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Items 1 to 100 of about 12699
1. Zhu Y, Xie ZX: [Nitric oxide synthase expression and multiple drug resistance in patients with acute leukemia]. Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2004 Feb;29(1):25-7
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  • [Title] [Nitric oxide synthase expression and multiple drug resistance in patients with acute leukemia].
  • OBJECTIVE: To determine the relationship between nitric oxide synthase (NOS) expression and Pgp/mdr-1.
  • RESULTS: NOS expression increased in patients with acute leukemia compared with that of the controls.
  • CONCLUSION: NO may influcence multiple drug resistance in patients with acute leukemia.
  • [MeSH-major] Drug Resistance, Multiple / genetics. Leukemia / enzymology. Nitric Oxide Synthase / biosynthesis. P-Glycoprotein / biosynthesis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Drug Resistance, Neoplasm / genetics. Female. Genes, MDR / genetics. Humans. Male. Middle Aged. Nitric Oxide Synthase Type II / biosynthesis. Nitric Oxide Synthase Type II / genetics. Nitric Oxide Synthase Type III / biosynthesis. Nitric Oxide Synthase Type III / genetics

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  • (PMID = 16136998.001).
  • [ISSN] 1672-7347
  • [Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
  • [ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / P-Glycoprotein; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nitric Oxide Synthase Type III
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2. Styczyński J, Haus O: [Cytogenetics and in vitro drug resistance of acute leukemia in children and adults]. Postepy Hig Med Dosw (Online); 2006;60:527-37

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  • [Title] [Cytogenetics and in vitro drug resistance of acute leukemia in children and adults].
  • In spite of continuous progress in the therapy of acute leukemia, relapses still occur frequently both in children and adults.
  • The presence of cytogenetic aberrations in leukemic cells at presentation is an important prognostic factor in acute leukemia.
  • The translocation t(9;22) and the 11q23/MLL rearrangement are related to poor prognosis, while hyperdiploidy >50 chromosomes and the translocation t(12;21) are indicators of good prognosis in acute lymphoblastic leukemia (ALL).
  • In acute myeloid leukemia (AML), t(8;21), t(15;17), and inv(16) indicate good prognosis, whereas 5/5q-, 7/7q-, and complex karyotype indicate poor prognosis.
  • It seems that the prognostic value of cytogenetic changes is related to differences in cellular drug resistance in ALL and, to lesser extent, in AML.
  • Genetic profiling based on microarray analysis confirms the correlation between cytogenetic changes in leukemic cells and drug resistance in ALL.
  • The cytogenetic profile possibly determines cellular drug resistance and final therapy outcome.
  • Knowledge on the karyotype-related drug resistance profile might enable the use of targeted therapy in resistant/refractory acute leukemia both in children and adults.

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  • (PMID = 17060894.001).
  • [ISSN] 1732-2693
  • [Journal-full-title] Postepy higieny i medycyny doswiadczalnej (Online)
  • [ISO-abbreviation] Postepy Hig Med Dosw (Online)
  • [Language] POL
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Multidrug Resistance-Associated Proteins
  • [Number-of-references] 74
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3. Fujimaki S, Funato T, Harigae H, Fujiwara J, Kameoka J, Meguro K, Kaku M, Sasaki T: Quantitative analysis of a MDR1 transcript for prediction of drug resistance in acute leukemia. Clin Chem; 2002 Jun;48(6 Pt 1):811-7
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  • [Title] Quantitative analysis of a MDR1 transcript for prediction of drug resistance in acute leukemia.
  • BACKGROUND: Assessing the drug resistance of leukemic cells is important for treatment of leukemia.
  • We developed a quantitative reverse transcription (RT)-PCR method for multidrug resistance 1 (MDR1) and multidrug resistance-related protein 1 (MRP1) transcripts to evaluate drug resistance, and applied it to clinical samples.
  • To confirm that the cutoffs reflected biological resistance, we established vincristine (VCR)-resistant K562 sublines that showed various degrees of drug resistance and examined the correlation between the copy numbers of these transcripts and the biological resistance of these clones.
  • In addition, we compared the sensitivity and specificity of quantitative RT-PCR to a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometric (FCM) analysis.
  • RESULTS: The defined cutoff for copy numbers of MDR1 transcripts corresponded with the degree of biological resistance of VCR-resistant K562 sublines.
  • Clinical study revealed that the concentrations of MDR1 mRNA in all relapsed patients with acute myelogenous leukemia (AML) were above the cutoff.
  • Moreover, both AML and acute lymphoblastic leukemia patients with high MDR1 mRNA expression at diagnosis tended to show a low remission rate and short remission periods.
  • CONCLUSION: These results suggest the efficacy of this quantitative analysis of MDR1 transcripts for the prediction of clinical drug resistance in acute leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. Multidrug Resistance-Associated Proteins / genetics. P-Glycoprotein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Flow Cytometry. Humans. Neoplasm Recurrence, Local. Phenotype. Reverse Transcriptase Polymerase Chain Reaction. Sensitivity and Specificity. Tumor Cells, Cultured

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  • (PMID = 12028995.001).
  • [ISSN] 0009-9147
  • [Journal-full-title] Clinical chemistry
  • [ISO-abbreviation] Clin. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / multidrug resistance-associated protein 1
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4. Jun KR, Jang S, Chi HS, Lee KH, Lee JH, Choi SJ, Seo JJ, Moon HN, Im HJ, Park CJ: Relationship between in vitro chemosensitivity assessed with MTT assay and clinical outcomes in 103 patients with acute leukemia. Korean J Lab Med; 2007 Apr;27(2):89-95
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  • [Title] Relationship between in vitro chemosensitivity assessed with MTT assay and clinical outcomes in 103 patients with acute leukemia.
  • BACKGROUND: Cellular drug resistance is supposed to play a major role in chemotherapy failure or relapse.
  • The purpose of this study was to analyze the relationship between in vitro chemosensitivity test results using a 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and clinical response on chemotherapy, and to find the possibility of optimizing the treatment protocol for individual patients according to their actual drug resistance.
  • METHODS: For MTT assay, we obtained bone marrow aspirates from 103 patients with acute leukemia at the time of initial diagnosis or relapse.
  • The following drugs were tested: cytarabine, vincristine, methotrexate, daunorubicin, dexamethasone, L-asparaginase, and mitoxantrone.
  • CONCLUSIONS: Although it does not provide the insight into the mechanisms that cause drug resistance, the MTT assay may be a useful tool in individually optimizing the chemotherapy of patients with acute leukemia.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antibiotics, Antineoplastic / therapeutic use. Child. Child, Preschool. Coloring Agents. Cytarabine / therapeutic use. Daunorubicin / therapeutic use. Drug Evaluation, Preclinical. Drug Resistance, Neoplasm. Female. Humans. Infant. Male. Middle Aged. Tetrazolium Salts. Thiazoles. Treatment Outcome

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  • (PMID = 18094557.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Coloring Agents; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 298-93-1 / thiazolyl blue; ZS7284E0ZP / Daunorubicin
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5. Wang T, Chen FY, Han JY, Shao NX, Ou-Yuang RR: [Study of CYP3A5 in drug resistance mechanisms in acute leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2003 Jun;24(6):286-9
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  • [Title] [Study of CYP3A5 in drug resistance mechanisms in acute leukemia].
  • OBJECTIVE: To investigate if CYP3A5 is involved in drug resistances mechanisms of acute leukemia.
  • METHODS: By using RT-PCR, immunohistochemistry and MTT assay, CYP3A5 mRNA and protein were detected in leukemia cell lines and acute leukemia patients, meanwhile transcriptional regulation of CYP3A5 induced by daunorubicin was observed.
  • A pcDNA3-CYP3A5 reconstituted plasmid and its stably transfected cell line HL-60/CYP3A5 were both established.
  • Bone marrow CYP3A5 positive blast cell percentage at the time of diagnosis in primary drug resistance group (17.2%) was significantly higher than that of continuous complete remission (CCR) group (0.4%) and secondary drug resistance group (5.4%).
  • HL-60/CYP3A5 cell was significantly resistant to daunorubicin and vincristine than HL-60 cells did (3.0 and 4.0 times, respectively).
  • CONCLUSION: CYP3A5 expressed in leukemia cells may cause in situ metabolization of many kinds of anticancer drugs, thus led to drug resistance.
  • [MeSH-major] Cytochrome P-450 Enzyme System / physiology. Leukemia / drug therapy
  • [MeSH-minor] Cytochrome P-450 CYP3A. Daunorubicin / pharmacology. Drug Resistance, Neoplasm. Humans. RNA, Messenger / analysis. Tumor Cells, Cultured

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  • (PMID = 12859862.001).
  • [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
  • [Publication-country] China
  • [Chemical-registry-number] 0 / RNA, Messenger; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / CYP3A protein, human; EC 1.14.14.1 / CYP3A5 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A; ZS7284E0ZP / Daunorubicin
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6. Kaya P, Gündüz U, Arpaci F, Ural AU, Guran S: Identification of polymorphisms on the MDR1 gene among Turkish population and their effects on multidrug resistance in acute leukemia patients. Am J Hematol; 2005 Sep;80(1):26-34
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  • [Title] Identification of polymorphisms on the MDR1 gene among Turkish population and their effects on multidrug resistance in acute leukemia patients.
  • Multidrug-resistance (MDR) phenotype is a serious limitation to the effective chemotherapeutic treatment of many cancer types, including leukemia.
  • One of the most important proteins, the over-expression of which is responsible for the multidrug-resistance phenotype in many cancer types, is P-glycoprotein.
  • This protein is the product of the MDR1 gene.
  • It was suggested that this might have an advantage in cancer chemotherapy by resulting in a low drug-resistance phenotype.
  • The frequencies of these SNPs were studied in 45 acute leukemia patients (25 of which were primary refractory and 20 of which were drug-sensitive) and 17 healthy individuals, forming a Turkish population of 62 individuals.
  • In the second part of this study, drug-resistant and drug-sensitive acute leukemia patients were compared for these SNPs.
  • These polymorphisms did not seem to have a significant effect on P-glycoprotein-mediated drug resistance in the patients studied.
  • [MeSH-major] Drug Resistance, Multiple / genetics. Leukemia / genetics. P-Glycoprotein / genetics. Polymorphism, Genetic. Polymorphism, Single Nucleotide
  • [MeSH-minor] Acute Disease. Antigens, CD / immunology. DNA, Neoplasm / blood. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Humans. Immunophenotyping. Reference Values. Turkey

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16138358.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / DNA, Neoplasm; 0 / P-Glycoprotein
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7. Styczyński J, Wysocki M, Debski R, Kurylak A, Balwierz W, Rokicka-Milewska R, Matysiak M, Balcerska A, Kowalczyk J, Wachowiak J, Sońta-Jakimczyk D, Chybicka A: The influence of intracellular idarubicin and daunorubicin levels on drug cytotoxicity in childhood acute leukemia. Acta Biochim Pol; 2002;49(1):99-107
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  • [Title] The influence of intracellular idarubicin and daunorubicin levels on drug cytotoxicity in childhood acute leukemia.
  • Uptake and efflux of two anthracyclines, idarubicin (IDA) and daunorubicin (DNR), was studied in childhood acute leukemia samples.
  • A comparison of IDA and DNR transport phenomena in relation to drug cytotoxicity and expression of P-glycoprotein (PGP) was made.
  • Intracellular content of IDA/DNR was determined by flow cytometry using the fluorescent properties of the drugs.
  • In vitro drug cytotoxicity was measured by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay.
  • The uptake and efflux rates were non-significantly higher for IDA than DNR.
  • There were no differences between three types of leukemia with respect to drug content during accumulation and retention.
  • After correction for the cell volume, intracellular concentration of both drugs in each moment of uptake and efflux was significantly lower in relapsed ALL and AML samples in comparison with initial ALL cells.
  • Efflux, but not uptake, of both drugs was inversely correlated with PGP expression and IDA, but not DNR, cytotoxicity.
  • The cytotoxicity was correlated with drug accumulation for both drugs and with drug retention for IDA.
  • In conclusion, it seems that (1) intracellular content was related to the lipophilic properties of the drugs rather than to the type of leukemia, (2) decreased intracellular concentration of both drugs might have an impact on compromised therapy results in AML and relapsed ALL children, (3) IDA presents higher cytotoxicity, which possibly might be decreased by the presence of PGP.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Daunorubicin / pharmacokinetics. Idarubicin / pharmacokinetics. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 12136962.001).
  • [ISSN] 0001-527X
  • [Journal-full-title] Acta biochimica Polonica
  • [ISO-abbreviation] Acta Biochim. Pol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / P-Glycoprotein; 0 / Tetrazolium Salts; 0 / Thiazoles; 298-93-1 / thiazolyl blue; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin
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8. Hubeek I, Peters GJ, Broekhuizen R, Zwaan CM, Kaaijk P, van Wering ES, Gibson BE, Creutzig U, Janka-Schaub GE, den Boer ML, Pieters R, Kaspers GJ: In vitro sensitivity and cross-resistance to deoxynucleoside analogs in childhood acute leukemia. Haematologica; 2006 Jan;91(1):17-23
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  • [Title] In vitro sensitivity and cross-resistance to deoxynucleoside analogs in childhood acute leukemia.
  • BACKGROUND AND OBJECTIVES: Cytarabine (ara-C) is a key drug in the treatment of acute leukemia.
  • DESIGN AND METHODS: Using the MTT assay, we determined in vitro sensitivity and cross-resistance to deoxynucleoside analogs in 362 acute leukemia samples from untreated children and 32 normal bone marrow mononuclear cell samples.
  • RESULTS: Normal bone marrow samples were significantly more resistant to ara-C, cladribine and fludarabine than were acute myeloid leukemia (AML) samples and significantly more resistant to ara-C and fludarabine than were acute lymphoblastic leukemia (ALL) samples.
  • The only drug to which AML samples were more sensitive in vitro than ALL was cladribine.
  • T-ALL was significantly more resistant to cladribine than B-cell precursor ALL.
  • INTERPRETATION AND CONCLUSIONS: Cladribine appears to be a useful drug in AML, particularly in FAB M5.
  • We observed cross-resistance between ara-C and other deoxynucleoside analogs, as well as between ara-C and drugs with different modes of action in childhood acute leukemia.
  • [MeSH-major] Drug Resistance, Multiple. Leukemia / drug therapy. Nucleosides / therapeutic use
  • [MeSH-minor] Acute Disease. Child. Cytarabine / therapeutic use. Drug Screening Assays, Antitumor. Humans

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  • (PMID = 16434366.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nucleosides; 04079A1RDZ / Cytarabine
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9. Lin XM, Xie ZX, Zhu Y: [Expression of multidrug resistance P-170 and MRP and their correlation with clinical drug resistance in acute leukemia]. Hunan Yi Ke Da Xue Xue Bao; 2002 Dec 28;27(6):522-4
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  • [Title] [Expression of multidrug resistance P-170 and MRP and their correlation with clinical drug resistance in acute leukemia].
  • OBJECTIVE: To investigate the relevance between the expression of P-170 and MRP and clinical drug resistance in acute leukemia.
  • METHODS: The expression of P-170 and MRP in mononuclear cells of bone marrows was analyzed by the immunohistochemical technique in 72 acute leukemia patients.
  • RESULTS: The expression of P-170 was positive in 46 and negative in 26 of the 72 post-chemotherapy acute leukemia patients.
  • The expression of MRP was positive in 39 and negative in 33 of the 72 post-chemotherapy acute leukemia patients.
  • The expression of P-170 and MRP had a significant concordance (Kappa = 0.427, P < 0.01).
  • The sensitivity of P-170 and MRP which were analyzed simultaneously was 97.5%, which was higher than that of P-170 (90%) or MRP (77.5%) analyzed respectively in drug resistance patients.
  • CONCLUSION: The expression of P-170 and/or MRP was significantly related with drug resistance in clinical chemotherapy.
  • These data suggest that P-170 and MRP analyzed simultaneously can improve the value of diagnosis and prognosis in patients with drug resistance leukemia.
  • [MeSH-major] Glycoproteins / biosynthesis. Leukemia, Myeloid, Acute / metabolism. Multidrug Resistance-Associated Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Adolescent. Adult. Drug Resistance, Multiple. Female. Humans. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Prognosis

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  • (PMID = 12658928.001).
  • [ISSN] 1000-5625
  • [Journal-full-title] Hunan yi ke da xue xue bao = Hunan yike daxue xuebao = Bulletin of Hunan Medical University
  • [ISO-abbreviation] Hunan Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Glycoproteins; 0 / Multidrug Resistance-Associated Proteins; 0 / p-170 glycoprotein, human
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10. Ma J, Xu S, Lai Y, Lu Y: [The correlation of cyclin A gene expression with drug resistance in adult acute leukemia patients]. Zhonghua Xue Ye Xue Za Zhi; 2002 May;23(5):243-6
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  • [Title] [The correlation of cyclin A gene expression with drug resistance in adult acute leukemia patients].
  • OBJECTIVE: To investigate the relationship between the expression of cyclin A and drug resistance in patients with adult acute leukemias.
  • METHODS: The mRNA expressions of cyclin A, mdr1, Topo II alpha and bcl-2 were measured in 64 patients with adult acute leukemia (AL) and 20 normal subjects by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS:.
  • There was no cyclin A mRNA expression in the 20 normal subjects under the same experiment condition. (2) The mdr1 and bcl-2 mRNA expression levels in the resistant group were significantly higher than that in sensitive group (P < 0.01). (3) Cyclin A and Topo II alpha gene expression levels were positively correlated (r = 0.794, P = 0.000) in the 64 AL patients, and there was a negative correlation between the gene expression levels of cyclin A and mdr1 (r = -0.337, P = 0.029) in the drug resistant group. (4) Ten AL patients with low expressions of both cyclin A and Topo II alpha were all in the resistant group.
  • Logistic regression of binary analysis showed a significant correlation between the low expression of cyclin A and drug resistance.
  • CONCLUSION: Low expression of cyclin A gene might be a unfavorable prognostic factor for patients with AL and measurement of both cyclin A and Topo II alpha gene expression would predict drug resistance for AL patients.
  • [MeSH-major] Cyclin A / metabolism. DNA Topoisomerases, Type II / metabolism. Drug Resistance, Multiple / physiology. Drug Resistance, Neoplasm / physiology. Leukemia / metabolism
  • [MeSH-minor] Acute Disease. Adult. Antigens, Neoplasm. DNA-Binding Proteins. Female. Humans. Logistic Models. Male. P-Glycoprotein / genetics. P-Glycoprotein / metabolism. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / biosynthesis

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  • (PMID = 12133445.001).
  • [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] Comparative Study; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cyclin A; 0 / DNA-Binding Proteins; 0 / P-Glycoprotein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
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11. Chauncey TR: Drug resistance mechanisms in acute leukemia. Curr Opin Oncol; 2001 Jan;13(1):21-6
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  • [Title] Drug resistance mechanisms in acute leukemia.
  • Markers of anticancer drug resistance are predictive of treatment response and outcome in patients with acute myeloid leukemia.
  • Immunologic detection of the drug efflux pumps, P-glycoprotein (Pgp) and multidrug resistance-associated protein 1 (MRP1), correlate with functional assays of drug resistance.
  • These accumulation defects also appear operable in acute lymphoblastic leukemia.
  • Other markers such as lung-resistance protein, bcl-2, and breast cancer-resistance protein, have been described in acute myeloid leukemia patients although their pathophysiology and clinical relevance are less clear and the methodology for their quantification are not well standardized.
  • Preclinical studies have shown that small molecules capable of reversing efflux can restore drug sensitivity in resistant tumor models.
  • Although one large randomized study has demonstrated a proven survival advantage without increased toxicity using cyclosporine, the inconsistent results with other modulators raise doubt as to the utility and overall strategy of using drug efflux blockers in patients with established Pgp overexpression.
  • Preventing or delaying development of drug resistance in chemosensitive patients represents another therapeutic strategy to be tested.
  • [MeSH-major] ATP-Binding Cassette Transporters / pharmacology. ATP-Binding Cassette, Sub-Family B, Member 1 / pharmacology. Biomarkers, Tumor / analysis. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Leukemia / drug therapy
  • [MeSH-minor] Drug Interactions. Gene Expression Regulation, Neoplastic. Humans. Multidrug Resistance-Associated Proteins. Phenotype. Prognosis. Randomized Controlled Trials as Topic. Survival Analysis

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  • (PMID = 11148681.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Biomarkers, Tumor; 0 / Multidrug Resistance-Associated Proteins
  • [Number-of-references] 65
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12. Nørgaard JM, Hokland P: Biology of multiple drug resistance in acute leukemia. Int J Hematol; 2000 Oct;72(3):290-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biology of multiple drug resistance in acute leukemia.
  • Since the early 1970s, multiple drug resistance (MDR) has been known to exist in cancer cells and is thought to be attributable to a membrane-bound, energy-dependent pump protein (P-glycoprotein [P-gp]) capable of extruding various related and unrelated chemotherapeutic drugs.
  • At the cellular level, the function of P-gp has been extensively investigated in human cancer.
  • Although innumerable reports have been published in which P-gp has been shown to confer MDR to malignant (including leukemia) cells, so far, large-scale studies in the clinical setting have not convincingly proven that MDR1 plays a major role in clinical drug resistance when the influence of other known prognostic factors in human leukemia are taken into account.
  • At present, results from phase 3 clinical trials evaluating the efficiency of inhibiting (or reversing) the function of P-gp in hematologic malignancies are eagerly awaited.
  • Moreover, the horizon of cellular drug resistance in human cancer has during recent years widened dramatically.
  • Thus, an array of different molecules and mechanisms by which resistant cells can escape the cytotoxic effect of anticancer drugs has now been identified.
  • These molecules and mechanisms include apoptosis-related proteins.
  • In this article, we review the different methods for determining MDR and, in particular, methods for determining P-gp/MDR1, with special reference to their potential importance for therapeutic strategies in human acute leukemia.
  • [MeSH-major] Drug Resistance, Multiple / genetics. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans

  • MedlinePlus Health Information. consumer health - Leukemia.
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  • [ErratumIn] Int J Hematol 2001 Jan;73(1):132
  • (PMID = 11185984.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Number-of-references] 93
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13. Li L, Xiao ZJ: [Research update on pharmacogenomics in acute leukemia - review]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Jun;16(3):704-11
MedlinePlus Health Information. consumer health - Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Research update on pharmacogenomics in acute leukemia - review].
  • Pharmacogenomics, a new subject aiming to elucidate genetic basis for inter individual differences in response on a drug and to predict the safety and efficacy of drugs by the genetic information, which guides to clinical individual therapy, breaks a new way to apply drugs rationally to acute leukemia.
  • This article reviewed the enzymes related to metabolism, transport and acting point of the drugs used in the treatment of acute leukemia and discussed the influence of their coding gene's polymorphism on drug adverse effects and disease prognosis.

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  • (PMID = 18549659.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] China
  • [Number-of-references] 44
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14. Borthakur G, Faderl S, Ravandi F, Padmanabhan S, Stock W, Wu K, Li J, Curt G, Tallman M, Minden M: Clinical, pharmacokinetic (PK), and pharmacodynamic findings from a phase I trial of an Eg5 inhibitor (AZD4877) in patients with refractory acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):3580

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical, pharmacokinetic (PK), and pharmacodynamic findings from a phase I trial of an Eg5 inhibitor (AZD4877) in patients with refractory acute myeloid leukemia (AML).
  • Eg5 inhibition is thus specific for dividing cells, resulting in monoastral mitotic spindles (monoasters) and apoptotic cell death.
  • Preclinically, hematologic tumor cell lines were generally more sensitive to AZD4877 than those derived from solid tumors.
  • METHODS: AZD4877 was administered IV daily x 3 as induction for up to 2 cycles, followed by consolidation (daily x 2) for up to 4 cycles.
  • The T<sub>1/2</sub> of AZD4877 ranged from 26 to 42 hr; PK were linear and drug levels non-cumulative.

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  • (PMID = 27961757.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Schwartz S, Borner K, Müller K, Fischer L, Korfel A, Atkinson T, Melton R, Thiel E: Rescue with recombinant Carboxypeptidase G2 (CPG2) in high-dose methotrexate (HD-MTX) induced renal failure: Results in 42 patients from a German emergency protocol. J Clin Oncol; 2004 Jul 15;22(14_suppl):8067

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: 42 pts. (age: 10-78 years) with lymphoma (29), acute lymphoblastic leukemia (12) or germ cell tumor (1) were enroled.
  • MTX serum levels rapidly declined from a median of 5.11μmol/l (range: 0.35-165.86) to 1μmol/l or less within 7-50 minutes after CPG2 administration.
  • The remaining 19 pts. had median peak serum creatinine levels of 283μmol/l which subsequently declined to a median of 150μmol/l by days 1-58 after CPG2.
  • Further studies are needed to evaluate the efficacy of CPG2 with respect to clinical endpoints, as well as the role of this novel drug as a standard rescue agent.

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  • (PMID = 28015873.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Pigazzi M, Manara E, Baron E, Beghin A, Basso G: The inducible cyclic adenosine 3',5'-monophosphate early repressor (ICER) enhances drug sensitivity in acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e22045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The inducible cyclic adenosine 3',5'-monophosphate early repressor (ICER) enhances drug sensitivity in acute myeloid leukemia.
  • CREB was previously demonstrated to be overexpressed in acute leukemia, whereas ICER was found rapidly degradated being unable to control gene transcription.
  • ICER exogenous expression was demonstrated to repress CREB targets preventing leukemia progression.
  • We hypothesized that ICER restoration deserves a special consideration for playing a role in CREB oncogenic feature and in modeling leukemic cell phenotype.
  • We monitored transcription and translation of a series of genes involved in different pathways by quantitative gene expression and western blot analysis.
  • We investigate ICER's role in cell death after treatment with chemotherapic drugs.
  • RESULTS: We revealed that ICER was able to control gene expression in leukemia, principally of genes involved in cell death and survival.
  • HL60+ICER after being treated with drugs increased apoptosis.
  • Cell cycle analyses revealed a block in G2 phase, a lowered cell proliferation and clonogenic potential with respect to HL60 treated at the same conditions.
  • CONCLUSIONS: Finally, we described an enhanced sensibility to drugs in HL60 induced by ICER exogenous expression and that p38 stress signaling pathway is the direct target of this phenomenon.

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  • (PMID = 27963227.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Pratz KW, Cho E, Karp J, Levis M, Zhao M, Rudek M, Wright J, Smith BD: Phase I dose escalation trial of sorafenib as a single agent for adults with relapsed and refractory acute leukemias. J Clin Oncol; 2009 May 20;27(15_suppl):7065

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I dose escalation trial of sorafenib as a single agent for adults with relapsed and refractory acute leukemias.
  • Based on preclinical activity in FLT3 mutant AML, sorafenib was studied in refractory acute leukemia.
  • METHODS: The primary objective was to determine the safety and tolerability of sorafenib in refractory acute leukemias.
  • RESULTS: Fifteen patients (13 = AML, 2 = ALL) were enrolled (ages 37-85) and treated on three dosing schedules (400 mg BID x 14 d, 400 mg BID x 21 days, 600 mg BID x 21days) of single agent sorafenib.
  • No patients met criteria for complete or partial response, but 11 of 15 (73%) patients experienced stable disease as best response, with 6 showing a reduction in bone marrow blasts after only one cycle, half of who experienced a >50% reduction in bone marrow blasts.
  • Interestingly, 2 pts with FLT3-ITD mutations both showed marrow blast response (1 pt >50%).
  • Clinical activity as a single agent was limited to transient reductions in bone marrow blast counts and dose escalation was limited due to toxicities.

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  • (PMID = 27961441.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Kadia TM, Faderl S, Estrov Z, Konopleva M, George S, Lee W, Puzanov I, Chen A, Kantarjian H, Ravandi F: Final results of phase I and pharmacokinetic study of SJG-136 administered on a daily x 5 schedule. J Clin Oncol; 2009 May 20;27(15_suppl):e13506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here we report the results of a CTEP-sponsored phase I trial of SJG-136 administered on a daily x 5 schedule in pts with relapsed or refractory (R/R) leukemias.
  • METHODS: Previously treated pts with R/R acute leukemias (AML, ALL, high risk MDS, CML blast phase) or R/R CLL with adequate organ function and ECOG performance status of ≤ 2 were eligible for the study.
  • Other manifestations of vascular leak including grade I, II hypoalbuminemia, edema, and pleural effusions were seen in a number of patients starting at dose level 24 mcg/m<sup>2</sup> and above.
  • Other non-dose limiting toxicities included nausea, dyspnea, fatigue, bloating, and insomnia.
  • One pt had a PR, 8 pts had stable disease, and 6 had progression.
  • CONCLUSIONS: SJG-136 is safe and active in patients with advanced leukemias.
  • Edema and other vascular leak syndromes are characteristic toxicities of the agent at higher dose levels.

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  • (PMID = 27961262.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Arellano M, Waller EK: GM-CSF + INF-alpha induce a graft-versus-leukemia effect in BMT patients with relapsed AML and ALL. J Clin Oncol; 2004 Jul 15;22(14_suppl):6634

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GM-CSF + INF-alpha induce a graft-versus-leukemia effect in BMT patients with relapsed AML and ALL.
  • : 6634 Background: Relapse of acute leukemia following allogeneic hematopoietic progenitor cell transplantation (HPCT) has a poor prognosis.
  • GM-CSF and Interferon-alpha (IFN) activate dendritic cells and induce leukemia cells to express co-stimulatory molecules and enhance allo-antigen presentation, potentially inducing graft-versus-leukemia effects.
  • We hypothesized GM-CSF and IFN induce anti-leukemic effects in patients with relapsed acute leukemia.
  • Overall survival rates of cytokine-treated patients were compared with relapsed leukemia patients who did not receive cytokine immunotherapy.
  • RESULTS: Six patients received GM-CSF and IFN injections following the diagnosis of ALL or AML relapsed after allogeneic HPCT.
  • Two of 3 surviving patients remain without evidence of disease on no immunosuppressive drugs.
  • Cytokine-treated patients had better survival compared to 91 non-cytokine-treated patients with relapsed ALL or AML (median survival of 52 days, one-year survival of 8%, p=0.02).
  • CONCLUSIONS: The administration of GM-CSF and IFN may induce remissions in patients with acute leukemia who have relapsed after allogeneic HPCT.

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  • (PMID = 28016350.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Heffner LT Jr, Damon LE, Larson ML, Schiller G, Stock W, Kantarjian HM, Lu B, Imperiale SM, O'Brien S: A phase II study of the tolerability and activity of weekly vincristine sulfate liposomes injection (VSLI) in adults with Philadelphia chromosome-negative (Ph-) acute lymphoblastic leukemia (ALL) in second relapse or progressing following two antileukemia treatment lines. J Clin Oncol; 2009 May 20;27(15_suppl):7046

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of the tolerability and activity of weekly vincristine sulfate liposomes injection (VSLI) in adults with Philadelphia chromosome-negative (Ph-) acute lymphoblastic leukemia (ALL) in second relapse or progressing following two antileukemia treatment lines.
  • METHODS: Eligible adult subjects received single agent intravenous VSLI at a dose of 2.25 mg/m<sup>2</sup> weekly with no dose cap.
  • CONCLUSIONS: These results are encouraging, as VSLI was given as a single agent to a heavily pretreated patient population who nearly universally received prior VCR.
  • This population typically has a very low response rate to anti-leukemia therapies.
  • VSLI was well tolerated in these patients in the context of universal prior vincristine treatment.

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  • (PMID = 27961424.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Cheng PC, Crane J, Hunter T: Combination of bortezomib with a FLT3 inhibitor potentiates inhibition of proliferation and apoptosis of AML in vitro. J Clin Oncol; 2009 May 20;27(15_suppl):e14551

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14551 Background: FLT3 receptor tyrosine kinase activating mutations contribute to leukemogenesis and poor prognosis in approximately 30% of acute myeloid leukemia (AML).
  • An internal tandem duplication (ITD) mutation in the juxtamembrane domain of FLT3 results in loss of autoinhibition that leads to constitutive, ligand-independent activation of the receptor, with subsequent activation of multiple downstream signaling pathways, including RAS/MAPK and STAT5.
  • METHODS: In the course of conducting a synthetic lethality screen with a FLT3 inhibitor on the Ba/F3 murine cell line stably expressing human FLT3 or FLT3-ITD, we identified bortezomib, a proteasome inhibitor, as having potent activity against FLT3-ITD cells.
  • The effects of drugs on proliferation, apoptosis, and phosphosignaling were quantified in Ba/F3 cells and in the HL60 (WT FLT3) and MV4-11 (FLT3-ITD) human cell lines, using an MTS- based colorimetric assay, caspase 3 and 7 activity assays, and immunoblotting, respectively.
  • Surprisingly, bortezomib abrogated tyrosine phosphorylation of FLT3, STAT5, and ERK within 60 min of adding drug.
  • When the FLT3 inhibitor and bortezomib were used at IC25 concentrations, a more pronounced inhibition of cell proliferation was observed when they were used in combination than with either alone.
  • CONCLUSIONS: Bortezomib preferentially kills FLT3- ITD cells, showing a four-fold more potent inhibition of cell proliferation, induces apoptosis, and abrogates activation of FLT3 and its downstream effector pathways.

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  • (PMID = 27963616.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Tsimberidou AM, Tirado-Gomez M, Andreeff M, O'Brien S, Kantarjian HM, Keating MJ, Lopez-Berestein G, Estey E: Single agent liposomal-encapsulated (Lipo) all-trans retinoic acid (ATRA) can cure patients with untreated acute promyelocytic leukemia (APL): An update and comparison with an ATRA+idarubicin induction regimen. J Clin Oncol; 2004 Jul 15;22(14_suppl):6513

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Single agent liposomal-encapsulated (Lipo) all-trans retinoic acid (ATRA) can cure patients with untreated acute promyelocytic leukemia (APL): An update and comparison with an ATRA+idarubicin induction regimen.
  • : 6513 Background: There is interest in using "targeted therapy" in leukemia in order to avoid non-specific toxicity.
  • CONCLUSIONS: These results, which are considerably superior to those reported with single agent oral ATRA (Fenaux, Leukemia, 6, Suppl.

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  • (PMID = 28016919.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Faderl S, Thomas DA, Gandhi V, Huang X, Borthakur G, O'Brien S, Ravandi F, Plunkett W, Bretz JL, Kantarjian HM: Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL). J Clin Oncol; 2009 May 20;27(15_suppl):7020

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL).
  • Single agent CLO in adult ALL was less active so that combinations of CLO with other active agents are pursued.
  • As CLO inhibits DNA repair following exposure to DNA damaging agents, we designed a phase I study of the combination of CLO with CY.
  • Twenty-one pts had pre-B ALL, 5 pts pre-T/T ALL, 1 pt mature B ALL, and 3 pts biphenotypic acute leukemias.
  • One (20%) pt in cohort 1 and 9 (36%) in cohort 2 experienced DLTs (≥ grade 3) including transaminase elevations, diarrhea, hyperbilirubinemia, and (1 pt each) elevation of creatinine/renal failure, lipase elevation, rash, nausea/vomiting.

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  • (PMID = 27961382.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Remick S, Sweeney C, Takimoto C, Douer D, Bernareggi A: Pharmacokinetics (PK) of arsenic trioxide in cancer patients (pts) with renal dysfunction: Preliminary results. J Clin Oncol; 2004 Jul 15;22(14_suppl):2018

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2018 Background: Trisenox (arsenic trioxide- ATO) is approved for treatment of relapsed/refractory acute promyelocytic leukemia.
  • METHODS: 14 pts (median age 66 yrs, 29-85) in 4 renal function (RF) groups (normal- CL<sub>CR</sub> >80 mL/min; mild dysfunction: 50-80; moderate: 30-49; severe: <30) received IV ATO 0.15 mg/kg/d twice weekly for 4 wks, followed by 2 weeks without drug.
  • The only severe drug-related toxicity was 1 grade 3 hyperglycemia.

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  • (PMID = 28015604.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Flinn IW, Byrd JC, Furman RR, Brown JR, Lin TS, Bello C, Giese NA, Yu AS: Preliminary evidence of clinical activity in a phase I study of CAL-101, a selective inhibitor of the p1108 isoform of phosphatidylinositol 3-kinase (P13K), in patients with select hematologic malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):3543

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 3543 Background: The class I PI3Ks regulate a variety of cellular functions relevant to oncogenesis, including metabolism, proliferation and survival.
  • The PI3K p110δ isoform is highly expressed in cells of hematopoietic origin and plays a key role in B cell maturation and function.
  • In vitro studies of 0.1 to 10 μM CAL-101 showed inhibition of pAKT expression and/or apoptotic effects against primary chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML) cells and against a range of leukemia and lymphoma cell lines.
  • METHODS: In an ongoing phase 1 dose escalation study in sequential cohorts of 3 patients with relapsed/refractory CLL or select B-cell non-Hodgkin's lymphoma, CAL-101 is administered orally twice daily for 28 days per cycle.
  • Mean trough drug levels in the 50 and 100 mg cohorts were 0.3 and 1 μM, respectively, which are in the range required to inhibit PI3K p110δ in vitro.
  • Two of 6 patients attained partial response and 4 have stable disease.
  • Partial responses were observed after 2 cycles of 50 mg in a patient with mantle cell lymphoma with 6 prior therapies, and after 1 cycle of 100 mg in a patient with follicular lymphoma with 6 prior therapies, including autologous stem cell transplant.
  • Disease specific cohort expansion will occur at the maximally tolerated dose, and patients with AML will be added.
  • CONCLUSIONS: Early results from a phase 1 study of the oral PI3K p110δ inhibitor CAL-101 show that it is well tolerated and has preliminary clinical activity in patients with B-cell malignancies.

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  • (PMID = 27961357.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Crump M, Leber B, Kassis J, Hedley D, Minden M, Buckstein R, McIntosh L, Eisenhauer E, Seymour L: A randomized phase I clinical and biologic study of two schedules of BAY 43-9006 in patients with myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML): A National Cancer Institute of Cancer Clinical Trials Group Study. J Clin Oncol; 2004 Jul 15;22(14_suppl):6611

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A randomized phase I clinical and biologic study of two schedules of BAY 43-9006 in patients with myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML): A National Cancer Institute of Cancer Clinical Trials Group Study.
  • Phospho-ERK levels were assessed in bone marrow (BM) blasts at baseline, day 15 and 28 by immunohistochemistry and in stem cell factor (SCF) stimulated peripheral blood (PB) blasts by a flow cytometry assay.
  • Biologic activity (inhibition of pERK in SCF stimulated PB blasts) has been assessed in 14 pts and shows drug-related inhibition in 5/14, all at 400 mg bid.
  • Early clinical and biological activity is evident.

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  • (PMID = 28016333.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Te Loo DM, van Schie RM, Hoogerbrugge PM: Effect of azole antifungal therapy on vincristine toxicity in childhood acute lymphoblastic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):10049

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of azole antifungal therapy on vincristine toxicity in childhood acute lymphoblastic leukemia.
  • : 10049 Background: Vincristine is one of the corner stitches in the treatment of children with acute lymphoblastic leukemia (ALL).
  • Drugs interfering with the metabolism of vincristine might potentiate these side effects.
  • A group of drugs that interact with the metabolism of vincristine are azoles.
  • METHODS: In total, twenty pediatric patients with de novo ALL were included in this study.

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  • (PMID = 27962456.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Mulhern RK, Khan R, Kaplan S, Xiong X, Wu S, Helton S, Brown R, Bonner M, Christensen R, Reddick W: A randomized, double-blind, placebo-controlled trial of methylphenidate for attentional problems in survivors of childhood cancer. J Clin Oncol; 2004 Jul 15;22(14_suppl):8510

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A randomized, double-blind, placebo-controlled trial of methylphenidate for attentional problems in survivors of childhood cancer.
  • : 8510 Background: Children surviving acute lymphoblastic leukemia (ALL) and malignant brain tumors (BT) have a higher incidence of attention and learning problems in school than their healthy peers.
  • RESULTS: The 30 male and 24 female patients ranged from 0.54 to 12.57 (M=5.25) years of age at diagnosis and 6.83 to 17.49 (M=11.63) years of age at participation.
  • CONCLUSIONS: Short-term treatment with low-dose MPH can reduce attentional problems among survivors of childhood ALL and BT.
  • Forty-five of the 54 (83%) patients showed a positive response to MPH and continue on medication.

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  • (PMID = 28013790.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Epenetos AA, Kousparou C, Stylianou S: Inhibition of Notch and tumor regression. J Clin Oncol; 2009 May 20;27(15_suppl):e14623

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14623 Background: Notch signaling is an evolutionary-conserved pathway in vertebrates and invertebrates which is involved many developmental processes, including cell fate decisions, apoptosis, proliferation, and stem-cell self renewal.
  • Increasing evidence suggests that the Notch signaling pathway is frequently up regulated in many forms of cancer including acute T-cell lymphoblastic leukemia, cervical, prostate, lung, breast and others.
  • RESULTS: Our data show that ANTP/DN MAML fusion protein, TR4 contains signals for proper cell targeting, internalization and nuclear transport.
  • Furthermore, TR4 inhibits human mammary and colon xenograft tumor growth and metastases in immuno deficient mice.TR4 presence and activity was also detected in the brains of treated animals demonstrating that TR4 can cross the blood-brain barrier and potentially eliminate brain tumors and metastases, unlike other anticancer drugs and biological such as monoclonal antibodies that cannot cross the blood brain barrier.
  • TR4 was found to be non- immunogenic following repeat administration in healthy animals.
  • It is non- immunogenic following repeat administration and has acceptable toxicity profile.

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  • (PMID = 27964214.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Barret J, Dumontet C, Annereau J, Brel V, Breillout F, Guminski Y, Imbert T, Guilbaud N, Bailly C: A functional procedure using fresh samples to select patients with acute myeloid leukemia prior to treatment with the novel targeted cytotoxic agent F14512. J Clin Oncol; 2009 May 20;27(15_suppl):11087

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A functional procedure using fresh samples to select patients with acute myeloid leukemia prior to treatment with the novel targeted cytotoxic agent F14512.
  • : 11087 Background: The Polyamine Transport System (PTS) is an energy-dependent machinery generally hyper-active in cancer cells with a high demand for polyamines.
  • This study was undertaken to investigate the potential of N-methyl-spermine-NBD, a proprietary fluorescent polyamine conjugate, designed to select patients with PTS-positive leukemic cells.
  • METHODS: The uptake of this probe was first measured by flow cytometry in a panel of human leukemia cell lines.
  • RESULTS: Data showed that high level of fluorescence was detected in F14512 -sensitive cancer cell lines whereas leukemia cells responding poorly to F14512 generally exhibited very low levels of PTS.
  • We then demonstrated that human leukocytes incorporate N-methyl-spermine-NBD in a time, concentration and temperature dependent manner, confirming the active transport of polyamines in these cells.
  • A panel of 50 fresh human acute myeloid leukemia samples showed a larger inter-individual variation and, interestingly, incorporation of the fluorescent probe was generally higher in leukemia blasts than in lymphocytes.

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  • (PMID = 27963178.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Cunningham CC, Nemunaitis J, Senzer N, Vukelja S, Weiss J, Ferrier A, Vukovic V, Weitman S, Richards D: Clofarabine administered weekly to adult patients with advanced solid tumors in a phase I dose-finding study. J Clin Oncol; 2004 Jul 15;22(14_suppl):3115

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 3115 Background: Clofarabine, a next-generation nucleoside analogue that inhibits DNA synthesis, has demonstrated activity in acute leukemia in Phase I and II trials.
  • The agent has also shown potent cytotoxic activity in a wide range of solid tumor cell lines and therapeutic activity in murine tumor models.
  • To avoid the dose limiting toxicity of myelosuppression observed with the daily × 5 administration used for hematologic malignancies, clofarabine is administered IV on days 1, 8, and 15 of a 28-day cycle.
  • Tumor types include colorectal (5); non-small cell lung (3); squamous cell larynx, transitional cell bladder, and prostate (2 each); and adenosquamous gallbladder, bronchioalveolar, hepatocellular/cholangiocarcinoma, leiomysarcoma, melanoma, pancreas, and squamous cell esophagus (1 each).
  • Data on 20 of the 21 patients show that 7 had stable disease (SD) as their best response; 1 prostate cancer patient had a drop in PSA level from 7975 ng/mL at baseline to 934 ng/mL at end of study.

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  • (PMID = 28014838.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Tsai DE, Wang W, Reshef R, Vogl D, Stadtmauer E, Andreadis C, Carlson A, Luger S: Effect of bexarotene on platelet counts in patients undergoing cancer treatment: An analysis of clinical trials in lung cancer and leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e20533

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of bexarotene on platelet counts in patients undergoing cancer treatment: An analysis of clinical trials in lung cancer and leukemia.
  • : e20533 Background: Bexarotene (Bex) is an oral retinoid X receptor agonist with activity against cutaneous T cell lymphoma and currently under investigation for other malignancies.
  • In patients receiving this agent for acute myeloid leukemia (AML), we noted increases in platelet counts.
  • METHODS: We analyzed platelet count data from 3 Bex clinical trials encompassing non-small cell lung cancer (NSCLC) and AML.

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  • (PMID = 27960979.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Ritchie EK, Roboz G, Hinchcliff K, Curcio T, Scandura J, Feldman E: Phase I trial of laromustine in combination with infusional ara-C in elderly patients over age 60 with newly diagnosed AML or high-grade MDS. J Clin Oncol; 2009 May 20;27(15_suppl):7054

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7054 Background: Laromustine is a novel sulfonylhydrazine-alkylating agent with activity in acute myeloid leukemia (AML).
  • Laromustine in phase I and II trials shows activity in patients with relapsed/refractory leukemia (1) and elderly patients with new AML (2).
  • METHODS: Laromustine 300 mg/m2 (cohort 1, n = 6), 400 mg/m2 (cohort 2, n = 5) and 500 mg/m2 (cohort 3) was administered by IV infusion over 1 hour on day 1 in combination with ara-C 100 mg/m2/day as a continuous infusion for 7 days.
  • Patients achieving CR after induction therapy were offered up to 2 cycles of consolidation therapy for a maximum cumulative laromustine dose of 1,000 mg/m2.
  • One patient had grade 2 dyspnea possibly related to drug and improved with a short course of steroids.
  • After 2 consolidation cycles, there was possible drug-related pulmonary toxicity with 3 episodes of grade 3 hypoxia.

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  • (PMID = 27961420.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Raza A, Galili N, Borthakur G, Carter TH, Claxton DF, Erba HP, DeAngelo DJ, Berger MS, Schimmer A: A safety and schedule seeking trial of Bcl-2 inhibitor obatoclax in previously untreated older patients with acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):3579

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A safety and schedule seeking trial of Bcl-2 inhibitor obatoclax in previously untreated older patients with acute myeloid leukemia (AML).
  • : 3579 Background: Obatoclax (Ob) is a small-molecule inhibitor of all Bcl-2 prosurvival proteins.
  • This study evaluated the single-agent response rate in older patients with previously untreated AML.
  • Evidence of biological activity was seen with the 3-hr infusion schedule but not with the 24-hr infusion schedule, suggesting that efficacy may be improved with the 3-hr infusion schedule and may be related to PK differences.

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  • (PMID = 27961704.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Plunkett W, Thomas DA, O'Brien SM, Federl S, Giles FJ, Nicol SJ, Gill J, Zhao L, Ravandi F, Kantarjian H: Phase I study of pemetrexed in patients with relapsed or refractory acute leukemia or lymphoid blast phase chronic myelogenous leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7068

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of pemetrexed in patients with relapsed or refractory acute leukemia or lymphoid blast phase chronic myelogenous leukemia.
  • The purpose of this phase I trial was to define the dose-limiting toxicity (DLT), maximum tolerated dose (MTD), and recommended phase II dose (RP2D) of pemetrexed given with vitamin supplementation to patients with relapsed or refractory leukemia.
  • METHODS: Patients ≥15 years of age were enrolled with relapsed or refractory leukemia, Eastern Cooperative Oncology Group performance status ≤2, adequate renal and hepatic function, and life expectancy of ≥6 weeks.
  • RESULTS: Twenty-two patients entered the trial; median age was 50 years (range: 18-75); 15 patients had acute myeloid leukemia and 7 patients had acute lymphocytic leukemia (ALL).
  • Two patients were ineligible and did not receive study drug.
  • Two patients died during the study due to disease progression and 1 patient discontinued due to a subdural hematoma of unknown cause.

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  • (PMID = 27961463.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Ghavamzadeh A, Allahyari A, Alimoghaddam K, Karimi A, Shamshiri A, Abolhasani R, Manookian A, Asadi M, Khatami F: Outpatient versus inpatient autologous stem cell transplantation for malignant hematologic disorders. J Clin Oncol; 2009 May 20;27(15_suppl):7042

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outpatient versus inpatient autologous stem cell transplantation for malignant hematologic disorders.
  • : 7042 Background: High-dose chemotherapy with autologous stem cell support is utilized for the treatment of a variety of malignancies including Hodgkin/non-Hodgkins lymphoma and acute leukemias.
  • The aim of this study was to compare the time of engraftment and mortality rate and cost of neutropenic treatment in outpatient versus inpatient autologous stem cell transplantation (SCT).
  • They received conditioning regimen (CEAM for NHL and HL, busulfan and etoposide for AML) and stem cell infusion in hospital.
  • For inpatient group the cost of drugs, just for neutropenic fever antibiotic therapy was six times than outpatient group.

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  • (PMID = 27961405.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. Evans WE, Relling MV: Pharmacogenomics of childhood acute lymphoblastic leukemia (ALL). J Clin Oncol; 2009 May 20;27(15_suppl):s3

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pharmacogenomics of childhood acute lymphoblastic leukemia (ALL).
  • : s3 Childhood ALL is a model for drug-responsive cancer: it is successfully cured with medications in 85%-90% of patients, but relapse remains unacceptably high for some subgroups, and therapy is complicated by the occurrence of adverse effects.
  • Based on these studies, candidate gene genotyping has been already incorporated into the treatment of childhood ALL and integrated with electronic medical records at St. Jude to optimize use of a few medications.
  • Additional genotyping is conducted on a research basis and has identified SLCO1B1 as important for methotrexate disposition, IL15 as related to antileukemic drug response, ITPA as important for thiopurine toxicity, and a genomic basis to race-related differences in relapse risk.
  • Because prognostic factors (including genomic variations) depend upon the details of therapy, collection of blood (for germ-line DNA) should be part of every cancer clinical trial to advance genomic research.

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  • (PMID = 27962369.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. Lopez-Enriquez AT: Acute promielocytic leukemia: 14 years experience at the University Hospital, San Juan, Puerto Rico. J Clin Oncol; 2009 May 20;27(15_suppl):e18006

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute promielocytic leukemia: 14 years experience at the University Hospital, San Juan, Puerto Rico.
  • : e18006 Background: Acute promielocytic leukemias (APL) are a unique example in carcinogenesis, of maturation arrest at the promielocytic stage, associated with a chromosomal reciprocal translocation of a portion of chromosome 15 and 17 with the formation of fusion proteins between the PML gene and the alpha-retinoic acid receptor site.
  • METHODS: Since 1994 when transretinoic acid (ATRA) became available to us, we developed a protocol incorporating this drug to the standard regime of induction chemotherapy for acute leukemias used in our institution of 7 days of continuous infusion of cytosine arabinoside (Ara-C) and three days of daunorubicine (7+3), starting the ATRA on day 14 at 45 mg/m2 and continued daily for 120 days.
  • Nineteen of eighty-nine (19/89) died early in the first two weeks of treatment mainly secondary to bleeding and sepsis for a 21% early death rate.
  • Sixty-seven of seventy (67/70) patients went into complete remission for a 98% rate.
  • Fifty-three (53) has remained in complete remission with a range of 6months to 14 years, for a rate of 76%.
  • Thirteen of 17 (13/17) relapsed after receiving Dauno x3 x3 as consolidation chemotherapy for a 76% relapsed rate.
  • Daunorubicine as a single agent in consolidation is inappropriate in our population.

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  • (PMID = 27963993.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Laille E, Ward R, Nasser A, Stoltz M, Cogle C, Gore S, Skikne BS, Garcia-Manero G: The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7087

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML).
  • : 7087 Background: 5-azacitidine (AZA), through its effects on DNA metabolism, gene expression, and cell differentiation, has proven beneficial in treatment of MDS and AML and AZA therapy significantly increases survival in higher-risk MDS and AML compared to conventional care.
  • PK parameters of AZA were derived from drug concentrations in plasma and urine collected after the first and last dose (day 7) of AZA.
  • CONCLUSIONS: The AZA AUC<sub>inf</sub> after SC doses is similar to the published AUC value (1044 hr*ng/mL) after 75 mg/m<sup>2</sup> IV doses indicating approximating 100% systemic bioavailability.

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  • (PMID = 27961481.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Medeiros BC, Gotlib JR, Coutre SE, Jones C, Khan SA, Rajwanshi R, Rajwanshi R, Zehnder J, Zehnder J: Interim results of protracted low doses of temozolomide in high-risk acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7052

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interim results of protracted low doses of temozolomide in high-risk acute myeloid leukemia.
  • : 7052 Background: High treatment-related mortality and low response rates often discourage elderly patients with acute myeloid leukemia from receiving treatment.
  • De novo AML was diagnosed in eight patients and five patients had s-AML.
  • Drug-related hematologic toxicities were difficult to distinguish from disease-related cytopenias.
  • Seven patients have died from disease progression, while two patients died of neutropenic sepsis (early deaths).

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  • (PMID = 27961417.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. Sampat KR, Garcia-Gutierrez V, Rossi A, Pierce S, Cortes J, Kantarjian H, Garcia-Manero G: Prevalence and therapeutic relationships of pericardial effusions in patients with leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7067

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence and therapeutic relationships of pericardial effusions in patients with leukemia.
  • : 7067 Background: Little is known regarding the prevalence and natural history of pericardial disease in patients with leukemia.
  • Although a direct causal relationship has not been established yet, this complication may have a significant impact for the future development of this class of drugs.
  • To study this issue, we retrospectively analyzed a large cohort of patients with leukemia, who were evaluated at MD Anderson Cancer Center (MDACC), to determine the prevalence, timing, and characteristics of PEf in leukemia.
  • METHODS: We reviewed 3,327 patients with acute myeloid leukemia (AML, N = 1,809, 54%), acute lymphocytic leukemia (ALL, N = 494, 15%), or myelodysplastic syndrome (MDS, N =1,024, 31%), who were seen at MDACC from August 2003 to July 2008.
  • Data regarding diagnosis, timing, effusion size, and prior therapy was collected in the 401 patients (20.2%) that had echocardiographic evidence of PEf.
  • In the 401 total patients with PEf, 22.8%, 25.0%, and 18.4% (p = 0.33) of these effusions were found before treatment in the three disease categories, respectively.
  • The rest occurred after some form of chemotherapy, accounting for 77.2%, 75.0%, and 81.6% (p = 0.73) of the total PEf by disease, respectively.
  • No differences in effusion characteristics, including severity, were observed among different types of therapies including HDACi.
  • CONCLUSIONS: PEf are relatively common in patients with leukemia at initial presentation and are usually asymptomatic.
  • Their incidence increases with therapy administration although it appears that this is not a process related to specific classes of treatment or type of leukemia.

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  • (PMID = 27961462.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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42. Villano JL, Letarte N, Yu JM, Shakir AR, Bressler L: Hematologic adverse events associated with temozolomide (TMZ). J Clin Oncol; 2009 May 20;27(15_suppl):2053

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2053 Background: Secondary acute myeloid leukemia (AML) is reported to occur in 3%-10% of patients treated with alkylating agents for Hodgkin's lymphoma, non-Hodgkin's lymphoma, ovarian cancer, breast cancer, and multiple myeloma.
  • TMZ is a pro-drug of methyl-triazeno-imidazole-carboxamide (MTIC), an alkylating metabolite of dacarbazine.
  • The FDA, in a Drug Safety Newsletter, described 18 cases of aplastic anemia reported between 1999 and 2006.
  • Among these patients, we identified 140 cases that we labeled as major hematologic adverse events: agranulocytosis (8 cases), aplasia (42), aplastic anemia (52), leukemia (26), MDS (6), and lymphoma (6).
  • Risk of leukemia/MDS from our review may also be significant, but length of follow-up is insufficient and the real risk is likely still unknown.

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  • (PMID = 27964671.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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43. List AF, Schiller GJ, Mason J, Douer D, Ellison R: Arsenic trioxide in patients with myelodysplastic syndromes (MDS): Preliminary results of a phase II clinical study. J Clin Oncol; 2004 Jul 15;22(14_suppl):6512

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenic trioxide in patients with myelodysplastic syndromes (MDS): Preliminary results of a phase II clinical study.
  • : 6512 Background: Trisenox (arsenic trioxide -ATO) is a novel anticancer agent approved for the treatment of relapsed or refractory acute promyelocytic leukemia.
  • ATO has unique mechanisms of action that impact apoptotic threshold and differentiation in leukemia cell lines and hematopoietic malignancies.
  • METHODS: Pts received ATO at 0.25 mg/kg via a 1-2 hour IV infusion, Monday to Friday, 2 consecutive wks every 28 days.
  • Disease response and toxicity were assessed using the International Working Group (IWG) criteria and NCI CTC v2, respectively.
  • RESULTS: 53 pts are enrolled: 4 received no study drug and 3 are too early in treatment to assess.
  • The median interval from diagnosis to first dose was 7 months (0-81).
  • Thirty-five pts were transfusion-dependent (TD).
  • Responses included 9 erythroid (5 major, including 1 CR), 3 major platelet, and 2 major neutrophil.
  • Stable disease lasting >8 weeks was observed in 8 additional HR pts.
  • Grades (gr) 3-4 adverse events considered drug-related that were observed in ≥2 pts included fatigue, febrile neutropenia, dyspnea, urinary tract infection, hyperglycemia, congestive heart failure, hypoxia, herpes infection, and pleural effusion.

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  • (PMID = 28016925.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Vey N, Bourhis J, Dombret H, Bordessoule D, Prebet T, Charbonnier A, Squiban P, Damholt B, Blaise D, Olive D: A phase I study of the anti-natural killer inhibitory receptor (KIR) monoclonal antibody (1-7F9, IPH2101) in elderly patients with acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):3015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of the anti-natural killer inhibitory receptor (KIR) monoclonal antibody (1-7F9, IPH2101) in elderly patients with acute myeloid leukemia (AML).
  • To mimic this effect with a pharmaceutical agent, a fully human IgG4 anti-KIR mAb specific for KIR2DL1/2/3 (HLA-C specific KIRs) was generated.
  • We present the results of the first-in-human phase I trial of this agent in patients with AML in complete remission (CR).
  • METHODS: Patients aged 60-80 years with non promyelocytic AML in first CR following induction and 1-6 cycles of consolidation chemotherapy, normal renal, and hepatic functions, KIR-expression on patient NK-cells and who signed informed consent were eligible.Dose escalation (0.0003, 0.003, 0.015, 0.075, 0.3, 1, 3 mg/kg) was studied using a 3+3 scheme.
  • Side effects that could be related to drug administration were mild and transient.
  • As expected for an IgG4, NK cell numbers were unaffected by the treatment.

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  • (PMID = 27962059.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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45. Maris MB, Ravandi F, Stuart R, Stone R, Cripe L, Cooper M, Strickland S, Turturro F, Stock W, Berman C: A phase II study of voreloxin as single agent therapy for elderly patients (pts) with newly diagnosed acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of voreloxin as single agent therapy for elderly patients (pts) with newly diagnosed acute myeloid leukemia (AML).
  • Interim results of REVEAL-1, a phase II study of single agent voreloxin in newly diagnosed elderly AML pts, are reported.
  • B) 72 mg/m<sup>2</sup>qw X 2; or C) 72 mg/m<sup>2</sup>/dose on D1 and D4.
  • Eligibility: newly diagnosed AML (de novo or secondary AML), pts age ≥ 60 and ≥ 1 additional adverse risk factor (age ≥ 70, secondary AML, intermediate or unfavorable cytogenetics, or PS 2).
  • Voreloxin PK were similar to those in an earlier single agent phase I study in relapsed/refractory AML.

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  • (PMID = 27961427.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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46. Yeh C, Ma W, Kantarjian H, Zhang ZJ, Cortes J, Albitar M: BCR-ABL truncation due to premature translation termination as a mechanism of resistance to kinase inhibitors. J Clin Oncol; 2009 May 20;27(15_suppl):7028

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7028 Background: The major mechanism underlying imatinib resistance in patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with point mutations in the BCR-ABL tyrosine kinase.
  • We describe three novel ABL premature termination mutations leading to BCR-ABL truncation in leukemia patients with multidrug (imatinib/nilotinib/dasatinib) resistance.
  • METHODS: Peripheral blood or bone marrow samples from drug-resistant CML patients were collected.
  • Total nucleic acids were purified and subjected to two rounds of PCR analysis, with the first PCR designed to eliminate amplification of the wild-type, non-translocated ABL gene.
  • HL60 cells (a Ph-negative myeloid leukemia cell line) and peripheral blood of healthy subjects were used as negative controls; a human CML cell line (K562) was used as a positive control.
  • RESULTS: We identified an exon 7 deletion in three CML patients, a 4-nt insertion (908insCAGG) near the exon 5/6 junction in one CML case, and an exon 6 point mutation (997C>T) in one patient with acute lymphoblastic leukemia (ALL).
  • These mutations all create premature stop codons and cause termination at residues 381, 315, and 333, respectively, leading to truncated proteins with only the first quarter of the kinase domain (P-loop) or lacking the C-terminus of ABL including the A-loop.
  • (2) abolish the regulatory element in the ABL kinase domain and the downstream C-terminal region; and (3) confer significant drug resistance.

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  • (PMID = 27961401.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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47. Jeha S, Razzouk B, Gaynon P, Kadota R, Rheingold S, Luchtman-Jones L, Arceci R, Fernandez M, Weitman S, Steinherz P: Clofarabine therapy for the treatment of relapsed or refractory pediatric acute leukemias. J Clin Oncol; 2004 Jul 15;22(14_suppl):8504

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  • [Title] Clofarabine therapy for the treatment of relapsed or refractory pediatric acute leukemias.
  • : 8504 Background: Despite marked improvement in pediatric leukemia outcome, children with refractory disease or early relapse have a dismal prognosis with the current salvage regimens.
  • Leukemia remains the leading cause of disease-related death in children.
  • Clofarabine, a next-generation nucleoside analogue, has shown clinical activity when used as a single agent in heavily pretreated children with relapsed or refractory acute leukemias.
  • As determined by independent review, preliminary data indicate overall response rates of 28% in ALL (4 CR, 3 CRp, and 4 PR) and 24% in AML (1 CRp and 6 PR).
  • One responding AML patient had previously failed an induction therapy regimen that included cladribine, and 5 other responding patients (2 ALL, 3 AML) had received prior fludarabine as part of a conditioning regimen for BMT.
  • Most drug-related adverse events were transient including fever, nausea/vomiting, headache, skin rash, hand-foot syndrome, elevation in liver enzymes and bilirubin, and infusion-related flushing and anxiety.
  • CONCLUSIONS: Clofarabine, a next-generation nucleoside analogue, is active in multiply relapsed or refractory pediatric leukemia patients, including those who have failed prior nucleoside therapies such as cladribine or fludarabine.

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  • (PMID = 28014535.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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48. Ciceri F, Bonini C, Bondanza A, Magnani Z, Bernardi M, Peccatori J, Crippa F, Gallo Stampino C, Bregni M, Bordignon C: Early immune reconstitution and abrogation of GvHD after infusion of HSV-TK engineered donor lymphocytes after haplo-identical hemopoietic stem cell transplantation. J Clin Oncol; 2004 Jul 15;22(14_suppl):6515

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  • [Title] Early immune reconstitution and abrogation of GvHD after infusion of HSV-TK engineered donor lymphocytes after haplo-identical hemopoietic stem cell transplantation.
  • : 6515 Background: Haplo-identical stem cell transplantation (haplo-SCT) is a therapeutic option for patients with high risk hematologic malignancies lacking an HLA matched donor.
  • Infusion of small numbers of donor T cells, aimed at providing immune reconstitution, results in severe forms of graft-versus-host-disease (GvHD).
  • Immune reconstitution resulted in complete control of viral infections and complete remission of leukemia in the majority of patients.
  • In 1 pt a grade II biopsy-proven acute GvHD, involving skin and liver was observed.
  • Multiple doses of ganciclovir (10 mg/kg/die), in the absence of immunosuppressive drugs, quickly resulted in the complete resolution of all signs of GvHD.
  • CONCLUSIONS: Tk-DLI at a dose of 10e7/kg is a promising tool for preventing disease relapse and promoting immune reconstitution after haplo-SCT while providing an effective and selective treatment for GvHD.

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  • (PMID = 28016921.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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49. Erba HP, Kantarjian HM, Claxton DF, Arellano M, Lyons RM, Kovacsovics TJ, Gabrilove J, Eckert S, Faderl S: Updated remission duration and survival results of single-agent clofarabine in previously untreated older adult patients with acute myelogenous leukemia (AML) unlikely to benefit from standard induction chemotherapy due to unfavorable baseline risk factor(s). J Clin Oncol; 2009 May 20;27(15_suppl):7062

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Updated remission duration and survival results of single-agent clofarabine in previously untreated older adult patients with acute myelogenous leukemia (AML) unlikely to benefit from standard induction chemotherapy due to unfavorable baseline risk factor(s).
  • We now report updated duration of remission (DOR), disease-free survival (DFS), and overall survival (OS).
  • METHODS: Single arm, multi-center, phase II, open-label, 2-stage study of patients with untreated AML, ≥60 years old, and at least one adverse prognostic factor: age ≥70 years, antecedent hematologic disorder (AHD), PS = 2, and/or intermediate/unfavorable risk karyotype.
  • CONCLUSIONS: These data expand on the previously reported efficacy and safety data of single agent CLO in adult AML.
  • These results suggest that single agent CLO is an effective and tolerable treatment option for older adult patients with untreated AML and 1 or more unfavorable baseline prognostic factor(s).

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  • (PMID = 27961436.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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50. Casorelli I, Offman J, Mele L, Pagano L, Sica S, D'Errico M, Giannini G, Leone G, Bignami M, Karran P: Drug treatment in the development of mismatch repair defective acute leukemia and myelodysplastic syndrome. DNA Repair (Amst); 2003 May 13;2(5):547-59
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  • [Title] Drug treatment in the development of mismatch repair defective acute leukemia and myelodysplastic syndrome.
  • DNA from therapy-related acute leukemia/myelodysplastic syndrome cases (tAL/MDS) from the GIMEMA [Gruppo Italiano Malattie Ematologiche Maligne dell'Adulto] Archive was examined for the microsatellite instability (MSI(+)) phenotype that is diagnostic for defective DNA mismatch repair.
  • More than 60% (16/25) of tAL/MDS cases were MSI(+) in contrast to <4% (0/28) of de novo cases. hMLH1 gene silencing was rare and evidence of promoter methylation was found in less than one-third of the MSI(+) cases.
  • Among the GIMEMA patients who had been treated for breast cancer there was an apparent trend towards early onset primary breast disease.
  • In view of the established relationship between drug resistance and mismatch repair defects, we suggest that selection for therapeutic drug resistance may contribute to the incidence of MSI(+) tAL/MDS.
  • [MeSH-major] Base Pair Mismatch. DNA Repair. Leukemia / drug therapy. Myelodysplastic Syndromes / drug therapy. Neoplasms / drug therapy
  • [MeSH-minor] Acute Disease. Adaptor Proteins, Signal Transducing. Adult. Age Factors. Aged. Bone Marrow Cells. Breast Neoplasms / genetics. Carrier Proteins. DNA / metabolism. DNA Damage. DNA Methylation. DNA Sequence, Unstable. Exons. Female. Heterozygote. Homozygote. Humans. Male. Microsatellite Repeats. Middle Aged. Mutation. Neoplasm Proteins / genetics. Nuclear Proteins. Phenotype. Promoter Regions, Genetic. Recombination, Genetic


51. Crawford MW, Pehora C, Lopez AV: Drug-induced acute pancreatitis in children receiving chemotherapy for acute leukemia: does propofol increase the risk? Anesth Analg; 2009 Aug;109(2):379-81
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  • [Title] Drug-induced acute pancreatitis in children receiving chemotherapy for acute leukemia: does propofol increase the risk?
  • BACKGROUND: The use of propofol is controversial in patients with a history of acute pancreatitis or those taking drugs, including certain chemotherapeutic drugs, that are associated with pancreatitis.
  • METHODS: To investigate this issue, we reviewed the medical records of all children who were diagnosed with pancreatitis while receiving chemotherapy for acute leukemia during a 5-year period.
  • RESULTS: A temporal relationship between propofol use and development of acute pancreatitis could not be established.
  • CONCLUSION: Propofol can be considered for general anesthesia in children who are receiving chemotherapeutic drugs that are themselves associated with acute pancreatitis or those who have a history of chemotherapy-induced pancreatitis.
  • [MeSH-major] Anesthetics, Intravenous / adverse effects. Antineoplastic Agents / adverse effects. Leukemia / complications. Pancreatitis / chemically induced. Pancreatitis / epidemiology. Propofol / adverse effects
  • [MeSH-minor] Acute Disease. Adolescent. Anesthesia, General / adverse effects. Child. Child, Preschool. Dose-Response Relationship, Drug. Female. Humans. Intraoperative Complications / epidemiology. Male. Risk Assessment

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  • (PMID = 19608806.001).
  • [ISSN] 1526-7598
  • [Journal-full-title] Anesthesia and analgesia
  • [ISO-abbreviation] Anesth. Analg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anesthetics, Intravenous; 0 / Antineoplastic Agents; YI7VU623SF / Propofol
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52. Styczynski J, Wysocki M, Kurylak A, Juraszewska E, Malinowska I, Stanczak E, Płoszynska A, Stefaniak J, Mazur B, Szczepanski T, Ras M: In vitro activity of glufosfamide in childhood acute leukemia. Anticancer Res; 2002 Jan-Feb;22(1A):247-50
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  • [Title] In vitro activity of glufosfamide in childhood acute leukemia.
  • Glufosfamide is a new agent for cancer chemotherapy.
  • The objective of the study was the comparison of the in vitro drug resistance profile of glufosfamide with other oxazaphosphorines in 106 samples of childhood acute leukemia by means of the MTT assay.
  • The following drugs were tested: glufosfamide, 4-HOO-ifosfamide, 4-HOO-cyclophosphamide, mafosfamide cyclohexylamine salt, prednisolone, vincristine, L-asparaginase, daunorubicin and cytarabine.
  • In the group of initial Acute Lymphoblastic Leukemia (ALL) samples, equivalent cytotoxicity values for glufosfamide, 4-HOO-ifosfamide, 4-HOO-cyclophosphamide and mafosfamide were 5.95, 9.92, 4.60 and 3.90 microg/ml, respectively.
  • In comparison to initial ALL samples, the relative resistance for glufosfamide and 4-HOO-ifosfamide in relapsed ALL samples were 1.9 (p=0.049) and 1.3 (ns), and in initial Acute Myeloblastic Leukemia (AML) samples, respectively, 31 (p<0.001) and 5 (p=0.001).
  • Glufosfamide shows high activity against lymphoblasts both on diagnosis and on relapse, however it cannot circumvent resistance to other oxazaphosphorines.
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacology. Cyclophosphamide / analogs & derivatives. Ifosfamide / analogs & derivatives. Leukemia, Myeloid, Acute / drug therapy. Phosphoramide Mustards / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 12017297.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Phosphoramide Mustards; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / beta-D-glucosylisophosphoramide mustard; 298-93-1 / thiazolyl blue; 5970HH9923 / mafosfamide; 67292-64-2 / 4-hydroxyifosfamide; 8N3DW7272P / Cyclophosphamide; IY9XDZ35W2 / Glucose; UM20QQM95Y / Ifosfamide
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53. Huang BT, Xiao Z, Shi YT, Ha S, Zhao WH, Gao D, Yan XH, Yang H: [Expressions of LRP, GST-pi and MRP1 in acute leukemia patients and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Apr;15(2):262-6
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  • [Title] [Expressions of LRP, GST-pi and MRP1 in acute leukemia patients and its clinical significance].
  • This study was purposed to investigate the relationship of expressions of gluthatione-S-transferase-pi (GST-pi), multidrug resistance protein-1 (MRP-1), lung resistance protein (LRP) with multidrug resistance of acute leukemia (AL), the correlation between 3 kinds protein expressions and the correlation of their protein expression with clinical features of AL patients.
  • The S-P immunohistochemical staining method was used to determine the expressions of GST-pi, MRP1 and LRP proteins in 80 AL patients and 30 normal subjects.
  • The results showed that there was the correlation between GST-pi, MRP1, LRP protein expression and chemotherapy resistance, meanwhile CR rates of patients with positive expression of those proteins were lower than that of patients with negative expression (P<0.05), so those protein expressions may be accounted for poor prognosis.
  • It is concluded that co-examination of GST-pi and MRP1 has greater significance than examination of one kind of protein in evaluating poor prognosis of leukemia patients.
  • LRP protein expression increase obviously when WBC counts >or= 10 x 10(9)/L (63.6%, P<0.05), therefore LRP protein has great judging value for evaluating drug resistance and prognosis of acute leukemia patients whose peripheral blood WBC counts were high.

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  • (PMID = 17493328.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan 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 / P-Glycoprotein; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; EC 2.5.1.18 / Glutathione S-Transferase pi
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54. Ma WD, Xu SR, Guo XN, Gao XL, Ma J, Qiao SK: [The relationship between cyclin B1 and multidrug resistance in adult patients with acute leukemia]. Zhonghua Nei Ke Za Zhi; 2003 Mar;42(3):169-72
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  • [Title] [The relationship between cyclin B1 and multidrug resistance in adult patients with acute leukemia].
  • OBJECTIVE: To investigate the relation between the expression of cyclin B1 and multidrug resistance in adult patients with acute leukemia.
  • METHODS: The proteins expression of cyclin B1, p170 was measured with flow cytometric analysis in 85 adult de novo acute leukemia patients (AL) and 17 normal control (NC).
  • CONCLUSIONS: Low expression of cyclin B1 might be a unfavorable prognostic factor for patients with AL and measurement of both cyclin B1 and TOPOIIalpha, TOPOIIbeta gene expression would predict drug resistance in adult acute leukemia patients.
  • [MeSH-major] Cyclin B / biosynthesis. Drug Resistance, Neoplasm. Leukemia, Myeloid, Acute / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Adolescent. Adult. Antigens, Neoplasm. Cyclin B1. DNA Topoisomerases, Type II / biosynthesis. DNA Topoisomerases, Type II / genetics. DNA-Binding Proteins. Female. Glycoproteins / biosynthesis. Glycoproteins / genetics. Humans. Male. Middle Aged. P-Glycoprotein / biosynthesis. P-Glycoprotein / genetics. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / genetics. RNA, Messenger / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 12816698.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / CCNB1 protein, human; 0 / Cyclin B; 0 / Cyclin B1; 0 / DNA-Binding Proteins; 0 / Glycoproteins; 0 / P-Glycoprotein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / p-170 glycoprotein, human; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha; EC 5.99.1.3 / DNA topoisomerase II beta
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55. Jabbour E, Giralt S, Kantarjian H, Garcia-Manero G, Jagasia M, Kebriaei P, de Padua L, Shpall EJ, Champlin R, de Lima M: Low-dose azacitidine after allogeneic stem cell transplantation for acute leukemia. Cancer; 2009 May 1;115(9):1899-905
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  • [Title] Low-dose azacitidine after allogeneic stem cell transplantation for acute leukemia.
  • BACKGROUND: : The authors hypothesized that low doses of the hypomethylating agent 5-azacitidine may maximize the graft-versus-leukemia effect and may be tolerated well after allogeneic transplantation (HSCT).
  • METHODS: : The drug was given to 17 patients with acute leukemia as salvage for disease recurrence after HSCT (n = 9 patients) or as maintenance therapy (n = 8 patients).
  • RESULTS: : Five of 9 patients with recurrent disease responded.
  • Four of 13 responding patients developed disease recurrence while they were receiving 5-azacitidine after a median of 10 months.
  • There were no extramedullary toxicities, and no graft-versus-host disease exacerbation was observed.
  • CONCLUSIONS: : Low-dose 5-azacitidine may induce durable remissions for patients who develop disease recurrence after HSCT.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Azacitidine / administration & dosage. Hematopoietic Stem Cell Transplantation. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Combined Modality Therapy. Drug Administration Schedule. Humans. Middle Aged. Recurrence. Retrospective Studies. Transplantation, Homologous

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  • (PMID = 19235255.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ NIHMS588939; NLM/ PMC4086213
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56. Zhang ZM, Xie ZX, Tan DR, Huang CH: [Detection of glutathione S-transferase and lung resistance-related proteins in acute leukemia and its clinical significance]. Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2005 Jun;30(3):292-4
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  • [Title] [Detection of glutathione S-transferase and lung resistance-related proteins in acute leukemia and its clinical significance].
  • OBJECTIVE: To explore the relationship among intracellular glutathione S-transferase activity (GST), the expression of lung resistance-related proteins (LRP) in acute leukemia, and its clinical effects.
  • METHODS: The GST activity of bone marrow mononuclear cells and LRP expression in 57 acute leukemia patients were detected by the spectrophotometry assay and immuno-cytochemistry (SABC), respectively.
  • RESULTS: The GST activity of bone marrow mononuclear cells in the acute leukemia group was significantly higher than that of the control group (P < 0.01).
  • The GST activity of mononuclear cells in acute leukemia was positively correlated with the percentage of blast in the bone marrow (r = 0.30, P < 0.05).
  • The GST activity of mononuclear cells in the untreated acute leukemia group was obviously higher than that of the complete remission group (P <0.01).
  • The GST activity in the refractory or relapsed acute leukemia group was significantly higher than that of the complete remission group and untreated leukemia group (P <0.05).
  • In post-chemotherapy 13 of 17 the LRP-positive patients were the non-remission, 12 of the 20 LRP-negative patients were the complete remission.
  • The GST activities of non-remission patients in the LRP-positive and LRP-negative group obviously increased.
  • CONCLUSION: The increase of GST activity in the bone marrow mononuclear cells is related to the clinical curative effects and the proliferation of blast in acute leukemia.
  • Detection of LRP and GST activities in acute leukemia may have a reference value in judging the leukemia with drug resistance and estimating the prognosis.
  • [MeSH-major] Glutathione Transferase / metabolism. Leukemia, Myeloid, Acute / metabolism. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Vault Ribonucleoprotein Particles / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Bone Marrow Cells / metabolism. Child. Female. Humans. Male. Middle Aged. Multidrug Resistance-Associated Proteins / metabolism

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  • (PMID = 16045016.001).
  • [ISSN] 1672-7347
  • [Journal-full-title] Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
  • [ISO-abbreviation] Zhong Nan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; EC 2.5.1.18 / Glutathione Transferase
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57. Fazlina N, Maha A, Jamal R, Zarina AL, Cheong SK, Hamidah H, Ainoon O, Zulkifli SZ, Hamidah NH: Expression of multidrug resistance (MDR) proteins and in vitro drug resistance in acute leukemias. Hematology; 2007 Feb;12(1):33-7
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  • [Title] Expression of multidrug resistance (MDR) proteins and in vitro drug resistance in acute leukemias.
  • The expression of the multidrug resistance (MDR) proteins may influence the outcome of treatment in patients with acute leukemia.
  • The aim of this study was to determine the IC50 of cytotoxic drugs (cytosine arabinoside, ara-C and daunorubicin, dnr) using the in vitro 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)2H-tetrazolium, inner salt (MTS) assay method.
  • A total of 82 newly diagnosed acute leukemia cases (43 adult myeloid leukaemia, AML cases and 39 acute lymphoblastic leukaemia, ALL cases) and 16 relapsed cases (8 AML cases and 8 ALL cases) were studied.
  • The MTS assay was performed using two cytotoxic drugs, dnr and ara-C.
  • Cells were incubated with different concentrations of drugs for 4 days and the IC50 was extrapolated from the viability curve.
  • However, there was no correlation between IC50 values of these drugs tested with clinical outcome.
  • In conclusion, we found that MTS assay is an easy, rapid and non laborious method to study in vitro drug resistance in acute leukaemia cases.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Leukemia / metabolism. Neoplasm Proteins / metabolism. P-Glycoproteins / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Cell Survival. Child. Child, Preschool. Coloring Agents / analysis. Cytarabine / pharmacology. Daunorubicin / pharmacology. Female. Humans. Infant. Inhibitory Concentration 50. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / metabolism. Male. Methylphenazonium Methosulfate / pharmacology. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Recurrence. Staining and Labeling / methods. Tetrazolium Salts / analysis. Thiazoles / analysis. Treatment Outcome. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / ultrastructure

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  • (PMID = 17364990.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Coloring Agents; 0 / Neoplasm Proteins; 0 / P-Glycoproteins; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 138169-43-4 / 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium; 299-11-6 / Methylphenazonium Methosulfate; ZS7284E0ZP / Daunorubicin
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58. Appelbaum FR, Rosenblum D, Arceci RJ, Carroll WL, Breitfeld PP, Forman SJ, Larson RA, Lee SJ, Murphy SB, O'Brien S, Radich J, Scher NS, Smith FO, Stone RM, Tallman MS: End points to establish the efficacy of new agents in the treatment of acute leukemia. Blood; 2007 Mar 1;109(5):1810-6
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  • [Title] End points to establish the efficacy of new agents in the treatment of acute leukemia.
  • Federal regulations provide 2 pathways for approval of new agents for the treatment of acute leukemia, regular and accelerated approval.
  • The acute leukemias are a heterogeneous and relatively uncommon group of diseases.
  • To explore some of the issues pertinent to the choice of end points for drug approval in acute leukemia, the Food and Drug Administration invited the American Society of Hematology to participate in the organization and conduct of a joint workshop.
  • [MeSH-major] Hematologic Agents / therapeutic use. Leukemia / drug therapy. Randomized Controlled Trials as Topic / methods
  • [MeSH-minor] Acute Disease. Drug Approval / methods. Humans. Quality of Life. Societies, Medical. Stem Cell Transplantation. United States. United States Food and Drug Administration

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  • (PMID = 17095617.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hematologic Agents
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59. Zhao XS, Sun Zq, Jiang B, Wang de B: [The assay of intracelluar cytidine deaminase activity and its clinical significance in patient with acute leukemia]. Beijing Da Xue Xue Bao; 2008 Apr;40(2):181-4
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  • [Title] [The assay of intracelluar cytidine deaminase activity and its clinical significance in patient with acute leukemia].
  • OBJECTIVE: To investigate the relationship between the intracellular cytidine deaminase (CDD) activity and drug resistance in acute leukemia (AL) of different stage.
  • CONCLUSION: Intracellular CDD activity in AL patients may be related to the stages of the disease.
  • It seemed that CDD might not be considered as an independent predictive factor for the drug healing efficacy of Ara-C.
  • [MeSH-major] Cytidine Deaminase / metabolism. Drug Resistance, Neoplasm. Intracellular Fluid / enzymology. Leukemia / enzymology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antimetabolites, Antineoplastic / pharmacology. Cytarabine / pharmacology. Female. Humans. Male. Middle Aged. Young Adult

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  • (PMID = 18458696.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine; EC 3.5.4.5 / Cytidine Deaminase
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60. Dalle F, Lafon I, L'ollivier C, Ferrant E, Sicard P, Labruère C, Jebrane A, Laubriet A, Vagner O, Caillot D, Bonnin A: A prospective analysis of the genotypic diversity and dynamics of the Candida albicans colonizing flora in neutropenic patients with de novo acute leukemia. Haematologica; 2008 Apr;93(4):581-7
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  • [Title] A prospective analysis of the genotypic diversity and dynamics of the Candida albicans colonizing flora in neutropenic patients with de novo acute leukemia.
  • We report the result of a prospective study aimed at investigating the dynamics and heterogeneity of C. albicans flora in patients with de novo acute leukemia.
  • DESIGN AND METHODS: Between 2001 and 2003, 66 consecutive adults with newly diagnosed acute leukemia were monitored for Candida colonization.
  • The genotypic profile was not altered by topical and/or systemic use of antifungal agents in any of the patients.
  • CONCLUSIONS: In patients with de novo acute leukemia, genetic evolution of the colonizing C. albicans flora and selection of variants or replacement of the original strain upon antifungal drug pressure or nosocomial transmission are rare events.
  • [MeSH-major] Candida albicans / genetics. Candidiasis / microbiology. Genome, Fungal. Leukemia / complications. Neutropenia / complications
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antifungal Agents / pharmacology. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Fungal / genetics. Female. Genetic Variation. Genotype. Humans. Immunocompromised Host. Male. Middle Aged. Myeloablative Agonists / adverse effects. Myeloablative Agonists / therapeutic use. Organ Specificity. Patient Isolation. Sampling Studies

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  • (PMID = 18322258.001).
  • [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 / Antifungal Agents; 0 / Myeloablative Agonists
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61. Ren JH, Du XY, Guo XN, Wang Y, Zhang JN, Lin FR, Dong ZR: [Relationship between resistance to chemotherapy and expression of breast cancer resistance protein (BCRP) gene in patients with acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2004 Feb;12(1):55-8
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  • [Title] [Relationship between resistance to chemotherapy and expression of breast cancer resistance protein (BCRP) gene in patients with acute leukemia].
  • In order to investigate the relationship between the expression of breast cancer resistance protein (BCRP) gene and drug resistance in patients with acute leukemia (AL), semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to examine the expression of BCRP mRNA in AL patients and 15 normal subjects.
  • The expression levels of BCRP mRNA in drug resistance group and drug sensitive group were 0.962 +/- 0.426 and 0.315 +/- 0.296 respectively (P = 0.0001).
  • It is concluded that high expression of BCRP mRNA leads to clinical drug resistance and is an unfavorable factor for prognosis of AL patients except acute promyelocytic leukemia.
  • [MeSH-major] ATP-Binding Cassette Transporters / genetics. Leukemia / drug therapy. Neoplasm Proteins / genetics
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Acute Disease. Adolescent. Adult. Aged. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. RNA, Messenger / analysis

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  • (PMID = 14989769.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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62. Bolufer P, Collado M, Barragán E, Cervera J, Calasanz MJ, Colomer D, Roman-Gómez J, Sanz MA: The potential effect of gender in combination with common genetic polymorphisms of drug-metabolizing enzymes on the risk of developing acute leukemia. Haematologica; 2007 Mar;92(3):308-14
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  • [Title] The potential effect of gender in combination with common genetic polymorphisms of drug-metabolizing enzymes on the risk of developing acute leukemia.
  • BACKGROUND AND OBJECTIVES: We examined common polymorphisms in the genes for glutathione S-transferase (GST), cytochrome P450 (CYP), quinone oxoreductase (NQO1), methylene tetrahydrofolate reductase (MTHFR), and thymidylate synthetase (TYMS) and the role of gender associated with the susceptibility to de novo acute leukemia (AL).
  • DESIGN AND METHODS: We conducted a case-control study analyzing the prevalence of the polymorphisms CYP1A1*2A, CYP2E1*5B, CYP3A4*1B, del{GSTT1}, del{GSTM1}, NQO1*2, MTHFR C6777, and TYMS 2R/3R in 443 patients with AL [302 with acute myeloblastic leukemia (AML) and 141 with acute lymphoblastic leukemia (ALL)] and 454 control volunteers, using polymerase chain reaction (PCR)-based methods.
  • RESULTS: We found a higher incidence of del{GSTT1} in patients with AML than among controls (25.6% vs. 13.7%, OR=2.2, p<0.001) and a higher incidence of NQO1*2 homozygosity (NQO1*2hom.) in males with the M3 FAB subtype than in control males (8.6% vs. 2.2%, OR=4.9, p=0.02).
  • The del{GSTT1} and NQO1*2hom. polymorphisms increased the risk of ALL (OR=2.2 and 3.0, p=0.001 and 0.003, respectively).
  • The higher risk conferred by NQO1*2hom. and del{GSTT1} mainly affected males (OR=6.1 and 2.4; p=0.002 and 0.005, respectively).
  • INTERPRETATION AND CONCLUSIONS: Males harboring NQO1*2hom. and del{GSTT1} polymorphisms showed a higher risk than females of developing AL.
  • [MeSH-major] Leukemia / epidemiology. Polymorphism, Genetic. Sex Factors
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Aged. Aged, 80 and over. Case-Control Studies. Cell Transformation, Neoplastic / genetics. Child. Child, Preschool. Cytochrome P-450 CYP1A1 / genetics. Cytochrome P-450 CYP2E1 / genetics. Cytochrome P-450 CYP3A. Cytochrome P-450 Enzyme System / genetics. DNA Mutational Analysis. Disease Susceptibility. Female. Gene Frequency. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Humans. Infant. Leukemia, Myeloid / epidemiology. Leukemia, Myeloid / genetics. Leukemia, Myeloid / physiopathology. Male. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Middle Aged. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology. Risk. Spain / epidemiology. Thymidylate Synthase / genetics

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  • (PMID = 17339179.001).
  • [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] 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.13.- / Cytochrome P-450 CYP2E1; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.14.14.1 / Cytochrome P-450 CYP3A; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2); EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.1.1.45 / Thymidylate Synthase; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase
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63. Ma J, Xu S, Lai Y, Lu Y, Yao E: Correlation between cyclin A gene expression in adult patients with acute leukemia and drug resistance. J Huazhong Univ Sci Technolog Med Sci; 2003;23(3):245-8
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  • [Title] Correlation between cyclin A gene expression in adult patients with acute leukemia and drug resistance.
  • In order to investigate the relationship between the expression of cyclin A and drug resistance in adult patients with acute leukemia (AL), the mRNA expression of cyclin A, mdr1, Top II alpha, bcl-2 was detected in 64 adult patients with AL and 20 normal controls by semi-reverse transcription polymerase chain reaction (semi-RT-PCR).
  • It was found that the cyclin A and Top II alpha mRNA expression levels in drug resistant group were significantly lower than in sensitive group (P < 0.01).
  • In drug resistant group there was a negative correlation between the gene expression levels of cyclin A and mdr1 (rs = -0.337, P = 0.029).
  • The 10 AL patients with positive lower expression of both cyclin A and Top II alpha were all resistant to drugs.
  • Logistic regression of Binary analysis showed the correlation between the lower expression of cyclin A and drug resistance.
  • It was concluded that lower expression of cyclin A gene might be an unfavorable prognostic factor for patients with AL, and detection of both cyclin A and Top II alpha gene expression would predict drug resistance in AL patients.
  • [MeSH-major] Cyclin A / genetics. Drug Resistance, Neoplasm / genetics. Genes, MDR. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Drug Resistance, Multiple / genetics. Female. Humans. Leukemia, Promyelocytic, Acute / genetics. Male. Middle Aged. P-Glycoprotein / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 14526424.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cyclin A; 0 / P-Glycoprotein; 0 / RNA, Messenger
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64. Cheok MH, Lugthart S, Evans WE: Pharmacogenomics of acute leukemia. Annu Rev Pharmacol Toxicol; 2006;46:317-53
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  • [Title] Pharmacogenomics of acute leukemia.
  • Over the past four decades, treatment of acute leukemia in children has made remarkable progress, from this disease being lethal to now achieving cure rates of 80% for acute lymphoblastic leukemia and 45% for acute myeloid leukemia.
  • This progress is largely owed to the optimization of existing treatment modalities rather than the discovery of new agents.
  • However, the annual number of patients with leukemia who experience relapse after initial therapy remains greater than that of new cases of most childhood cancers.
  • The aim of pharmacogenetics is to develop strategies to personalize medications and tailor treatment regimens to individual patients, with the goal of enhancing efficacy and safety through better understanding of the person's genetic makeup.
  • In this review, we summarize recent pharmacogenomic studies related to the treatment of pediatric acute leukemia.
  • These strategies illustrate the promise of pharmacogenomics to further advance the treatment of human cancers, with childhood leukemia serving as a paradigm.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia / drug therapy. Leukemia / genetics. Pharmacogenetics
  • [MeSH-minor] Acute Disease. Animals. Gene Expression Profiling. Humans

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  • (PMID = 16402908.001).
  • [ISSN] 0362-1642
  • [Journal-full-title] Annual review of pharmacology and toxicology
  • [ISO-abbreviation] Annu. Rev. Pharmacol. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 207
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65. Ansari M, Krajinovic M: Pharmacogenomics of acute leukemia. Pharmacogenomics; 2007 Jul;8(7):817-34
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  • [Title] Pharmacogenomics of acute leukemia.
  • Such an approach is particularly needed in cancer therapy, as most chemotherapeutics drugs affect both tumor and normal cells, are ineffective in many patients and exhibit serious side effects.
  • Leukemia exists in two different forms, myeloid and lymphoid.
  • Acute lymphoblastic leukemia more frequently occurs in children, whereas the risk of acute myeloid leukemia is more common in adults.
  • Prognosis is particularly poor in adult acute myeloid leukemia.
  • Treatment failure in childhood acute lymphoblastic leukemia due to drug resistance remains the leading cause of cancer-related death in children.
  • Here, we provide an overview of pharmacogenetics studies carried out in children and adults with acute lymphoblastic leukemia and acute myeloid leukemia, attempting to find the associations between treatment responses and polymorphisms in the genes whose products are needed for metabolism, and effects of drugs used in the treatment of leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Pharmacogenetics
  • [MeSH-minor] Child. Humans. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18240908.001).
  • [ISSN] 1744-8042
  • [Journal-full-title] Pharmacogenomics
  • [ISO-abbreviation] Pharmacogenomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 130
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66. Nikougoftar M, Farhadi M, Pourfathollah AA: P-glycoprotein quantitation in acute leukemia. Iran J Allergy Asthma Immunol; 2003 Jun;2(2):57-60

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  • [Title] P-glycoprotein quantitation in acute leukemia.
  • Multi drug resistance(MDR) is a major problem in the treatment ofcancer and hematological malignancies.
  • This resistance is multi factorial and is the result of decreased intra cellular drug accumulation.
  • This is partly due to the presence of a 170KD intra membranous protein termed P-glycoprotein(P-gp) that is an energy- dependent efflux pump which has increased expression on drug-resistance cells.
  • In this study we identified the presence of P-gp by staining with Fluorescent Iso Thio Cyanate (FITC) conjugated anti P-gp in acute leukemia patients and flow cytometry in addition to performing immunophenotype analysis and French, American British (FAB) classification.
  • Results revealed that one fifth of leukemic patients expressed P-gp and this phenotype was more prevalent in Acute Undifferentiated Leukemia(AUL) and Acute Myelogenous Leukemia (AML) than in Acute Lymphoblastic Leukemia(ALL).
  • The accumulation of P-gp molecule that was stated as Mean Fluorescence Intensity (MFI) on the blasts' membrane of AUL and AML patients showed marked increase in comparison to ALL.
  • Kepvords: Leukemia, Drug resistance, P-glycoprotein, Flowcytometry, FAB classification, Immunophenotyping, Mean Fluorescence Intensity.

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  • (PMID = 17301357.001).
  • [ISSN] 1735-1502
  • [Journal-full-title] Iranian journal of allergy, asthma, and immunology
  • [ISO-abbreviation] Iran J Allergy Asthma Immunol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Iran
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67. Emerenciano M, Koifman S, Pombo-de-Oliveira MS: Acute leukemia in early childhood. Braz J Med Biol Res; 2007 Jun;40(6):749-60

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  • [Title] Acute leukemia in early childhood.
  • Acute leukemia in early childhood is biologically and clinically distinct.
  • The particular characteristics of this malignancy diagnosed during the first months of life have provided remarkable insights into the etiology of the disease.
  • The pro-B, CD10 negative immunophenotype is typically found in infant acute leukemia, and the most common genetic alterations are the rearrangements of the MLL gene.
  • The environmental exposure to damaging agents that give rise to genetic changes prenatally may be accurately determined in infants since the window of exposure is limited and known.
  • The Brazilian Collaborative Study Group of Infant Acute Leukemia has found that mothers exposed to dipyrone, pesticides and hormones had an increased chance to give birth to babies with infant acute leukemia [OR = 1.48 (95%CI = 1.05-2.07), OR = 2.27 (95%CI = 1.56-3.31) and OR = 9.08 (95%CI = 2.95-27.96)], respectively.
  • This review aims to summarize recent clues that have facilitated the elucidation of the biology of early childhood leukemias, with emphasis on infant acute leukemia in the Brazilian population.

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  • (PMID = 17581672.001).
  • [ISSN] 0100-879X
  • [Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • [ISO-abbreviation] Braz. J. Med. Biol. Res.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 60
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68. Styczyński J, Wysocki M, Debski R, Balwierz W, Rokicka-Milewska R, Matysiak M, Balcerska A, Kowalczyk J, Wachowiak J, Sońta-Jakimczyk D, Chybicka A: In vitro activity of oxazaphosphorines in childhood acute leukemia: preliminary report. Acta Biochim Pol; 2002;49(1):221-5
The Lens. Cited by Patents in .

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  • [Title] In vitro activity of oxazaphosphorines in childhood acute leukemia: preliminary report.
  • Glufosfamide (beta-D-glucosyl-ifosfamide mustard) is a new agent for cancer chemotherapy.
  • The aim of the study was a comparison of the drug resistance profiles of glufosfamide and other oxazaphosphorines in childhood acute leukemias.
  • Leukemic cells, taken from children with ALL on diagnosis (n = 41), ALL on relapse (n = 12) and AML on diagnosis (n = 13) were analyzed by means of the MTT assay.
  • The following drugs were tested: glufosfamide (GLU), 4-HOO-ifosfamide (IFO), 4-HOO-cyclophosphamide (CYC) and mafosfamide cyclohexylamine salt (MAF).
  • Glufosfamide presented high activity against lymphoblasts both on diagnosis and on relapse.
  • [MeSH-major] Cyclophosphamide / analogs & derivatives. Cyclophosphamide / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Phosphoramide Mustards / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Glucose / analogs & derivatives. Humans. Ifosfamide / analogs & derivatives. In Vitro Techniques. Infant. Male. Tumor Cells, Cultured / drug effects

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  • (PMID = 12136944.001).
  • [ISSN] 0001-527X
  • [Journal-full-title] Acta biochimica Polonica
  • [ISO-abbreviation] Acta Biochim. Pol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / 4-hydroxyperoxycyclophosphamide; 0 / Phosphoramide Mustards; 0 / beta-D-glucosylisophosphoramide mustard; 88746-71-8 / Asta Z 7557; 8N3DW7272P / Cyclophosphamide; IY9XDZ35W2 / Glucose; UM20QQM95Y / Ifosfamide
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69. Svingen PA, Karp JE, Krajewski S, Mesner PW Jr, Gore SD, Burke PJ, Reed JC, Lazebnik YA, Kaufmann SH: Evaluation of Apaf-1 and procaspases-2, -3, -7, -8, and -9 as potential prognostic markers in acute leukemia. Blood; 2000 Dec 01;96(12):3922-31
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  • [Title] Evaluation of Apaf-1 and procaspases-2, -3, -7, -8, and -9 as potential prognostic markers in acute leukemia.
  • In this study, immunoblotting was used to examine levels of apoptotic protease activating factor-1 (Apaf-1) and procaspases-2, -3, -7, -8, and -9 in bone marrow samples (at least 80% leukemia) harvested before chemotherapy from adults with newly diagnosed acute myelogenous leukemia (AML, 42 patients) and acute lymphocytic leukemia (ALL, 18 patients).
  • In further studies, 16 paired samples (13 AML, 3 ALL), the first harvested before induction therapy and the second harvested at the time of leukemia regrowth, were also examined.
  • There were no systematic alterations in levels of Apaf-1 or procaspases at relapse compared with diagnosis.
  • These results indicate that levels of initiator caspases vary widely among different leukemia specimens but cast doubt on the hypothesis that this variation is a major determinant of drug sensitivity for acute leukemia in the clinical setting. (Blood.
  • [MeSH-major] Caspases / metabolism. Enzyme Precursors / metabolism. Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptotic Protease-Activating Factor 1. Biomarkers, Tumor / immunology. Biomarkers, Tumor / metabolism. Bone Marrow Cells / chemistry. Bone Marrow Cells / enzymology. Cohort Studies. HL-60 Cells. Humans. Immunoblotting. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / therapy. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Prognosis. Proteins / drug effects. Proteins / immunology. Proteins / metabolism

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  • (PMID = 11090079.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA069008; United States / NCI NIH HHS / CA / CA13106; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / CA69008
  • [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 / APAF1 protein, human; 0 / Apoptotic Protease-Activating Factor 1; 0 / Biomarkers, Tumor; 0 / Enzyme Precursors; 0 / Proteins; EC 3.4.22.- / Caspases
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70. Batova A, Shao LE, Diccianni MB, Yu AL, Tanaka T, Rephaeli A, Nudelman A, Yu J: The histone deacetylase inhibitor AN-9 has selective toxicity to acute leukemia and drug-resistant primary leukemia and cancer cell lines. Blood; 2002 Nov 1;100(9):3319-24
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  • [Title] The histone deacetylase inhibitor AN-9 has selective toxicity to acute leukemia and drug-resistant primary leukemia and cancer cell lines.
  • The novel prodrug of butyric acid, pivaloyloxymethyl butyrate (AN-9), a histone deacetylase inhibitor, shows great promise as an effective and relatively nontoxic anticancer agent for solid malignancies.
  • In this study, we show that 21 primary samples of acute leukemia were sensitive to the antiproliferative effects of AN-9, with a 50% inhibitory concentration (IC(50)) of 45.8 +/- 4.1 microM.
  • In colony-forming assays, primary T-cell acute lymphoblastic leukemia (T-ALL) cells were 3-fold more sensitive to AN-9 than the normal hematopoietic progenitors, erythroid burst-forming units and granulocyte/monocyte colony-forming units.
  • AN-9 induced apoptosis in the T-ALL cell line CEM.
  • A common problem with cancer is chemoresistance, which is often typical of relapsed cancers.
  • Remarkably, a T-ALL sample at diagnosis and an acute myeloid leukemia sample at relapse that were resistant to doxorubicin in vitro were sensitive to AN-9, with an IC(50) of 50 microM for both samples.
  • More strikingly, samples from 2 infants with t(4;11) ALL obtained at diagnosis and relapse each were the most sensitive to AN-9, with IC(50) values of 25 microM and 17 microM, respectively.
  • AN-9 induced the expression of p21 in an infant leukemia sample with 11q23 rearrangement, but not in T- or B-precursor ALL.
  • Collectively, our results suggest that AN-9 is a selective agent for hematopoietic malignancies that can circumvent the mechanisms of chemoresistance limiting most conventional chemotherapy.
  • [MeSH-major] Butyrates / pharmacology. Drug Resistance, Neoplasm. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Leukemia / pathology. Neoplasm Proteins / antagonists & inhibitors. Neoplasms / pathology. Neoplastic Stem Cells / drug effects
  • [MeSH-minor] Acetylation / drug effects. Acute Disease. Apoptosis / drug effects. Cell Division / drug effects. Child. Cyclin-Dependent Kinase Inhibitor p21. Cyclins / biosynthesis. Cyclins / genetics. Doxorubicin / pharmacology. Drug Resistance, Multiple / genetics. Drug Screening Assays, Antitumor. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Genes, MDR. HL-60 Cells / drug effects. Hematopoietic Stem Cells / drug effects. Hematopoietic Stem Cells / enzymology. Histones / metabolism. Humans. Infant. Inhibitory Concentration 50. Leukemia, Myeloid / enzymology. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Leukemia-Lymphoma, Adult T-Cell / enzymology. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Protein Processing, Post-Translational / drug effects. Transfection. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / enzymology. Tumor Stem Cell Assay

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  • (PMID = 12384433.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 79951; United States / NCRR NIH HHS / RR / M01 RR 00827
  • [Publication-type] Comparative Study; 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 / Butyrates; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclins; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Neoplasm Proteins; 122110-53-6 / pivalyloxymethyl butyrate; 80168379AG / Doxorubicin
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71. 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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72. Weise A, Liehr T, Efferth T, Kuechler A, Gebhart E: Comparative M-FISH and CGH analyses in sensitive and drug-resistant human T-cell acute leukemia cell lines. Cytogenet Genome Res; 2002;98(2-3):118-25

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparative M-FISH and CGH analyses in sensitive and drug-resistant human T-cell acute leukemia cell lines.
  • Cell lines of human T-cell acute lymphoblastic leukemias (T-ALL) have gained high interest for study of mechanisms of cytostatic drug resistance.
  • Therefore, comparative genomic hybridization (CGH) and 24-color-fluorescence-in-situ-hybridization (M-FISH) were applied to eight sublines of CCRF-CEM leukemia cells selected in vitro for drug resistance and to their drug-sensitive parental counterparts.
  • All cell lines were characterized by altered chromosome numbers and by a variety of chromosomal structural aberrations as shown by M-FISH.
  • Amplifications of 5q13 in the six methotrexate-resistant cell lines, a del(9)(p21pter) in all lines examined, and a gain of chromosome 20 in 9 of the 10 lines examined were readily detected by both techniques.
  • The same held true for losses of chromosomes 17 and 18 in the near tetraploid cell lines which could also be confirmed by CGH.
  • Some imbalances of genomic material detected by CGH were, however, not observed by means of M-FISH, possibly due to the limited extension of the corresponding chromosomal segment involved or the small subpopulation of cells affected.
  • A comparison of chromosomal alterations in drug-resistant and parental cell lines showed not only amplifications of chromosomal segments harboring well-known drug resistance genes, e.g., the dihydrofolate reductase gene, but also chromosomal changes which may involve novel genes associated with drug resistance.
  • Their combination allowed a distinct improvement of the definition of the complex karyotypes of drug-resistant cell lines.
  • [MeSH-major] Chromosome Aberrations. Drug Resistance, Neoplasm / genetics. In Situ Hybridization, Fluorescence. Leukemia-Lymphoma, Adult T-Cell / genetics. Nucleic Acid Hybridization

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  • [Copyright] Copyright 2002 S. Karger AG, Basel
  • (PMID = 12697993.001).
  • [ISSN] 1424-8581
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
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73. Mintzer DM, Billet SN, Chmielewski L: Drug-induced hematologic syndromes. Adv Hematol; 2009;2009:495863

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Drug-induced hematologic syndromes.
  • Objective. Drugs can induce almost the entire spectrum of hematologic disorders, affecting white cells, red cells, platelets, and the coagulation system.
  • This paper aims to emphasize the broad range of drug-induced hematological syndromes and to highlight some of the newer drugs and syndromes.
  • Methods. Medline literature on drug-induced hematologic syndromes was reviewed.
  • Most reports and reviews focus on individual drugs or cytopenias.
  • Results. Drug-induced syndromes include hemolytic anemias, methemoglobinemia, red cell aplasia, sideroblastic anemia, megaloblastic anemia, polycythemia, aplastic anemia, leukocytosis, neutropenia, eosinophilia, immune thrombocytopenia, microangiopathic syndromes, hypercoagulability, hypoprothrombinemia, circulating anticoagulants, myelodysplasia, and acute leukemia.
  • Some of the classic drugs known to cause hematologic abnormalities have been replaced by newer drugs, including biologics, accompanied by their own syndromes and unintended side effects.
  • Conclusions. Drugs can induce toxicities spanning many hematologic syndromes, mediated by a variety of mechanisms.
  • Physicians need to be alert to the potential for iatrogenic drug-induced hematologic complications.

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  • (PMID = 19960059.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2778502
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74. Kwaan HC, Huyck T: Thromboembolic and bleeding complications in acute leukemia. Expert Rev Hematol; 2010 Dec;3(6):719-30
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thromboembolic and bleeding complications in acute leukemia.
  • The risk of both thromboembolic and bleeding complications is high in acute leukemia.
  • This double hazard has a significant negative impact on the morbidity and mortality of patients with this disease.
  • The clinical manifestations of both complications show special features specific to the form of acute leukemia.
  • Recognition of these characteristics is important in the diagnosis and management of acute leukemia.
  • In this article, several additional issues are addressed, including the features of bleeding and thrombosis in acute promyelocytic leukemia, the current understanding of the leukostasis syndrome and the iatrogenic complications including catheter-associated thrombosis, and the adverse effects of therapeutic agents used in acute leukemia.
  • Corrective measures, including recent guidelines on platelet transfusions, are provided.
  • [MeSH-major] Hemorrhage / etiology. Leukemia / complications. Thromboembolism / etiology
  • [MeSH-minor] Acute Disease. Blood Vessels / pathology. Drug-Related Side Effects and Adverse Reactions. Humans. Thrombophilia. Thrombosis / complications. Thrombosis / epidemiology

  • MedlinePlus Health Information. consumer health - Bleeding.
  • MedlinePlus Health Information. consumer health - Leukemia.
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  • (PMID = 21091148.001).
  • [ISSN] 1747-4094
  • [Journal-full-title] Expert review of hematology
  • [ISO-abbreviation] Expert Rev Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
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75. Thomas X: Chemotherapy of acute leukemia in adults. Expert Opin Pharmacother; 2009 Feb;10(2):221-37
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  • [Title] Chemotherapy of acute leukemia in adults.
  • BACKGROUND: General therapeutic options for adult patients with acute leukemia are reviewed and specific new treatment strategies are described.
  • RESULTS/CONCLUSION: In the past years, striking new developments have been noticeable in the treatment of adult acute leukemia.
  • However, the overall outcome of adult acute leukemia remains poor, particularly in older patients.
  • Intensive chemotherapy remains the standard for leukemia treatment but several approaches using new cytotoxic agents seem promising.
  • Therapeutic targeting of specific biologic abnormalities present in the leukemia cell population might, in a near future, improve outcome of adult leukemia patients.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19236195.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 120
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76. Savchenko VG: [Acute leukemia and pregnancy--some postulates]. Ter Arkh; 2009;81(7):5-7
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  • [Title] [Acute leukemia and pregnancy--some postulates].
  • The aim of chemotherapy of acute leukemia in pregnant women is to save two lives.
  • Abortion is not mandatory in acute leukemia as this disease is curable by chemotherapy.
  • Effective treatment of pregnant women with acute leukemia diagnosis is now practiced not only by large clinics, it is also provided by regional centers.
  • Overall 5-year actual survival for acute myeloid leukemia is 64%, for APL and ALL - 25%.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia / drug therapy. Pregnancy Complications, Neoplastic / drug therapy
  • [MeSH-minor] Acute Disease. Disease-Free Survival. Embryonic Development / drug effects. Female. Fetal Development / drug effects. Humans. Pregnancy. Pregnancy Outcome

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  • (PMID = 19708566.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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77. Furukawa Y, Sutheesophon K, Wada T, Nishimura M, Saito Y, Ishii H, Furukawa Y: Methylation silencing of the Apaf-1 gene in acute leukemia. Mol Cancer Res; 2005 Jun;3(6):325-34
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  • [Title] Methylation silencing of the Apaf-1 gene in acute leukemia.
  • Apaf-1 is important for tumor suppression and drug resistance because it plays a central role in DNA damage-induced apoptosis.
  • Inactivation of the Apaf-1 gene is implicated in disease progression and chemoresistance of some malignancies.
  • Apaf-1 mRNA levels were below the detection limit or very low in 5 of 20 human leukemia cell lines (25%) and 5 of 12 primary acute myeloblastic leukemia cells (42%).
  • Methylation of CpG in the region between +87 and +128 of the Apaf-1 gene was almost exclusively observed in Apaf-1-defective cell lines.
  • In conclusion, methylation silencing is a mechanism of the inactivation of Apaf-1 in acute leukemia, and Dnmt1 overexpression may underlie hypermethylation of the Apaf-1 gene.
  • [MeSH-major] DNA Methylation. Gene Silencing. Leukemia, Myeloid, Acute / genetics. Proteins / metabolism
  • [MeSH-minor] 5' Untranslated Regions. Antimetabolites, Antineoplastic / pharmacology. Apoptotic Protease-Activating Factor 1. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Cell Line, Tumor. CpG Islands / genetics. DNA (Cytosine-5-)-Methyltransferase / metabolism. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. HL-60 Cells. Histone Deacetylase Inhibitors. Humans. Jurkat Cells. K562 Cells. Promoter Regions, Genetic. RNA, Messenger / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. U937 Cells

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  • (PMID = 15972851.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5' Untranslated Regions; 0 / APAF1 protein, human; 0 / Antimetabolites, Antineoplastic; 0 / Apoptotic Protease-Activating Factor 1; 0 / Histone Deacetylase Inhibitors; 0 / Proteins; 0 / RNA, Messenger; 776B62CQ27 / decitabine; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA (cytosine-5-)-methyltransferase 1; M801H13NRU / Azacitidine
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78. Ren J, Dong Z, Guo X, Wang F, Du X, Zhang X, Lin F, Yao E: [The clinical significance of lung resistance protein (LRP) gene expression in patients with acute leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2000 Jan;21(1):10-3
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  • [Title] [The clinical significance of lung resistance protein (LRP) gene expression in patients with acute leukemia].
  • OBJECTIVE: To investigate the relationship between the expression of lung resistance protein (LRP) gene and drug resistance in patients with acute leukemias (AL).
  • CONCLUSION: High expression of LRP gene leads to clinical drug resistance and is an unfavorable factor to AL patients of prognosis.
  • [MeSH-major] Leukemia / metabolism. Neoplasm Proteins / genetics. Vault Ribonucleoprotein Particles / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Drug Resistance, Neoplasm. Female. Gene Expression. Genes, MDR. Humans. Male. Middle Aged. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 11876952.001).
  • [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
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein
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79. Advani AS, Hunger SP, Burnett AK: Acute leukemia in adolescents and young adults. Semin Oncol; 2009 Jun;36(3):213-26
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  • [Title] Acute leukemia in adolescents and young adults.
  • In many areas of medicine adolescents are regarded as a discrete group with specific therapeutic, psychological, educational, and resource needs.
  • In the treatment of acute leukemia age is a predictor of response.
  • Thus, in acute lymphoblastic leukemia (ALL) there is a clearly poorer treatment outcome after puberty, while in acute myeloid leukaemia (AML), which is more common in older adults, age is a continuous variable with poorer outcomes in each successive decade.
  • Here we discuss the outcome of acute leukemia in adolescents and young adults, particularly with respect to whether they respond similarly to children or other adults.
  • [MeSH-major] Leukemia, Myeloid, Acute. Precursor Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Adolescent. Adult. Age Factors. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Leukemia, Promyelocytic, Acute. Stem Cell Transplantation. Survival Rate

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  • (PMID = 19460579.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 66
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80. Wu HJ, Chen Y: [Biological characteristics of hyperleukocytic acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Jun;14(3):450-4
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  • [Title] [Biological characteristics of hyperleukocytic acute leukemia].
  • The study was to investigate the biological characteristics of hyperleucocyte acute leukemia (HAL) and its clinical significance.
  • In AML, monocytic leukemia is easier to become into HAL than other leukemias.
  • In ALL, T-lineage antigens of HAL group are more easily expressed than those of NHAL group; the leukemia cells of HAL group are naiver than those of NHAL group, meanwhile the prognosis of HAL is poor.

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  • (PMID = 16800918.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Antigens, CD79; 0 / Antigens, CD8; 0 / Sialic Acid Binding Ig-like Lectin 2
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81. Blank C, Wagner HM, Hohenleutner U, Andreesen R: Unusual manifestations of acute leukemia. Case 2. Leukemia and rash: paraneoplastic or drug-induced? J Clin Oncol; 2000 Oct 01;18(19):3437-9
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  • [Title] Unusual manifestations of acute leukemia. Case 2. Leukemia and rash: paraneoplastic or drug-induced?
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Drug Eruptions / etiology. Hidradenitis / etiology. Leukemia, Myeloid, Acute / complications. Paraneoplastic Syndromes / etiology
  • [MeSH-minor] Diagnosis, Differential. Humans. Male. Middle Aged

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  • (PMID = 11013285.001).
  • [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] Case Reports; Journal Article
  • [Publication-country] United States
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82. Agliano A, Martin-Padura I, Mancuso P, Marighetti P, Rabascio C, Pruneri G, Shultz LD, Bertolini F: Human acute leukemia cells injected in NOD/LtSz-scid/IL-2Rgamma null mice generate a faster and more efficient disease compared to other NOD/scid-related strains. Int J Cancer; 2008 Nov 1;123(9):2222-7
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  • [Title] Human acute leukemia cells injected in NOD/LtSz-scid/IL-2Rgamma null mice generate a faster and more efficient disease compared to other NOD/scid-related strains.
  • Transplantation of human acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) primary cells and cell lines in different strains of immunodeficient mice has led to preclinical models extensively used to investigate acute leukemia stem cells, biology and drug sensitivity.
  • We studied the engraftment kinetics of AML and ALL cell lines and primary cells in 3 strains of NOD.CB17-Prkdc(scid) (NOD/scid, NS)-related mice (NOD.Cg-Prkdc(scid)B2m(tm1Unc)/J, abbreviated NOD/scid/beta2 null, NSB; and NOD.Cg-Prkdc(scid)Il2rg(tm1Wjll)/SzJ, abbreviated NOD/scid/IL-2Rgamma null, NSG).
  • In NSG mice, we observed a significantly faster development of leukemia-related symptoms and a higher percentage of leukemia cells in the blood, in the marrow and in the spleen.
  • The leukemia-related angiogenic switch (measured as the number of circulating endothelial cells and progenitors) was faster in NSG compared to NS and NSB mice.
  • These models will be instrumental to studies on leukemia-initiating stem cells, leukemia biology, preclinical treatment studies, and to obtain patient-specific preclinical models to design and investigate patient-tailored therapies.
  • [MeSH-major] Disease Models, Animal. Interleukin Receptor Common gamma Subunit / physiology. Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology
  • [MeSH-minor] Animals. Cell Line, Tumor. Humans. Immunohistochemistry. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Polymerase Chain Reaction. Transplantation, Heterologous


83. Seiter K, Katragadda S, Ponce D, Rasul M, Ahmed N: Temozolomide and cisplatin in relapsed/refractory acute leukemia. J Hematol Oncol; 2009;2:21
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  • [Title] Temozolomide and cisplatin in relapsed/refractory acute leukemia.
  • Cisplatin depletes MGMT and increases the sensitivity of leukemia cells to temozolomide.
  • We performed a phase I study of cisplatin and temozolomide in patients with relapsed and refractory acute leukemia.
  • Fifteen patients had AML, 3 had ALL, and 2 had biphenotypic leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Dacarbazine / analogs & derivatives. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adult. Aged. Drug Resistance, Neoplasm / drug effects. Female. Humans. Male. Middle Aged. Recurrence. Salvage Therapy. Treatment Failure. Young Adult

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  • (PMID = 19463179.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2694825
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84. Sinigaglia R, Gigante C, Bisinella G, Varotto S, Zanesco L, Turra S: Musculoskeletal manifestations in pediatric acute leukemia. J Pediatr Orthop; 2008 Jan-Feb;28(1):20-8
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  • [Title] Musculoskeletal manifestations in pediatric acute leukemia.
  • BACKGROUND: In children, acute leukemia (AL) at presentation can mimic several orthopaedic pathologies, so that a variable delay of the correct diagnosis is often reported.
  • METHODS: To define more clearly the clinical and radiological musculoskeletal manifestations of leukemia in children, 122 affected children referred from 1984 to 1999 to our Pediatric Onco-Hematologic Clinic were retrospectively reviewed.
  • Average age at diagnosis was 6.6 years (from 7 months to 17 years).
  • One hundred two (83.6%) had acute lymphoblastic leukemia, 20 (16.4%) had acute myeloid leukemia.
  • RESULTS: At presentation, complaints related to the musculoskeletal system were frequent (38.3%), including pain (34.4%), functional impairment (22.9%), limping (12.3%), swelling (10.6%), and joint effusion (5.7%).
  • At presentation, 40.2% of children had at least 1 radiographic abnormality.
  • Different from previous reports, late radiographic lesions were uncommon (5.7%), probably because of milder newer medication protocols.
  • Radiographic abnormalities (P = 0.400), type of leukemia (P = 0.291), sex (P = 0.245), and white blood cell count at presentation (P = 0.877) were not prognostic factors.
  • As early diagnosis significantly decreases morbidity and mortality of AL, the orthopaedist should suspect AL in any child with unexplained persistent skeletal pain or radiographic alterations.
  • Accurate history, general physical examination, and complete blood cell count tests should address the suspicion, which is confirmed by a peripheral and/or iliac crest bone marrow biopsy.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Musculoskeletal Diseases / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Infant. Leukocyte Count. Male. Prevalence. Retrospective Studies. Survival Rate. Time Factors

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  • (PMID = 18157042.001).
  • [ISSN] 0271-6798
  • [Journal-full-title] Journal of pediatric orthopedics
  • [ISO-abbreviation] J Pediatr Orthop
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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85. Swords R, Giles F: Troxacitabine in acute leukemia. Hematology; 2007 Jun;12(3):219-27
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  • [Title] Troxacitabine in acute leukemia.
  • It was obtained by exchanging the sulphur endocyclic atom with oxygen in the structure of lamivudine, following the discovery that this agent had cytotoxic, as well as anti-viral activity.
  • The initial trials with troxacitabine have established its efficacy in both solid and haematological malignancies, including those resistant to ara-C (cytarabine).
  • [MeSH-major] Cytosine / analogs & derivatives. Dioxolanes / therapeutic use. Leukemia / drug therapy
  • [MeSH-minor] Antineoplastic Agents. Humans. Treatment Outcome

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  • [CommentIn] Hematology. 2007 Oct;12(5):471 [17891602.001]
  • (PMID = 17558697.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Duplicate Publication; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Dioxolanes; 60KQZ0388Y / troxacitabine; 8J337D1HZY / Cytosine
  • [Number-of-references] 46
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86. Kriukov AI, Karel'skaia NA: [Therapeutic and diagnostic policy in nasal bleeding in patients with acute leukemia]. Vestn Otorinolaringol; 2007;(1):37-40
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  • [Title] [Therapeutic and diagnostic policy in nasal bleeding in patients with acute leukemia].
  • The algorithm of the otorhinolaryngologist's actions in nasal bleeding (NB) in acute leukemia (AL) patients is presented.
  • A working classification and an original technique of nasal tamponade using the drug tahocomb in AL patients with nasal bleeding are proposed.
  • [MeSH-major] Algorithms. Aprotinin / therapeutic use. Epistaxis. Fibrinogen / therapeutic use. Health Policy. Leukemia / diagnosis. Leukemia / epidemiology. Thrombin / therapeutic use
  • [MeSH-minor] Acute Disease. Drug Combinations. Humans. Otolaryngology / methods. Tampons, Surgical

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  • (PMID = 17495802.001).
  • [ISSN] 0042-4668
  • [Journal-full-title] Vestnik otorinolaringologii
  • [ISO-abbreviation] Vestn. Otorinolaringol.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / tachocomb; 9001-32-5 / Fibrinogen; 9087-70-1 / Aprotinin; EC 3.4.21.5 / Thrombin
  • [Number-of-references] 12
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87. Uggla B, Tina E, Nahi H, Paul C, Höglund M, Sirsjö A, Tidefelt U: Topoisomerase IIalpha mRNA and protein expression vs. in vitro drug resistance and clinical outcome in acute leukaemia. Int J Oncol; 2007 Jul;31(1):153-60
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  • [Title] Topoisomerase IIalpha mRNA and protein expression vs. in vitro drug resistance and clinical outcome in acute leukaemia.
  • The objective of this study was to correlate the expression of topoisomerase (topo) IIalpha to in vitro drug sensitivity and to the clinical outcome in patients with acute leukaemia.
  • In both groups, chemosensitivity testing by a bioluminescence ATP assay was performed to a variable extent for both topo IIalpha poisons and non-topo IIalpha targeting drugs.
  • Cell samples from patients with a high (>median value) percentage of topo IIalpha-positive cells were significantly more sensitive to the topo IIalpha active drugs etoposide and daunorubicin, and showed a borderline value for idarubicin (p=0.08), while there was no difference for non-topo IIalpha targeting drugs.
  • We conclude that expression of topo IIalpha, determined as percentage of topo IIalpha-positive cells, in leukaemic cells correlates to chemosensitivity in vitro against topoisomerase poisons but that it does not predict clinical outcome in acute leukaemia.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Antigens, Neoplasm / metabolism. DNA Topoisomerases, Type II / metabolism. DNA-Binding Proteins / metabolism. Drug Resistance, Neoplasm. Leukemia, Myeloid / enzymology. Leukemia, Myeloid / mortality
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Blood Cells / drug effects. Blood Cells / enzymology. Bone Marrow Cells / drug effects. Bone Marrow Cells / enzymology. Cell Survival. Daunorubicin. Etoposide / pharmacology. Female. Humans. Male. Middle Aged. Prognosis. RNA, Messenger / analysis. RNA, Messenger / metabolism

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  • (PMID = 17549416.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 6PLQ3CP4P3 / Etoposide; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha; ZS7284E0ZP / Daunorubicin
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88. Gong H, Liu W, Zhou J, Xu H: Methylation of gene CHFR promoter in acute leukemia cells. J Huazhong Univ Sci Technolog Med Sci; 2005;25(3):240-2
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  • [Title] Methylation of gene CHFR promoter in acute leukemia cells.
  • In order to explore whether gene CHFR was inactivated by methylation in leukemia cells, the expression of CHFR was examined before and after treatment with demethylation agent in Molt-4, Jurkat and U937 leukemia cell lines by means of RT-PCR.
  • The methylation of promoter in Molt-4, Jurkat and U937 cells as well as 41 acute leukemia patients was analyzed by MS-PCR.
  • The results showed that methylation of CHFR promoter was inactivated and could be reversed by treatment with a demethylating agent in Molt-4, Jurkat and U937.
  • CHFR promoter methylation was detected in 39% of acute leukemia patients.
  • There was no difference in incidence of CHFR promoter methylation between acute myelocytic leukemia and acute lymphocytic leukemia.
  • In conclusion, CHFR is frequently inactivated in acute leukemia and is a good candidate for the leukemia supper gene.
  • By affecting mitotic checkpoint function, CHFR inactivation likely plays a key role in tumorigenesis in acute leukemia.
  • Moreover, the methylation of gene CHFR appears to be a good index with which to predict the sensitivity of acute leukemia to microtubule inhibitors.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA Methylation. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics

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  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6 [8790415.001]
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  • [Cites] Carcinogenesis. 2003 Jan;24(1):47-51 [12538348.001]
  • (PMID = 16201259.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins
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89. Zhou RQ, Gong YP, Zheng BH, Yang X: [Effects of bortezomib combined with daunorubicin on proliferation and apoptosis in primary adult acute leukemia]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2010 Sep;41(5):789-92
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  • [Title] [Effects of bortezomib combined with daunorubicin on proliferation and apoptosis in primary adult acute leukemia].
  • OBJECTIVE: To assess effects of proteasome inhibitor Bortezomib (Bor) in combination with Daunorubicin (DNR) on proliferation, apoptosis and the expression of Bcl-2 mRNA in primary leukemia cells in vitro.
  • METHODS: Primary leukemia cells were isolated from bone marrow of adult acute leukemia patients using Ficoll liquid, then the primary leukemia cells were treated with different concentration of these two drugs (Bor 5, 10, 20, 50 nmol/L, DNR 50, 100, 200, 500 nmol/L, and Bor 5, 10 nmol/L combined with DNR 50, 100, 200, 500 nmol/L respectively ).
  • RESULTS: Growth inhibition ratio of all the types of acute leukemia cells were increased with the treatment of DNR and Bor in dose-dependent manner.
  • Combined with Bor (5, 10 nmol/L),the IC50 of DNR decreased from (102 +/- 27) nmol/L to (73 +/- 26), (55 +/- 22) nmol/L respectively.
  • Compared with control group and single drug (DNR or Bor) group, there were obvious increase of apoptosis ratio and obvious decrease of Bcl-2 in the group of DNR 100 nmol/L combined with Bor 20 nmol/L after 24 h or 48 h cultivation (P < 0.05).
  • CONCLUSION: Bor combined with DNR shows synergetic effect in promoting the apoptosis of adult acute leukemia primary cells as well as inhibitory effect on the proliferation of leukemia cells.
  • [MeSH-major] Apoptosis / drug effects. Boronic Acids / pharmacology. Daunorubicin / pharmacology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Pyrazines / pharmacology
  • [MeSH-minor] Adult. Antibiotics, Antineoplastic / pharmacology. Antineoplastic Agents / pharmacology. Bortezomib. Drug Synergism. Female. Humans. Male. Middle Aged. Tumor Cells, Cultured. Young Adult

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  • (PMID = 21302442.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 69G8BD63PP / Bortezomib; ZS7284E0ZP / Daunorubicin
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90. Su WL, Liu JY, Kao WY: Management of pregnancy-associated acute leukemia. Eur J Gynaecol Oncol; 2003;24(3-4):251-4
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  • [Title] Management of pregnancy-associated acute leukemia.
  • Since leukocystosis and anemia are common findings in pregnancy, pathological alterations in hematopoesis, such as leukemias, can sometimes proceed undetected.
  • Chemotherapy during pregnancy carries the risk of teratogenic effects on the fetus, and there is little data to guide chemotherapeutic regimens for leukemia during pregnancy.
  • The following paper describes our experience in treating two women with acute leukemia during pregnancy and the immediate postpartum period, and reviews the relevant literature.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / drug therapy. Pregnancy Complications, Neoplastic / diagnosis. Pregnancy Complications, Neoplastic / drug therapy. Pregnancy Outcome

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  • (PMID = 12807234.001).
  • [ISSN] 0392-2936
  • [Journal-full-title] European journal of gynaecological oncology
  • [ISO-abbreviation] Eur. J. Gynaecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 28
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91. Nakajima A, Tauchi T, Sashida G, Sumi M, Abe K, Yamamoto K, Ohyashiki JH, Ohyashiki K: Telomerase inhibition enhances apoptosis in human acute leukemia cells: possibility of antitelomerase therapy. Leukemia; 2003 Mar;17(3):560-7
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  • [Title] Telomerase inhibition enhances apoptosis in human acute leukemia cells: possibility of antitelomerase therapy.
  • We examined the impact of telomerase inhibition by the dominant-negative human catalytic subunit of telomerase (DN-hTERT) on the biological features of acute leukemia.
  • We introduced vectors encoding dominant- negative (DN)-hTERT, wild-type (WT)-hTERT, or a control vector expressing only a drug-resistant marker into a telomerase-positive human acute lymphoblastic leukemia cell line, HAL-01.
  • Expression of DN-hTERT dramatically inhibited telomerase activity, leading to apoptotic cell death.
  • Furthermore, the G-quadruplex-interactive telomerase-specific inhibitor, telomestatin, shortened the telomere length and induced apoptosis in freshly isolated primary acute leukemia cells.
  • These results suggest that antitelomerase therapy may be useful in some acute leukemias in combination with antileukemic agents such as daunorubicin.
  • [MeSH-major] Apoptosis / drug effects. Leukemia / pathology. Telomerase / antagonists & inhibitors. Telomerase / genetics. Telomerase / pharmacology
  • [MeSH-minor] Acute Disease. Animals. DNA-Binding Proteins. Daunorubicin / pharmacology. Drug Synergism. Genes, Dominant. Genetic Therapy. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Mutation. Telomere / drug effects. Telomere / ultrastructure. Transfection. Tumor Cells, Cultured

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  • (PMID = 12646945.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; EC 2.7.7.49 / Telomerase; ZS7284E0ZP / Daunorubicin
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92. Pea F, Russo D, Michieli M, Baraldo M, Ermacora A, Damiani D, Baccarani M, Furlanut M: Liposomal daunorubicin plasmatic and renal disposition in patients with acute leukemia. Cancer Chemother Pharmacol; 2000;46(4):279-86
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  • [Title] Liposomal daunorubicin plasmatic and renal disposition in patients with acute leukemia.
  • DaunoXome (DNX, NeXstar) is a liposomal-encapsulated preparation of daunorubicin registered for treatment of Kaposi's sarcoma that during prior in vitro studies showed a toxicity to leukemic cells at least comparable to that of free daunorubicin.
  • The aim of our study was to determine DNX pharmacokinetics in 11 poor-risk patients with acute leukemia treated with DNX 60 mg/m2 IV on days 1, 3, and 5.
  • The main pharmacokinetic parameters (t1/2alpha 4.54 +/- 0.87 h; VdSS 2.88 +/- 0.93 l/m2; Cl 0.47 +/- 0.26 l/h/m2) showed that in patients with acute leukemia liposomal-entrapped daunorubicin pharmacokinetics greatly differed from that observed for the conventional formulation.
  • In fact, DNX produced mean plasma AUC levels (t-DNR AUC0-infinity 456.27 +/- 182.64 microg/ml/h) about 100- to 200-fold greater than those reported for the free drug at comparable doses due to a very much lower total body clearance.
  • Volume of distribution at steady state was 200-to 500-fold lower than for the free drug.
  • Therefore, pharmacokinetic characteristics suggest that DNX may be more convenient than free daunorubicin in the treatment of acute leukemia.
  • In fact, liposomal formulation may allow a reduction of daunorubicin captation in normal tissues. thus minimizing toxicity at least for the parent drug, and guarantee an unimpeded access to leukemic cells in the bloodstream and bone marrow, thus theoretically improving efficacy.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Antibiotics, Antineoplastic / pharmacokinetics. Daunorubicin / administration & dosage. Daunorubicin / pharmacokinetics. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Calibration. Drug Carriers. Female. Humans. Kidney / metabolism. Liposomes. Male. Middle Aged. Pilot Projects. Spectrometry, Fluorescence

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  • (PMID = 11052625.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Drug Carriers; 0 / Liposomes; ZS7284E0ZP / Daunorubicin
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93. Wu SJ, Du X, Chen YX, Jiang WL, Zhong LY, Lin W, Huang ZL: [Relationship between cyclins and prognosis of acute leukemia]. Ai Zheng; 2003 Aug;22(8):852-5
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  • [Title] [Relationship between cyclins and prognosis of acute leukemia].
  • BACKGROUND & OBJECTIVE: Cell proliferation and differentiation are directed by cell cycle mechanism.
  • When tumor cells proliferate abnormally, cyclins, which are positive agents of cell cycle, may be expressed abnormally at the same time.
  • This study was designed to investigate the relationship between expression of cyclins and prognosis of acute leukemia.
  • METHODS: Sixty-eight cases of acute leukemia were enrolled.
  • All samples were divided into three groups: acute leukemia in complete remission (12 cases), newly diagnosed acute leukemia (16 cases) and refractory leukemia (40 case).
  • There was no difference of expression of cyclin D and cyclin E mRNA among CR patients with acute leukemia(P >0.05), while the expression of cyclin D mRNA is significantly higher than that of cyclin E in refractory leukemia group.
  • Furthermore the expression of cyclin D mRNA in recurrent refractory leukemia patients is significantly higher than that newly diagnosed cases (P< 0.05).
  • No difference was found between complete remission group and refractory leukemia group (P >0.05).
  • CONCLUSION: Cyclin D may act as a prognostic marker for acute leukemia.
  • The amount of cyclins expressed cannot be used as a prognostic factor for acute leukemia.
  • [MeSH-major] Cyclins / genetics. Leukemia / metabolism. RNA, Messenger / analysis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Cyclin A / genetics. Cyclin D. Cyclin E / genetics. Female. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 12917034.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cyclin A; 0 / Cyclin D; 0 / Cyclin E; 0 / Cyclins; 0 / RNA, Messenger
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94. Mannelli F, De Simone P, Gianfaldoni G, Nozzoli C, Filipponi F, Bosi A: Atypical acute leukemia early after liver transplantation. Transplant Proc; 2009 Nov;41(9):3945-6
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  • [Title] Atypical acute leukemia early after liver transplantation.
  • Acute myeloid leukemia (AML) has been rarely reported after transplantation, namely seven cases described so far.
  • The putative mechanism of action is long-standing immunosuppression, even though no clear correlation with the type of drug has ever been demonstrated.
  • We report the case of a 28-year-old male patient who presented with a early onset of AML after liver transplantation for hepatitis B virus-related acute liver failure.
  • The AML was characterized by aggressive clinical features with extrahematologic sites of involvement and an atypical immunophenotype; the laboratory findings were consistent with the diagnosis of monocytic acute leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / pathology. Liver Failure / surgery. Liver Transplantation / adverse effects

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  • (PMID = 19917419.001).
  • [ISSN] 1873-2623
  • [Journal-full-title] Transplantation proceedings
  • [ISO-abbreviation] Transplant. Proc.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA Antigens
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95. Pérez-Sanchez I, Anguita J, Martín-Rabadan P, Muñoz P, Serrano D, Escudero A, Pintado T: Blastoschizomyces capitatus infection in acute leukemia patients. Leuk Lymphoma; 2000 Sep;39(1-2):209-12
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  • [Title] Blastoschizomyces capitatus infection in acute leukemia patients.
  • Most of the patients had acute leukemia (AL) or related disorders and had received chemotherapy treatment.
  • Due to BC's resistance to currently used antifungal agents, this infection represents a therapeutic challenge and serious complication in the treatment of hematology malignancies.
  • Here we report our experience with BC infection in four patients with acute leukemia or related disorders.
  • [MeSH-major] Leukemia / parasitology. Mycoses / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Amphotericin B / administration & dosage. Antifungal Agents / administration & dosage. Female. Humans. Immunosuppression / adverse effects. Male. Middle Aged. Neutropenia / chemically induced. Trichosporon

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  • (PMID = 10975401.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 0 / Antifungal Agents; 7XU7A7DROE / Amphotericin B
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96. Xu Z, Wang M, Wang L, Wang Y, Zhao X, Rao Q, Wang J: Aberrant expression of TSC2 gene in the newly diagnosed acute leukemia. Leuk Res; 2009 Jul;33(7):891-7
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  • [Title] Aberrant expression of TSC2 gene in the newly diagnosed acute leukemia.
  • The tuberous sclerosis (TSC) genes, TSC1 and TSC2, encode hamartin and tuberin, respectively, and are putative tumor suppressor genes that were originally identified due to their involvement in the inherited autosomal dominant disorder tuberous sclerosis.
  • It has been elucidated that the two proteins form an intracellular heterodimer participating in signaling pathway of the mammalian Target of Rapamycin (mTOR).
  • Recent studies showed that mTOR pathway was frequently activated in blasts from acute myeloid leukemia (AML) patient and associated with proliferation, survival, and drug-resistance of these cells.
  • These phenomena led us to hypothesize that TSC gene might be involved in acute leukemia (AL).
  • [MeSH-major] DNA Methylation. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Antimetabolites, Antineoplastic / pharmacology. Azacitidine / pharmacology. Base Sequence. Blotting, Western. Bone Marrow / metabolism. Case-Control Studies. Child. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Humans. Infant. Male. Middle Aged. Molecular Sequence Data. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sequence Homology, Nucleic Acid. Survival Rate. Young Adult

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  • [CommentIn] Leuk Res. 2009 Jul;33(7):883-5 [19286253.001]
  • (PMID = 19250671.001).
  • [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
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins; 4JG2LF96VF / tuberous sclerosis complex 2 protein; M801H13NRU / Azacitidine
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97. Rao DN, Anuradha C, Vishnupriya S, Sailaja K, Surekha D, Raghunadharao D, Rajappa S: Association of an MDR1 gene (C3435T) polymorphism with acute leukemia in India. Asian Pac J Cancer Prev; 2010;11(4):1063-6
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  • [Title] Association of an MDR1 gene (C3435T) polymorphism with acute leukemia in India.
  • The multidrug resistance (MDR1) gene product P-glycoprotein is a membrane bound protein that functions as an ATP-dependent efflux pump, transporting exogenous and endogenous substrates from the cells.
  • Our main objective was to study the MDR1gene polymorphism at C3435T with reference to development and progression of acute leukemia.
  • The present study included 290 acute leukemia cases, comprising of 147 acute lymphocytic leukemia (ALL), 143 acute myeloid leukemia and 249 age-sex matched control samples for the analysis of MDR1 C3435T polymorphism, by the PCR-RFLP method.
  • The mean white blood cell count, blast% and LDH levels were increased in ALL patients with the CC genotype.
  • No deviation was observed with respect to hematoglobin, platelet count and disease free survival in ALL patients.
  • The association of CC genotype with clinical variables in ALL indicated that the CC genotype with high expression might be eliminating antileukemic drugs (anthracyclines, Daunorubicin, Vincristeine, Mitoxanthrone) which are P-gp substrates, leading to lower intra cellular drug concentrations and a poor prognosis.
  • In conclusion, these results suggested that the MDR1 TT genotype might influence risk of development of acute lympoblastic leukemia and the CC genotype might be linked to a poor prognosis of ALL.
  • [MeSH-major] Genes, MDR / genetics. Leukemia, Myeloid, Acute / genetics. P-Glycoprotein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 21133625.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / P-Glycoprotein; 0 / P-Glycoproteins
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98. Barbui T, Falanga A: Disseminated intravascular coagulation in acute leukemia. Semin Thromb Hemost; 2001 Dec;27(6):593-604
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  • [Title] Disseminated intravascular coagulation in acute leukemia.
  • Life-threatening bleeding is frequent in acute leukemias, particularly in acute promyelocytic leukemia (APL).
  • An important pathogenetic role is attributed to the leukemic cell properties interfering with the hemostatic mechanisms.
  • However, chemotherapy and intercurrent infections also contribute to the bleeding risk in the patient with leukemia.
  • In this article, we will attempt to describe what is currently known about the coagulopathy of acute leukemia, summarize the various aspects of the hemostatic abnormalities underlying this disorder, and revise the principal pathogenetic mechanisms.
  • We will also try to provide information on the current therapeutic tools and recommendations for the management of life-threatening bleeding in this disease.
  • Finally, a special focus will be devoted to the management of this complication in the era of all-trans retinoic acid (ATRA), a drug now indispensable in curing APL that has completely changed the natural history of APL and its coagulation/bleeding syndrome.
  • [MeSH-major] Disseminated Intravascular Coagulation. Leukemia / complications
  • [MeSH-minor] Acute Disease. Humans

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  • (PMID = 11740683.001).
  • [ISSN] 0094-6176
  • [Journal-full-title] Seminars in thrombosis and hemostasis
  • [ISO-abbreviation] Semin. Thromb. Hemost.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 109
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99. Thall PF, Estey EH: Some ethical issues in phase II trials in acute leukemia. Clin Adv Hematol Oncol; 2005 Dec;3(12):943-8
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  • [Title] Some ethical issues in phase II trials in acute leukemia.
  • Although we discuss chemotherapy trials in acute leukemia, the issues pertain to a much larger class of early-phase clinical trials.
  • Our focus is on the manner in which numerical values of standard and targeted response rates of a statistical design are specified, the number of interim tests that are applied, and the effects of these design features on early stopping probabilities and the treatments that patients actually receive.
  • These points are illustrated by numerical comparisons of alternative designs for a particular phase II trial of a new drug for relapsed or refractory acute myelogenous leukemia.
  • The general conclusions are that statistical designs have both scientific and ethical implications, and that science, statistics, and ethics cannot be treated as separate issues.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Clinical Trials, Phase II as Topic / ethics. Ethics, Research. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Ethics, Medical. Humans

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  • [CommentIn] Clin Adv Hematol Oncol. 2006 Feb;4(2):95 [16739255.001]
  • [RetractionIn] Clin Adv Hematol Oncol. 2006 Feb;4(2):95 [16739302.001]
  • (PMID = 16555436.001).
  • [ISSN] 1543-0790
  • [Journal-full-title] Clinical advances in hematology & oncology : H&O
  • [ISO-abbreviation] Clin Adv Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Retracted Publication; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 17
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100. Sarkodee-Adoo CB, Merz WG, Karp JE: Management of infections in patients with acute leukemia. Oncology (Williston Park); 2000 May;14(5):659-66, 671-2; discussion 672-7
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  • [Title] Management of infections in patients with acute leukemia.
  • Several recent studies have addressed the management of infectious problems in patients with acute leukemia.
  • This article describes recent developments in the management of infectious illnesses in patients who are neutropenic due to leukemia or its treatment.
  • The discussion will focus on the increasing armamentarium of antimicrobial drugs and adjunctive agents.
  • These expanding therapeutic options must be viewed in the context of newly emerging resistant organisms and special problems, such as the increased use of indwelling venous catheters.
  • [MeSH-major] Anti-Infective Agents / therapeutic use. Antineoplastic Agents / adverse effects. Leukemia / drug therapy. Neutropenia / complications. Opportunistic Infections / drug therapy. Opportunistic Infections / prevention & control
  • [MeSH-minor] Acute Disease. Antifungal Agents / therapeutic use. Bacterial Infections / drug therapy. Bacterial Infections / prevention & control. Humans. Mycoses / drug therapy. Mycoses / prevention & control

  • MedlinePlus Health Information. consumer health - Leukemia.
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  • (PMID = 10853459.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Antifungal Agents; 0 / Antineoplastic Agents
  • [Number-of-references] 116
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