mitoxantrone 10 and 100 micro g/L inhibited myelin degradation by leucocytes and peritoneal macrophages derived from mice with acute EAE by approximately 60% and 100%.
  • The drug exhibits triexponential pharmacokinetics, with a rapid initial distribution (alpha) phase, an intermediate distribution (beta) phase and a much slower elimination (gamma) phase.
  • Mitoxantrone persists for prolonged periods in tissues and was detectable in autopsy tissue from patients who last received the drug up to 272 days before death.
  • At concentrations of 10-10000 ng/mL, the drug was 70-80 % bound to plasma proteins in dogs.
  • Renal clearance accounts for 10 % of the total clearance of the drug.
  • The drug appears to have a low potential for interaction with other concomitantly administered agents.
  • Intravenous mitoxantrone (infusion of > or = 5 minutes), either as monotherapy or in combination with intravenous methylprednisolone, delayed the progression of the disease in patients with secondary-progressive (SP) or worsening relapsing-remitting (RR) MS (the latter is also termed progressive-relapsing MS) in comparative, randomised, multicentre trials.
  • The drug also significantly reduced the mean number of corticosteroid-treated relapses per patient and prolonged the time to the first treated relapse.
  • Mitroxantrone was also more effective than placebo according to secondary endpoints in this study, with fewer mitoxantrone recipients experiencing a relapse, a deterioration of > or =1 EDSS point or a confirmed deterioration in EDSS score over a 3-month period.
  • Mitoxantrone recipients also showed less deterioration in quality-of-life ratings and had fewer hospital admissions, whereas more placebo recipients had new gadolinium-enhanced lesions at study end (the latter parameter was assessed using magnetic resonance imaging [MRI] in a subgroup of 110 patients, including 40 patients who received an exploratory 5 mg/m(2) dose).
  • After 6 months, significantly more combination therapy recipients had no new gadolinium-enhanced lesions (90.5% vs 31.3% with monotherapy; p < 0.001) [primary endpoint].
  • Eight percent of patients discontinued treatment in the mitoxantrone 12 mg/m(2) group due to an adverse event versus 3% of placebo recipients.
  • The incidence of drug-related acute myelogenous leukaemia was very low (0.12%) in a cohort of 802 patients with MS receiving mitoxantrone.
  • After 1 year of monotherapy, 3.4% of mitoxantrone recipients had a reduction in left ventricular ejection fraction (LVEF) to < or =50% compared with 0% of placebo recipients; at the end of the second year, respective incidences were 1.9% and 2.9% (total cumulative dose of mitoxantrone per patient was 96 mg/m(2) after 2 years' treatment). (ABSTRACT TRUNCATED)
  • [MeSH-major] Drug Evaluation. Mitoxantrone / therapeutic use. Multiple Sclerosis / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / economics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Clinical Trials as Topic / methods. Databases as Topic. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Therapy, Combination. Drug Tolerance. Humans. In Vitro Techniques. MEDLINE

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  • (PMID = 15089110.001).
  • [ISSN] 1172-7047
  • [Journal-full-title] CNS drugs
  • [ISO-abbreviation] CNS Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents; BZ114NVM5P / Mitoxantrone
  • [Number-of-references] 80
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32. Legrand O, Perrot JY, Simonin G, Baudard M, Marie JP: JC-1: a very sensitive fluorescent probe to test Pgp activity in adult acute myeloid leukemia. Blood; 2001 Jan 15;97(2):502-8
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  • [Title] JC-1: a very sensitive fluorescent probe to test Pgp activity in adult acute myeloid leukemia.
  • One of the best-characterized resistance mechanisms in acute myeloid leukemia (AML) is the drug extrusion mediated by P-glycoprotein (Pgp).
  • Nevertheless, the I group has an intermediate expression of Pgp (0.39, 0.29, and 0.19 for the R, I, and S groups, respectively, P =.002), an intermediate biologic profile (percentage of CD34, 95%, 67%, and 44%, respectively, P <.0001; in vitro resistance to daunorubicin, 94 microM, 20 microM, and 12 microM, respectively, P =.
  • 02), and an intermediate prognosis (achievement of complete remission, 55%, 65%, and 87%, P =.006; 3-year disease-free survival, 11%, 16%, and 36%, respectively, P =.005; and 3-year overall survival, 0%, 20%, and 51%, respectively, P <.0001).
  • [MeSH-major] Benzimidazoles. Carbocyanines. Leukemia, Myeloid / pathology. P-Glycoprotein / metabolism
  • [MeSH-minor] Acute Disease. Adult. Aged. Antibodies, Monoclonal. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cohort Studies. Disease-Free Survival. Flow Cytometry. Fluorescent Dyes. Humans. Immunoassay / methods. Immunoassay / standards. Immunophenotyping. Middle Aged. Multivariate Analysis. Neoplasm Proteins / immunology. Neoplasm Proteins / metabolism. Prognosis. Rhodamines. Sensitivity and Specificity. Stem Cells / chemistry. Stem Cells / pathology. Survival Rate. Treatment Outcome

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  • (PMID = 11154229.001).
  • [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 / Antibodies, Monoclonal; 0 / Benzimidazoles; 0 / Carbocyanines; 0 / Fluorescent Dyes; 0 / Neoplasm Proteins; 0 / P-Glycoprotein; 0 / Rhodamines; 21527-78-6 / 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine
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33. Liesveld JL: Acute promyelocytic leukemia-mobile and infiltrative. Leuk Res; 2007 Jan;31(1):5-7
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  • [Title] Acute promyelocytic leukemia-mobile and infiltrative.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / pathology
  • [MeSH-minor] Antigens, CD / physiology. Antigens, CD11 / physiology. Antigens, CD18 / physiology. Blast Crisis. Cell Differentiation / drug effects. Humans

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  • [CommentOn] Leuk Res. 2007 Jan;31(1):49-57 [16764927.001]
  • (PMID = 16978695.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD11; 0 / Antigens, CD18
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34. Shieh DE, Cheng HY, Yen MH, Chiang LC, Lin CC: Baicalin-induced apoptosis is mediated by Bcl-2-dependent, but not p53-dependent, pathway in human leukemia cell lines. Am J Chin Med; 2006;34(2):245-61
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  • [Title] Baicalin-induced apoptosis is mediated by Bcl-2-dependent, but not p53-dependent, pathway in human leukemia cell lines.
  • Acute lymphoblastic leukemia (ALL), especially T-acute lymphoblastic leukemia (T-ALL), is a common childhood malignant neoplastic disorder.
  • Chemotherapy agents, particularly those that can induce apoptosis, are the major intervening strategy in the treatment of ALL.
  • In this study, we investigated in T-ALL cell line, CCRF-CEM, the in vitro cytotoxic effect and the mechanism of action of baicalin, a compound extracted from Scutellaria baicalensis Georgi and S. rivularis Benth (Labiateae).
  • It triggered apoptotic effect by fragmentizing cellular DNA and arrested the cell cycle at G(0)/G(1) phase.
  • In conclusion, baicalin was found to induce apoptosis in T-ALL cell lines through multiple pathways.
  • This finding encourages further investigation of baicalin in its role as a potential candidate for chemotherapeutic agents in T-ALL.
  • [MeSH-major] Apoptosis / drug effects. Flavonoids / pharmacology. Leukemia / pathology. Proto-Oncogene Proteins c-bcl-2 / physiology. Tumor Suppressor Protein p53 / physiology
  • [MeSH-minor] Caspase 3. Caspases / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cytochromes c / metabolism. DNA / drug effects. Flow Cytometry. Humans. Membrane Potentials

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  • (PMID = 16552836.001).
  • [ISSN] 0192-415X
  • [Journal-full-title] The American journal of Chinese medicine
  • [ISO-abbreviation] Am. J. Chin. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Singapore
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 347Q89U4M5 / baicalin; 9007-43-6 / Cytochromes c; 9007-49-2 / DNA; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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35. Keating MJ, Cazin B, Coutré S, Birhiray R, Kovacsovics T, Langer W, Leber B, Maughan T, Rai K, Tjønnfjord G, Bekradda M, Itzhaki M, Hérait P: Campath-1H treatment of T-cell prolymphocytic leukemia in patients for whom at least one prior chemotherapy regimen has failed. J Clin Oncol; 2002 Jan 01;20(1):205-13
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  • [Title] Campath-1H treatment of T-cell prolymphocytic leukemia in patients for whom at least one prior chemotherapy regimen has failed.
  • PURPOSE: We conducted a retrospective analysis to evaluate the safety and efficacy of Campath-1H, an anti-CD52 humanized monoclonal antibody, in previously treated T-prolymphocytic leukemia (T-PLL) patients in a compassionate-use program.
  • PATIENTS AND METHODS: Seventy-six patients with T-PLL (including four chemotherapy-naive patients) received 3, 10, and 30 mg of Campath-1H on sequential days, followed by 30 mg three times weekly, as 2-hour intravenous infusions, for 4 to 12 weeks.
  • The most common Campath-1H-related adverse events were acute reactions during or immediately after infusions.
  • CONCLUSION: Campath-1H is an active drug in T-PLL patients for whom first-line therapy has failed.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, T-Cell / drug therapy. Salvage Therapy / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Consumer Product Safety. Female. Hematologic Diseases / chemically induced. Hematologic Diseases / epidemiology. Humans. Infusions, Intravenous. Male. Middle Aged. Opportunistic Infections / chemically induced. Opportunistic Infections / epidemiology. Retrospective Studies. Survival Rate. Time Factors

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  • (PMID = 11773171.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
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36. Mossallam GI, Abdel Hamid TM, Samra MA: Glutathione S-transferase GSTM1 and GSTT1 polymorphisms in adult acute myeloid leukemia; its impact on toxicity and response to chemotherapy. J Egypt Natl Canc Inst; 2006 Sep;18(3):264-73
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  • [Title] Glutathione S-transferase GSTM1 and GSTT1 polymorphisms in adult acute myeloid leukemia; its impact on toxicity and response to chemotherapy.
  • Pharmacogenomics, the study of inherited differences in drug disposition and effects, is emerging as a tool to predict efficacy and toxicity of drugs.
  • In this study, we investigated the impact of these polymorphisms on response and side effects of chemotherapy in adult acute myeloid leukaemia (AML) patients.
  • Overall survival and disease-free survival were similar in patients with and without the genes.
  • Studies on larger numbers are needed focusing on selection of anticancer agents to avoid adverse reactions and therapeutic failure, with special emphasis on drug toxicity and dose adjustment.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Glutathione Transferase / genetics. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / mortality. Polymorphism, Genetic
  • [MeSH-minor] Acute Disease. Adult. Aged. Female. Humans. Male. Middle Aged. Treatment Failure. Treatment Outcome

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  • (PMID = 17671537.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase
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37. Sperr WR, Hauswirth AW, Wimazal F, Knöbl P, Geissler K, Valent P: Treatment concepts for elderly patients with acute myeloid leukemia. Wien Klin Wochenschr; 2003 Aug 14;115(13-14):505-14
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  • [Title] Treatment concepts for elderly patients with acute myeloid leukemia.
  • The majority of patients with acute myeloid leukemia (AML) are over 60 years of age at diagnosis.
  • Unlike treatment options for younger adults, those for older patients are limited to non-myeloablative therapy, and many patients are not treatable because of poor performance status.
  • In responding patients (up to 60%) the disease-free survival may be almost comparable to that of younger adults.
  • The therapeutic efficiency and toxicity-profiles of these novel drugs are currently under investigation in clinical trials.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Adult. Age Factors. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic. Disease-Free Survival. Etoposide / administration & dosage. Etoposide / therapeutic use. Follow-Up Studies. Forecasting. Humans. Idarubicin / administration & dosage. Idarubicin / therapeutic use. Middle Aged. Palliative Care. Patient Selection. Randomized Controlled Trials as Topic. Thioguanine / administration & dosage. Thioguanine / therapeutic use. Time Factors

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  • (PMID = 13677269.001).
  • [ISSN] 0043-5325
  • [Journal-full-title] Wiener klinische Wochenschrift
  • [ISO-abbreviation] Wien. Klin. Wochenschr.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Austria
  • [Chemical-registry-number] 6PLQ3CP4P3 / Etoposide; FTK8U1GZNX / Thioguanine; ZRP63D75JW / Idarubicin; ETI protocol
  • [Number-of-references] 111
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38. Mazzucconi MG, Redi R, Bernasconi S, Bizzoni L, Dragoni F, Latagliata R, Santoro C, Mandelli F: A long-term study of young patients with essential thrombocythemia treated with anagrelide. Haematologica; 2004 Nov;89(11):1306-13
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  • BACKGROUND AND OBJECTIVES: Essential thrombocythemia (ET) can be complicated by life-threatening thrombosis and has a risk of converting into acute leukemia.
  • Herein, we report the results of a long-term study of patients with ET treated with anagrelide to control thrombocytosis.
  • RESULTS: A complete response (platelets < 450x10(9)/L for >1 month) was seen in 15 /34 (44%) patients and a partial response (platelets 450-600x10(9)/L for >1 month) was seen in 17/34 ( 50%), so that the some kind of response was seen in 32/34 (94%) of the patients at a median time of 4.2 months after starting treatment.
  • Seventeen patients (50%) are still being treated and have achieved platelet control for a maximum follow-up of 12.5 years.
  • This drug may be used in patients younger than 60 years, with the exclusion of women of child-bearing potential and subjects aged 40-60 years with a history of major thrombotic events.
  • [MeSH-major] Platelet Aggregation Inhibitors / therapeutic use. Quinazolines / therapeutic use. Thrombocythemia, Essential / drug therapy

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  • (PMID = 15531452.001).
  • [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 / Hemoglobins; 0 / Platelet Aggregation Inhibitors; 0 / Quinazolines; 0 / anagrelide
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39. Lü S, Chen Z, Yang J, Chen L, Zhou H, Xu X, Li J, Han F, Wang J: The effects of proteasome inhibitor bortezomib on a P-gp positive leukemia cell line K562/A02. Int J Lab Hematol; 2010 Feb;32(1 Pt 1):e123-31
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  • [Title] The effects of proteasome inhibitor bortezomib on a P-gp positive leukemia cell line K562/A02.
  • The aim of this study is to clarify the efficacy of proteasome inhibitor bortezomib to multidrug resistant (MDR) acute leukemia cells.
  • We observed the effects of bortezomib on a P-glycoprotein (P-gp) positive leukemia line K562/A02.
  • The results showed that bortezomib has significant effects on P-gp positive K562/A02 cells including cytotoxicity (48 h IC(50): 171.36 nM), induction of apoptosis (31.71 +/- 1.07% apoptotic cells after 24 h treatment at 100 nM), and inhibition of proteasome chymotrypsin-like activity (relative activity to untreated controls: 20.07 +/- 0.66% at 24 h with 10 nM bortezomib).
  • Bortezomib shows a promising effect for the treatment of refractory/relapsed leukemia, but it does not improve the effect of anthracycline to MDR leukemia cells.
  • [MeSH-major] Apoptosis / drug effects. Boronic Acids / pharmacology. Pyrazines / pharmacology
  • [MeSH-minor] Bortezomib. Chymotrypsin / antagonists & inhibitors. Drug Resistance, Multiple. Drug Resistance, Neoplasm / drug effects. Humans. Inhibitory Concentration 50. K562 Cells. Leukemia / drug therapy. P-Glycoprotein / metabolism

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  • (PMID = 19254348.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / P-Glycoprotein; 0 / Pyrazines; 69G8BD63PP / Bortezomib; EC 3.4.21.1 / Chymotrypsin
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40. Pauley JL, Panetta JC, Schmidt J, Kornegay N, Relling MV, Pui CH: Late-onset delayed excretion of methotrexate. Cancer Chemother Pharmacol; 2004 Aug;54(2):146-52
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  • We describe the clinical course and pharmacokinetics of MTX in a patient with acute lymphoblastic leukemia who experienced pleural effusions, ascites, and renal failure during the weeks after treatment with high-dose MTX (1.63 g/m2 i.v. over 24 h).
  • This unusual finding of an undetectable plasma MTX concentration that subsequently rose to persistent, potentially toxic levels was explained only by a pharmacokinetic model that accounted both for a third space at the time of treatment and for the subsequent decrease in the systemic elimination rate.
  • Therefore, the finding of a physiologic third space during MTX administration combined with the detection of renal dysfunction in the following weeks should be an indication for prolonged therapeutic drug monitoring.
  • [MeSH-major] Antimetabolites, Antineoplastic / blood. Antimetabolites, Antineoplastic / pharmacokinetics. Ascites / complications. Methotrexate / blood. Methotrexate / pharmacokinetics. Pleural Effusion / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Renal Insufficiency / complications

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  • (PMID = 15148625.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA78224
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
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41. Mistry AR, Pedersen EW, Solomon E, Grimwade D: The molecular pathogenesis of acute promyelocytic leukaemia: implications for the clinical management of the disease. Blood Rev; 2003 Jun;17(2):71-97
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  • [Title] The molecular pathogenesis of acute promyelocytic leukaemia: implications for the clinical management of the disease.
  • Acute promyelocytic leukaemia (APL) is characterised by chromosomal rearrangements of 17q21, leading to fusion of the gene encoding retinoic acid receptor alpha (RARalpha) to a number of alternative partner genes (X), the most frequent of which are PML (>95%), PLZF (0.8%) and NPM (0.5%).
  • Over the last few years, it has been established that the X-RARalpha fusion proteins play a key role in the pathogenesis of APL through recruitment of co-repressors and the histone deacetylase (HDAC)-complex to repress genes implicated in myeloid differentiation.
  • Paradoxically, the X-RARalpha fusion protein has the potential to mediate myeloid differentiation at pharmacological doses of its ligand (all trans-retinoic acid (ATRA)), which is dependent on the dissociation of the HDAC/co-repressor complex.
  • Arsenic compounds have also been shown to be promising therapeutic agents, leading to differentiation and apoptosis of APL blasts.
  • Patients at high risk of relapse can be identified by minimal residual disease monitoring.
  • The challenge for future studies is to improve complete remission rates through reduction of induction deaths, particularly due to haemorrhage, identification of patients at high risk of relapse who would benefit from additional therapy, and identification of a favourable-risk group, for which treatment intensity could be reduced, thereby reducing risks of treatment toxicity and development of secondary leukaemia/myelodysplasia.
  • With the advent of ATRA and arsenic, APL has already provided the first example of successful molecularly targeted therapy; it is hoped that with further understanding of the pathogenesis of the disease, the next decade will yield further improvements in the outlook for these patients.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / pathology
  • [MeSH-minor] Animals. Gene Rearrangement. Humans. Models, Biological. Mutation. Neoplasm, Residual / genetics. Neoplasm, Residual / pathology. Receptors, Retinoic Acid / genetics. Receptors, Retinoic Acid / metabolism. Translocation, Genetic

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  • [Copyright] Copyright 2003 Elsevier Science Ltd.
  • (PMID = 12642121.001).
  • [ISSN] 0268-960X
  • [Journal-full-title] Blood reviews
  • [ISO-abbreviation] Blood Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor alpha
  • [Number-of-references] 265
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42. Kharas MG, Okabe R, Ganis JJ, Gozo M, Khandan T, Paktinat M, Gilliland DG, Gritsman K: Constitutively active AKT depletes hematopoietic stem cells and induces leukemia in mice. Blood; 2010 Feb 18;115(7):1406-15
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  • [Title] Constitutively active AKT depletes hematopoietic stem cells and induces leukemia in mice.
  • Human cancers, including acute myeloid leukemia (AML), commonly display constitutive phosphoinositide 3-kinase (PI3K) AKT signaling.
  • However, the exact role of AKT activation in leukemia and its effects on hematopoietic stem cells (HSCs) are poorly understood.
  • Several members of the PI3K pathway, phosphatase and tensin homolog (Pten), the forkhead box, subgroup O (FOXO) transcription factors, and TSC1, have demonstrated functions in normal and leukemic stem cells but are rarely mutated in leukemia.
  • In our murine bone marrow transplantation model using a myristoylated AKT1 (myr-AKT), recipients develop myeloproliferative disease, T-cell lymphoma, or AML.


43. Tisdale JF, Dunn DE, Maciejewski J: Cyclophosphamide and other new agents for the treatment of severe aplastic anemia. Semin Hematol; 2000 Jan;37(1):102-9
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  • [Title] Cyclophosphamide and other new agents for the treatment of severe aplastic anemia.
  • Current accepted therapeutic strategies include allogeneic stem-cell transplantation and immunosuppression, both resulting in long-term survival in the majority of patients.
  • Although human leukocyte antigen (HLA)-matched sibling stem-cell transplantation is highly effective, the 25% probability of finding a suitable sibling donor within a family renders this approach available to only a minority of patients.
  • Late evolution of aplastic anemia to other serious hematologic disorders, including paroxysmal nocturnal hemoglobinuria (PNH), myelodysplasia, and acute leukemia, is also a significant problem following treatment with ATG/CSA.
  • Recently, results of immunosuppression in SAA with another potent immunosuppressive agent, cyclophosphamide, were reported in a small number of patients.
  • The overall response rate was similar to that seen with ATG/CSA, but relapse and late clonal disease were not observed during a long period of follow-up.
  • Additionally, a number of protocols designed to test the efficacy of alternative immunosuppressive or immunomodulatory agents are being developed.
  • [MeSH-major] Anemia, Aplastic / drug therapy. Cyclophosphamide / therapeutic use. Immunosuppressive Agents / therapeutic use

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  • (PMID = 10676915.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunosuppressive Agents; 0 / Receptors, Interleukin-2; 8N3DW7272P / Cyclophosphamide; 9242ECW6R0 / mycophenolate mofetil; HU9DX48N0T / Mycophenolic Acid; W36ZG6FT64 / Sirolimus; WM0HAQ4WNM / Tacrolimus
  • [Number-of-references] 75
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44. Christiansen N, Taylor KM, Duggan C: Oral chemotherapy in paediatric oncology in the UK: problems, perceptions and information needs of parents. Pharm World Sci; 2008 Oct;30(5):550-5
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  • [Title] Oral chemotherapy in paediatric oncology in the UK: problems, perceptions and information needs of parents.
  • OBJECTIVE: To identify problems, perceptions and information needs of parents and carers regarding oral chemotherapy.
  • MAIN OUTCOME MEASURES: Awareness and knowledge of medicines, information needs and handling procedures.
  • Knowledge of acute lymphoblastic leukaemia maintenance treatment was assessed in 47 interviewees; 31 parents were able to explain the reasons for maintenance chemotherapy.
  • The data suggest the majority of parents had a great interest in understanding the disease and treatment, with 91% using the internet to access further information.
  • Three-quarters of parents faced some kind of difficulty when dealing with oral chemotherapy, including problems with the patient not taking the drug, technical and supply problems and problems following the drug regimen.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Health Knowledge, Attitudes, Practice. Parents / psychology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Administration, Oral. Adult. Cancer Care Facilities. Caregivers / psychology. Child. Child, Preschool. Female. Humans. Male. Medication Adherence / psychology. Surveys and Questionnaires. United Kingdom / epidemiology

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  • (PMID = 18379895.001).
  • [ISSN] 0928-1231
  • [Journal-full-title] Pharmacy world & science : PWS
  • [ISO-abbreviation] Pharm World Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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45. Faderl S, Harris D, Van Q, Kantarjian HM, Talpaz M, Estrov Z: Granulocyte-macrophage colony-stimulating factor (GM-CSF) induces antiapoptotic and proapoptotic signals in acute myeloid leukemia. Blood; 2003 Jul 15;102(2):630-7
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  • [Title] Granulocyte-macrophage colony-stimulating factor (GM-CSF) induces antiapoptotic and proapoptotic signals in acute myeloid leukemia.
  • High levels of cytokines are associated with a poor prognosis in acute myeloid leukemia (AML).
  • However, cytokines may induce, on one hand, survival factor expression and cell proliferation and, on the other hand, expression of inhibitory signals such as up-regulation of suppressors of cytokine signaling (SOCS) and induce apoptotic cell death.
  • In the GM-CSF-responsive OCIM2 AML cell line, GM-CSF induced signal transducer and activator of transcription 5 (Stat 5) phosphorylation, up-regulated cyclin D2, and stimulated cell cycle progression.
  • Concurrently, GM-CSF stimulated expression of SOCS-2 and -3 and of procaspases 2 and 3 and induced caspase 3 activation, poly(ADP[adenosine 5'-diphosphate]-ribose) polymerase (PARP) cleavage, and apoptotic cell death.
  • GM-CSF also increased procaspase 3 protein levels in OCI/AML3 and Mo7e cells, suggesting that this phenomenon is not restricted to a single leukemia cell line.
  • Our data suggest that GM-CSF exerts a dual effect: it stimulates cell division but contemporaneously up-regulates Jak-Stat-dependent proapoptotic proteins.
  • [MeSH-major] Apoptosis / drug effects. DNA-Binding Proteins. Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology. Leukemia, Myeloid / pathology. Repressor Proteins. Trans-Activators. Transcription Factors
  • [MeSH-minor] Acute Disease. Caspases / biosynthesis. Caspases / genetics. Cell Division / drug effects. Enzyme Induction / drug effects. Enzyme Inhibitors / pharmacology. Enzyme Precursors / biosynthesis. Enzyme Precursors / genetics. Gene Expression Regulation, Neoplastic / drug effects. Genes, bcl-2. Humans. Inhibitor of Apoptosis Proteins. Leukemia, Erythroblastic, Acute / pathology. Microtubule-Associated Proteins / biosynthesis. Microtubule-Associated Proteins / genetics. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Poly(ADP-ribose) Polymerases / metabolism. Protein Biosynthesis. Proteins / genetics. Proto-Oncogene Proteins / biosynthesis. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / genetics. Recombinant Proteins / pharmacology. Signal Transduction / drug effects. Suppressor of Cytokine Signaling Proteins. Tumor Cells, Cultured / cytology. Tumor Cells, Cultured / drug effects. Tumor Stem Cell Assay. Tyrphostins / pharmacology. X-Linked Inhibitor of Apoptosis Protein. bcl-2-Associated X Protein. bcl-X Protein

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  • (PMID = 12663443.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA49639; United States / NCI NIH HHS / CA / P01 CA55164
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / BCL2L1 protein, human; 0 / BIRC5 protein, human; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Enzyme Precursors; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Recombinant Proteins; 0 / Repressor Proteins; 0 / SOCS2 protein, human; 0 / SOCS3 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tyrphostins; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human; 0 / alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspases
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46. Curbo S, Karlsson A: Nelarabine: a new purine analog in the treatment of hematologic malignancies. Rev Recent Clin Trials; 2006 Sep;1(3):185-92
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  • It has been shown that nelarabine has activity as a single agent in patients with T-cell malignancies that have relapsed or are refractory to other therapy.
  • Food and Drug Administration (FDA) for treatment of patients with T-cell acute lymphoblastic leukemia and lymphoblastic lymphoma who have not responded to or whose disease has progressed during treatment with at least two standard regimens.
  • It is likely that nelarabine will be a useful drug in the treatment of leukemic diseases in the future and therefore nelarabine is an interesting drug to study further.
  • [MeSH-major] Arabinonucleosides / therapeutic use. Hematologic Neoplasms / drug therapy
  • [MeSH-minor] Clinical Trials as Topic. DNA Repair / drug effects. Dose-Response Relationship, Drug. Drug Resistance. Drug Therapy, Combination. Humans. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Phosphorylation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Treatment Outcome. Vidarabine / analogs & derivatives. Vidarabine / pharmacology. Vidarabine / therapeutic use

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  • (PMID = 18473971.001).
  • [ISSN] 1574-8871
  • [Journal-full-title] Reviews on recent clinical trials
  • [ISO-abbreviation] Rev Recent Clin Trials
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Arabinonucleosides; 38819-10-2 / 9-arabinofuranosylguanine; 60158CV180 / nelarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Number-of-references] 47
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47. Park S, Han SS, Park CH, Hahm ER, Lee SJ, Park HK, Lee SH, Kim WS, Jung CW, Park K, Riordan HD, Kimler BF, Kim K, Lee JH: L-Ascorbic acid induces apoptosis in acute myeloid leukemia cells via hydrogen peroxide-mediated mechanisms. Int J Biochem Cell Biol; 2004 Nov;36(11):2180-95
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  • [Title] L-Ascorbic acid induces apoptosis in acute myeloid leukemia cells via hydrogen peroxide-mediated mechanisms.
  • L-Ascorbic acid (LAA) is being investigated clinically for the treatment of patients with acute myeloid leukemia (AML) based on the observed effects of LAA on AML progenitor cells in vitro.
  • LAA at concentrations of 0.25-1.0 mM induced a dose- and time-dependent inhibition of proliferation in three AML cell lines and also in leukemic cells from peripheral blood specimens obtained from three patients with AML.
  • In contrast, ovarian cancer cell lines were only minimally affected.
  • Flow cytometric analysis showed that LAA at concentrations of 0.25-1.0 mM could significantly induce apoptosis in the AML cell lines.
  • [MeSH-major] Apoptosis / drug effects. Ascorbic Acid / pharmacology. Cell Proliferation / drug effects. Leukemia, Myeloid, Acute / drug therapy. Mitochondria / metabolism
  • [MeSH-minor] Caspase 3. Caspase 9. Caspases / metabolism. Cytochromes c / metabolism. Enzyme Activation / drug effects. Enzyme Activation / physiology. Glutathione / metabolism. HL-60 Cells. Humans. Hydrogen Peroxide / metabolism. Oxidation-Reduction / drug effects. Tumor Cells, Cultured

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  • (PMID = 15313465.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 9007-43-6 / Cytochromes c; BBX060AN9V / Hydrogen Peroxide; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases; GAN16C9B8O / Glutathione; PQ6CK8PD0R / Ascorbic Acid
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48. Mayani H, Flores-Figueroa E, Chávez-González A: In vitro biology of human myeloid leukemia. Leuk Res; 2009 May;33(5):624-37
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  • [Title] In vitro biology of human myeloid leukemia.
  • For about 40 years, the biology of human myeloid leukemia (ML) has been studied in different in vitro systems.
  • Throughout this time, semisolid colony assays, Dexter-type long-term cultures and liquid suspension cultures have contributed to our understanding of the mechanisms involved in the origin and progression of this hematological disorder.
  • By using such systems, it has been possible to identify the cells in which leukemia originates; to recognize a functional hierarchy within the hematopoietic system of leukemia patients; to identify factors, soluble and cell-associated, that regulate leukemic growth; and to study the effects of different antineoplastic drugs.
  • Still, many questions and problems remain unsolved regarding the biology of myeloid leukemia in vitro.
  • This article presents a comprehensive review on the behavior of leukemic stem and progenitor cells, both from acute and chronic myeloid leukemia, in the different culture systems mentioned above.
  • [MeSH-major] Leukemia, Myeloid / pathology
  • [MeSH-minor] Cell Division. Humans. Tumor Cells, Cultured

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  • (PMID = 19108888.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 199
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49. Cataland SR, Daugherty CK, Weseman EC, Larson RA: Preliminary experience with a new chemotherapy regimen for adults with acute lymphoblastic leukemia. Leuk Lymphoma; 2001 Apr;41(3-4):297-307
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  • [Title] Preliminary experience with a new chemotherapy regimen for adults with acute lymphoblastic leukemia.
  • We treated 11 consecutive adult patients who presented with acute lymphoblastic leukemia to the University of Chicago with a novel, intensified chemotherapy regimen to evaluate the feasibility and toxicity of this program.
  • Following a 5-drug induction therapy (course A), patients received sequential courses (B and C) of high-dose antimetabolite therapies, in part to replace cranial irradiation for CNS prophylaxis.
  • The Cancer and Leukemia Group B is presently evaluating the efficacy of this regimen in a large phase II trial (CALGB study 19802).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cause of Death. Cyclophosphamide / administration & dosage. Cytogenetic Analysis. Disease-Free Survival. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Male. Methotrexate / blood. Methotrexate / pharmacokinetics. Middle Aged. Pilot Projects

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  • (PMID = 11378542.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 8N3DW7272P / Cyclophosphamide; YL5FZ2Y5U1 / Methotrexate
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50. George P, Bali P, Annavarapu S, Scuto A, Fiskus W, Guo F, Sigua C, Sondarva G, Moscinski L, Atadja P, Bhalla K: Combination of the histone deacetylase inhibitor LBH589 and the hsp90 inhibitor 17-AAG is highly active against human CML-BC cells and AML cells with activating mutation of FLT-3. Blood; 2005 Feb 15;105(4):1768-76
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  • Present studies show that LBH589, a novel cinnamic hydroxamic acid analog histone deacetylase inhibitor, induces acetylation of histone H3 and H4 and of heat shock protein 90 (hsp90), increases p21 levels, as well as induces cell-cycle G(1) phase accumulation and apoptosis of the human chronic myeloid leukemia blast crisis (CML-BC) K562 cells and acute leukemia MV4-11 cells with the activating length mutation of FLT-3.
  • In MV4-11 cells, this was associated with marked attenuation of the protein levels of p-FLT-3, FLT-3, p-AKT, and p-ERK1/2.
  • In the imatinib mesylate (IM)-refractory leukemia cells expressing Bcr-Abl with the T315I mutation, treatment with the combination attenuated the levels of the mutant Bcr-Abl and induced apoptosis.
  • Finally, cotreatment with LBH589 and 17-AAG also induced more apoptosis of IM-resistant primary CML-BC and acute myeloid leukemia (AML) cells (with activating mutation of FLT-3) than treatment with either agent alone.
  • [MeSH-major] Blast Crisis / metabolism. Enzyme Inhibitors / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Histone Deacetylase Inhibitors. Hydroxamic Acids / analogs & derivatives. Hydroxamic Acids / pharmacology. Leukemia, Myeloid / metabolism. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / genetics. Rifabutin / analogs & derivatives. Rifabutin / pharmacology
  • [MeSH-minor] Acute Disease. Apoptosis / drug effects. Benzamides. Benzoquinones. Cell Line, Tumor. Drug Combinations. Drug Synergism. Fusion Proteins, bcr-abl / antagonists & inhibitors. Fusion Proteins, bcr-abl / genetics. Fusion Proteins, bcr-abl / metabolism. Gene Deletion. Gene Expression Regulation. Humans. Imatinib Mesylate. Indoles. K562 Cells. Lactams, Macrocyclic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / enzymology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Piperazines / pharmacology. Point Mutation. Polyubiquitin / metabolism. Proteasome Endopeptidase Complex / metabolism. Pyrimidines / pharmacology. fms-Like Tyrosine Kinase 3

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  • (PMID = 15514006.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA95188
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Benzoquinones; 0 / Drug Combinations; 0 / Enzyme Inhibitors; 0 / HSP90 Heat-Shock Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Indoles; 0 / Lactams, Macrocyclic; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Pyrimidines; 120904-94-1 / Polyubiquitin; 1W306TDA6S / Rifabutin; 4GY0AVT3L4 / tanespimycin; 8A1O1M485B / Imatinib Mesylate; 9647FM7Y3Z / panobinostat; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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51. Muszyńska-Rosłan K, Krawczuk-Rybak M, Protas PT, Hołownia A: Level of tau protein in children treated for acute lymphoblastic leukemia. Pediatr Neurol; 2006 May;34(5):367-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Level of tau protein in children treated for acute lymphoblastic leukemia.
  • Long-term neuropsychological complications such as attention and concentration disturbances, poor school performance, hyperexcitability, and even leukoencephalopathy have been described in children after chemotherapy for acute lymphoblastic leukemia.
  • The aim of the study was to assess the level of cerebrospinal fluid tau protein in children with acute lymphoblastic leukemia.
  • The study included 26 patients with acute lymphoblastic leukemia and 19 patients with clinical symptoms of cerebrospinal meningitis (reference group).
  • The examination was performed at diagnosis, after induction treatment, during consolidation, and after reinduction, i.e. before maintenance therapy.
  • The mean tau protein value at diagnosis was 244.84 +/- 98.96 pg/mL in the study group (norm 300 pg/mL) and produced no correlation with initial leukocytosis, lactate dehydrogenase activity, or organomegaly at this point.
  • Dynamic analysis revealed a statistically significant increase in tau protein after induction treatment (431.25 +/- 232.50) as compared with its level at diagnosis (244.84 +/- 98.96, P < 0.008) and later during treatment.
  • This finding requires further studies, also in reference to other central nervous system proteins, and confirms the necessity of long-term follow-up of leukemia patients.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Brain Diseases / cerebrospinal fluid. Brain Diseases / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. tau Proteins / cerebrospinal fluid
  • [MeSH-minor] Adolescent. Biomarkers / cerebrospinal fluid. Child. Child, Preschool. Female. Humans. Infant. Leukemia, B-Cell / cerebrospinal fluid. Leukemia, B-Cell / drug therapy. Leukemia, T-Cell / cerebrospinal fluid. Leukemia, T-Cell / drug therapy. Male. Meningitis / cerebrospinal fluid

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  • (PMID = 16647996.001).
  • [ISSN] 0887-8994
  • [Journal-full-title] Pediatric neurology
  • [ISO-abbreviation] Pediatr. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers; 0 / tau Proteins
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52. Soki H, Nagase Y, Yamazaki K, Oda T, Kikuchi K: [Isolation of the yeast-like fungus Stephanoascus ciferrii by culturing the aural discharge of a patient with intractable otitis media. Case report]. Kansenshogaku Zasshi; 2010 Mar;84(2):210-2
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  • [Title] [Isolation of the yeast-like fungus Stephanoascus ciferrii by culturing the aural discharge of a patient with intractable otitis media. Case report].
  • As longer lives have become possible due to advances in medical technology and diagnostic technology in recent years, weakly toxic fungus have been emerging as causative agents of opportunistic infections, primarily in high-risk groups.
  • We report a case in which the yeast-like fungus Stephanoascus ciferii, which has morphological characteristics that differ from those of the more common Candida species, was isolated by culturing the aural discharge of a patient with intractable otitis media.
  • Drug susceptibility testing showed that it was resistant to fluconazole, flucytosine, and itraconazole, suggesting that it is a species that has a strong tendency to become resistant.
  • The principal sites of infection by Stephanoascus ciferii are thought to be in the ENT area, but in other countries it has been isolated from patients with acute myeloid leukemia and immunodeficiency as well as superficial mycoses, and it may also be a causative agent of deep mycoses.

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  • (PMID = 20420168.001).
  • [ISSN] 0387-5911
  • [Journal-full-title] Kansenshōgaku zasshi. The Journal of the Japanese Association for Infectious Diseases
  • [ISO-abbreviation] Kansenshogaku Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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53. Hoang T: Of mice and men: how an oncogene transgresses the limits and predisposes to T cell acute lymphoblastic leukemia. Sci Transl Med; 2010 Mar 3;2(21):21ps10
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  • [Title] Of mice and men: how an oncogene transgresses the limits and predisposes to T cell acute lymphoblastic leukemia.
  • The gene encoding LIM-only 2 (LMO2), an oncogenic transcription factor, is frequently activated in T cell acute lymphoblastic leukemia (T-ALL), but how LMO2 transforms primary hematopoietic cells to induce T-ALL remains an open question.
  • These leukemia-initiating cells are resistant to irradiation, indicating the need to develop new therapeutic drugs that specifically target the oncogene itself.
  • [MeSH-major] DNA-Binding Proteins / genetics. Genetic Predisposition to Disease. Metalloproteins / genetics. Oncogenes / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Humans. LIM Domain Proteins. Mice. Proto-Oncogene Proteins. T-Lymphocytes / metabolism. T-Lymphocytes / pathology

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  • (PMID = 20374994.001).
  • [ISSN] 1946-6242
  • [Journal-full-title] Science translational medicine
  • [ISO-abbreviation] Sci Transl Med
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins
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54. Kees UR, Ford J, Watson M, Murch A, Ringńer M, Walker RL, Meltzer P: Gene expression profiles in a panel of childhood leukemia cell lines mirror critical features of the disease. Mol Cancer Ther; 2003 Jul;2(7):671-7
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  • [Title] Gene expression profiles in a panel of childhood leukemia cell lines mirror critical features of the disease.
  • The development of new drugs against cancer requires established cell lines.
  • They are needed for in vitro studies to identify candidate drugs and in xenograft models to measure drug efficacy in vivo.
  • Specific criteria need to be fulfilled by cell lines used in the evaluation of potential novel therapeutic agents.
  • In this study, we have examined these aspects for pediatric acute lymphoblastic leukemia.
  • A panel of 13 leukemia cell lines recently established in our laboratory was analyzed.
  • Importantly, the panel of lines displayed the critical genetic features identified in clinically important acute lymphoblastic leukemia subtypes in childhood leukemia patients.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Leukemic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 12883040.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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55. Kim SH, Cho SS, Simkhada JR, Lee HJ, Kim SW, Kim TS, Yoo JC: Enhancement of 1,25-dihydroxyvitamin D3- and all-trans retinoic acid-induced HL-60 leukemia cell differentiation by Panax ginseng. Biosci Biotechnol Biochem; 2009 May;73(5):1048-53
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  • [Title] Enhancement of 1,25-dihydroxyvitamin D3- and all-trans retinoic acid-induced HL-60 leukemia cell differentiation by Panax ginseng.
  • Meyer) has a wide range of therapeutic uses including cancer treatment.
  • Human promyelocytic leukemia cells differentiate into monocytes or granulocytes when treated with 1,25-dihydroxyvitamin D(3) [1,25-(OH)(2)D(3)] or all-trans retinoic acid (ATRA).
  • Treatment of HL-60 cells with zero to 100 microg/ml of a methanol extract of ginseng for 72 h induced a small increase in cell differentiation.
  • The inhibitors of protein kinase C (PKC) and extracellular signal-regulated kinase (ERK), but not of phosphoinositide 3-kinase (PI3-K), inhibited the HL-60 differentiation induced by the extract in combination with ATRA or 1,25-(OH)(2)D(3), signifying that PKC and ERK were involved in the cell differentiation enhancement by the extract.
  • These results suggest that the ability of a methanol extract of ginseng to enhance the differentiation potential of ATRA or 1,25-(OH)(2)D(3) may improve the ultimate outcome of acute promyelocytic leukemia therapy.
  • [MeSH-major] Calcitriol / pharmacology. Cell Differentiation / drug effects. Panax / chemistry. Plant Extracts / pharmacology. Tretinoin / pharmacology
  • [MeSH-minor] Dose-Response Relationship, Drug. HL-60 Cells. Humans. Methanol / chemistry. Protein Kinase Inhibitors / pharmacology

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  • (PMID = 19420713.001).
  • [ISSN] 1347-6947
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Plant Extracts; 0 / Protein Kinase Inhibitors; 5688UTC01R / Tretinoin; FXC9231JVH / Calcitriol; Y4S76JWI15 / Methanol
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56. Cortes J, Kantarjian HM: Promising approaches in acute leukemia. Invest New Drugs; 2000 Feb;18(1):57-82
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  • [Title] Promising approaches in acute leukemia.
  • In the last few decades, there has been a significant improvement in the prognosis of patients with acute leukemias.
  • In recent years there has been a great surge in the understanding of the molecular mechanisms of disease which have provided us with new targets for anti-leukemia therapy.
  • These range from chemotherapeutic agents with novel mechanisms of action, such as topoisomerase I inhibitors or demethylating agents, to reversal of drug-resistance mechanisms, to monoclonal antibodies directed against specific antigens, and targeted therapy that inhibit the function of molecules such as tyrosine kinases or Ras.
  • The research on many of these agents is still in the early phases, but these new approaches offer the promise of finding a cure for the majority of patients with leukemia in the near future.
  • Here we describe some of the promising approaches that are currently being investigated in the treatment of acute leukemias.
  • [MeSH-major] Leukemia / therapy
  • [MeSH-minor] Acute Disease. Animals. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Humans. Immunotherapy. Leukemia, Experimental / drug therapy

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  • (PMID = 10830141.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents
  • [Number-of-references] 284
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57. Nurmio M, Keros V, Lähteenmäki P, Salmi T, Kallajoki M, Jahnukainen K: Effect of childhood acute lymphoblastic leukemia therapy on spermatogonia populations and future fertility. J Clin Endocrinol Metab; 2009 Jun;94(6):2119-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of childhood acute lymphoblastic leukemia therapy on spermatogonia populations and future fertility.
  • CONTEXT: Isolation of spermatogonial stem cells before potentially sterilizing cancer therapy, followed by transplantation of these cells into the testis after such treatment, may be an effective approach to prevent infertility among prepubertal boys suffering from acute lymphoblastic leukemia (ALL).
  • A key clinical consideration in this context is the timing of biopsy, if collection of spermatogonia could be delayed from diagnosis to the later phase of leukemia treatment, better patient selection could be offered.
  • OBJECTIVE: The objective of the study was to examine the routine testicular biopsy material collected to detect testicular leukemia to evaluate if treatment for leukemia affects numbers and maturation of the spermatogonia during the prepubertal period.
  • OUTCOME MEASURE: Samples were stained immunohistochemically to evaluate the expression of the spermatogonial markers MAGE 4A, OCT4, CD9, and AP2gamma, and of the Sertoli cell marker WT-1.
  • No significant alteration in spermatogonial numbers was associated with testicular leukemia.
  • CONCLUSION: Treatment for childhood leukemia without high-dose cyclophosphamide seldom depletes the spermatogonial stem cell pool totally.
  • [MeSH-major] Cyclophosphamide / adverse effects. Fertility / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sperm Count. Spermatogonia / pathology
  • [MeSH-minor] Adolescent. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Alkylating / therapeutic use. Child. Child, Preschool. Humans. Infertility, Male / chemically induced. Infertility, Male / pathology. Infertility, Male / prevention & control. Male. Puberty / drug effects. Puberty / physiology. Testis / pathology. Testis / physiology

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
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  • (PMID = 19318447.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
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58. Ersvaer E, Kittang AO, Hampson P, Sand K, Gjertsen BT, Lord JM, Bruserud O: The protein kinase C agonist PEP005 (ingenol 3-angelate) in the treatment of human cancer: a balance between efficacy and toxicity. Toxins (Basel); 2010 01;2(1):174-94
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  • Direct pro-apoptotic effects of this drug have been demonstrated in several malignant cells, including melanoma cell lines and primary human acute myelogenous leukemia cells.
  • At micromolar concentrations required to kill melanoma cells this agent causes PKC-independent secondary necrosis.
  • However, in addition to this pro-apoptotic effect the agent seems to have immunostimulatory effects, including: (i) increased chemokine release by malignant cells;.
  • (ii) a general increase in proliferation and cytokine release by activated T cells, including T cells derived from patients with chemotherapy-induced lymphopenia;.
  • (iii) local infiltration of neutrophils after topical application with increased antibody-dependent cytotoxicity; and (iv) development of specific anti-cancer immune responses by CD8(+) T cells in animal models.
  • Published studies mainly describe effects from in vitro investigations or after topical application of the agent, and careful evaluation of the toxicity after systemic administration is required before the possible use of this agent in the treatment of malignancies other than skin cancers.
  • [MeSH-minor] Animals. Humans. Isoenzymes / metabolism. Melanoma. Necrosis

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  • (PMID = 22069553.001).
  • [ISSN] 2072-6651
  • [Journal-full-title] Toxins
  • [ISO-abbreviation] Toxins (Basel)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.7.11.13 / Protein Kinase C-delta
  • [Other-IDs] NLM/ PMC3206618
  • [Keywords] NOTNLM ; cancer-protein kinase C-PEP005 (major topic)
  • [General-notes] NLM/ Original DateCompleted: 20111110
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59. van der Kolk DM, de Vries EG, Müller M, Vellenga E: The role of drug efflux pumps in acute myeloid leukemia. Leuk Lymphoma; 2002 Apr;43(4):685-701
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  • [Title] The role of drug efflux pumps in acute myeloid leukemia.
  • A major problem in the treatment of patients with acute myeloid leukemia (AML) is the occurrence of resistance to structurally and functionally unrelated chemotherapeutic agents, called multidrug resistance (MDR).
  • Permeability-glycoprotein (P-gp), the best characterized of the human drug efflux pumps, has been shown to be associated with poor treatment outcome in AML patients.
  • Alternative transporter proteins, such as the MRP1 homologues MRP2, MRP3, MRP5 and MRP6, and the breast cancer resistance protein (BCRP), have been shown to be expressed at variable levels in AML patient cells.
  • The latter proteins have been described to confer resistance to chemotherapeutic agents, such as daunorubicin, mitoxantrone, etoposide and 6-mercaptopurine, which are generally used in the treatment of AML patients; however, theyhave not yet proven to play a role in drug resistance in AML.
  • The present review gives an overview of the current knowledge concerning these drug transporters, with a focus on the role of the transporter proteins in AML.
  • [MeSH-major] ATP-Binding Cassette Transporters / physiology. ATP-Binding Cassette, Sub-Family B, Member 1 / physiology. Drug Resistance, Multiple. Leukemia, Myeloid, Acute / drug therapy. Neoplasm Proteins
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Animals. Biological Transport. Drug Resistance, Neoplasm. Hematopoiesis. Humans. Mice

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  • (PMID = 12153153.001).
  • [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; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Neoplasm Proteins
  • [Number-of-references] 231
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60. Piccaluga PP, Visani G, Martinelli G, Isidori A, Malagola M, Rondoni M, Baccarani M, Tura S: Liposomal daunorubicin (DaunoXome) for treatment of relapsed meningeal acute myeloid leukemia. Leukemia; 2002 Sep;16(9):1880-1
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  • [Title] Liposomal daunorubicin (DaunoXome) for treatment of relapsed meningeal acute myeloid leukemia.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Daunorubicin / administration & dosage. Leukemia, Myeloid / drug therapy. Meningeal Neoplasms / diagnosis
  • [MeSH-minor] Acute Disease. Adult. Drug Carriers. Female. Humans. Liposomes. Male. Neoplasm Recurrence, Local / drug therapy

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  • (PMID = 12200714.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Drug Carriers; 0 / Liposomes; ZS7284E0ZP / Daunorubicin
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61. Qian WB, Lin MF: [Study on the up-regulation of B7 molecules expression and immunogenicity of acute leukemia cells induced by interleukin 7]. Zhonghua Xue Ye Xue Za Zhi; 2005 May;26(5):289-92
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  • [Title] [Study on the up-regulation of B7 molecules expression and immunogenicity of acute leukemia cells induced by interleukin 7].
  • OBJECTIVE: To investigate the effects of interleukin 7 (IL-7) on B7 molecules expression and immunogenicity of acute leukemia (AL) cells.
  • METHODS: The B7 molecules expression on fresh acute leukemia cells and on the IL-7 exposed leukemia cells was detected by FACScan cytometer.
  • The stimulation of proliferation of allogeneic peripheral blood mononuclear cells (PBMNC) by IL-7 treated leukemia cells was detected by MTT method.
  • IL-7 treated leukemia cells could stimulate PBMNC proliferation and promote their IFN-gamma production.
  • The IL-7-treated leukemia cells can significantly stimulate the proliferation of allogeneic PBMNC and induce their IFN gamma secretion.
  • [MeSH-major] Antigens, CD80 / metabolism. Antigens, CD86 / metabolism. Interleukin-7 / pharmacology. Leukemia / metabolism
  • [MeSH-minor] Humans. RNA, Messenger / genetics. Tumor Cells, Cultured. Up-Regulation / drug effects

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  • (PMID = 15949292.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Antigens, CD86; 0 / Interleukin-7; 0 / RNA, Messenger
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62. Elhasid R, Sahar D, Merling A, Zivony Y, Rotem A, Ben-Arush M, Izraeli S, Bercovich D, Larisch S: Mitochondrial pro-apoptotic ARTS protein is lost in the majority of acute lymphoblastic leukemia patients. Oncogene; 2004 Jul 15;23(32):5468-75
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  • [Title] Mitochondrial pro-apoptotic ARTS protein is lost in the majority of acute lymphoblastic leukemia patients.
  • Here, we report that the expression of ARTS is lost in all lymphoblasts of more than 70% of childhood acute lymphoblastic leukemia (ALL) patients.
  • The loss of ARTS is specific, as the related non-apoptotic protein H5, bearing 83% identity to ARTS, is unaffected.
  • Two leukemic cell lines, ALL-1 and HL-60 lacking ARTS, were resistant to apoptotic induction by ara-C.
  • Transfection of ARTS into these cells restored their ability to undergo apoptosis in response to this chemotherapeutic agent.
  • [MeSH-major] Mitochondria / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Bone Marrow / metabolism. Cytoskeletal Proteins / genetics. Cytoskeletal Proteins / metabolism. GTP Phosphohydrolases / genetics. GTP Phosphohydrolases / metabolism. Humans. RNA, Messenger / blood. RNA, Messenger / metabolism. Septins

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  • [ErratumIn] Oncogene. 2004 Dec 16;23(58):9450
  • (PMID = 15122323.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / RNA, Messenger; EC 3.6.1.- / GTP Phosphohydrolases; EC 3.6.1.- / SEPT4 protein, human; EC 3.6.1.- / Septins
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63. Cortes J, Giles F, O'Brien S, Thomas D, Albitar M, Rios MB, Talpaz M, Garcia-Manero G, Faderl S, Letvak L, Salvado A, Kantarjian H: Results of imatinib mesylate therapy in patients with refractory or recurrent acute myeloid leukemia, high-risk myelodysplastic syndrome, and myeloproliferative disorders. Cancer; 2003 Jun 1;97(11):2760-6
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  • [Title] Results of imatinib mesylate therapy in patients with refractory or recurrent acute myeloid leukemia, high-risk myelodysplastic syndrome, and myeloproliferative disorders.
  • BACKGROUND: Imatinib mesylate is a selective tyrosine kinase inhibitor of c-abl, bcr/abl, c-kit, and platelet-derived growth factor-receptor (PDGF-R).
  • c-kit is expressed in most patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) and PDGF has been implicated in the pathogenesis of myeloproliferative disorders (MPD).
  • Forty-eight patients with AML (n = 10), MDS (n = 8), myelofibrosis (n = 18), atypical chronic myeloid leukemia (CML; n = 7), chronic myelomonocytic leukemia (CMML; n = 3), or polycythemia vera (n = 2) were treated with imatinib 400 mg daily.
  • CONCLUSIONS: Within these small subgroups of disease types, single-agent imatinib did not achieve a significant clinical response among patients with AML, MDS, atypical CML, or CMML without PDGF-R fusion genes.
  • Therefore, a combination treatment regimen including imatinib may be more effective.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Myeloproliferative Disorders / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Benzamides. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelomonocytic, Chronic / drug therapy. Middle Aged. Polycythemia Vera / drug therapy. Primary Myelofibrosis / drug therapy. Recurrence


64. Safa M, Kazemi A, Zand H, Azarkeivan A, Zaker F, Hayat P: Inhibitory role of cAMP on doxorubicin-induced apoptosis in pre-B ALL cells through dephosphorylation of p53 serine residues. Apoptosis; 2010 Feb;15(2):196-203
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  • Exposure of cells to chemotherapeutic drug doxorubicin, a DNA-damaging agent, induces an increase in the levels and activity of the wild-type p53 protein.
  • Here we show that elevation of cAMP in pre-B acute lymphoblastic leukemia NALM-6 cells significantly attenuated phosphorylation state of p53 at Ser6, Ser9, Ser15, Ser20, Ser37, Ser46 and Ser392 upon exposure to doxorubicin.
  • Increased cAMP levels also shifted the ratio of the death promoter to death repressor genes via alteration of Bcl-2 and Bax proteins expression.
  • [MeSH-major] Apoptosis / drug effects. Cyclic AMP / pharmacology. Doxorubicin / pharmacology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Serine / metabolism
  • [MeSH-minor] Ataxia Telangiectasia Mutated Proteins. Caspase 3 / metabolism. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Checkpoint Kinase 2. DNA Damage. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Leukemic / drug effects. Humans. Intracellular Space / drug effects. Intracellular Space / metabolism. Okadaic Acid / pharmacology. Phosphoprotein Phosphatases / metabolism. Phosphorylation / drug effects. Phosphoserine / metabolism. Protein Phosphatase 1 / metabolism. Protein Phosphatase 2 / metabolism. Protein-Serine-Threonine Kinases / metabolism. Tumor Suppressor Protein p53 / metabolism. Tumor Suppressor Proteins / metabolism. bcl-2-Associated X Protein / metabolism

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  • (PMID = 19882354.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / bcl-2-Associated X Protein; 17885-08-4 / Phosphoserine; 1W21G5Q4N2 / Okadaic Acid; 452VLY9402 / Serine; 80168379AG / Doxorubicin; E0399OZS9N / Cyclic AMP; EC 2.7.1.11 / Checkpoint Kinase 2; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / CHEK2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 1; EC 3.1.3.16 / Protein Phosphatase 2; EC 3.1.3.16 / protein phosphatase 2C; EC 3.4.22.- / Caspase 3
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65. Baker SK, Lipson DM: Vincristine-induced peripheral neuropathy in a neonate with congenital acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2010 Apr;32(3):e114-7
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  • [Title] Vincristine-induced peripheral neuropathy in a neonate with congenital acute lymphoblastic leukemia.
  • We report the case of a 46-day-old boy with a fulminant vincristine-induced peripheral neuropathy after treatment for congenital acute lymphoblastic leukemia.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Peripheral Nervous System Diseases / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / congenital. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vincristine / adverse effects
  • [MeSH-minor] Acetylcysteine / therapeutic use. Carnitine / therapeutic use. Drug Therapy, Combination. Free Radical Scavengers / therapeutic use. Humans. Infant. Male. Pyridoxine / therapeutic use. Vitamin B Complex / therapeutic use

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  • (PMID = 20216233.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Free Radical Scavengers; 12001-76-2 / Vitamin B Complex; 5J49Q6B70F / Vincristine; KV2JZ1BI6Z / Pyridoxine; S7UI8SM58A / Carnitine; WYQ7N0BPYC / Acetylcysteine
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66. Lahaye T, Riehm B, Berger U, Paschka P, Müller MC, Kreil S, Merx K, Schwindel U, Schoch C, Hehlmann R, Hochhaus A: Response and resistance in 300 patients with BCR-ABL-positive leukemias treated with imatinib in a single center: a 4.5-year follow-up. Cancer; 2005 Apr 15;103(8):1659-69
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  • [Title] Response and resistance in 300 patients with BCR-ABL-positive leukemias treated with imatinib in a single center: a 4.5-year follow-up.
  • BACKGROUND: The advent of imatinib has considerably changed the treatment of chronic myeloid leukemia (CML).
  • Early studies demonstrated high rates of hematologic and cytogenetic responses in all phases of the disease after limited observation periods.
  • METHODS: The authors evaluated long-term outcome, rates of response, and resistance in 300 patients with BCR-ABL-positive leukemias (CML in chronic phase after failure to respond to interferon-alpha [CP], n = 139; accelerated phase [AP], n = 80; myeloid blast crisis [BC], n = 76; lymphoid BC and Philadelphia chromosome-positive acute lymphoblastic leukemia, n = 5) who entered clinical trials with imatinib in a single center after an observation time of 4.5 years.
  • In myeloid BC, the median survival period after the start of imatinib and after diagnosis of BC was 6 and 9 months, respectively.
  • CONCLUSIONS: The data emphasized the need for a prolonged follow-up of patients treated with imatinib to define the clinical potential of the drug and to establish methods to optimize therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Fusion Proteins, bcr-abl / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Neoplasm Recurrence, Local / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Benzamides. Blast Crisis. Cytogenetic Analysis. Female. Humans. Imatinib Mesylate. Interferon-alpha / adverse effects. Male. Middle Aged. Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction. Salvage Therapy. Survival Rate. Treatment Outcome

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  • [Copyright] (c) 2005 American Cancer Society.
  • (PMID = 15747376.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Interferon-alpha; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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67. Rodig SJ, Abramson JS, Pinkus GS, Treon SP, Dorfman DM, Dong HY, Shipp MA, Kutok JL: Heterogeneous CD52 expression among hematologic neoplasms: implications for the use of alemtuzumab (CAMPATH-1H). Clin Cancer Res; 2006 Dec 1;12(23):7174-9
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  • The humanized monoclonal antibody alemtuzumab (CAMPATH-1H) is specific for CD52 and is Food and Drug Administration - approved for the treatment of relapsed or refractory chronic lymphocytic leukemia (CLL).
  • RESULTS: The vast majority of low-grade B cell lymphoproliferative disorders (CLL/small lymphocytic leukemia, follicular lymphoma, lymphoplasmacytic lymphoma, hairy cell leukemia, and mucosa-associated lymphoid tissue lymphomas) express CD52.
  • In addition, we found that the majority of precursor B cell acute lymphoblastic leukemia/lymphomas express this antigen.
  • In contrast, there is surprising heterogeneity in CD52 expression among more aggressive B cell lymphomas, with 25% of cases of diffuse large B cell lymphoma and Burkitt lymphoma demonstrating no detectable CD52.
  • In addition, the majority of neoplasms of the T cell lineage are negative for the antigen, including most cases of precursor T cell acute lymphoblastic leukemia/lymphoma, anaplastic large cell lymphoma, and peripheral T cell lymphoma, not otherwise specified.
  • Finally, the vast majority of cases of acute myeloid leukemia, Hodgkin lymphoma, and multiple myeloma are negative for CD52 expression.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antigens, CD / biosynthesis. Antigens, Neoplasm / biosynthesis. Glycoproteins / biosynthesis. Leukemia, Myeloid. Lymphoma, B-Cell. Lymphoma, T-Cell. Lymphoproliferative Disorders
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal, Humanized. Humans. Immunohistochemistry. Treatment Outcome

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  • (PMID = 17145843.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
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68. Nasr R, de Thé H: Eradication of acute promyelocytic leukemia-initiating cells by PML/RARA-targeting. Int J Hematol; 2010 Jun;91(5):742-7
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  • [Title] Eradication of acute promyelocytic leukemia-initiating cells by PML/RARA-targeting.
  • Acute promyelocytic leukemia (APL) is characterized by a t(15;17) translocation that yields a PML/RARA fusion protein.
  • RA also triggers growth arrest and progressive clearance of leukemia initiating cells (LIC), both ex vivo and in vivo.
  • Suboptimal RA concentrations or expression of the PLZF/RARA variant allows complete RA-induced differentiation, but neither LIC clearance nor disease remission.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Granulocyte Precursor Cells / drug effects. Leukemia, Promyelocytic, Acute / drug therapy. Oncogene Proteins, Fusion / genetics. Oxides / therapeutic use. Tretinoin / therapeutic use
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Oncogenes / drug effects

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  • (PMID = 20455087.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / Oncogene Proteins, Fusion; 0 / Oxides; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; S7V92P67HO / arsenic trioxide
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69. Figueroa ME, Wouters BJ, Skrabanek L, Glass J, Li Y, Erpelinck-Verschueren CA, Langerak AW, Löwenberg B, Fazzari M, Greally JM, Valk PJ, Melnick A, Delwel R: Genome-wide epigenetic analysis delineates a biologically distinct immature acute leukemia with myeloid/T-lymphoid features. Blood; 2009 Mar 19;113(12):2795-804
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  • [Title] Genome-wide epigenetic analysis delineates a biologically distinct immature acute leukemia with myeloid/T-lymphoid features.
  • Acute myeloid leukemia is a heterogeneous disease from the molecular and biologic standpoints, and even patients with a specific gene expression profile may present clinical and molecular heterogeneity.
  • We studied the epigenetic profiles of a cohort of patients who shared a common gene expression profile but differed in that only half of them harbored mutations of the CEBPA locus, whereas the rest presented with silencing of this gene and coexpression of certain T-cell markers.
  • CEBPA-silenced leukemias also displayed marked hypermethylation compared with normal CD34(+) hematopoietic cells, whereas CEBPA mutant cases showed only mild changes in DNA methylation compared with these normal progenitors.
  • Biologically, CEBPA-silenced leukemias presented with a decreased response to myeloid growth factors in vitro.

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  • (PMID = 19168792.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE14417
  • [Grant] United States / NIGMS NIH HHS / GM / GM007288; United States / NCI NIH HHS / CA / R01 CA118316; United States / NCI NIH HHS / CA / CA118316; United States / NIGMS NIH HHS / GM / T32 GM007288; United States / NICHD NIH HHS / HD / R01 HD044078; United States / NCI NIH HHS / CA / R01 CA104348
  • [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 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / DNA, Neoplasm; 0 / Interleukin-3; 0 / Neoplasm Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2945920
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70. Quintás-Cardama A, Cortes J: Evaluation of the L-stereoisomeric nucleoside analog troxacitabine for the treatment of acute myeloid leukemia. Expert Opin Investig Drugs; 2007 Apr;16(4):547-57
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  • [Title] Evaluation of the L-stereoisomeric nucleoside analog troxacitabine for the treatment of acute myeloid leukemia.
  • These characteristics make troxacitabine a suitable alternative for patients with acute myelogenous leukemia as a potential way for overcoming resistance to ara-C therapy, which is the mainstay of acute myelogenous leukemia therapy at present.
  • Clinically significant activity has been reported in Phase I studies in patients with advanced hematologic malignancies and has prompted troxacitabine to enter a series of Phase II trials in patients with refractory and relapsed acute myelogenous leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cytosine / analogs & derivatives. Dioxolanes / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Animals. Drug Evaluation, Preclinical. Humans. Nucleosides / chemistry. Nucleosides / therapeutic use. Stereoisomerism

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  • (PMID = 17371201.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dioxolanes; 0 / Nucleosides; 60KQZ0388Y / troxacitabine; 8J337D1HZY / Cytosine
  • [Number-of-references] 45
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71. Bermúdez M, Fuster JL, Llinares E, Galera A, Gonzalez C: Itraconazole-related increased vincristine neurotoxicity: case report and review of literature. J Pediatr Hematol Oncol; 2005 Jul;27(7):389-92
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  • Itraconazole is particularly attractive in fungal prophylaxis for cancer patients due to its broad spectrum, including Candida and Aspergillus.
  • A 3-year-old boy diagnosed with acute lymphoblastic leukemia received induction chemotherapy.
  • The authors suggest that in the absence of any proven benefit of itraconazole prophylaxis, and given the interaction of this drug with vincristine leading to severe and even potentially fatal toxicities, the combination use of these drugs should be avoided.
  • [MeSH-major] Antifungal Agents / therapeutic use. Antineoplastic Agents, Phytogenic / toxicity. Itraconazole / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vincristine / toxicity
  • [MeSH-minor] Child, Preschool. Drug Antagonism. Humans. Male. Treatment Outcome

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  • (PMID = 16012330.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Antineoplastic Agents, Phytogenic; 304NUG5GF4 / Itraconazole; 5J49Q6B70F / Vincristine
  • [Number-of-references] 20
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72. LaRosa C, McMullen L, Bakdash S, Ellis D, Krishnamurti L, Wu HY, Moritz ML: Acute renal failure from xanthine nephropathy during management of acute leukemia. Pediatr Nephrol; 2007 Jan;22(1):132-5
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  • [Title] Acute renal failure from xanthine nephropathy during management of acute leukemia.
  • We report a case of oliguric acute renal failure due to bilateral xanthine nephropathy in an 11-year-old girl as a complication of tumor lysis syndrome during the treatment of T-cell acute lymphoblastic leukemia.
  • Xanthine nephropathy should be considered in patients who develop acute renal failure following aggressive chemotherapy with appropriate tumor lysis syndrome prophylaxis.
  • Urine measurements for xanthine could aid in the diagnosis of patients with nephrolithiasis complicating tumor lysis syndrome.
  • [MeSH-major] Acute Kidney Injury / etiology. Nephrolithiasis / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Xanthine / adverse effects
  • [MeSH-minor] Allopurinol / adverse effects. Allopurinol / therapeutic use. Child. Enzyme Inhibitors / adverse effects. Enzyme Inhibitors / therapeutic use. Female. Humans. Tumor Lysis Syndrome / complications. Tumor Lysis Syndrome / drug therapy

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  • (PMID = 17039332.001).
  • [ISSN] 0931-041X
  • [Journal-full-title] Pediatric nephrology (Berlin, Germany)
  • [ISO-abbreviation] Pediatr. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 1AVZ07U9S7 / Xanthine; 63CZ7GJN5I / Allopurinol
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73. Robak T, Wierzbowska A, Robak E: Recent clinical trials of cladribine in hematological malignancies and autoimmune disorders. Rev Recent Clin Trials; 2006 Jan;1(1):15-34
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  • The purine nucleoside analog - cladribine (2-chlorodeoxyadenosine, 2-CdA) is a cytotoxic agent with high activity in lymphoid and myeloid malignancies.
  • It is also an effective drug in some autoimmune disorders.
  • Recently however, new formulation of this agent has been developed for subcutaneous and oral administration.
  • 2-CdA is widely established as first line standard treatment for hairy cell leukemia.
  • Moreover several clinical trials have demonstrated that this agent, used alone or in combination with other cytotoxic drugs, showed good efficacy and acceptable toxicity profile in the treatment of chronic lymphocytic leukemia, Waldenström macroglobulinemia, low-grade non-Hodgkin's lymphoma and acute myeloid leukemia.
  • Moreover, some studies indicate that 2-CdA has some activity in progressive multiple sclerosis and other autoimmune disorders including autoimmune hemolytic anemia, rheumatoid arthritis, systemic lupus erythematosus, psoriasis and in patients with refractory factor VIII inhibitors.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Autoimmune Diseases / drug therapy. Cladribine / administration & dosage. Hematologic Neoplasms / drug therapy. Multiple Sclerosis / drug therapy

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  • (PMID = 18393777.001).
  • [ISSN] 1574-8871
  • [Journal-full-title] Reviews on recent clinical trials
  • [ISO-abbreviation] Rev Recent Clin Trials
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 47M74X9YT5 / Cladribine
  • [Number-of-references] 150
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74. Grigoryan RS, Panosyan EH, Seibel NL, Gaynon PS, Avramis IA, Avramis VI: Changes of amino acid serum levels in pediatric patients with higher-risk acute lymphoblastic leukemia (CCG-1961). In Vivo; 2004 Mar-Apr;18(2):107-12
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  • [Title] Changes of amino acid serum levels in pediatric patients with higher-risk acute lymphoblastic leukemia (CCG-1961).
  • BACKGROUND: Deamination of asparagine (Asn) and glutamine (Gln) by asparaginases (ASNase) is associated with good prognosis in acute lymphoblastic leukemia (ALL).
  • Chemotherapy drugs used for ALL may accelerate catabolism of other amino acids (AA).
  • Asparaginase may indirectly cause moderate depletion of serum Arg and Ser levels, providing an enhancement in leukemia blasts apoptosis.
  • Toxicity from the ASNase and other drugs could enhance the decrease of AA serum levels.
  • [MeSH-major] Amino Acids / blood. Asparaginase / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / blood. Child. Citric Acid Cycle / drug effects. Citric Acid Cycle / physiology. Humans

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  • (PMID = 15113036.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; EC 3.5.1.1 / Asparaginase
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75. Douer D, Estey E, Santillana S, Bennett JM, Lopez-Bernstein G, Boehm K, Williams T: Treatment of newly diagnosed and relapsed acute promyelocytic leukemia with intravenous liposomal all-trans retinoic acid. Blood; 2001 Jan 1;97(1):73-80
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  • [Title] Treatment of newly diagnosed and relapsed acute promyelocytic leukemia with intravenous liposomal all-trans retinoic acid.
  • A novel intravenous liposomal formulation of all-trans retinoic acid (ATRA) was evaluated in 69 patients with acute promyelocytic leukemia (APL): 32 new diagnoses, 35 relapses, and 2 oral ATRA failures.
  • Liposomal ATRA (90 mg/m(2)) was administered every other day until complete remission (CR) or a maximum of 56 days.
  • Remission failure in newly diagnosed patients was not from resistant disease.
  • Several patients in CR became polymerase chain reaction (PCR) negative for promyelocytic leukemia/retinoic acid receptor-alpha (PML/RARalpha) after liposomal ATRA alone.
  • It provides a reliable dosage of ATRA for patients with APL unable to swallow or absorb medications and can induce molecular remissions without chemotherapy.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / drug therapy. Liposomes / administration & dosage. Tretinoin / administration & dosage. Tretinoin / toxicity
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Bone Marrow / metabolism. Child. Child, Preschool. Continental Population Groups. DNA / metabolism. Disease-Free Survival. Drug Compounding / standards. Female. Humans. Injections, Intravenous. Male. Middle Aged. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Prospective Studies. Recurrence. Remission Induction. Risk Factors. Treatment Outcome

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  • (PMID = 11133744.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Liposomes; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin; 9007-49-2 / DNA
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76. Côté S, Zhou D, Bianchini A, Nervi C, Gallagher RE, Miller WH Jr: Altered ligand binding and transcriptional regulation by mutations in the PML/RARalpha ligand-binding domain arising in retinoic acid-resistant patients with acute promyelocytic leukemia. Blood; 2000 Nov 1;96(9):3200-8
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  • [Title] Altered ligand binding and transcriptional regulation by mutations in the PML/RARalpha ligand-binding domain arising in retinoic acid-resistant patients with acute promyelocytic leukemia.
  • Acute promyelocytic leukemia (APL) is characterized by a specific translocation, t(15;17), that fuses the promyelocytic leukemia (PML) gene with the RA receptor RARalpha.
  • Pharmacologic doses of retinoic acid (RA) induce differentiation in human APL cells and complete clinical remissions.
  • These mutant PML/RARalpha proteins have been expressed in vitro, which shows that they cause a diversity of alterations in binding to ligand and to nuclear coregulators of transcription, leading to varying degrees of inhibition of retinoid-induced transcription.
  • This contrasts with the nearly complete dominant negative activity of mutations in PML/RARalpha previously characterized in cell lines developing RA resistance in vitro.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Leukemia, Promyelocytic, Acute / genetics. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / chemistry. Oncogene Proteins, Fusion / genetics. Transcription, Genetic. Tretinoin / therapeutic use

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  • (PMID = 11050004.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA56771
  • [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 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin
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77. Yee KW, Cortes J, Ferrajoli A, Garcia-Manero G, Verstovsek S, Wierda W, Thomas D, Faderl S, King I, O'brien SM, Jeha S, Andreeff M, Cahill A, Sznol M, Giles FJ: Triapine and cytarabine is an active combination in patients with acute leukemia or myelodysplastic syndrome. Leuk Res; 2006 Jul;30(7):813-22
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  • [Title] Triapine and cytarabine is an active combination in patients with acute leukemia or myelodysplastic syndrome.
  • Triapine, an iron chelator and a potent inhibitor of ribonucleotide reductase, has significant anti-leukemia activity.
  • A phase I study of Triapine in combination with ara-C was conducted in 32 patients with refractory acute leukemia and high-risk MDS.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cytarabine / administration & dosage. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Pyridines / administration & dosage. Thiosemicarbazones / administration & dosage
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Combinations. Female. Humans. Injections, Intravenous. Male. Maximum Tolerated Dose. Middle Aged. Recurrence. Risk Factors. Treatment Outcome


78. Momota H, Narita Y, Miyakita Y, Hosono A, Makimoto A, Shibui S: Acute lymphoblastic leukemia after temozolomide treatment for anaplastic astrocytoma in a child with a germline TP53 mutation. Pediatr Blood Cancer; 2010 Sep;55(3):577-9
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  • [Title] Acute lymphoblastic leukemia after temozolomide treatment for anaplastic astrocytoma in a child with a germline TP53 mutation.
  • We present a case of a 12-year-old female with a germline TP53 mutation who presented with anaplastic astrocytoma and subsequent acute lymphoblastic leukemia (ALL) 13 months after starting treatment with temozolomide (TMZ).
  • Although alkylating agents such as TMZ are known to induce secondary hematologic malignancy, only several cases of treatment-related acute leukemia have been reported after TMZ-alone chemotherapy for malignant gliomas.
  • [MeSH-major] Antineoplastic Agents, Alkylating / adverse effects. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Dacarbazine / analogs & derivatives. Frontal Lobe. Genes, p53 / genetics. Germ-Line Mutation. Neoplasms, Second Primary / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced


79. Reichert A, Heisterkamp N, Daley GQ, Groffen J: Treatment of Bcr/Abl-positive acute lymphoblastic leukemia in P190 transgenic mice with the farnesyl transferase inhibitor SCH66336. Blood; 2001 Mar 1;97(5):1399-403
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  • [Title] Treatment of Bcr/Abl-positive acute lymphoblastic leukemia in P190 transgenic mice with the farnesyl transferase inhibitor SCH66336.
  • The Philadelphia (Ph) chromosome is found in approximately 3% of pediatric patients with acute lymphoblastic leukemia (ALL) and the percentage markedly increases in adult patients.
  • The Ph-translocation joins the BCR and ABL genes and leads to expression of a chimeric Bcr/Abl protein with enhanced tyrosine kinase activity.
  • Ras proteins have to undergo a series of posttranslational modifications to become biologically active.
  • We studied the effect of the farnesyl transferase inhibitor SCH66336 in an in vivo murine model of Bcr/Abl-positive acute lymphoblastic leukemia.
  • All animals of the control groups died of leukemia/lymphoma within 103 days (range, 18-103 days).
  • In contrast, 80% of the drug-receiving group survived without any signs of leukemia or lymphoma until termination of treatment, after a median treatment period of 200 days (range, 179-232 days).
  • We conclude that farnesyl transferase inhibitor SCH66336 is able to revert early signs of leukemia and significantly prolongs survival in a murine ALL model.
  • [MeSH-major] Alkyl and Aryl Transferases / antagonists & inhibitors. Genes, abl / genetics. Piperidines / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyridines / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Bone Marrow. Farnesyltranstransferase. Mice. Mice, Transgenic. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate

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  • (PMID = 11222386.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA47456; United States / NCI NIH HHS / CA / CA50248
  • [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 / Antineoplastic Agents; 0 / Piperidines; 0 / Pyridines; 0 / RNA, Messenger; 193275-84-2 / lonafarnib; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase
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80. Trinks C, Djerf EA, Hallbeck AL, Jönsson JI, Walz TM: The pan-ErbB receptor tyrosine kinase inhibitor canertinib induces ErbB-independent apoptosis in human leukemia (HL-60 and U-937) cells. Biochem Biophys Res Commun; 2010 Feb 26;393(1):6-10
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  • [Title] The pan-ErbB receptor tyrosine kinase inhibitor canertinib induces ErbB-independent apoptosis in human leukemia (HL-60 and U-937) cells.
  • Our study was initiated in order to determine the effect of the pan-ErbB receptor tyrosine kinase inhibitor, canertinib (CI-1033), on growth and survival of human leukemia (HL-60 and U-937) cells.
  • We show that treatment of HL-60 and U-937 cells with canertinib significantly inhibits growth of both cell lines in a dose-dependent manner; half maximal effective dose (IC(50)) in HL-60 and U-937 cells was approximately 2.5 microM and 1.0 microM, respectively.
  • Treatment with 2 microM canertinib promoted a G(1) cell cycle arrest, whereas doses of 5 microM or more induced apoptosis as determined by the Annexin V method and cleavage of poly-(ADP-ribose) polymerase (PARP).
  • However, none of the corresponding ErbB-receptor proteins could be detected by Western blot analysis.
  • Our results suggest that canertinib could be of potential clinical interest in the treatment of acute myeloid leukemia.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Leukemia, Myeloid, Acute / enzymology. Morpholines / pharmacology. Protein Kinase Inhibitors / pharmacology. Receptor, ErbB-2 / antagonists & inhibitors
  • [MeSH-minor] G1 Phase / drug effects. HL-60 Cells. Humans. Poly(ADP-ribose) Polymerases / metabolism

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20096663.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Morpholines; 0 / Protein Kinase Inhibitors; C78W1K5ASF / Canertinib; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.10.1 / Receptor, ErbB-2
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81. Mahoney DH Jr, Shuster JJ, Nitschke R, Lauer S, Steuber CP, Camitta B: Intensification with intermediate-dose intravenous methotrexate is effective therapy for children with lower-risk B-precursor acute lymphoblastic leukemia: A Pediatric Oncology Group study. J Clin Oncol; 2000 Mar;18(6):1285-94
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  • [Title] Intensification with intermediate-dose intravenous methotrexate is effective therapy for children with lower-risk B-precursor acute lymphoblastic leukemia: A Pediatric Oncology Group study.
  • PURPOSE: To determine whether early intensification with 12 courses of intravenous (IV) methotrexate (MTX) and IV mercaptopurine (MP) is superior to 12 courses of IV MTX alone for prevention of relapse in children with lower-risk B-lineage acute lymphoblastic leukemia (ALL).
  • Patients were randomized to receive intensification with IV MTX 1,000 mg/m(2) plus IV MP 1,000 mg/m(2) (regimen A) or IV MTX 1,000 mg/m(2) alone (regimen C).
  • CONCLUSION: Intensification with 12 courses of IV MTX is an effective therapy for prevention of relapse in children with B-precursor ALL who are at lower risk for relapse but may be associated with an increased risk for neurotoxicity.
  • Prolonged infusions of MP combined with IV MTX did not provide apparent advantage.
  • [MeSH-major] 6-Mercaptopurine / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Methotrexate / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Drug Administration Schedule. Female. Humans. Infant. Infusions, Intravenous. Male. Proportional Hazards Models. Survival Analysis

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  • (PMID = 10715299.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; E7WED276I5 / 6-Mercaptopurine; YL5FZ2Y5U1 / Methotrexate
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82. Tan TW, Tsai HY, Chen YF, Chung JG: Induction of apoptosis in human promyelocytic leukemia HL-60 cells by Ampelopsis cantoniensis crude extract. In Vivo; 2004 Jul-Aug;18(4):457-62
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  • [Title] Induction of apoptosis in human promyelocytic leukemia HL-60 cells by Ampelopsis cantoniensis crude extract.
  • The crude extract of Ampelopsis cantoniensis induced apoptosis in human promyelocytic leukemia HL-60 cells and this induction was investigated by flow cytometric analysis, DNA gel electrophoresis and poly (ADP-ribose) fluorescence staining.
  • [MeSH-major] Ampelopsis / chemistry. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Drugs, Chinese Herbal / pharmacology. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Caspase 3. Caspases / genetics. Caspases / metabolism. Cell Survival / drug effects. DNA Fragmentation. DNA, Neoplasm / analysis. Dose-Response Relationship, Drug. Flow Cytometry. HL-60 Cells / drug effects. HL-60 Cells / pathology. Humans. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15369184.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Neoplasm; 0 / Drugs, Chinese Herbal; 0 / RNA, Neoplasm; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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83. Cros E, Jordheim L, Dumontet C, Galmarini CM: Problems related to resistance to cytarabine in acute myeloid leukemia. Leuk Lymphoma; 2004 Jun;45(6):1123-32
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  • [Title] Problems related to resistance to cytarabine in acute myeloid leukemia.
  • First-line chemotherapy treatment in acute-myeloid leukemia patients usually consists of a combination of cytarabine (ara-C) and an anthracycline.
  • However, clinical outcome is unsatisfactory, as most of the patients who achieve a CR will relapse within 2 years from diagnosis, often with resistant disease and poor response to subsequent therapy.
  • Thus, understanding the factors which contribute to the emergence of chemoresistant leukemic cells is essential to improve outcome in patients suffering from this disease.
  • Ara-C combined with agents modulating apototic responses are expected to provide additional benefit.
  • In the same way that combination chemotherapy has provided curative treatment of AML, a multifactorial approach of ara-C resistance should allow significant progress in the treatment of currently chemoresistant disease.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Cytarabine / therapeutic use. Drug Resistance, Neoplasm. Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid / drug therapy. Ribonucleotide Reductases / antagonists & inhibitors
  • [MeSH-minor] Acute Disease. Humans

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  • (PMID = 15359991.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Enzyme Inhibitors; 04079A1RDZ / Cytarabine; EC 1.17.4.- / Ribonucleotide Reductases
  • [Number-of-references] 125
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84. Abe S, Funato T, Takahashi S, Yokoyama H, Yamamoto J, Tomiya Y, Yamada-Fujiwara M, Ishizawa K, Kameoka J, Kaku M, Harigae H, Sasaki T: Increased expression of insulin-like growth factor i is associated with Ara-C resistance in leukemia. Tohoku J Exp Med; 2006 Jul;209(3):217-28
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  • [Title] Increased expression of insulin-like growth factor i is associated with Ara-C resistance in leukemia.
  • Resistance to cytosine arabinoside (Ara-C) is a major problem in the treatment of patients with acute myeloid leukemia (AML).
  • In order to investigate the mechanisms involved in Ara-C resistance, the gene expression profile of Ara-C-resistant K562 human myeloid leukemia cells (K562/AC cells) was compared to that of Ara-C-sensitive K562 cells (K562 cells) by using a cDNA microarray platform.
  • The biological significance of IGF-I overexpression was further examined in vitro.
  • Moreover, from the analysis of 27 AML patients, we have shown that IGF-I expression levels are higher in patients at refractory stage, after Ara-C combined chemotherapy, than those in patients at diagnosis.
  • [MeSH-major] Cytarabine / therapeutic use. Drug Resistance, Neoplasm / genetics. Insulin-Like Growth Factor I / metabolism. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Apoptosis / drug effects. Female. Gene Expression Profiling. Humans. K562 Cells. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Oncogene Protein v-akt / metabolism. Receptor, IGF Type 1 / metabolism. Suramin / pharmacology. Up-Regulation

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  • (PMID = 16778368.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6032D45BEM / Suramin; 67763-96-6 / Insulin-Like Growth Factor I; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.11.1 / Oncogene Protein v-akt
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85. Oliver JW, Farnsworth B, Tonk VS: Juvenile myelomonocytic leukemia in a child with Crohn disease. Cancer Genet Cytogenet; 2006 May;167(1):70-3
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  • [Title] Juvenile myelomonocytic leukemia in a child with Crohn disease.
  • Intestinal adenocarcinoma is a well-known complication of inflammatory bowel disease.
  • Hematologic malignancies, most commonly lymphoma or acute myeloid leukemia, represent a much less well-recognized complication of these disorders; these typically occur in adults with ulcerative colitis.
  • We report a fatal case of juvenile myelomonocytic leukemia associated with monosomy 7 in a young child with a clinical history of Crohn disease.
  • Neither the leukemia nor the cytogenetic aberration has been previously reported in a patient with inflammatory bowel disease.
  • The aggressive disease course emphasizes the need for proper recognition and further study of this unusual complication.
  • [MeSH-major] Crohn Disease / complications. Crohn Disease / diagnosis. Leukemia, Myelomonocytic, Chronic / complications. Leukemia, Myelomonocytic, Chronic / diagnosis
  • [MeSH-minor] Biopsy. Chromosome Aberrations. Chromosomes, Human, Pair 7. Cytogenetic Analysis. Drug Therapy. Fatal Outcome. Hematopoietic Stem Cells / cytology. Humans. Infant. Male. Monosomy. Stem Cell Transplantation


86. Li H, Lu Y, Piao L, Wu J, Liu S, Marcucci G, Ratnam M, Lee RJ: Targeting human clonogenic acute myelogenous leukemia cells via folate conjugated liposomes combined with receptor modulation by all-trans retinoic acid. Int J Pharm; 2010 Dec 15;402(1-2):57-63
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  • [Title] Targeting human clonogenic acute myelogenous leukemia cells via folate conjugated liposomes combined with receptor modulation by all-trans retinoic acid.
  • Our previous data demonstrated that folate receptor β (FR-β) targeted liposomal doxorubicin (FT-L-DOX) showed enhanced cytotoxicity relative to non-targeted liposomal doxorubicin (CON-L-DOX), and the effect was enhanced by selective FR-β upregulation by all-trans retinoic acid (ATRA) in AML blast cells.
  • Moreover, FT-L-DOX was more toxic to AML clonogenic cells than to AML blast cells.

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  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
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  • (PMID = 20883757.001).
  • [ISSN] 1873-3476
  • [Journal-full-title] International journal of pharmaceutics
  • [ISO-abbreviation] Int J Pharm
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA080183; United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / R01 CA080183; United States / NCI NIH HHS / CA / R01CA095673; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NCI NIH HHS / CA / R01 CA095673; United States / NCI NIH HHS / CA / CA095673-05; United States / NCI NIH HHS / CA / R01 CA095673-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Fluoresceins; 0 / Folate Receptor 2; 5688UTC01R / Tretinoin; 80168379AG / Doxorubicin; V0YM2B16TS / fluorexon
  • [Other-IDs] NLM/ NIHMS249454; NLM/ PMC2982872
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87. Callies S, de Alwis DP, Mehta A, Burgess M, Aarons L: Population pharmacokinetic model for daunorubicin and daunorubicinol coadministered with zosuquidar.3HCl (LY335979). Cancer Chemother Pharmacol; 2004 Jul;54(1):39-48
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  • PURPOSE: The impact of zosuquidar.3HCl, an inhibitor of P-glycoprotein, on the pharmacokinetics of daunorubicin and daunorubicinol was examined in a phase I trial using a population approach.
  • Of a total of 18 patients entered, 16 with acute leukemia completed the study.
  • CONCLUSIONS: The decrease in daunorubicin and daunorubicinol clearance in the presence of zosuquidar.3HCl likely reflects inhibition of P-glycoprotein in the bile canaliculi impeding their biliary excretion.
  • [MeSH-minor] Bile Canaliculi. Dose-Response Relationship, Drug. Drug Interactions. Drug Resistance, Multiple. Humans. P-Glycoprotein

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  • (PMID = 15045528.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Dibenzocycloheptenes; 0 / P-Glycoprotein; 0 / Quinolines; 813AGY3126 / zosuquidar trihydrochloride; YDU8YIP30L / daunorubicinol; ZS7284E0ZP / Daunorubicin
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88. Soriano AO, Yang H, Faderl S, Estrov Z, Giles F, Ravandi F, Cortes J, Wierda WG, Ouzounian S, Quezada A, Pierce S, Estey EH, Issa JP, Kantarjian HM, Garcia-Manero G: Safety and clinical activity of the combination of 5-azacytidine, valproic acid, and all-trans retinoic acid in acute myeloid leukemia and myelodysplastic syndrome. Blood; 2007 Oct 1;110(7):2302-8
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  • [Title] Safety and clinical activity of the combination of 5-azacytidine, valproic acid, and all-trans retinoic acid in acute myeloid leukemia and myelodysplastic syndrome.
  • The combination of a DNA hypomethylating agent with a histone deacetylase inhibitor has synergistic antileukemia activity and may restore sensitivity to all-trans retinoic acid (ATRA).
  • We conducted a phase 1/2 study of the combination of 5-azacitidine (5-AZA), valproic acid (VPA), and ATRA in patients with acute myeloid leukemia or high-risk myelodysplastic syndrome.
  • [MeSH-major] Azacitidine / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / drug therapy. Tretinoin / therapeutic use. Valproic Acid / therapeutic use
  • [MeSH-minor] Acetylation. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. DNA Methylation. Dose-Response Relationship, Drug. Drug Therapy, Combination. Drug-Related Side Effects and Adverse Reactions. Gene Expression Regulation. Histones / metabolism. Humans. Middle Aged. RNA, Messenger / genetics


89. Guillem V, Tormo M: Influence of DNA damage and repair upon the risk of treatment related leukemia. Leuk Lymphoma; 2008 Feb;49(2):204-17
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  • [Title] Influence of DNA damage and repair upon the risk of treatment related leukemia.
  • Therapy-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) are malignancies occurring after exposure to chemotherapy and/or radiotherapy.
  • Several studies have addressed cumulative dose, dose intensity and exposure to specific agents of preceding cytotoxic therapy in relation to the risk of developing such leukemia.
  • Since only a small percentage of patients exposed to cytotoxic therapy develop t-MDS/AML, it has been suggested that some genetic predisposition may be involved, specifically associated to polymorphisms in certain genes involved in chemotherapy/radiotherapy response - fundamentally genes intervening in drug detoxification and DNA synthesis and repair.
  • A review is made of the genetic studies related to t-MDS/AML predisposition, focusing on the mechanistic findings of how specific chemotherapeutic drug exposure produces DNA damage and induces the chromosomal abnormalities characteristic of t-MDS/AML, the molecular pathways involved in repairing such drug induced damage, and the way in which they influence t-MDS/AML genesis.
  • Specific issues are (a) the interaction of topoisomerase II inhibitors, alkylators and antimetabolite drugs with DNA repair mechanisms and their impact on t-MDS/AML leukemogenicity and (b) the influence of DNA polymorphisms in genes involved in DNA repair, drug metabolization and nucleotide synthesis, paying special attention to the relevance of folate metabolism.
  • Finally, we discuss some aspects relating to study design that are most suitable for characterizing associations between drug exposure and genotypes related to t-MDS/AML risk - stressing the importance of the inclusion of chemotherapy-exposed control groups.
  • [MeSH-major] Antineoplastic Agents / adverse effects. DNA Damage. DNA Repair / genetics. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Antimetabolites, Antineoplastic. Antineoplastic Agents, Alkylating. Genetic Predisposition to Disease. Humans. Polymorphism, Genetic. Topoisomerase II Inhibitors

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  • (PMID = 18231906.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Topoisomerase II Inhibitors
  • [Number-of-references] 111
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90. Tronstad KJ, Bruserud Ø, Berge K, Berge RK: Antiproliferative effects of a non-beta-oxidizable fatty acid, tetradecylthioacetic acid, in native human acute myelogenous leukemia blast cultures. Leukemia; 2002 Nov;16(11):2292-301
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  • [Title] Antiproliferative effects of a non-beta-oxidizable fatty acid, tetradecylthioacetic acid, in native human acute myelogenous leukemia blast cultures.
  • The lipid metabolism is important in the regulation of cell proliferation.
  • We have examined effects of a fatty acid analogue, tetradecylthioacetic acid (TTA), on the functional phenotype of native, human AML cells.
  • TTA inhibited AML blast proliferation in the presence of single cytokines (GM-CSF and SCF: P > 0.05, 35 patients with detectable proliferation) and a combination of cytokines (P < 0.005, n = 21).
  • AML blast populations varied significantly in their levels and activities of metabolites and enzymes characterizing oxidative status and fatty acid metabolism, and there was no significant correlation between the intrinsic oxidative status and the effects of PA and TTA on blast proliferation.
  • Although TTA reduced the proliferation of mitogen-stimulated normal T cells derived from healthy individuals (P < 0.05, n = 8), no adverse effects were seen on peripheral blood cell counts (reticulocytes, platelets, total white blood cells, differential leukocyte counts) for healthy volunteers receiving TTA (oral administration of 1000 mg/day for 7 consecutive days).
  • Our results suggest that TTA can inhibit AML blast proliferation through pathways that are unrelated to autocrine cytokine secretion and intrinsic oxidative status.
  • [MeSH-major] Antioxidants / pharmacology. Cell Division / drug effects. Cytokines / metabolism. Enzyme Inhibitors / pharmacology. Leukemia