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Items 1 to 100 of about 2345
1. Li H, Diao YT, Li HQ, Ma Q, Cui J, Zhou YZ, Li D: The association between serum levels of oxLDL-lgG and oxLDL-lgM autoantibody with adult acute myeloblastic leukaemia. Lipids Health Dis; 2010;9:11
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  • [Title] The association between serum levels of oxLDL-lgG and oxLDL-lgM autoantibody with adult acute myeloblastic leukaemia.
  • AIM: To evaluate the relationship between serum antibodies against ox-LDL levels and adult acute myeloblastic leukemia (AML).
  • METHODS: Forty three patients with AML and 52 normal controls were enrolled in this study in the Department of Hematology, Tumor Center of Qilu Hospital of Shandong University from Feb.
  • Binary logistic regression showed the odds ratios of association of oxLD-lgG and oxLD-lgM with adult AML were 0.72(95%CI: 0.55-0.94) and 1.11(95%CI: 1.01-1.21) respectively after adjusted for potential confounders.
  • CONCLUSION: In the preliminary investigation we found a descensive oxLDL- lgG and an elevated oxLDL-lgM serum levels for the adult AML.
  • Future studies need to confirm the hypothesis whether they related to the development and progression of adult AML.
  • [MeSH-major] Autoantibodies / immunology. Immunoglobulin G / blood. Immunoglobulin M / blood. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / immunology. Lipoproteins, LDL / blood
  • [MeSH-minor] Adolescent. Adult. Aged. Case-Control Studies. Disease Progression. Enzyme-Linked Immunosorbent Assay / methods. Female. Humans. Male. Middle Aged

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  • [Cites] Arterioscler Thromb Vasc Biol. 2000 Jan;20(1):204-9 [10634819.001]
  • [Cites] Prog Lipid Res. 2003 Jul;42(4):318-43 [12689622.001]
  • [Cites] Circulation. 2003 Oct 28;108(17):2107-12 [14530200.001]
  • [Cites] Bratisl Lek Listy. 1990 Jan;91(1):70-6 [2322871.001]
  • [Cites] Clin Immunol. 2010 Jan;134(1):55-65 [19427818.001]
  • [Cites] Br J Cancer. 2006 Jan 16;94(1):156-60 [16404369.001]
  • [Cites] Clin Immunol. 2008 Jun;127(3):394-400 [18533284.001]
  • [Cites] Arch Med Res. 2008 Nov;39(8):760-7 [18996289.001]
  • [Cites] Nihon Koshu Eisei Zasshi. 1994 May;41(5):393-403 [8049507.001]
  • (PMID = 20113525.001).
  • [ISSN] 1476-511X
  • [Journal-full-title] Lipids in health and disease
  • [ISO-abbreviation] Lipids Health Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Autoantibodies; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Lipoproteins, LDL; 0 / oxidized low density lipoprotein
  • [Other-IDs] NLM/ PMC2834680
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2. Fazlina N, Maha A, Zarina AL, Hamidah A, Zulkifli SZ, Cheong SK, Ainoon O, Jamal R, Hamidah NH: Assessment of P-gp and MRP1 activities using MultiDrugQuant Assay Kit: a preliminary study of correlation between protein expressions and its functional activities in newly diagnosed acute leukaemia patients. Malays J Pathol; 2008 Dec;30(2):87-93
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessment of P-gp and MRP1 activities using MultiDrugQuant Assay Kit: a preliminary study of correlation between protein expressions and its functional activities in newly diagnosed acute leukaemia patients.
  • Multidrug resistance (MDR) is believed to be responsible for poor response of patients towards chemotherapy particularly patients with acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL).
  • We studied P-gp and multidrug resistance-associated protein 1 (MRP1) expression and functional activities in 43 newly diagnosed acute leukemia cases (19 paediatric ALL cases and 24 adult AML cases).
  • In adult AML cases, all cases expressed MRP1 and its functional activities but only 58.3% were positive for P-gp and its functional activities.
  • We were able to show a significant correlation between the expression of the multidrug resistant protein (P-gp and MRP1) and their functional activity in adult AML and paediatric ALL samples.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. Multidrug Resistance-Associated Proteins / biosynthesis. P-Glycoprotein / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Reagent Kits, Diagnostic

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  • (PMID = 19291917.001).
  • [ISSN] 0126-8635
  • [Journal-full-title] The Malaysian journal of pathology
  • [ISO-abbreviation] Malays J Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Malaysia
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / Reagent Kits, Diagnostic; 0 / multidrug resistance-associated protein 1
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3. Falini B, Mecucci C, Saglio G, Lo Coco F, Diverio D, Brown P, Pane F, Mancini M, Martelli MP, Pileri S, Haferlach T, Haferlach C, Schnittger S: NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities: a comparative analysis of 2562 patients with acute myeloid leukemia. Haematologica; 2008 Mar;93(3):439-42
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  • [Title] NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities: a comparative analysis of 2562 patients with acute myeloid leukemia.
  • Acute myeloid leukemia carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc(+) acute myeloid leukemia) represents one-third of adult AML (50-60% of all acute myeloid leukemia with normal karyotype) and shows distinct biological, pathological and clinical features.
  • We confirm in 2562 patients with acute myeloid leukemia our previous observation that NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities.
  • Taken together, these findings make NPMc+ acute myeloid leukemia a good candidate for inclusion in the upcoming World Health Organization classification.
  • [MeSH-major] Cytoplasm / chemistry. Leukemia, Myeloid / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Bone Marrow / pathology. Cell Nucleus / chemistry. Chromosome Aberrations. Chromosome Inversion. Cohort Studies. DNA Mutational Analysis. Germany / epidemiology. Humans. In Situ Hybridization, Fluorescence. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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  • (PMID = 18268276.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin
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4. Bao LY, Wang JS: [Correlation of adult AML Npm1 mutations with prognosis and its relationship with gene mutation of FLT3 and CEBPA]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Feb;18(1):19-24
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  • [Title] [Correlation of adult AML Npm1 mutations with prognosis and its relationship with gene mutation of FLT3 and CEBPA].
  • This study was aimed to investigate the correlation of 12th exon mutations in the npm1 gene with prognosis of adult AML patients and to explore the relationship of 12th exon mutation with other gene mutations.
  • The specimen of bone marrow and peripheral blood from AML patients, the informations of medical history, symptoms, related image examinations, blood routine examination, NAP, oxygen saturation level in artery blood and EPO level in serum were collected; the bcr/abl fusion gene was detected by routine examination of bone marrow + biopsy + chromosome mapping + FISH.
  • The results indicated that the npm1 heterozygote gene mutation was found in 72 out of 150 AML patients with normal cytogenetics (48%, 72/150).
  • The AML patients with npm1 gene mutation had specific clinical, phenotypic and genetic characteristics.
  • It is concluded that npm1 mutation is a favorable independent prognostic factor for adult AML patients with normal cytogenetics under conditions without FIT3 gene mutation.

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  • (PMID = 20137111.001).
  • [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 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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5. Lee JN, Kim HR, Shin JH, Joo YD: [Prevalence of FLT3 internal tandem duplication in adult acute myelogenous leukemia]. Korean J Lab Med; 2007 Aug;27(4):237-43
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  • [Title] [Prevalence of FLT3 internal tandem duplication in adult acute myelogenous leukemia].
  • An internal tandem duplication of the FLT3 gene (FLT3/ITD) has been reported in acute myelogenous leukemia (AML) and may be associated with a poor prognosis.
  • In this study we determined the prevalence and prognostic significance of FLT3/ITD in adult AML patients.
  • METHODS: This study included 52 adult de novo AML.
  • RESULTS: FLT3/ITD was found in 15 (28.8%) of the 52 AML patients.
  • CONCLUSIONS: Our data indicate that FLT3/ITD is a common alteration in adult AML patients.
  • Although based on a study with a limited number of AML patients, FLT3/ITD is a prognostic marker in patients with AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 17. Female. Humans. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Survival Analysis

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  • (PMID = 18094582.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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6. van den Heuvel-Eibrink MM, van der Holt B, Sonneveld P: Role of BCRP and its expression with MDR1 in adult AML. Leuk Res; 2005 Jan;29(1):115

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of BCRP and its expression with MDR1 in adult AML.
  • [MeSH-minor] Drug Resistance, Multiple. Gene Expression. Humans. Leukemia, Myeloid, Acute

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  • [CommentOn] Leuk Res. 2004 Apr;28(4):367-72 [15109536.001]
  • (PMID = 15541485.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / Neoplasm Proteins; 0 / P-Glycoprotein
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7. Ho PA, Alonzo TA, Kopecky KJ, Miller KL, Kuhn J, Zeng R, Gerbing RB, Raimondi SC, Hirsch BA, Oehler V, Hurwitz CA, Franklin JL, Gamis AS, Petersdorf SH, Anderson JE, Reaman GH, Baker LH, Willman CL, Bernstein ID, Radich JP, Appelbaum FR, Stirewalt DL, Meshinchi S: Molecular alterations of the IDH1 gene in AML: a Children's Oncology Group and Southwest Oncology Group study. Leukemia; 2010 May;24(5):909-13
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular alterations of the IDH1 gene in AML: a Children's Oncology Group and Southwest Oncology Group study.
  • Recent whole-genome sequencing efforts led to the identification of IDH1(R132) mutations in acute myeloid leukemia (AML) patients.
  • We studied the prevalence and clinical implications of IDH1 genomic alterations in pediatric and adult AML.
  • Diagnostic DNA from 531 AML patients treated on Children's Oncology Group trial COG-AAML03P1 (N=257), and Southwest Oncology Group trials SWOG-9031, SWOG-9333 and SWOG-9500 (N=274), were tested for IDH1 mutations.
  • Codon R132 mutations were absent in the pediatric cohort, but were found in 12 of 274 adult patients (4.4%, 95% CI 2.3-7.5).
  • IDH1 mutations were not detected in pediatric AML, and are uncommon in adult AML.

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  • [Cites] Science. 2009 Apr 10;324(5924):261-5 [19359588.001]
  • [Cites] Cell Cycle. 2009 Jun 1;8(11):1806-7 [19411854.001]
  • [Cites] Arthritis Res Ther. 2009;11(2):219 [19435530.001]
  • [Cites] Int J Cancer. 2009 Jul 15;125(2):353-5 [19378339.001]
  • [Cites] Blood. 2009 Jun 25;113(26):6558-66 [19304957.001]
  • [Cites] Adv Cancer Res. 2009;102:19-65 [19595306.001]
  • [Cites] Acta Neuropathol. 2009 Oct;118(4):469-74 [19554337.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3589-95 [11369655.001]
  • [Cites] J Cell Mol Med. 2009 Sep;13(9A):2780-6 [19674190.001]
  • [Cites] N Engl J Med. 2009 Feb 19;360(8):765-73 [19228619.001]
  • [Cites] Acta Neuropathol. 2008 Dec;116(6):597-602 [18985363.001]
  • [Cites] Hum Mutat. 2009 Jan;30(1):7-11 [19117336.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1058-66 [19657110.001]
  • [Cites] Blood. 2002 Dec 1;100(12):3869-76 [12393614.001]
  • [Cites] Blood. 1997 May 1;89(9):3323-9 [9129038.001]
  • [Cites] Blood. 2006 May 1;107(9):3724-6 [16368883.001]
  • [Cites] Am J Hematol. 2007 Dec;82(12):1056-62 [17696203.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • (PMID = 20376086.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA027057; United States / NCI NIH HHS / CA / CA18029; United States / NCI NIH HHS / CA / U10 CA032102-30; United States / NCI NIH HHS / CA / U10 CA098543-03; United States / NCI NIH HHS / CA / CA12213; United States / NCI NIH HHS / CA / CA20319; United States / NCI NIH HHS / CA / K23 CA92405; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / N01 CA032102; United States / NCI NIH HHS / CA / R21 CA10262-01; United States / NCI NIH HHS / CA / R01 CA114563-01; United States / NCI NIH HHS / CA / K23 CA092405; United States / NCI NIH HHS / CA / CA114563; United States / NCI NIH HHS / CA / U10 CA032102; United States / NCI NIH HHS / CA / CA32102; United States / NCI NIH HHS / CA / CA38926; United States / NCI NIH HHS / CA / N01 CA038926; United States / NCI NIH HHS / CA / N01 CA027057; United States / NCI NIH HHS / CA / R01 CA114563; United States / NCI NIH HHS / CA / U10 CA020319; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / U10 CA038926; United States / NCI NIH HHS / CA / R21 CA102624; United States / NCI NIH HHS / CA / CA27057; United States / NCI NIH HHS / CA / R01 CA114563-04; United States / NCI NIH HHS / CA / U10 CA98543
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Codon; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ NIHMS184578; NLM/ PMC2945692
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8. Tamai H, Yamaguchi H, Takahashi S, Tojo A, Hamaguchi H, Kobayashi T, Akiyama H, Sakamaki H, Okumura H, Nakao S, Arai A, Miura O, Tajika K, Inokuchi K, Dan K: Treatment of adult AML with t(6;11)(q27;q23) by allogeneic hematopoietic SCT in the first CR. Bone Marrow Transplant; 2008 Oct;42(8):553-4
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  • [Title] Treatment of adult AML with t(6;11)(q27;q23) by allogeneic hematopoietic SCT in the first CR.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / mortality
  • [MeSH-minor] Adolescent. Adult. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 6 / genetics. Disease-Free Survival. Female. Humans. Male. Middle Aged. Retrospective Studies. Survival Rate. Translocation, Genetic / genetics. Transplantation, Homologous

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  • (PMID = 18622415.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
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9. Dupret C, Asnafi V, Leboeuf D, Millien C, Ben Abdelali R, Preudhomme C, Beldjord K, Delabesse E, Macintyre E: IgH/TCR rearrangements are common in MLL translocated adult AML and suggest an early T/myeloid or B/myeloid maturation arrest, which correlates with the MLL partner. Leukemia; 2005 Dec;19(12):2337-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IgH/TCR rearrangements are common in MLL translocated adult AML and suggest an early T/myeloid or B/myeloid maturation arrest, which correlates with the MLL partner.
  • [MeSH-major] Cell Lineage. Leukemia, Myeloid / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. B-Lymphocytes / pathology. Gene Rearrangement. Genes, T-Cell Receptor. Humans. Immunoglobulin Heavy Chains / genetics. Myeloid Cells / pathology. T-Lymphocytes / pathology

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  • (PMID = 16304577.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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10. Stock W: Clinical trials in adult AML. Clin Adv Hematol Oncol; 2009 Jun;7(6):8-10
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  • [Title] Clinical trials in adult AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Drugs, Investigational / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Age Factors. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Double-Blind Method. Hematopoietic Stem Cell Transplantation. Humans. Middle Aged. Multicenter Studies as Topic. Randomized Controlled Trials as Topic. Treatment Outcome

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  • (PMID = 19645130.001).
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Investigational
  • [Number-of-references] 30
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11. Uggla B, Ståhl E, Wågsäter D, Paul C, Karlsson MG, Sirsjö A, Tidefelt U: BCRP mRNA expression v. clinical outcome in 40 adult AML patients. Leuk Res; 2005 Feb;29(2):141-6
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BCRP mRNA expression v. clinical outcome in 40 adult AML patients.
  • Efflux pumps are considered being mechanisms behind drug resistance in acute myeloid leukaemia (AML).
  • A recently described efflux pump, breast cancer resistance protein (BCRP), can be expressed in AML, but its clinical importance is uncertain.
  • In this study BCRP mRNA expression was determined in samples from 40 AML patients by real-time RT-PCR.
  • There was no difference in BCRP mRNA expression between patients responding to induction treatment and non-responders.
  • This suggests a possible role of BCRP in drug resistance in AML.
  • [MeSH-major] ATP-Binding Cassette Transporters / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Adult. Aged. Cell Line, Tumor. Drug Resistance, Neoplasm / physiology. Female. Gene Expression Regulation, Leukemic. Humans. Male. Middle Aged. Predictive Value of Tests. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Treatment Outcome

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  • (PMID = 15607361.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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12. Basecke J, Whelan JT, Griesinger F, Bertrand FE: The MLL partial tandem duplication in acute myeloid leukaemia. Br J Haematol; 2006 Nov;135(4):438-49

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The MLL partial tandem duplication in acute myeloid leukaemia.
  • Mixed lineage leukaemia gene-partial tandem duplications (MLL-PTD) characterise acute myeloid leukaemia (AML) with trisomy 11 and AML with a normal karyotype.
  • MLL-PTD confer a worse prognosis with shortened overall and event free survival in childhood and adult AML.
  • This review summarises clinical studies on MLL-PTD positive AML and recent experimental findings on the putative leukaemogenic role of MLL-PTD.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Tandem Repeat Sequences
  • [MeSH-minor] Acute Disease. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 11 / genetics. DNA, Neoplasm / genetics. Genetic Predisposition to Disease. Histone-Lysine N-Methyltransferase. Humans. Prognosis. Trisomy

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  • (PMID = 16965385.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 81
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13. Styczynski J: Drug resistance in childhood acute myeloid leukemia. Curr Pharm Biotechnol; 2007 Apr;8(2):59-75
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  • [Title] Drug resistance in childhood acute myeloid leukemia.
  • Therapy results in childhood AML differ from those of ALL.
  • The development of drug resistance is the limiting factor in the therapy of AML.
  • Different problems of drug resistance in childhood AML, with emphasis to age and in comparison to adult AML are presented.
  • Taking into account both children and adults, it seems that age is adversely related to therapy outcome in AML, and the percentage of patients with favorable cytogenetics decreases with age; however, age is positively correlated with multi-drug resistance and the proportion of patients with unfavorable cytogenetics.
  • AML is considered a stem cell disease.
  • Cellular drug resistance in AML cells seems to be similar throughout all other age groups, however the higher the age, the worse the outcome.
  • In childhood AML, no drug is more effective in comparison to ALL, and cellular drug resistance is partially related to chromosomal abnormalities.
  • Pediatric AML is equally resistant as adult AML.
  • Pediatric and adult AML, respectively, are possibly equally drug resistant on initial diagnosis and at relapse.
  • In contrast to ALL, the prognostic value of in vitro drug resistance in childhood AML has not been well documented yet.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / epidemiology. Neoplasm Recurrence, Local / epidemiology. Neoplasm Recurrence, Local / prevention & control

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  • (PMID = 17430154.001).
  • [ISSN] 1873-4316
  • [Journal-full-title] Current pharmaceutical biotechnology
  • [ISO-abbreviation] Curr Pharm Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 165
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14. 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).
  • 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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15. McHayleh WM, Redner R, Sehgal R, Raptis A, Agha M, Natale J, Luong T, Schlesselman JJ, Foon K, Boyiadzis M: Etoposide and mitoxantrone in newly diagnosed acute myeloid leukemia patients with persistent leukemia after a course of induction therapy with cytarabine and idarubicin. J Clin Oncol; 2009 May 20;27(15_suppl):7073

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Etoposide and mitoxantrone in newly diagnosed acute myeloid leukemia patients with persistent leukemia after a course of induction therapy with cytarabine and idarubicin.
  • : 7073 Background: The goal of induction chemotherapy in acute myeloid leukemia (AML) is complete remission with restoration of normal bone marrow.
  • If residual leukemia is present after the first course of induction therapy, patients receive a second course identical to the first or receive a non-cross resistant antileukemic regimen.
  • METHODS: In a retrospective study of adult patients with newly-diagnosed AML treated at the University of Pittsburgh Cancer Institute between December 2002 and May 2008, we evaluated the efficacy and toxicity of mitoxantrone (10 mg/m<sup>2</sup>/d) and etoposide (100 mg/m<sup>2</sup>/d), both administered intravenously within 5 days as second course therapy of patients not responding to first-course induction therapy with cytarabine and idarubicin.
  • RESULTS: 74 AML patients (mean age 56 years, range: 18-73 years) completed treatment with etoposide and mitoxantrone; 29 (39%) achieved CR.
  • CONCLUSIONS: Our study suggests that the combination of etoposide and mitoxantorne is an active and well-tolerated regimen as second-course therapy in newly diagnosed AML patients who have persistent leukemia after a first course of induction therapy with cytarabine and idarubicin.

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  • (PMID = 27961456.001).
  • [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. Bloomfield CD: Importance of genetic heterogeneity in curing adult acute leukemia (AL). J Clin Oncol; 2009 May 20;27(15_suppl):s1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Importance of genetic heterogeneity in curing adult acute leukemia (AL).
  • : s1 Forty-five years ago adult AL was incurable.
  • Publication of the French-American-British classification 34 years ago resulted in acceptance that morphology and cytochemistry separated AL into two different diseases, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), that required separate treatment.
  • During the next 15-20 years the importance of cytogenetics in dissecting ALL and AML into entities requiring different therapies became widely accepted, resulting in 2001 in their first incorporation into the World Health Organization (WHO) classification of AL.
  • The most striking example of increased curability of AL is acute promyelocytic leukemia, in which targeted therapy combined with chemotherapy has increased survival from a 2-week median to an 80% cure rate.
  • Recognition of increased sensitivity of a genetic subtype of AML to high-dose cytarabine (HiDAC) has increased the cure rate of core-binding factor (CBF) AML from <10%-25% to 55%-60%.
  • Recent discovery of the adverse impact of KIT mutations in CBF AML may allow the addition of tyrosine kinase inhibitors to HiDAC to substantially further increase cure.
  • Among adult de novo AML 40%-45% are cytogenetically normal (CN); the striking molecular heterogeneity of CN-AML is now being recognized and promises to allow individualized approaches that improve substantially upon the current cure rate of 40%.
  • In adult ALL the major adverse subgroup has a Philadelphia chromosome (PH+).
  • New molecularly targeted approaches are allowing remissions in over 90% of PH+ elderly patients and appear likely to substantially cure an increasing fraction of younger PH+ adults.
  • New approaches to studying the leukemia genome and epigenome should improve our understanding of AL heterogeneity, identify new therapeutic targets, and allow the cure of most patients.

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  • (PMID = 27962366.001).
  • [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. Shepard RC, Talluto CC, Jacob G: Phase I study results of nanomolecular liposomal annamycin in refractory ALL. J Clin Oncol; 2009 May 20;27(15_suppl):7066

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7066 Background: There continues to be no effective second-line therapy for refractory AML or ALL and the cure rate with current therapy has not significantly improved in decades.
  • The first-line therapy for adult AML has remained the same 7 + 3 that it was a generation ago.
  • CONCLUSIONS: Nanomolecular liposomal annamycin appears to be effective through its innate resistance to MDR even as a single agent in refractory adult ALL.
  • We are now testing it in a phase I study in children and young adults with refractory ALL or AML.

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  • (PMID = 27961442.001).
  • [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. Pemmaraju N, Kantarjian H, Ravandi F, O'Brien S, Wierda W, Thomas D, Garcia-Manero G, Borthakur G, Pierce S, Cortes J: Acute myeloid leukemia (AML) in adolescents and young adults (AYA): The M. D. Anderson Cancer Center (MDACC) experience. J Clin Oncol; 2009 May 20;27(15_suppl):7051

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia (AML) in adolescents and young adults (AYA): The M. D. Anderson Cancer Center (MDACC) experience.
  • : 7051 Background: AML is a heterogeneous group of hematopoietic neoplasms demonstrating clonal proliferation of myeloid precursors and is typically a disease of older adults.
  • Little is known about outcomes of AYA with AML.
  • METHODS: We retrospectively analyzed all patients (pts) with AML treated at MDACC from 1965 to 2008.
  • RESULTS: Among 3,934 adult AML pts treated during this period, 163 pts (4%) were AYA with median age of 19 yrs.
  • This cohort included 27 (17%) pts with Core Binding Factor (CBF)-AML [inv(16), t(8:21)] and 19 pts (12%) with acute promyelocytic leukemia (APL).
  • Complete remission (CR) rates were 89% for CBF AML, 79% for APL, and 75% for all other pts.
  • Outcome is better for pts with CBF leukemia (3 yr survival 56%, sustained CR 49%) and APL (3 yr survival 51%, sustained CR 36%) compared to other AML (3 yr survival 28%, sustained CR 24%).
  • To compare outcomes of AYA with older adults, we focused on those with diploid cytogenetics.CR for pts ages 16-21 was 81%, with 3 yr survival of 46%; for ages 22-45, CR was 75% and 3 yr survival 36%; for ages 46-60 CR was 68% with 3 yr survival 28%; and for pts age greater than 60, CR was 54% with 3 yr survival of 22%.
  • CONCLUSIONS: The outcome of AYA pts with AML is significantly better than for older adults with AML.
  • Despite the advances in treatments over time, there is still significant room for improvement, particularly among those AYA with AML other than CBF and APL.

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  • (PMID = 27961415.001).
  • [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. 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.
  • METHODS: Adult patients with MDS or AML and ECOG status 0-2 were treated with 7 consecutive daily SC doses of 75 mg/m<sup>2</sup> AZA during their first treatment cycle.

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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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20. Giles FJ, O'Brien S, Rizzieri DA, Vey N, Krug U, Sekeres M, Jacobsen TF, Nilsson BI, Staudacher K: A phase II study with CP-4055 in patients with second salvage AML. J Clin Oncol; 2009 May 20;27(15_suppl):7047

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study with CP-4055 in patients with second salvage AML.
  • The aim of this study was to assess efficacy and safety of CP-4055 when given as second salvage therapy to patients (pts) with acute myeloid leukemia (AML).
  • METHODS: Adult pts who received two previous chemotherapy regimens and who had refractory/relapsed AML (CR after first salvage therapy lasting less than 6 months) were enrolled.
  • Clinical activity (IWG criteria for AML), 2 CR (1 with no CR1 or CR2), and 1 CRp (CR rate 15%), were reported.
  • CONCLUSIONS: CP-4055 given as second salvage therapy to AML pts show manageable toxicity when administered at 2,000 mg/m<sup>2</sup>/d, 24 h CIV, in a d1-5 q3w schedule.
  • Clinical activity (2 CR and 1 CRp) has been reported among the first 20 late stage AML pts.

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  • (PMID = 27961426.001).
  • [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. Marcucci G, Maharry K, Whitman SP, Paschka P, Baldus CD, Langer C, Mrózek K, Kolitz JE, Larson RA, Bloomfield CD, Cancer and Leukemia Group B (CALGB): Improving the molecular risk classification for younger (&lt;60 years) de novo cytogenetically normal acute myeloid leukemia (CN AML) patients (pts). J Clin Oncol; 2009 May 20;27(15_suppl):7002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improving the molecular risk classification for younger (<60 years) de novo cytogenetically normal acute myeloid leukemia (CN AML) patients (pts).
  • : 7002 Background: CN AML pts are currently stratified into Low-risk [FLT3-ITD negative (neg)/NPM1 mutated (mut)] and High-risk [FLT3-ITD positive (pos) or NPM1 wild type (wt)] groups (FLT3-ITD/NPM1-only classification).
  • Here, we assess if adding CEBPA and WT1 mutation and ERG expression testing improves the currently used CN AML molecular risk classification.
  • METHODS: FLT3, NPM1, CEBPA and WT1 mutations and ERG and BAALC expression were tested at diagnosis in 143 CN AML adults enrolled on CALGB treatment protocols 9621 and 19808.
  • CONCLUSIONS: Prognostic classification of younger de novo CN AML pts is improved by adding CEBPA and WT1 mutation and ERG expression testing.

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  • (PMID = 27961374.001).
  • [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. Schwind S, Marcucci G, Maharry K, Radmacher MD, Whitman SP, Paschka P, Mrózek K, Kolitz JE, Larson RA, Bloomfield CD, Cancer and Leukemia Group B (CALGB): MicroRNA 181a (miR-181a) expression as a prognosticator in cytogenetically normal acute myeloid leukemia (CN AML). J Clin Oncol; 2009 May 20;27(15_suppl):7001

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA 181a (miR-181a) expression as a prognosticator in cytogenetically normal acute myeloid leukemia (CN AML).
  • : 7001 Background: We showed recently that CEBPA mutations (mut) in CN AML are associated with better outcome and a unique microRNA expression profile, including miR-181a upregulation.
  • METHODS: We analyzed 187 de novo CN AML adult patients (pts) aged <60 years (y; median 45) similarly treated on CALGB 9621 and 19808.
  • Of these, 122 had molecular high risk [FLT3-ITD or NPM1 wild type (wt)] and 65 low risk (no FLT3-ITD, NPM1 mut) CN AML.
  • CONCLUSIONS: miR-181a expression is a prognostic marker in CN AML, mainly in the molecular high risk group, where it predicts outcome independently of other variables including CEBPA mutations.
  • As miR-181a↑ confer better treatment response, novel approaches increasing miR-181a levels might benefit not only CN but also other AML pts.

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  • (PMID = 27961373.001).
  • [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. Fernandez HF, Sun Z, Litzow MR, Luger SM, Paietta EM, Dewald G, Ketterling RP, Rowe JM, Lazarus HM, Tallman MS: A randomized trial of anthracycline dose intensification during induction of younger patients with acute myeloid leukemia: Results of Eastern Cooperative Oncology Group study E1900. J Clin Oncol; 2009 May 20;27(15_suppl):7003

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A randomized trial of anthracycline dose intensification during induction of younger patients with acute myeloid leukemia: Results of Eastern Cooperative Oncology Group study E1900.
  • : 7003 Background: In younger adults with newly diagnosed acute myeloid leukemia (AML), anthracycline dose intensification during induction may improve complete remission (CR) rates; however, an improvement in overall survival (OS) in a randomized trial has not been demonstrated.
  • METHODS: Adult patients with previously untreated AML were randomized to receive either SDD (45 mg/m<sup>2</sup>/d) or HDD (90 mg/m<sup>2</sup>/d) each for 3days combined with standard-dose cytarabine (100 mg/m<sup>2</sup>/d) for 7 days by continuous intravenous infusion.
  • In younger AML patients a higher dose of anthracycline in induction should be considered the new standard of care.

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  • (PMID = 27961375.001).
  • [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. Fang YH, Liu HX, Tong CR: [Long-term survival analysis in 89 adult patients with acute myeloid leukemia of fusion gene aml1/eto positive]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2009 Jun;17(3):750-5
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  • [Title] [Long-term survival analysis in 89 adult patients with acute myeloid leukemia of fusion gene aml1/eto positive].
  • This study was aimed to investigate various factors influencing long-term survival in adult AML patients with fusion gene aml1/eto positive.
  • A single institutional retrospective study with long-term follow-up was performed to better define the prognostic factors for AML patients with aml1/eto positive.
  • Newly diagnosed 89 adult AML patients with aml1/eto positive were followed up for 1 to 42 months (median 24 months) from January 2004 to July 2008.
  • Univariate and multivariate analysis of potential factors influencing survival and prognosis were carried out by using Log-Rank and Cox regression method, including sex, age, initial WBC counts, extramedullary leukemic disease, central nervous system leukemia (CNSL), chromosome aberrations, immunophenotype, first induction regimen, chemotherapy course to complete remission (CR), time from induction therapy to CR, negative or positive rate of aml1/eto and allogeneic hematopoietic stem cell transplantation and so on.
  • It is concluded that Chinese adult AML patients with fusion gene aml1/eto positive have some different characteristics as compared with patients from other countries, a relatively poor outcome is observed in patients, HSCT should be recommended to adult AML patients.

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  • (PMID = 19549401.001).
  • [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 / AML1-ETO fusion protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion
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25. Xu X, Talbott EO, Zborowski JV, Rager JR: Cigarette smoking and the risk of adult leukemia: results from the Three Mile Island cohort study. Arch Environ Occup Health; 2007;62(3):131-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cigarette smoking and the risk of adult leukemia: results from the Three Mile Island cohort study.
  • Smoking is an unconfirmed risk factor for the development of leukemia.
  • The authors identified all incident leukemia cases through the Pennsylvania Department of Health Cancer Registry.
  • They used the Cox proportional hazards model to evaluate the relationships and observed 42 incident leukemia cases, including 15 acute myeloid leukemia (AML) cases, in the cohort.
  • After controlling for other confounding factors, the authors found current smoking to be associated with an increased risk of adult AML (relative risk = 3.47; 95% confidence interval = 1.002-11.99).
  • The authors also observed a marginally significant linear trend of risk of AML associated with the number of years smoked (p = .06).
  • The results from this study suggested that cigarette smoking was associated with an increased risk of adult AML.
  • [MeSH-major] Leukemia / etiology. Smoking / adverse effects
  • [MeSH-minor] Adult. Cohort Studies. Confounding Factors (Epidemiology). Dose-Response Relationship, Drug. Female. Humans. Leukemia, Myeloid, Acute / etiology. Male. Middle Aged. Pennsylvania / epidemiology. Proportional Hazards Models. Registries. Risk Assessment. Risk Factors

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  • (PMID = 18400653.001).
  • [ISSN] 1933-8244
  • [Journal-full-title] Archives of environmental & occupational health
  • [ISO-abbreviation] Arch Environ Occup Health
  • [Language] eng
  • [Grant] United States / NCATS NIH HHS / TR / UL1 TR000005
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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26. Bruserud Ø, Stapnes C, Tronstad KJ, Ryningen A, Anensen N, Gjertsen BT: Protein lysine acetylation in normal and leukaemic haematopoiesis: HDACs as possible therapeutic targets in adult AML. Expert Opin Ther Targets; 2006 Feb;10(1):51-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Protein lysine acetylation in normal and leukaemic haematopoiesis: HDACs as possible therapeutic targets in adult AML.
  • Several new therapeutic strategies are now considered for acute myelogenous leukaemia (AML), including modulation of protein lysine acetylation through inhibition of histone deacetylases (HDACs): a large group of enzymes that alters the acetylation and, thereby, the function of a wide range of nuclear and cytoplasmic proteins.
  • The only HDAC inhibitors that have been investigated in clinical studies of AML are butyrate derivatives, valproic acid and depsipeptide.
  • In the first studies, the drugs have usually been used as continuous therapy for several weeks or months, and in most studies the drugs were used alone or in combination with all-trans retinoic acid for treatment of patients with relapsed or primary resistant AML.
  • Complete haematological remission lasting for several months has been reported for a few patients (< 5% of included patients), whereas increased peripheral blood platelet counts seem more common and have been described both for patients with AML and myelodysplastic syndromes.
  • Taken together, these studies suggest that HDAC inhibition can mediate antileukaemic effects in AML, but for most patients the clinical benefit seems limited and further studies of combination therapy are required.
  • [MeSH-major] Drug Delivery Systems / methods. Hematopoiesis / drug effects. Histone Deacetylases / metabolism. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / enzymology. Lysine / metabolism
  • [MeSH-minor] Acetylation / drug effects. Adult. Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Histone Deacetylase Inhibitors. Humans

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  • (PMID = 16441228.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; EC 3.5.1.98 / Histone Deacetylases; K3Z4F929H6 / Lysine
  • [Number-of-references] 136
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27. Li Y, Moysich KB, Baer MR, Weiss JR, Brasure J, Graham S, McCann SE: Intakes of selected food groups and beverages and adult acute myeloid leukemia. Leuk Res; 2006 Dec;30(12):1507-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intakes of selected food groups and beverages and adult acute myeloid leukemia.
  • Few studies have explored the association between diet and adult acute myeloid leukemia (AML).
  • In a hospital-based case-control study among 111 cases and 439 controls, AML risk was negatively associated with milk intake among women (OR 0.25, 95% CI 0.08-0.73) and tea (OR 0.50, 95% CI 0.23-1.09), and positively associated among women with beer (OR 2.48, 95% CI 1.05-5.85), wine (OR 2.32, 95% CI 1.05-5.09), and beef (OR 4.78, 95% CI 1.35-16.94).
  • Our findings support a role of diet in adult AML; however, further research is needed to explore gender differences in risk.
  • [MeSH-major] Beverages. Diet. Eating. Food Preferences. Leukemia, Myeloid / etiology. Leukemia, Myeloid / prevention & control
  • [MeSH-minor] Acute Disease. Case-Control Studies. Enzyme Inhibitors / adverse effects. Female. Humans. Male. Middle Aged. Risk Factors. Topoisomerase II Inhibitors. United States / epidemiology

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  • (PMID = 16678899.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Topoisomerase II Inhibitors
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28. Damiani D, Tiribelli M, Michelutti A, Geromin A, Cavallin M, Fabbro D, Pianta A, Malagola M, Damante G, Russo D, Fanin R: Fludarabine-based induction therapy does not overcome the negative effect of ABCG2 (BCRP) over-expression in adult acute myeloid leukemia patients. Leuk Res; 2010 Jul;34(7):942-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fludarabine-based induction therapy does not overcome the negative effect of ABCG2 (BCRP) over-expression in adult acute myeloid leukemia patients.
  • Over-expression of multidrug resistance (MDR) proteins PGP and BCRP has a negative prognostic impact in acute myeloid leukemia (AML) patients.
  • We investigated the role of BCRP in 138 adult AML patients receiving induction therapy with fludarabine.
  • [MeSH-major] ATP-Binding Cassette Transporters / physiology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm / drug effects. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / drug therapy. Neoplasm Proteins / physiology. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Male. Middle Aged. Multidrug Resistance-Associated Proteins / physiology. P-Glycoprotein / physiology. Remission Induction. Young Adult

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20122734.001).
  • [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 / ABCG2 protein, human; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 0 / P-Glycoprotein; 0 / multidrug resistance-associated protein 1; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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29. Owen C, Fitzgibbon J, Paschka P: The clinical relevance of Wilms Tumour 1 (WT1) gene mutations in acute leukaemia. Hematol Oncol; 2010 Mar;28(1):13-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinical relevance of Wilms Tumour 1 (WT1) gene mutations in acute leukaemia.
  • Recurrent genetic aberrations are important predictors of outcome in acute myeloid leukaemia (AML).
  • WT1 mutations occur in approximately 10% of adult AML patients at diagnosis and are most frequent in the cytogenetically normal (CN) AML subgroup.
  • Herein, we discuss the importance of WT1 mutations in AML.

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  • (PMID = 20013787.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] ENG
  • [Grant] United Kingdom / Medical Research Council / / G0700052; United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / WT1 Proteins
  • [Number-of-references] 75
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30. Jabbour EJ, Estey E, Kantarjian HM: Adult acute myeloid leukemia. Mayo Clin Proc; 2006 Feb;81(2):247-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is a group of several different diseases, the treatment and outcome of which depend on several factors, including leukemia karyotype, patient age, and comorbid conditions.
  • Despite advances in understanding the molecular biology of AML, its treatment remains challenging.
  • Such targeted therapies offer the promise of better antileukemic activity in adult AML.
  • [MeSH-major] Leukemia, Myeloid / therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Anthracyclines / therapeutic use. Antineoplastic Agents / therapeutic use. Humans. Immunosuppressive Agents / therapeutic use. Middle Aged. Risk Factors

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  • [ErratumIn] Mayo Clin Proc. 2006 Apr;81(4):569
  • (PMID = 16471082.001).
  • [ISSN] 0025-6196
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents
  • [Number-of-references] 161
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31. Laane E, Derolf AR, Björklund E, Mazur J, Everaus H, Söderhäll S, Björkholm M, Porwit-MacDonald A: The effect of allogeneic stem cell transplantation on outcome in younger acute myeloid leukemia patients with minimal residual disease detected by flow cytometry at the end of post-remission chemotherapy. Haematologica; 2006 Jun;91(6):833-6
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  • [Title] The effect of allogeneic stem cell transplantation on outcome in younger acute myeloid leukemia patients with minimal residual disease detected by flow cytometry at the end of post-remission chemotherapy.
  • Minimal residual disease (MRD) levels were determined by multi-parameter flow cytometry in 45 younger adult patients ( pound60 years old) with acute myeloid leukemia (AML) in complete remission.
  • Therefore allogeneic SCT should be considered in younger adult AML patients with detectable MRD at the end of post-remission chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid / therapy. Neoplasm, Residual / therapy. Stem Cell Transplantation
  • [MeSH-minor] Acute Disease. Adult. Blast Crisis / pathology. Bone Marrow Cells / pathology. Flow Cytometry. Humans. Retrospective Studies. Transplantation, Homologous

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  • [CommentIn] Haematologica. 2006 Dec;91(12 Suppl):ELT14; author reply ELT15 [17194674.001]
  • (PMID = 16769587.001).
  • [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 / Antineoplastic Agents
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32. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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.
  • In newly diagnosed cases, we found that childhood ALL samples showed higher IC50 values of dnr (0.040 +/- 2.320) compared to adult AML samples (0.021 +/- 0.158).
  • In contrast, newly diagnosed adult AML samples showed higher IC50 values of ara-C (0.157 +/- 0.529) compared to childhood ALL samples (0.100 +/- 2.350).
  • In relapsed cases, two samples of childhood ALL showed IC50 values of dnr (0.910 +/- 1.760) and ara-C (1.310 +/- 2.390), which was higher compared to childhood AML samples (0.129 +/- 0.214 and 0.210 +/- 0.003, respectively).
  • 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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33. Leslie M, Case MC, Hall AG, Coulthard SA: Expression levels of asparagine synthetase in blasts from children and adults with acute lymphoblastic leukaemia. Br J Haematol; 2006 Mar;132(6):740-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression levels of asparagine synthetase in blasts from children and adults with acute lymphoblastic leukaemia.
  • L-asparaginase is active in the treatment of acute lymphoblastic leukaemia (ALL) through the depletion of serum asparagine.
  • Here we report that median asparagine synthetase (AS) mRNA levels were higher in acute myeloid leukaemia (AML) than ALL blasts in both children and adults, with intermediate levels in normal peripheral blood mononuclear cells (NPBMC).
  • NPBMC versus child ALL (Tukeys multiple comparison test, P < 0.05); child ALL versus child AML (P < 0.001) and adult ALL versus adult AML (P < 0.01) were all significant and support the hypothesis that selectivity to treatment with l-asparaginase is due, at least in part, to lower AS expression.
  • [MeSH-major] Aspartate-Ammonia Ligase / analysis. Lymphocytes / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Cell Line, Tumor. Child. Child, Preschool. Female. Humans. Infant. Leukemia, Myeloid / enzymology. Leukocytes, Mononuclear / enzymology. Male. Middle Aged. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 16487174.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 6.3.1.1 / Aspartate-Ammonia Ligase
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34. Majeti R, Chao MP, Alizadeh AA, Pang WW, Jaiswal S, Gibbs KD Jr, van Rooijen N, Weissman IL: CD47 is an adverse prognostic factor and therapeutic antibody target on human acute myeloid leukemia stem cells. Cell; 2009 Jul 23;138(2):286-99
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  • [Title] CD47 is an adverse prognostic factor and therapeutic antibody target on human acute myeloid leukemia stem cells.
  • Acute myeloid leukemia (AML) is organized as a cellular hierarchy initiated and maintained by a subset of self-renewing leukemia stem cells (LSC).
  • We hypothesized that increased CD47 expression on human AML LSC contributes to pathogenesis by inhibiting their phagocytosis through the interaction of CD47 with an inhibitory receptor on phagocytes.
  • We found that CD47 was more highly expressed on AML LSC than their normal counterparts, and that increased CD47 expression predicted worse overall survival in three independent cohorts of adult AML patients.
  • Furthermore, blocking monoclonal antibodies directed against CD47 preferentially enabled phagocytosis of AML LSC and inhibited their engraftment in vivo.
  • Finally, treatment of human AML LSC-engrafted mice with anti-CD47 antibody depleted AML and targeted AML LSC.
  • In summary, increased CD47 expression is an independent, poor prognostic factor that can be targeted on human AML stem cells with blocking monoclonal antibodies capable of enabling phagocytosis of LSC.
  • [MeSH-major] Antigens, CD47 / immunology. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Phagocytosis

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  • [Cites] J Immunol. 2005 Feb 15;174(4):2004-11 [15699129.001]
  • [Cites] N Engl J Med. 1999 Sep 30;341(14):1051-62 [10502596.001]
  • [Cites] Nat Biotechnol. 2005 Sep;23(9):1147-57 [16151408.001]
  • [Cites] Trends Cell Biol. 2005 Sep;15(9):494-501 [16084092.001]
  • [Cites] JAMA. 2005 Sep 21;294(11):1359-66 [16174694.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2548-56 [16291597.001]
  • [Cites] Nat Rev Immunol. 2006 Jun;6(6):457-64 [16691243.001]
  • [Cites] N Engl J Med. 2006 Sep 21;355(12):1253-61 [16990388.001]
  • [Cites] Nat Med. 2006 Oct;12(10):1167-74 [16998484.001]
  • [Cites] Lancet. 2006 Nov 25;368(9550):1894-907 [17126723.001]
  • [Cites] J Immunol. 2006 Dec 15;177(12):8550-9 [17142753.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Curr Opin Immunol. 2007 Apr;19(2):239-45 [17291742.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 20;104(12):5062-6 [17360380.001]
  • [Cites] Oncol Rep. 2007 May;17(5):1189-94 [17390064.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jun 26;104(26):11008-13 [17576927.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2659-66 [17609428.001]
  • [Cites] Nat Immunol. 2007 Dec;8(12):1313-23 [17982459.001]
  • [Cites] Cell Stem Cell. 2007 Dec 13;1(6):635-45 [18371405.001]
  • [Cites] Blood. 2008 May 1;111(9):4490-5 [18309032.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] Blood. 2008 May 15;111(10):5078-85 [18337557.001]
  • [Cites] Curr Drug Targets. 2008 Oct;9(10):842-50 [18855618.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4193-201 [18716133.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3396-401 [19218430.001]
  • [Cites] Leuk Res. 2005 Apr;29(4):445-50 [15725479.001]
  • [Cites] Nat Med. 1999 Nov;5(11):1277-84 [10545994.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3633-43 [10572074.001]
  • [Cites] Science. 2000 Jun 16;288(5473):2051-4 [10856220.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7521-6 [10861016.001]
  • [Cites] Leukemia. 2000 Oct;14(10):1777-84 [11021753.001]
  • [Cites] J Exp Med. 2001 Apr 2;193(7):855-62 [11283158.001]
  • [Cites] Trends Cell Biol. 2001 Mar;11(3):130-5 [11306274.001]
  • [Cites] J Immunol. 2001 Sep 1;167(5):2547-54 [11509594.001]
  • [Cites] J Exp Med. 2001 Aug 20;194(4):541-9 [11514609.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Nature. 2003 May 15;423(6937):255-60 [12714970.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Mar 19;315(4):912-8 [14985099.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1617-28 [15084694.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]
  • [Cites] Blood. 1997 Oct 1;90(7):2555-64 [9326221.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [CommentIn] Cell. 2009 Jul 23;138(2):226-8 [19632173.001]
  • (PMID = 19632179.001).
  • [ISSN] 1097-4172
  • [Journal-full-title] Cell
  • [ISO-abbreviation] Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009302; United States / NIAID NIH HHS / AI / T32 AI007290; United States / NCI NIH HHS / CA / R01 CA086017-07; United States / NCI NIH HHS / CA / R01 CA086017-06; United States / NCI NIH HHS / CA / R01 CA086017; United States / NCI NIH HHS / CA / R01CA86017; United States / NCI NIH HHS / CA / R01 CA086017-08; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / R01 CA086017-09; United States / NCI NIH HHS / CA / R01 CA086017-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD47; 0 / Ptpns1 protein, mouse; 0 / Receptors, Immunologic
  • [Other-IDs] NLM/ NIHMS122682; NLM/ PMC2726837
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35. Bhushan B, Chauhan PS, Saluja S, Verma S, Mishra AK, Siddiqui S, Kapur S: Aberrant phenotypes in childhood and adult acute leukemia and its association with adverse prognostic factors and clinical outcome. Clin Exp Med; 2010 Mar;10(1):33-40
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  • [Title] Aberrant phenotypes in childhood and adult acute leukemia and its association with adverse prognostic factors and clinical outcome.
  • Occurrence of aberrant phenotypes in childhood and adult acute leukemia (AL) differs considerably in independent studies and their association with prognostic factors is still controversial.
  • In the present study, 214 patients with AL (106 children and 108 adults) were evaluated for the aberrant expression of CD33 in ALL (B cell and T cell) and CD3, CD5, CD7, and CD19 in AML.
  • In B-ALL, aberrant expression of CD33 was found in 39 and 23% cases of adult and children, respectively.
  • In T-ALL, CD33 was seen in 33% cases of adults while in children CD33 was not observed.
  • In AML, aberrant expression of CD19 was expressed in 52 and 32% while CD7 was expressed in 14 and 15% cases of childhood and adult AML, respectively.
  • One adult patient (AML-M5) showed expression of CD3, CD5, and CD19.
  • In summary, aberrant phenotype was commonly seen in adults than childhood B-ALL while in AML, aberrant phenotype was more common in children than adults.
  • CD19 was most commonly expressed antigen followed by CD7 in both childhood and adult AML.
  • Interestingly, aberrant phenotype was not found in childhood T-ALL; however, it was seen in 33% cases of adults.
  • We did not find any association of aberrant phenotype with adverse prognosis factors, CD34 marker, and clinical outcome except the absence of auer rod which was found to be significantly associated with aberrant phenotype of childhood AML (P = 0.01).
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Adult. Antigens, CD / biosynthesis. Child. Child, Preschool. Female. Humans. Infant. Infant, Newborn. Male. Phenotype. Prognosis. Treatment Outcome. Young Adult

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  • (PMID = 19779962.001).
  • [ISSN] 1591-9528
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD
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36. Jamroziak K, Balcerczak E, Cebula B, Janus A, Mirowski M, Robak T: No influence of 3435C&gt;T ABCB1 (MDR1) gene polymorphism on risk of adult acute myeloid leukemia and P-glycoprotein expression in blast cells. Ther Drug Monit; 2006 Oct;28(5):707-11
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  • [Title] No influence of 3435C>T ABCB1 (MDR1) gene polymorphism on risk of adult acute myeloid leukemia and P-glycoprotein expression in blast cells.
  • Inherited differences in xenobiotic transport and metabolism may play an important role in the development of adult acute myeloid leukemia (AML) and response to the chemotherapy.
  • The aim of this study was to investigate the potential involvement of the ABCB1 gene exon 26 3435C>T single nucleotide polymorphism (SNP) in the genetic susceptibility to AML and regulation of P-gp expression and activity in AML cells.
  • A total of 180 adult AML patients and 180 sex-matched controls were genotyped using PCR-RFLP method.
  • Moreover, in 40 AML patients ABCB1 gene expression was studied by real-time RT-PCR and P-gp expression and activity were assessed by flow cytometry assays.
  • The authors conclude that isolated 3435C>T ABCB1 SNP is not a major factor of the genetic susceptibility to adult AML, and that genotyping of this polymorphism does not allow predicting P-gp expression or activity in AML cells.
  • [MeSH-major] Leukemia, Myeloid / genetics. Organic Anion Transporters / genetics. P-Glycoprotein / genetics
  • [MeSH-minor] Adult. Aged. Case-Control Studies. Female. Genotype. Humans. Male. Middle Aged. P-Glycoproteins. Polymorphism, Genetic

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  • (PMID = 17038891.001).
  • [ISSN] 0163-4356
  • [Journal-full-title] Therapeutic drug monitoring
  • [ISO-abbreviation] Ther Drug Monit
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Organic Anion Transporters; 0 / P-Glycoprotein; 0 / P-Glycoproteins
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37. Guan LJ, Zhang JH, Wang YX, Zhang N, Hu YP, Li ZG, Zhao W: [Expression of ubiquitin associated protein 1 gene and tumor-suppressor gene p16 in acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Oct;18(5):1119-23
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  • [Title] [Expression of ubiquitin associated protein 1 gene and tumor-suppressor gene p16 in acute leukemia].
  • In order to investigate the expression and the relationship of ubiquitin associated protein 1 (ubap1) gene and tumor-suppressor gene p16 in acute leukemia, 68 cases of acute leukemia and 22 control cases were selected in this experiment, FQ-PCR technique was used to detect the mRNA expression level of ubap1 gene and p16 gene in their bone marrow cells.
  • The results showed that as compared with the control group, the ubap1 gene in acute leukemia group highly expressed (p<0.01), while the p16 gene lowly expressed (p<0.01).
  • But grouping of patients according to FAB revealed that as compared with the control group, the ubap1 gene expression displayed statistical difference only in M4 and M5 of adult AML (p<0.05), while the p16 gene expression in all groups of adult AML showed significant difference (p<0.05) except M1 and M2.
  • It is concluded that the upregulation of ubap1 gene expression mainly and the downregulation of p16 gene expression mainly may simultaneously participate in the pathogenesis of acute leukemia.
  • High expression of ubap1 gene influences the M4 and M5 subtypes in AML.

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  • (PMID = 21129243.001).
  • [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 / Carrier Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Messenger; 0 / UBAP1 protein, human
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38. Velardi A, Ruggeri L, Mancusi A, Aversa F, Christiansen FT: Natural killer cell allorecognition of missing self in allogeneic hematopoietic transplantation: a tool for immunotherapy of leukemia. Curr Opin Immunol; 2009 Oct;21(5):525-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Natural killer cell allorecognition of missing self in allogeneic hematopoietic transplantation: a tool for immunotherapy of leukemia.
  • Donor-versus-recipient natural killer (NK) cell alloreactivity has been established as a key therapeutic element in HLA haplotype mismatched hematopoietic transplants in adult AML and pediatric ALL and as a possible beneficial effector in cord blood transplant for AML.
  • At present NK cell allotherapy for leukemia is deployed through stem cell transplantation (and ensuing NK cell reconstitution) across KIR ligand mismatches.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Killer Cells, Natural / immunology. Leukemia, Myeloid / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Acute Disease. Adult. Child. Humans. Immunotherapy / methods. Transplantation, Homologous

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  • (PMID = 19717293.001).
  • [ISSN] 1879-0372
  • [Journal-full-title] Current opinion in immunology
  • [ISO-abbreviation] Curr. Opin. Immunol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 PO1 CA100265
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 46
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39. Ahmad EI, Gawish HH, Al-Azizi NM, El-Hefni AM: The Prognostic Impact of K-RAS Mutations in Adult Acute Myeloid Leukemia Patients Treated with High Dose Cytarabine. J Egypt Natl Canc Inst; 2009 Dec;21(4):343-50

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Prognostic Impact of K-RAS Mutations in Adult Acute Myeloid Leukemia Patients Treated with High Dose Cytarabine.
  • It represents one of the most common genetic alterations in acute myeloid leukemia (AML).
  • However there is still controversy about its clinical relevance on the treatment outcome of this leukemia.
  • OBJECTIVE: This study aimed to clarify the biologic and prognostic impact of K-RAS mutations in relation to the dose of cytarabine (ara-C) used in post induction consolidation chemotherapy in adult AML patients.
  • PATIENTS AND METHODS: The study comprised 71de novo AML patients with a male: Female ratio of 1.4: 1; their ages ranged from 21-59 years with a median of 37 years.
  • The M4 subtype of AML and cases with Inv 16 showed significantly higher frequencies in mutRAS compared to wtRAS patients, (p=0.015, 0.003, respectively).
  • CONCLUSION: Adult AML patients carrying mutations in the K-RAS gene benefit from higher cytarabine doses more than wtRAS patients, so pretreatment mutation detection could be an important predictor for treatment strategy and survival of adult AML patients.
  • KEY WORDS: K-RAS mutations - Acute myeloid leukemia - Cytarabine.

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  • (PMID = 21415871.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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40. Bullinger L, Ehrich M, Döhner K, Schlenk RF, Döhner H, Nelson MR, van den Boom D: Quantitative DNA methylation predicts survival in adult acute myeloid leukemia. Blood; 2010 Jan 21;115(3):636-42
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  • [Title] Quantitative DNA methylation predicts survival in adult acute myeloid leukemia.
  • Acute myeloid leukemia (AML) is characterized by molecular heterogeneity that is not fully reflected in the current classification system.
  • Therefore, we investigated the prognostic impact of DNA methylation in AML.
  • To screen for promoter methylation in AML we applied a combination of base-specific cleavage biochemistry and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS), a powerful methodology allowing for quantitatively investigating DNA methylation status in a large series of both promoter regions and leukemia samples.
  • We analyzed 92 genomic regions in 182 patient samples, correlated findings with clinical and molecular data, and validated the results in an independent cohort of 74 AML samples.
  • Using this approach, we were able to identify novel leukemia subgroups based on distinct DNA methylation patterns.
  • Here, we report the first large-scale methylation-based outcome predictor in AML, and thereby our findings support the use of genomic methylation markers for improved molecular classification and prognostication in adult AML.
  • [MeSH-major] DNA Methylation. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / mortality. Sequence Analysis, DNA / methods
  • [MeSH-minor] Adult. Chromosomes, Human, Pair 17. CpG Islands / genetics. Cytogenetic Analysis / methods. DNA, Neoplasm / analysis. Gene Expression Profiling / methods. Humans. Multivariate Analysis. Oligonucleotide Array Sequence Analysis / methods. Prognosis. Promoter Regions, Genetic / genetics. Survival Analysis


41. Grandics P: Complete remission achieved in a case of both primary and recurrent adult acute myelogeneous leukemia by a novel nutritional therapy. J Altern Complement Med; 2006 Apr;12(3):311-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete remission achieved in a case of both primary and recurrent adult acute myelogeneous leukemia by a novel nutritional therapy.
  • OBJECTIVES: The aim of this study was to determine the possible clinical benefit of molasses-based dietary compositions (designated as MSQ 13, MSQ 15, and MSQ 18) in a case of both primary and recurrent adult AML.
  • OUTCOME MEASURES: Clinical improvement and regression of AML were the outcome measures.
  • CONCLUSIONS: Treatment with the MSQ dietary compositions resulted in disease regression and the reversal of clinical manifestations over two episodes of AML.
  • Therefore, further studies are warranted to evaluate the utility of this approach for the clinical management of AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / diet therapy. Molasses. Nutrition Therapy / methods
  • [MeSH-minor] Adult. Female. Humans. Remission Induction. Treatment Outcome

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  • (PMID = 16646731.001).
  • [ISSN] 1075-5535
  • [Journal-full-title] Journal of alternative and complementary medicine (New York, N.Y.)
  • [ISO-abbreviation] J Altern Complement Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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42. Kivivuori SM, Siitonen S, Porkka K, Vettenranta K, Alitalo R, Saarinen-Pihkala U: Expression of vascular endothelial growth factor receptor 3 and Tie1 tyrosine kinase receptor on acute leukemia cells. Pediatr Blood Cancer; 2007 Apr;48(4):387-92
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  • [Title] Expression of vascular endothelial growth factor receptor 3 and Tie1 tyrosine kinase receptor on acute leukemia cells.
  • Activation of vascular endothelial growth factor receptor 3 (VEGFR-3) and Tie1 tyrosine kinase receptor are known to promote leukemia cell survival.
  • PROCEDURE: We studied bone marrow samples from 73 patients with acute lymphoblastic (ALL) or myelogenous (AML) leukemia by using immunological methods.
  • RESULTS: Vascular endothelial growth factor receptor 3 expression was found in 15% of the samples, particularly in samples with pediatric lymphoblastic leukemias and monocytic AMLs.
  • Tie1 protein expression was found in 11% of the samples, all of which were from adult AML patients.
  • CONCLUSIONS: Our findings suggest that there are angiogenesis-related differences between pediatric and adult lymphoblastic leukemias as well as between lymphoid and myeloid leukemias.
  • [MeSH-major] Hematopoietic Stem Cells / enzymology. Leukemia, Myeloid / enzymology. Neoplastic Stem Cells / enzymology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Receptor, TIE-1 / analysis. Vascular Endothelial Growth Factor Receptor-3 / analysis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Factors. Antigens, CD / analysis. Antigens, CD34 / analysis. Bone Marrow / pathology. Child. Child, Preschool. Female. Glycoproteins / analysis. Humans. Immunophenotyping. Infant. Leukemia, Monocytic, Acute / enzymology. Leukemia, Monocytic, Acute / pathology. Male. Neovascularization, Pathologic / enzymology. Neovascularization, Pathologic / pathology. Peptides / analysis

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  • (PMID = 16685739.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Glycoproteins; 0 / Peptides; EC 2.7.10.1 / Receptor, TIE-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3
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43. Bedekovics J, Rejto L, Telek B, Udvardy M, Ujfalusi A, Oláh E, Hevessy Z, Kappelmayer J, Kajtár B, Méhes G: [Immunohistochemical demonstration of mutant nucleophosmin in acute myeloid leukemia: biological and clinical features related to NPMc expression]. Orv Hetil; 2009 May 31;150(22):1031-5
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  • [Title] [Immunohistochemical demonstration of mutant nucleophosmin in acute myeloid leukemia: biological and clinical features related to NPMc expression].
  • [Transliterated title] Mutáns nucleophosmin fehérje kimutatása akut myeloid leukaemiában: az NPMc+ AML biológiai és klinikai jellemzôi.
  • The mutation of the nucleophosmin gene (NPM1) is the most frequently occurring genetic aberration in acute myeloid leukemia (AML).
  • Due to the high frequency and the obvious impact on disease outcome, the current WHO classification also defines the new (tentative) entity of "AML with NPM mutation".
  • The present study focused on further biological and clinical characterization of NPMc+ AML determined by histological and cytological preparations of the bone marrow.
  • 41 adult AML cases were investigated in our center between 2005 and 2008, 6/41 cases were presented with cytoplasmic NPM immunostaining (14.6%).
  • All but one were female patients, and were diagnosed as de novo AML with no recurrent cytogenetic aberrations (6/23, 26.1%).
  • In conclusion, immunohistochemistry is well applicable for the identification of NPM mutated AML in the daily hematopathology practice.
  • [MeSH-major] Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Bone Marrow / chemistry. Leukemia, Myeloid, Acute / metabolism. Mutation. Nuclear Proteins / analysis. Nuclear Proteins / genetics

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  • (PMID = 19465351.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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44. Mehta PA, Alonzo TA, Gerbing RB, Elliott JS, Wilke TA, Kennedy RJ, Ross JA, Perentesis JP, Lange BJ, Davies SM, Children's Oncology Group: XPD Lys751Gln polymorphism in the etiology and outcome of childhood acute myeloid leukemia: a Children's Oncology Group report. Blood; 2006 Jan 1;107(1):39-45
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  • [Title] XPD Lys751Gln polymorphism in the etiology and outcome of childhood acute myeloid leukemia: a Children's Oncology Group report.
  • Polymorphisms in XPD, a member of the nucleotide excision repair pathway, have been associated with development of treatment-related acute myeloid leukemia (AML) and with poor outcome of AML in elderly patients.
  • We hypothesized that XPD Lys751Gln polymorphism may play a role in causation of AML in children and, as shown in adults, may affect the outcome of childhood AML therapy.
  • Genotyping of 456 children treated for de novo AML was performed at XPD exon 23.
  • Gene frequencies in AML patients and healthy controls were similar.
  • There were no significant differences in overall survival (P = .82), event-free survival (P = .78), treatment-related mortality (P = .43), or relapse rate (RR) (P = .92) between patients with XPD751AA versus 751AC versus 751CC genotypes, in contrast to reports in adult AML.
  • These data, representing the only data in pediatric AML, suggest that XPD genotype does not affect the etiology or outcome of childhood AML.
  • [MeSH-major] Leukemia, Myeloid / genetics. Polymorphism, Single Nucleotide. Xeroderma Pigmentosum Group D Protein / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Case-Control Studies. Child. Child, Preschool. Female. Gene Frequency. Genetic Testing. Genotype. Humans. Infant. Infant, Newborn. Male. Mutation, Missense. Survival Analysis. Treatment Outcome

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  • (PMID = 16150943.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human
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45. Oliansky DM, Appelbaum F, Cassileth PA, Keating A, Kerr J, Nieto Y, Stewart S, Stone RM, Tallman MS, McCarthy PL Jr, Hahn T: The role of cytotoxic therapy with hematopoietic stem cell transplantation in the therapy of acute myelogenous leukemia in adults: an evidence-based review. Biol Blood Marrow Transplant; 2008 Feb;14(2):137-80
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  • [Title] The role of cytotoxic therapy with hematopoietic stem cell transplantation in the therapy of acute myelogenous leukemia in adults: an evidence-based review.
  • Clinical research examining the role of hematopoietic stem cell transplantation (HSCT) in the therapy of acute myelogenous leukemia (AML) in adults is presented and critically evaluated in this systematic evidence-based review.
  • Treatment recommendations based on the evidence are presented in Table 3, entitled Summary of Treatment Recommendations Made by the Expert Panel for Adult Acute Myelogenous Leukemia, and were reached unanimously by a panel of AML experts.
  • The identified priority areas of needed future research in adult AML include:.
  • (3) What is the impact on survival outcomes of reduced intensity or nonmyeloablative versus conventional conditioning in older (>60 years) and intermediate (40-60 years) aged adults?
  • (4) What is the impact on survival outcomes of unrelated donor HSCT vesus chemotherapy in younger (<40 years) adults with high risk disease?
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy


46. Falini B, Bolli N, Shan J, Martelli MP, Liso A, Pucciarini A, Bigerna B, Pasqualucci L, Mannucci R, Rosati R, Gorello P, Diverio D, Roti G, Tiacci E, Cazzaniga G, Biondi A, Schnittger S, Haferlach T, Hiddemann W, Martelli MF, Gu W, Mecucci C, Nicoletti I: Both carboxy-terminus NES motif and mutated tryptophan(s) are crucial for aberrant nuclear export of nucleophosmin leukemic mutants in NPMc+ AML. Blood; 2006 Jun 1;107(11):4514-23
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  • [Title] Both carboxy-terminus NES motif and mutated tryptophan(s) are crucial for aberrant nuclear export of nucleophosmin leukemic mutants in NPMc+ AML.
  • We recently identified aberrant cytoplasmic expression of nucleophosmin (NPM) as the immunohistochemical marker of a large subgroup of acute myeloid leukemia (AML) (about one-third of adult AML) that is characterized by normal karyotype and mutations occurring at the exon-12 of the NPM gene.
  • All 29 AML-associated mutated NPM alleles so far identified encode abnormal proteins which have acquired at the C-terminus a nuclear export signal (NES) motif and lost both tryptophan residues 288 and 290 (or only the residue 290) which determine nucleolar localization.
  • [MeSH-major] Active Transport, Cell Nucleus / genetics. Leukemia / genetics. Mutation. Nuclear Export Signals / genetics. Nuclear Proteins / genetics. Tryptophan / genetics

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  • (PMID = 16455950.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Export Signals; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; 8DUH1N11BX / Tryptophan
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47. Haslam K, Chadwick N, Kelly J, Browne P, Vandenberghe E, Flynn C, Conneally E, Langabeer SE: Incidence and significance of FLT3-ITD and NPM1 mutations in patients with normal karyotype acute myeloid leukaemia. Ir J Med Sci; 2010 Dec;179(4):507-10
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  • [Title] Incidence and significance of FLT3-ITD and NPM1 mutations in patients with normal karyotype acute myeloid leukaemia.
  • BACKGROUND: Acute myeloid leukaemia (AML) is a heterogeneous clonal disorder of haematopoietic progenitor cells.
  • Approximately half of all adult AML patients have a normal karyotype (NK-AML) and an intermediate risk prognosis.
  • AIMS: To determine the incidence and prognostic significance of NPM1 and FLT3-ITD mutations in a population of patients with NK-AML.
  • METHODS: FLT3-ITD and NPM1 mutation status was retrospectively sought in presentation samples from 44 NK-AML patients.
  • CONCLUSIONS: FLT3-ITD and NPM1 mutation status can be defined in NK-AML.
  • Prospective screening for these mutations is advocated in all NK-AML patients, as the genotype is of clinical importance when considering treatment options including stem cell transplantation.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics. Phosphoproteins / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Electrophoresis, Agar Gel. Female. Genotype. Humans. Male. Middle Aged. Mutation. Prognosis. Retrospective Studies. Seroepidemiologic Studies. XYY Karyotype. Young Adult

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  • (PMID = 20803351.001).
  • [ISSN] 1863-4362
  • [Journal-full-title] Irish journal of medical science
  • [ISO-abbreviation] Ir J Med Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Phosphoproteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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48. Garzon R, Volinia S, Liu CG, Fernandez-Cymering C, Palumbo T, Pichiorri F, Fabbri M, Coombes K, Alder H, Nakamura T, Flomenberg N, Marcucci G, Calin GA, Kornblau SM, Kantarjian H, Bloomfield CD, Andreeff M, Croce CM: MicroRNA signatures associated with cytogenetics and prognosis in acute myeloid leukemia. Blood; 2008 Mar 15;111(6):3183-9
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  • [Title] MicroRNA signatures associated with cytogenetics and prognosis in acute myeloid leukemia.
  • To determine whether miRNAs are associated with cytogenetic abnormalities and clinical features in acute myeloid leukemia (AML), we evaluated the miRNA expression of CD34(+) cells and 122 untreated adult AML cases using a microarray platform.
  • An independent set of 60 untreated AML patients was used to validate the outcome signatures using real-time polymerase chain reaction.
  • We identified several miRNAs differentially expressed between CD34(+) normal cells and the AML samples. miRNA expression was also closely associated with selected cytogenetic and molecular abnormalities, such as t(11q23), isolated trisomy 8, and FLT3-ITD mutations.
  • Furthermore, patients with high expression of miR-191 and miR-199a had significantly worse overall and event-free survival than AML patients with low expression (overall survival: miR-191, P = .03; and miR-199a, P = .001, Cox regression).
  • In conclusion, miRNA expression in AML is closely associated with cytogenetics and FLT3-ITD mutations.

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  • [Cites] Leukemia. 2004 Oct;18(10):1565-8 [15452588.001]
  • [Cites] Oncogene. 2007 Sep 13;26(42):6133-40 [17404574.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] N Engl J Med. 1999 Sep 30;341(14):1051-62 [10502596.001]
  • [Cites] Nature. 2005 Feb 17;433(7027):769-73 [15685193.001]
  • [Cites] Cell. 2005 Mar 11;120(5):635-47 [15766527.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):834-8 [15944708.001]
  • [Cites] Leukemia. 2005 Sep;19(9):1550-7 [15973452.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13944-9 [16166262.001]
  • [Cites] N Engl J Med. 2005 Oct 27;353(17):1793-801 [16251535.001]
  • [Cites] Nucleic Acids Res. 2005;33(20):e179 [16314309.001]
  • [Cites] Cell. 2005 Dec 2;123(5):819-31 [16325577.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 13;102(50):18081-6 [16330772.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3589-95 [11369655.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Br J Haematol. 2002 Aug;118(2):357-64 [12139719.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15524-9 [12434020.001]
  • [Cites] Cancer Biol Ther. 2003 Mar-Apr;2(2):164-70 [12750556.001]
  • [Cites] Science. 2004 Jan 2;303(5654):83-6 [14657504.001]
  • [Cites] Cell. 2004 Jan 23;116(2):281-97 [14744438.001]
  • [Cites] Science. 2004 Apr 23;304(5670):594-6 [15105502.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 29;101(26):9740-4 [15210942.001]
  • [Cites] Cell. 2003 Dec 26;115(7):787-98 [14697198.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460.001]
  • [Cites] Cancer Cell. 2006 Mar;9(3):189-98 [16530703.001]
  • [Cites] Cell. 2006 Mar 24;124(6):1169-81 [16564011.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5078-83 [16549775.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7024-9 [16641092.001]
  • [Cites] Gastroenterology. 2006 Jun;130(7):2113-29 [16762633.001]
  • [Cites] Cancer Res. 2006 Dec 15;66(24):11590-3 [17178851.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Feb 20;104(8):2750-5 [17293455.001]
  • [Cites] Oncogene. 2007 Apr 26;26(19):2799-803 [17072344.001]
  • [Cites] Nature. 2007 Jun 28;447(7148):1130-4 [17554337.001]
  • [Cites] Blood. 1997 Jan 15;89(2):630-43 [9002967.001]
  • (PMID = 18187662.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / P01CA76259; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / P01 CA076259; United States / NCI NIH HHS / CA / P01CA81534; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / MicroRNAs
  • [Other-IDs] NLM/ PMC2265455
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49. Serrano E, Lasa A, Perea G, Carnicer MJ, Brunet S, Aventín A, Sierra J, Nomdedéu JF: Acute myeloid leukemia subgroups identified by pathway-restricted gene expression signatures. Acta Haematol; 2006;116(2):77-89
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  • [Title] Acute myeloid leukemia subgroups identified by pathway-restricted gene expression signatures.
  • Acute myeloid leukemia (AML) is a heterogeneous group of disorders characterized by abnormal proliferation of myeloid precursors and a maturation block.
  • Alternatively, we selected a pathway profiling strategy based on the current knowledge in order to stratify de novo AML patients and identify those cases which would potentially benefit from the use of new chemotherapeutic agents.
  • One hundred and thirty-two RNA samples obtained from de novo adult AML patients were tested for FLT3, FLT3-LG, NDST1, HDAC2, ATRX, FOS, DNMT1, DNMT3A, DNMT3B, NBS1, RAD50, MRE11A, Meis1 and Meis2 expression using quantitative PCR (qPCR) assays.
  • In accordance with previous results, Meis1 downregulation is a useful surrogate marker indicating a good prognosis in AML patients.
  • Simple qPCR platforms may help to identify different biologic subgroups in AML.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia, Myeloid / classification. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Female. Humans. Karyotyping. Male. Middle Aged. Mutation. Polymerase Chain Reaction. Prognosis. RNA, Neoplasm / genetics. RNA, Neoplasm / isolation & purification. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16914901.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / RNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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50. Liu LB, Li L, Zou P: Comparison of cytogenetics and clinical manifestations between M5a and M5b of acute monocytic leukemia. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Aug;14(4):654-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of cytogenetics and clinical manifestations between M5a and M5b of acute monocytic leukemia.
  • To compare the cytogenetic difference between M5a and M5b of acute monocytic leukemia and to study the correlation between karyotypes and clinical manifestations, a total of 58 cases of de novo adult AML M5 have been investigated.
  • The patients with AML M5 with aberrant karyotype had a higher incidence of hyperleukocytosis, extramedullary central nerve system infiltration, lower complete remission (CR) rate and shorter overall survival.
  • It is concluded that acute monocytic leukemia is a series of heterogeneous diseases, a distinctive cytogenetic features can be observed between patients with AML M5a and M5b, these results will provide insights into the classification and pathogenesis mechanism of AML M5 at molecular level.

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  • (PMID = 16928293.001).
  • [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] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] China
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51. Gorello P, Cazzaniga G, Alberti F, Dell'Oro MG, Gottardi E, Specchia G, Roti G, Rosati R, Martelli MF, Diverio D, Lo Coco F, Biondi A, Saglio G, Mecucci C, Falini B: Quantitative assessment of minimal residual disease in acute myeloid leukemia carrying nucleophosmin (NPM1) gene mutations. Leukemia; 2006 Jun;20(6):1103-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitative assessment of minimal residual disease in acute myeloid leukemia carrying nucleophosmin (NPM1) gene mutations.
  • Mutations in exon 12 of the nucleophosmin (NPM1) gene occur in about 60% of adult AML with normal karyotype.
  • In all 13 AML patients carrying NPM1 mutations at diagnosis, cDNA RQ-PCR showed >30 000 copies of NPM1-mutated transcript.
  • Thus, reliable, sensitive RQ-PCR assays for NPM1 mutations can now monitor and quantify MRD in AML patients with normal karyotype and NPM1 gene mutations.
  • [MeSH-major] Gene Dosage. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / genetics. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. DNA Mutational Analysis / methods. Gene Expression Profiling. Humans. Mutation. Predictive Value of Tests. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 16541144.001).
  • [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 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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52. Tajeddine N, Millard I, Gailly P, Gala JL: Real-time RT-PCR quantification of PRAME gene expression for monitoring minimal residual disease in acute myeloblastic leukaemia. Clin Chem Lab Med; 2006;44(5):548-55
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  • [Title] Real-time RT-PCR quantification of PRAME gene expression for monitoring minimal residual disease in acute myeloblastic leukaemia.
  • RESULTS: In paediatric acute myeloid leukaemia (AML) (n=22) and acute lymphoblastic leukaemia (ALL) (n=17), and in adult AML (n=20), abnormal PRAME expression was found in 41%, 35% and 40% of cases, respectively.
  • To assess the sensitivity of PRAME for monitoring MRD, PRAME-positive t(8;21) AML samples with detectable AML1/ETO expression by conventional RT-PCR (n=17) were assessed for quantitative expression of AML1/ETO and PRAME.

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  • (PMID = 16681423.001).
  • [ISSN] 1434-6621
  • [Journal-full-title] Clinical chemistry and laboratory medicine
  • [ISO-abbreviation] Clin. Chem. Lab. Med.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / PRAME protein, human
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53. Sakamaki H: [The role of gemtuzumab ozogamicin in the treatment of acute myeloid leukemia patients]. Gan To Kagaku Ryoho; 2008 Sep;35(9):1629-34
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  • [Title] [The role of gemtuzumab ozogamicin in the treatment of acute myeloid leukemia patients].
  • Gemtuzumab Ozogamicin (GO) targets leukemia cells expressing CD33 by means of a monoclonal antibody conjugated to a cytotoxic agent, calicheamicin.
  • GO has been approved in Japan as monotherapy for the treatment of patients with relapsed/refractory acute myeloid leukemia (AML)since 2005.
  • GO administered as a single agent has resulted in overall response rates of about 30% in previously relapsed adult AML.
  • Although caution is advised when administering GO within 115 days of a stem cell transplantation (SCT) procedure because of veno-occlusive disease, recent clinical studies overseas suggest that GO can be integrated into reduced-intensity conditioning therapy before allogeneic SCT in patients with relapsed AML.
  • [MeSH-major] Aminoglycosides / immunology. Aminoglycosides / therapeutic use. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / immunology. Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / immunology

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  • (PMID = 18799927.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / gemtuzumab
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54. Mullighan CG, Kennedy A, Zhou X, Radtke I, Phillips LA, Shurtleff SA, Downing JR: Pediatric acute myeloid leukemia with NPM1 mutations is characterized by a gene expression profile with dysregulated HOX gene expression distinct from MLL-rearranged leukemias. Leukemia; 2007 Sep;21(9):2000-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pediatric acute myeloid leukemia with NPM1 mutations is characterized by a gene expression profile with dysregulated HOX gene expression distinct from MLL-rearranged leukemias.
  • Somatic mutations in nucleophosmin (NPM1) occur in approximately 35% of adult acute myeloid leukemia (AML).
  • To assess the frequency of NPM1 mutations in pediatric AML, we sequenced NPM1 in the diagnostic blasts from 93 pediatric AML patients.
  • As dysregulated homeobox gene expression is also a feature of MLL-rearranged leukemia, the gene expression signatures of NPM1-mutated and MLL-rearranged leukemias were compared.
  • Significant differences were identified between these leukemia subtypes including the expression of different HOX genes, with NPM1-mutated AML showing higher levels of expression of HOXB2, B3, B6 and D4.
  • These results confirm recent reports of perturbed HOX expression in NPM1-mutated adult AML, and provide the first evidence that the NPM1-mutated signature is distinct from MLL-rearranged AML.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Child. Child, Preschool. Cohort Studies. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Male. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. Transcription Factors / genetics

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  • [CommentIn] Leukemia. 2007 Sep;21(9):1849-50 [17712359.001]
  • (PMID = 17597811.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / P01 CA71907-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HOXB2 protein, human; 0 / HOXB6 protein, human; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; 117896-08-9 / nucleophosmin; 140441-81-2 / HOXA10 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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55. Kim S, Lee J, Lee J, Kim D, Lim S, Lee Y, Kang Y, Seol M, Ryu S, Lee K: Pretransplant comorbidity as an outcome predictor in adult patients younger than 60 years of age receiving standard induction chemotherapy for de novo acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7055

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pretransplant comorbidity as an outcome predictor in adult patients younger than 60 years of age receiving standard induction chemotherapy for de novo acute myeloid leukemia.
  • : 7055 Background: Comorbidity has been evaluated as an outcome predictor in elderly patients receiving induction chemotherapy for acute myeloid leukemia (AML) as well as in patients undergoing allogeneic hematopoietic cell transplantation (HCT) for various hematologic disorders.
  • In this single-institute retrospective study, we investigated the prognostic significance of comorbidity in younger AML patients.
  • METHODS: A total of 276 patients, aged 14 to 59 years, who received standard induction chemotherapy consisting of cytarabine plus daunorubicin or idarubicin for de novo AML excluding M3 subtype between 2000 and 2007 were included.
  • Pre-treatment comorbidity score, assessed by the HCT specific comorbidity index (HCT-CI), was calculated using clinico- pathologic data, which were retrieved from Asan Medical Center Leukemia Registry Database.
  • CONCLUSIONS: Pre-treatment comorbidity may provide additional prognostic information over established prognostic factors in patients younger than 60 years of age receiving standard induction chemotherapy for de novo AML.

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  • (PMID = 27961421.001).
  • [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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56. Parkin B, Ouillette P, Wang Y, Liu Y, Wright W, Roulston D, Purkayastha A, Dressel A, Karp J, Bockenstedt P, Al-Zoubi A, Talpaz M, Kujawski L, Liu Y, Shedden K, Shakhan S, Li C, Erba H, Malek SN: NF1 inactivation in adult acute myelogenous leukemia. Clin Cancer Res; 2010 Aug 15;16(16):4135-47
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  • [Title] NF1 inactivation in adult acute myelogenous leukemia.
  • PURPOSE: This study was conducted to identify novel genes with importance to the biology of adult acute myelogenous leukemia (AML).
  • EXPERIMENTAL DESIGN: We analyzed DNA from highly purified AML blasts and paired buccal cells from 95 patients for recurrent genomic microdeletions using ultra-high density Affymetrix single nucleotide polymorphism 6.0 array-based genomic profiling.
  • Sequence analysis of all NF1 coding exons in the 11 AML cases with NF1 copy number changes identified acquired truncating frameshift mutations in two patients.
  • Subsequent expression analysis of NF1 mRNA in the entire AML cohort using fluorescence-activated cell sorting sorted blasts as a source of RNA identified six patients (one with a NF1 mutation) with absent NF1 expression.
  • The NF1 null states were associated with increased Ras-bound GTP, and short hairpin RNA-mediated NF1 suppression in primary AML blasts with wild-type NF1 facilitated colony formation in methylcellulose.
  • Primary AML blasts without functional NF1, unlike blasts with functional NF1, displayed sensitivity to rapamycin-induced apoptosis, thus identifying a dependence on mammalian target of rapamycin (mTOR) signaling for survival.
  • Finally, colony formation in methylcellulose ex vivo of NF1 null CD34+/CD38- cells sorted from AML bone marrow samples was inhibited by low-dose rapamycin.
  • CONCLUSIONS: NF1 null states are present in 7 of 95 (7%) of adult AML and delineate a disease subset that could be preferentially targeted by Ras or mammalian target of rapamycin-directed therapeutics.

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  • [Cites] Cancer Res. 2008 Feb 15;68(4):1012-21 [18281475.001]
  • [Cites] N Engl J Med. 1997 Jun 12;336(24):1713-20 [9180088.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 May 6;105(18):6708-13 [18458336.001]
  • [Cites] Leukemia. 2008 May;22(5):915-31 [18288131.001]
  • [Cites] Blood. 2008 Aug 1;112(3):814-21 [18490517.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Aug 19;105(33):11921-6 [18697940.001]
  • [Cites] Blood. 2008 Sep 1;112(5):1993-2003 [18436738.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4603-9 [18559876.001]
  • [Cites] Cancer Res. 2008 Dec 15;68(24):10349-57 [19074904.001]
  • [Cites] Cancer Cell. 2009 Jul 7;16(1):44-54 [19573811.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):12950-5 [19651600.001]
  • [Cites] Clin Cancer Res. 2009 Nov 1;15(21):6732-9 [19843663.001]
  • [Cites] J Exp Med. 2000 Jan 3;191(1):181-8 [10620616.001]
  • [Cites] Leukemia. 2000 Mar;14(3):513-7 [10720153.001]
  • [Cites] J Clin Invest. 2001 Sep;108(5):709-15 [11544276.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Blood. 2003 Aug 1;102(3):972-80 [12702506.001]
  • [Cites] Bioinformatics. 2004 May 22;20(8):1233-40 [14871870.001]
  • [Cites] Blood. 1991 Mar 1;77(5):925-9 [1704804.001]
  • [Cites] Am J Clin Pathol. 1993 Nov;100(5):534-40 [8249893.001]
  • [Cites] N Engl J Med. 1994 Mar 3;330(9):597-601 [8302341.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]
  • [Cites] J Biol Chem. 2004 Dec 3;279(49):50874-85 [15371411.001]
  • [Cites] Blood. 2005 Mar 15;105(6):2527-34 [15550488.001]
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3217-24 [15867216.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8573-8 [15937108.001]
  • [Cites] Biogerontology. 2005;6(3):185-92 [16041622.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):337-48 [16226708.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] J Biol Chem. 2005 Nov 25;280(47):39524-33 [16169856.001]
  • [Cites] Leukemia. 2006 Apr;20(4):635-44 [16467864.001]
  • [Cites] Leukemia. 2006 May;20(5):840-6 [16498392.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3887-94 [16864856.001]
  • [Cites] Clin Cancer Res. 2006 Sep 1;12(17):5165-73 [16951235.001]
  • [Cites] Cancer Cell. 2006 Sep;10(3):179-90 [16959610.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1224-31 [17377590.001]
  • [Cites] Clin Cancer Res. 2007 Aug 15;13(16):4777-85 [17699855.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1584-93 [17971485.001]
  • [Cites] Leukemia. 2008 Feb;22(2):240-8 [18200041.001]
  • [Cites] Blood. 2008 Apr 15;111(8):4322-8 [18172006.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):137-43 [8563750.001]
  • [Cites] Nat Genet. 1996 Feb;12(2):144-8 [8563751.001]
  • [CommentOn] Clin Cancer Res. 2010 Aug 15;16(16):4074-6 [20587590.001]
  • (PMID = 20505189.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA136537; United States / NCI NIH HHS / CA / 1R01 CA136537-01; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / R01 CA136537-02; United States / NCI NIH HHS / CA / CA136537-02
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS210184; NLM/ PMC2921448
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57. de Jonge HJ, Valk PJ, Veeger NJ, ter Elst A, den Boer ML, Cloos J, de Haas V, van den Heuvel-Eibrink MM, Kaspers GJ, Zwaan CM, Kamps WA, Löwenberg B, de Bont ES: High VEGFC expression is associated with unique gene expression profiles and predicts adverse prognosis in pediatric and adult acute myeloid leukemia. Blood; 2010 Sep 9;116(10):1747-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High VEGFC expression is associated with unique gene expression profiles and predicts adverse prognosis in pediatric and adult acute myeloid leukemia.
  • High VEGFC mRNA expression of acute myeloid leukemia (AML) blasts is related to increased in vitro and in vivo drug resistance.
  • We studied effect of VEGFC on treatment outcome and investigated gene expression profiles associated with VEGFC using microarray data of 525 adult and 100 pediatric patients with AML.
  • High VEGFC expression appeared strongly associated with reduced complete remission rate (P = .004), reduced overall and event-free survival (OS and EFS) in adult AML (P = .002 and P < .001, respectively).
  • Also, in pediatric AML high VEGFC was related to reduced OS (P = .041).
  • A unique series of differentially expressed genes was identified that distinguished AML with high VEGFC from AML with low VEGFC, that is, 331 up-regulated genes (representative of proliferation, vascular endothelial growth factor receptor activity, signal transduction) and 44 down-regulated genes (eg, related to apoptosis) consistent with a role in enhanced chemoresistance.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / genetics. Vascular Endothelial Growth Factor C / genetics
  • [MeSH-minor] Adolescent. Adult. Age Factors. Aged. Child. Child, Preschool. Humans. Infant. Infant, Newborn. Kaplan-Meier Estimate. Leukocyte Count. Middle Aged. Multivariate Analysis. Oligonucleotide Array Sequence Analysis. Predictive Value of Tests. Prognosis. Risk Factors. Young Adult


58. Malladi RK, Peniket AJ, Littlewood TJ, Towlson KE, Pearce R, Yin J, Cavenagh JD, Craddock C, Orchard KH, Olavarria E, McQuaker G, Collin M, Marks DI, British Society of Blood and Marrow Transplantation: Alemtuzumab markedly reduces chronic GVHD without affecting overall survival in reduced-intensity conditioning sibling allo-SCT for adults with AML. Bone Marrow Transplant; 2009 May;43(9):709-15
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  • [Title] Alemtuzumab markedly reduces chronic GVHD without affecting overall survival in reduced-intensity conditioning sibling allo-SCT for adults with AML.
  • By retrospective analysis of 88 patients from the British Society of Blood and Marrow Transplantation registry, we investigated the effect of in vivo T-cell depletion in HLA-identical sibling reduced-intensity conditioning (RIC) allografts for adult AML by comparing patients who received alemtuzumab with those without alemtuzumab conditioning.
  • The 2-year non-relapse mortality is 12% with alemtuzumab, and 17% without alemtuzumab (P=0.49).
  • Grades II-IV acute GVHD occurred in 22% (8/37) without alemtuzumab compared with 14% (7/51) given alemtuzumab (P=0.25).
  • Further studies are warranted before alemtuzumab can be recommended as standard in RIC allografts for AML.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Graft vs Host Disease / drug therapy. Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / therapeutic use. Chronic Disease. Drug Evaluation. Female. Humans. In Vitro Techniques. Lymphocyte Depletion / methods. Middle Aged. Registries. Retrospective Studies. Siblings. Survival Rate. Transplantation, Homologous. Young Adult

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  • (PMID = 19029965.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
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59. Tse WW, Zang SL, Bunting KD, Laughlin MJ: Umbilical cord blood transplantation in adult myeloid leukemia. Bone Marrow Transplant; 2008 Mar;41(5):465-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Umbilical cord blood transplantation in adult myeloid leukemia.
  • However, wide application of this procedure is limited by availability of suitable human leucocyte antigen (HLA)-matched adult donors.
  • The clinical experience of using UCB transplantation to treat pediatric acute leukemias has already shown that higher-level HLA-mismatched UCB can be equally as good as or even better than matched HSC.
  • Recently, large registries and multiple single institutional studies conclusively demonstrated that UCB is an acceptable source of HSCs for adult acute leukemia patients who lack HLA-matched donors.
  • These studies will impact the future clinical allogeneic stem cell transplantation for acute myeloid leukemia (AML), which is the most common acute leukemia in adults.
  • We anticipate that using UCB as a HSC source for allogeneic transplantation for adult AML will increase dramatically over the next 5 years, by expanding the available allogeneic donor pool.
  • Clinical studies are needed with focus on disease-specific UCB transplantation outcomes, including AML, acute lymphoblastic leukemia, and lymphoma.
  • [MeSH-major] Cord Blood Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Transplantation Conditioning / methods
  • [MeSH-minor] Adult. Blood Banks. Fetal Blood / physiology. Histocompatibility Testing. Humans

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  • (PMID = 18246116.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 60
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60. Wagner M, Schmelz K, Wuchter C, Ludwig WD, Dörken B, Tamm I: In vivo expression of survivin and its splice variant survivin-2B: impact on clinical outcome in acute myeloid leukemia. Int J Cancer; 2006 Sep 15;119(6):1291-7
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  • [Title] In vivo expression of survivin and its splice variant survivin-2B: impact on clinical outcome in acute myeloid leukemia.
  • Survivin, a member of the inhibitor of apoptosis protein family, is expressed in most human cancers, but undetectable in normal differentiated adult tissue in vivo.
  • To determine the expression and prognostic role of survivin in acute myeloid leukemia (AML), we investigated the mRNA expression pattern of survivin and of the splice variants survivin-2B and survivin-DeltaEx3 in adult (n = 74) and children (n = 31) with de novo AML using RT-PCR.
  • Survivin was the predominant transcript variant in AML cells, whereas significantly lower levels of survivin-2B and survivin-DeltaEx3 were observed (p < or = 0.0001).
  • For AML cases treated according to AMLCG92 (adult) and AML-BFM93 (children) protocols, respectively, expression patterns were correlated with clinical data: in adult AML (n = 51), low expression of survivin-2B correlated with a better overall survival (p = 0.05; mean survival time 19 months vs. 9 months) and a better eventfree survival (p < or = 0.01; 27 months vs. 10 months).
  • In childhood AML (n = 31), high survivin-DeltaEx3 expression was associated with a shorter overall survival (p < or = 0.05; 24 months vs. 43 months).
  • We conclude that certain survivin splice variants have potential prognostic impact for long-term therapy outcome in adult as well as childhood de novo AML.
  • [MeSH-major] Alternative Splicing. Leukemia, Myeloid / metabolism. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Acute Disease. Adult. Aged. Apoptosis. Case-Control Studies. DNA, Neoplasm / genetics. DNA, Neoplasm / metabolism. Disease-Free Survival. Female. Humans. Immunophenotyping. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Neoplasm Staging. Prognosis. RNA, Messenger / genetics. RNA, Messenger / metabolism

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  • (PMID = 16619249.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / DNA, Neoplasm; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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61. Walter MJ, Payton JE, Ries RE, Shannon WD, Deshmukh H, Zhao Y, Baty J, Heath S, Westervelt P, Watson MA, Tomasson MH, Nagarajan R, O'Gara BP, Bloomfield CD, Mrózek K, Selzer RR, Richmond TA, Kitzman J, Geoghegan J, Eis PS, Maupin R, Fulton RS, McLellan M, Wilson RK, Mardis ER, Link DC, Graubert TA, DiPersio JF, Ley TJ: Acquired copy number alterations in adult acute myeloid leukemia genomes. Proc Natl Acad Sci U S A; 2009 Aug 4;106(31):12950-5
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  • [Title] Acquired copy number alterations in adult acute myeloid leukemia genomes.
  • Cytogenetic analysis of acute myeloid leukemia (AML) cells has accelerated the identification of genes important for AML pathogenesis.
  • To complement cytogenetic studies and to identify genes altered in AML genomes, we performed genome-wide copy number analysis with paired normal and tumor DNA obtained from 86 adult patients with de novo AML using 1.85 million feature SNP arrays.
  • A total of 201 somatic CNAs were found in the 86 AML genomes (mean, 2.34 CNAs per genome), with French-American-British system M6 and M7 genomes containing the most changes (10-29 CNAs per genome).
  • Twenty-four percent of AML patients with normal cytogenetics had CNA, whereas 40% of patients with an abnormal karyotype had additional CNA detected by SNP array, and several CNA regions were recurrent.
  • Collectively, 34 of 86 AML genomes (40%) contained alterations not found with cytogenetics, and 98% of these regions contained genes.
  • In this study of 86 adult AML genomes, the use of an unbiased high-resolution genomic screen identified many genes not previously implicated in AML that may be relevant for pathogenesis, along with many known oncogenes and tumor suppressor genes.

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  • [Cites] Blood. 2001 Jun 1;97(11):3581-8 [11369654.001]
  • [Cites] Blood. 1999 Sep 1;94(5):1820-4 [10477709.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Jan;36(1):90-8 [12461753.001]
  • [Cites] Leukemia. 2003 Nov;17(11):2244-7 [12931227.001]
  • [Cites] Blood. 1993 Dec 1;82(11):3241-9 [8241496.001]
  • [Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]
  • [Cites] Oncogene. 2005 Jun 9;24(25):4129-37 [15806161.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):334-7 [16015648.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):305-19 [16075461.001]
  • [Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2355-8 [16239911.001]
  • [Cites] Leukemia. 2006 Apr;20(4):696-706 [16467868.001]
  • [Cites] Leukemia. 2006 May;20(5):840-6 [16498392.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3887-94 [16864856.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Leukemia. 2007 Mar;21(3):571-4 [17268525.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1224-31 [17377590.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1648-55 [17494858.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20007-12 [18077431.001]
  • [Cites] J Exp Med. 2007 Dec 24;204(13):3059-66 [18070937.001]
  • [Cites] Blood. 2008 May 1;111(9):4797-808 [18270328.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] Nat Genet. 2008 Jun;40(6):722-9 [18438408.001]
  • [Cites] Nature. 2008 Nov 6;456(7218):66-72 [18987736.001]
  • [Cites] Leukemia. 2009 Jan;23(1):85-94 [18818702.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1741-8 [19109227.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • (PMID = 19651600.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / K08 HL083012; United States / NCI NIH HHS / CA / P01 CA101937; United States / NHLBI NIH HHS / HL / T32 HL007088; United States / NCI NIH HHS / CA / U10 CA101140
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / NSD1 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Nuclear Proteins; 0 / Nup98 protein, human
  • [Other-IDs] NLM/ PMC2716381
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62. Breems DA, Boogaerts MA, Dekker AW, Van Putten WL, Sonneveld P, Huijgens PC, Van der Lelie J, Vellenga E, Gratwohl A, Verhoef GE, Verdonck LF, Löwenberg B: Autologous bone marrow transplantation as consolidation therapy in the treatment of adult patients under 60 years with acute myeloid leukaemia in first complete remission: a prospective randomized Dutch-Belgian Haemato-Oncology Co-operative Group (HOVON) and Swiss Group for Clinical Cancer Research (SAKK) trial. Br J Haematol; 2005 Jan;128(1):59-65
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  • [Title] Autologous bone marrow transplantation as consolidation therapy in the treatment of adult patients under 60 years with acute myeloid leukaemia in first complete remission: a prospective randomized Dutch-Belgian Haemato-Oncology Co-operative Group (HOVON) and Swiss Group for Clinical Cancer Research (SAKK) trial.
  • The question as to whether autologous stem cell transplantation (SCT) after consolidation chemotherapy improves the probability of survival of patients with acute myeloid leukaemia (AML) in first remission has not been settled.
  • Here, we present the results of a phase III study conducted in newly diagnosed adult AML patients aged <60 years.
  • [MeSH-major] Leukemia, Myeloid / surgery. Stem Cell Transplantation
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Belgium. Combined Modality Therapy. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Netherlands. Prospective Studies. Remission Induction. Survival Rate. Transplantation, Autologous

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  • (PMID = 15606550.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; Journal Article; Randomized Controlled Trial
  • [Publication-country] England
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63. Balgobind BV, Hollink IH, Reinhardt D, van Wering ER, de Graaf SS, Baruchel A, Stary J, Beverloo HB, de Greef GE, Pieters R, Zwaan CM, van den Heuvel-Eibrink MM: Low frequency of MLL-partial tandem duplications in paediatric acute myeloid leukaemia using MLPA as a novel DNA screenings technique. Eur J Cancer; 2010 Jul;46(10):1892-9
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  • [Title] Low frequency of MLL-partial tandem duplications in paediatric acute myeloid leukaemia using MLPA as a novel DNA screenings technique.
  • Mixed-lineage leukaemia (MLL)-partial tandem duplications (PTDs) are found in 3-5% of adult acute myeloid leukaemia (AML), and are associated with poor prognosis.
  • In adult AML, MLL-PTD is only detected in patients with trisomy 11 or internal tandem duplications of FLT3 (FLT3-ITD).
  • To date, studies in paediatric AML are scarce, and reported large differences in the frequency of MLL-PTD, frequently utilising mRNA RT-PCR only to detect MLL-PTDs.
  • We studied the frequency of MLL-PTD in a large cohort of paediatric AML (n=276) and the results from two different methods, i.e. mRNA RT-PCR, and multiplex ligation-dependent probe amplification (MLPA), a method designed to detect copy number differences of specific DNA sequences.
  • In paediatric AML, MLL-PTD was detected in 7/276 patients (2.5%).
  • Furthermore 4 of the 7 patients revealed a FLT3-ITD, which was significantly higher compared with the other AML cases (p=0.016).
  • In conclusion, using DNA-MLPA as a novel screenings technique in combination with mRNA RT-PCR a low frequency of MLL-PTD in paediatric AML was found.
  • Larger prospective studies are needed to further define the prognostic relevance of MLL-PTD in paediatric AML.
  • [MeSH-major] Gene Duplication. Genetic Testing / methods. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Tandem Repeat Sequences / genetics

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20233657.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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64. Gagyi E, Horváth E, Bödör C, Timár B, Matolcsy A, Pávai Z: Prognostic significance and detection of the internal tandem duplication of the FLT3 gene in acute myeloid leukemia. Rom J Morphol Embryol; 2006;47(4):331-7
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  • [Title] Prognostic significance and detection of the internal tandem duplication of the FLT3 gene in acute myeloid leukemia.
  • The FLT3/ITD is found in 20-40% of adult AML patients and is the most frequent mutation in leukemia.
  • Using native peripheral blood and bone marrow from AML and non-AML patients (total of 19 samples), and samples from the RNA bank (total of eight samples), the authors purpose was to work out a method for FLT3/ITD detection, which can be used in routine diagnostics.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 17392978.001).
  • [ISSN] 1220-0522
  • [Journal-full-title] Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
  • [ISO-abbreviation] Rom J Morphol Embryol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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65. Auewarakul CU, Lauhakirti D, Promsuwicha O, Munkhetvit C: C-kit receptor tyrosine kinase (CD117) expression and its positive predictive value for the diagnosis of Thai adult acute myeloid leukemia. Ann Hematol; 2006 Feb;85(2):108-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] C-kit receptor tyrosine kinase (CD117) expression and its positive predictive value for the diagnosis of Thai adult acute myeloid leukemia.
  • We examined the expression of c-kit receptor tyrosine kinase in 195 Thai adult patients with acute leukemia and determined its specificity and predictive values for the diagnosis of adult acute myeloid leukemia (AML).
  • Of 163 AML cases, 67% expressed CD117.
  • None of acute lymphoid leukemia (ALL) had CD117 expression, except one case of T-ALL.
  • The majority of AML patients carrying t(8;21), inv(16), and t(15;17) had high CD117 expression.
  • High proportion of AML cases without c-kit expressed monocytic markers.
  • Significant associations between CD117 and CD34 (P<0.001), CD13 (P=0.006), CD7 (P=0.034), and CD19 (P<0.001) were found in AML cases.
  • The calculated specificity of CD117 for the diagnosis of AML was 0.97, which was higher than CD13 (0.78) and CD33 (0.75) but comparable to MPO (0.97).
  • The positive predictive value (PPV) of CD117 for AML was 0.99, with the negative predictive value of 0.35.
  • In conclusion, the majority of Thai adult AML cases expressed c-kit.
  • C-kit is infrequently expressed in ALL and appeared to be specific for AML with high PPV.
  • Future targeting therapy using c-kit as a therapeutic target should benefit the majority of Thai AML patients who had high c-kit expression.
  • [MeSH-major] Biomarkers, Tumor. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis
  • [MeSH-minor] Acute Disease. Adult. Female. Flow Cytometry. Humans. Immunophenotyping. Karyotyping. Male. Predictive Value of Tests. Thailand


66. Gale RE, Green C, Allen C, Mead AJ, Burnett AK, Hills RK, Linch DC, Medical Research Council Adult Leukaemia Working Party: The impact of FLT3 internal tandem duplication mutant level, number, size, and interaction with NPM1 mutations in a large cohort of young adult patients with acute myeloid leukemia. Blood; 2008 Mar 1;111(5):2776-84
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  • [Title] The impact of FLT3 internal tandem duplication mutant level, number, size, and interaction with NPM1 mutations in a large cohort of young adult patients with acute myeloid leukemia.
  • An internal tandem duplication in the fms-like tyrosine kinase 3 gene (FLT3/ITD) is associated with poor prognosis in acute myeloid leukemia (AML), but the impact of mutant level, size, and interaction with nucleophosmin 1 (NPM1) mutations remains controversial.
  • We evaluated these characteristics in a large cohort of young adult AML patients.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid, Acute / genetics. Nuclear Proteins / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Adult. Clone Cells. Cohort Studies. Demography. Female. Humans. Karyotyping. Male. Middle Aged. Multivariate Analysis. Treatment Outcome. X Chromosome Inactivation


67. Garzon R, Garofalo M, Martelli MP, Briesewitz R, Wang L, Fernandez-Cymering C, Volinia S, Liu CG, Schnittger S, Haferlach T, Liso A, Diverio D, Mancini M, Meloni G, Foa R, Martelli MF, Mecucci C, Croce CM, Falini B: Distinctive microRNA signature of acute myeloid leukemia bearing cytoplasmic mutated nucleophosmin. Proc Natl Acad Sci U S A; 2008 Mar 11;105(10):3945-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinctive microRNA signature of acute myeloid leukemia bearing cytoplasmic mutated nucleophosmin.
  • Acute myeloid leukemia (AML) carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc+ AML) accounts for about one-third of adult AML and shows distinct features, including a unique gene expression profile.
  • Here, we investigated the role of miRNAs in the biology of NPMc+ AML.
  • The miRNA expression was evaluated in 85 adult de novo AML patients characterized for subcellular localization/mutation status of NPM1 and FLT3 mutations using a custom microarray platform.
  • Indeed, we confirmed that miR-204 targets HOXA10 and MEIS1, suggesting that the HOX up-regulation observed in NPMc+ AML may be due in part by loss of HOX regulators-miRNAs.
  • Our results identify a unique miRNA signature associated with NPMc+ AML and provide evidence that support a role for miRNAs in the regulation of HOX genes in this leukemia subtype.

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  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] Blood. 2005 Aug 1;106(3):899-902 [15831697.001]
  • [Cites] Leukemia. 2005 Oct;19(10):1760-7 [16079892.001]
  • [Cites] N Engl J Med. 2005 Oct 27;353(17):1793-801 [16251535.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3747-54 [16109776.001]
  • [Cites] Nucleic Acids Res. 2005;33(20):e179 [16314309.001]
  • [Cites] Cancer Cell. 2006 Mar;9(3):189-98 [16530703.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5078-83 [16549775.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7024-9 [16641092.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4514-23 [16455950.001]
  • [Cites] Nat Rev Cancer. 2006 Jul;6(7):493-505 [16794633.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1999-2005 [16720834.001]
  • [Cites] Trends Mol Med. 2006 Dec;12(12):580-7 [17071139.001]
  • [Cites] Blood. 2007 Feb 1;109(3):874-85 [17008539.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Feb 20;104(8):2750-5 [17293455.001]
  • [Cites] Leukemia. 2007 May;21(5):1099-103 [17301808.001]
  • [Cites] Leukemia. 2007 May;21(5):912-6 [17330104.001]
  • [Cites] Oncogene. 2007 Jun 14;26(28):4148-57 [17260024.001]
  • [Cites] Leukemia. 2007 Sep;21(9):2000-9 [17597811.001]
  • [Cites] Leukemia. 2008 Jan;22(1):195-8 [17637812.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]
  • [Cites] EMBO J. 2001 Feb 1;20(3):350-61 [11157742.001]
  • [Cites] Blood. 2002 Jan 1;99(1):310-8 [11756186.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Br J Haematol. 2002 Aug;118(2):357-64 [12139719.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2387-92 [12239146.001]
  • [Cites] Cell. 2003 Dec 26;115(7):787-98 [14697198.001]
  • [Cites] Science. 2004 Jan 2;303(5654):83-6 [14657504.001]
  • [Cites] Cell. 2004 Jan 23;116(2):281-97 [14744438.001]
  • [Cites] RNA. 2004 Oct;10(10):1507-17 [15383676.001]
  • [Cites] Trends Mol Med. 2004 Oct;10(10):500-7 [15464450.001]
  • [Cites] Mol Cell Biol. 1997 Jan;17(1):495-505 [8972230.001]
  • [Cites] Blood. 1999 May 1;93(9):3074-80 [10216104.001]
  • [Cites] N Engl J Med. 1999 Sep 30;341(14):1051-62 [10502596.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] J Exp Zool B Mol Dev Evol. 2005 Jan 15;304(1):75-85 [15643628.001]
  • [Cites] Nat Genet. 2005 May;37(5):495-500 [15806104.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 29;101(26):9740-4 [15210942.001]
  • (PMID = 18308931.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA076259; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / P01CA76259; United States / NCI NIH HHS / CA / P01CA81534
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / HOXB4 protein, human; 0 / Homeodomain Proteins; 0 / MicroRNAs; 0 / Mutant Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / myeloid ecotropic viral integration site 1 protein; 117896-08-9 / nucleophosmin; 140441-81-2 / HOXA10 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Other-IDs] NLM/ PMC2268779
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68. Walter RB, Pagel JM, Gooley TA, Petersdorf EW, Sorror ML, Woolfrey AE, Hansen JA, Salter AI, Lansverk E, Stewart FM, O'Donnell PV, Appelbaum FR: Comparison of matched unrelated and matched related donor myeloablative hematopoietic cell transplantation for adults with acute myeloid leukemia in first remission. Leukemia; 2010 Jul;24(7):1276-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of matched unrelated and matched related donor myeloablative hematopoietic cell transplantation for adults with acute myeloid leukemia in first remission.
  • Hematopoietic cell transplantation (HCT) from a matched related donor (MRD) benefits many adults with acute myeloid leukemia (AML) in first complete remission (CR1).
  • We retrospectively analyzed 226 adult AML CR1 patients undergoing myeloablative unrelated donor (URD) (10/10 match, n=62; 9/10, n=29) or MRD (n=135) HCT from 1996 to 2007.
  • The adjusted hazard ratios (HRs) were 1.43 (0.89-2.30, P=0.14) for overall mortality, 1.17 (0.66-2.08, P=0.60) for relapse and 1.79 (0.86-3.74, P=0.12) for NRM, respectively, and the adjusted odds ratio for grades 2-4 acute graft-versus-host disease was 1.50 (0.70-3.24, P=0.30).
  • These data indicate that URD HCT can provide long-term survival for CR1 AML; outcomes for 10/10 URD HCT, and possibly 9/10 URD HCT, suggest that this modality should be considered in the absence of a suitable MRD.

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  • [Cites] Blood Rev. 2004 Jun;18(2):115-36 [15010150.001]
  • [Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]
  • [Cites] J Clin Oncol. 2008 Nov 10;26(32):5183-91 [18768435.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2008;:412-7 [19074118.001]
  • [Cites] JAMA. 2009 Jun 10;301(22):2349-61 [19509382.001]
  • [Cites] N Engl J Med. 2001 Dec 20;345(25):1794-800 [11752355.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2976-80 [15251989.001]
  • [Cites] Bone Marrow Transplant. 1995 Jun;15(6):825-8 [7581076.001]
  • [Cites] Cancer. 2005 Apr 15;103(8):1652-8 [15742336.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6285-95 [16155011.001]
  • [Cites] Blood. 2005 Oct 15;106(8):2912-9 [15994282.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Dec;11(12):945-56 [16338616.001]
  • [Cites] Br J Haematol. 2006 Mar;132(6):755-69 [16487177.001]
  • [Cites] Best Pract Res Clin Haematol. 2006;19(2):321-8 [16516129.001]
  • [Cites] Best Pract Res Clin Haematol. 2006;19(2):333-9 [16516131.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3904-11 [16921041.001]
  • [Cites] J Clin Oncol. 2006 Dec 20;24(36):5695-702 [17116940.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] Curr Opin Hematol. 2007 Mar;14(2):152-61 [17255793.001]
  • [Cites] Best Pract Res Clin Haematol. 2007 Mar;20(1):67-75 [17336256.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 May;13(5):601-7 [17448920.001]
  • [Cites] Blood. 2007 May 1;109(9):3658-66 [17213292.001]
  • [Cites] Blood. 2007 Jul 1;110(1):409-17 [17374741.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4576-83 [17785583.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4606-13 [17873123.001]
  • [Cites] Best Pract Res Clin Haematol. 2008 Mar;21(1):85-92 [18342816.001]
  • [Cites] J Clin Oncol. 2003 Dec 15;21(24):4642-9 [14673054.001]
  • (PMID = 20485378.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / P01-AI33484; United States / NHLBI NIH HHS / HL / K99-HL088021; United States / NCI NIH HHS / CA / K08 CA095448; United States / NCI NIH HHS / CA / P01 CA018029-33; United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / K08 CA095448-01A2; United States / NCI NIH HHS / CA / K23-CA137161; United States / NCI NIH HHS / CA / K23 CA137161-01A2; United States / NIAID NIH HHS / AI / P01 AI033484-08; United States / NIAID NIH HHS / AI / P01 AI033484; United States / NCI NIH HHS / CA / K23 CA137161; United States / NCI NIH HHS / CA / K08-CA95448; United States / NCI NIH HHS / CA / R01 CA100019; United States / NHLBI NIH HHS / HL / K99 HL088021-01; United States / NCI NIH HHS / CA / P01-CA18029; United States / NHLBI NIH HHS / HL / K99 HL088021
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA Antigens
  • [Other-IDs] NLM/ NIHMS195191; NLM/ PMC3001162
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69. Kalinkovich A, Tavor S, Avigdor A, Kahn J, Brill A, Petit I, Goichberg P, Tesio M, Netzer N, Naparstek E, Hardan I, Nagler A, Resnick I, Tsimanis A, Lapidot T: Functional CXCR4-expressing microparticles and SDF-1 correlate with circulating acute myelogenous leukemia cells. Cancer Res; 2006 Nov 15;66(22):11013-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional CXCR4-expressing microparticles and SDF-1 correlate with circulating acute myelogenous leukemia cells.
  • Stromal cell-derived factor-1 (SDF-1/CXCL12) and its receptor CXCR4 are implicated in the pathogenesis and prognosis of acute myelogenous leukemia (AML).
  • In the present study, we investigated the putative relationships between the SDF-1/CXCR4 axis and microparticles in AML.
  • We detected CXCR4-expressing microparticles (CXCR4(+) microparticles) in the peripheral blood and bone marrow plasma samples of normal donors and newly diagnosed adult AML patients.
  • In samples from AML patients, levels of CXCR4(+) microparticles and total SDF-1 were elevated compared with normal individuals.
  • The majority of CXCR4(+) microparticles in AML patients were CD45(+), whereas in normal individuals, they were mostly CD41(+).
  • Importantly, we found a strong correlation between the levels of CXCR4(+) microparticle and WBC count in the peripheral blood and bone marrow plasma obtained from the AML patients.
  • Furthermore, our data indicate NH(2)-terminal truncation of the CXCR4 molecule in the microparticles of AML patients.
  • However, such microparticles were capable of transferring the CXCR4 molecule to AML-derived HL-60 cells, enhancing their migration to SDF-1 in vitro and increasing their homing to the bone marrow of irradiated NOD/SCID/beta2m(null) mice.
  • Our findings suggest that functional CXCR4(+) microparticles and SDF-1 are involved in the progression of AML.
  • We propose that their levels are potentially valuable as an additional diagnostic AML variable.
  • [MeSH-major] Chemokines, CXC / blood. Leukemia, Myeloid, Acute / blood. Receptors, CXCR4 / blood
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Bone Marrow / metabolism. Chemokine CXCL12. Female. HL-60 Cells. Humans. Leukocyte Count. Male. Middle Aged. U937 Cells

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  • (PMID = 17108140.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Receptors, CXCR4
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70. Staib P, Staltmeier E, Neurohr K, Cornely O, Reiser M, Schinköthe T: Prediction of individual response to chemotherapy in patients with acute myeloid leukaemia using the chemosensitivity index Ci. Br J Haematol; 2005 Mar;128(6):783-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prediction of individual response to chemotherapy in patients with acute myeloid leukaemia using the chemosensitivity index Ci.
  • As the response to chemotherapy in patients with acute myeloid leukaemia (AML) may still not be accurately determined by known prognostic factors, such as karyotype, the ex vivo chemosensitivity profile may help to predict the individual response.
  • We prospectively investigated the prognostic relevance of pre-therapeutic ex vivo chemosensitivity testing in primary cell cultures from adult AML patients by applying a new evaluation methodology, designated the chemosensitivity index, C(i).
  • Our data suggest that ex vivo chemosensitivity testing evaluated by the C(i) could serve as a powerful tool for assay-directed therapy strategies in AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Drug Screening Assays, Antitumor / methods. Drug Screening Assays, Antitumor / standards. Female. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Predictive Value of Tests. Prospective Studies. Sensitivity and Specificity. Survival Analysis. Thioguanine / administration & dosage. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 15755281.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; FTK8U1GZNX / Thioguanine; ZS7284E0ZP / Daunorubicin; DAT protocol 1; MAC chemotherapy protocol
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71. McCormack E, Bruserud O, Gjertsen BT: Review: genetic models of acute myeloid leukaemia. Oncogene; 2008 Jun 19;27(27):3765-79
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Review: genetic models of acute myeloid leukaemia.
  • The use of genetically engineered mice (GEM) have been critical in understanding disease states such as cancer, and none more so than acute myelogenous leukaemia (AML), a disease characterized by over 100 distinct chromosomal translocations.
  • Furthermore, little emphasis has been paid to the effect of chromosomal translocations other than recurrent genetic abnormalities, with no models reflecting the multiple abnormalities observed in high-risk cases of AML accounting for 8-10% of adult AML.
  • Here we review the differing technologies employed in generation of GEM of AML.
  • We discuss the relevance of GEM AML from embryonic stem cell-mediated (for example retinoic acid receptor-alpha fusions and AML1/ETO) models; through to the valuable retroviral-mediated gene transfer models.
  • The latter have been used to great effect in defining the transforming properties of chromosomal translocation products such as MLL (found in 5-6% of all AML cases) and NUP98 (denoting poor prognosis in therapy-related disease) and particularly when co-transduced with bad prognostic factors such as Flt3 mutations.
  • [MeSH-major] Animals, Genetically Modified / genetics. Leukemia, Myeloid, Acute / genetics. Models, Genetic
  • [MeSH-minor] Animals. Chromosome Aberrations. Disease Models, Animal. Exons. Humans. Leukemia, Promyelocytic, Acute / genetics. Mice. Mice, Transgenic. Prognosis

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  • (PMID = 18264136.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 111
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72. Cloos J, Goemans BF, Hess CJ, van Oostveen JW, Waisfisz Q, Corthals S, de Lange D, Boeckx N, Hählen K, Reinhardt D, Creutzig U, Schuurhuis GJ, Zwaan ChM, Kaspers GJ: Stability and prognostic influence of FLT3 mutations in paired initial and relapsed AML samples. Leukemia; 2006 Jul;20(7):1217-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stability and prognostic influence of FLT3 mutations in paired initial and relapsed AML samples.
  • In acute myeloid leukemia (AML), activating mutations in the fms-like tyrosine kinase 3 (FLT3) gene predict poor prognosis.
  • We determined FLT3 internal tandem duplications (FLT3/ITD) and D835 point mutations in paired initial and relapse samples from 80 pediatric and adult AML patients.
  • One D835 point mutation was found in an initial pediatric AML sample.
  • [MeSH-major] Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / genetics. Point Mutation. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Adult. Female. Genetic Markers. Genetic Predisposition to Disease / epidemiology. Humans. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Monocytic, Acute / genetics. Leukemia, Myelomonocytic, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Male. Neoplasm, Residual / epidemiology. Neoplasm, Residual / genetics. Prognosis. Recurrence. Risk Factors. Tandem Repeat Sequences

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  • (PMID = 16642044.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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73. Willman CL: Has gene expression profiling improved diagnosis, classification, and outcome prediction in AML? Best Pract Res Clin Haematol; 2008 Mar;21(1):21-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Has gene expression profiling improved diagnosis, classification, and outcome prediction in AML?
  • Gene expression profiling, the simultaneous measurement of the global patterns of gene expression in cells using microarray technologies, has held promise to improve diagnosis, risk classification, and outcome prediction in acute leukemias as well as in other human cancers.
  • But how much has gene expression profiling impacted or improved current diagnosis and risk classification schemes and therapeutic targeting in acute myeloid leukemia (AML)?
  • To date, gene expression profiling of AML has largely confirmed the presence of well-established recurring cytogenetic abnormalities, such as translocations, deletions, point mutations, or normal karyotypes, and has led to the identification of sets of genes reflective of these abnormalities.
  • Similarly, expression profiling has not led to the identification of many novel therapeutic targets in AML.
  • Using advanced statistical modeling techniques, our group has focused on expression profiling in adult AML patients with poor risk features in order to identify novel cluster groups and potential targets for therapy in this highly resistant form of disease.
  • To further advance the application of gene expression profiling and other comprehensive genomic and phosphoproteomic techniques to the study of AML, it would be ideal for the NCI Cooperative Groups to register all patients to common or intergroup collaborative clinical trials or registration studies in order to develop large, well-characterized cohorts of uniformly treated patients for future research studies.
  • [MeSH-major] Gene Expression Profiling. Leukemia, Myeloid, Acute. Registries

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  • (PMID = 18342809.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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74. Ferrara F, Izzo T, Criscuolo C, Riccardi C, Celentano M, Mele G: Day 15 bone marrow driven double induction in young adult patients with acute myeloid leukemia: feasibility, toxicity, and therapeutic results. Am J Hematol; 2010 Sep;85(9):687-90
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  • [Title] Day 15 bone marrow driven double induction in young adult patients with acute myeloid leukemia: feasibility, toxicity, and therapeutic results.
  • The strategy named double induction (DI) in acute myeloid leukemia (AML) consists of two courses of chemotherapy irrespective of the degree of cytoreduction in the bone marrow (BM) after the first course, unless severe complications prohibit its application.
  • Our study suggest that D15 driven DI represents a feasible and effective therapeutic strategy in young adult AML patients, improving therapeutic results and not compromising feasibility of allo-SCT.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Blast Crisis / therapy. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Bone Marrow / pathology. Chromosome Aberrations. Cytarabine / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Idarubicin / administration & dosage. Male. Middle Aged. Mutation. Remission Induction. Retrospective Studies. Survival Rate. Time Factors. Transplantation, Homologous. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Young Adult

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  • [Copyright] © 2010 Wiley-Liss, Inc.
  • (PMID = 20652967.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 6PLQ3CP4P3 / Etoposide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin
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75. Thiede C, Koch S, Creutzig E, Steudel C, Illmer T, Schaich M, Ehninger G: Prevalence and prognostic impact of NPM1 mutations in 1485 adult patients with acute myeloid leukemia (AML). Blood; 2006 May 15;107(10):4011-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence and prognostic impact of NPM1 mutations in 1485 adult patients with acute myeloid leukemia (AML).
  • Mutations of the nucleophosmin (NPM1) gene have recently been described in patients with acute myeloid leukemia (AML).
  • To clarify the prevalence as well as the clinical impact of this mutation, we investigated 1485 patients with AML for NPM1 exon 12 mutations using fragment analysis.
  • In conclusion, NPM1 mutations represent a common genetic abnormality in adult AML.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Adult. Amino Acid Sequence. Base Sequence. DNA Transposable Elements. Exons. Humans. Karyotyping. Microscopy, Confocal. Molecular Sequence Data. Polymerase Chain Reaction. Prevalence. Prognosis


76. Auewarakul CU, Lauhakirti D, Tocharoentanaphol C: Frequency of RAS gene mutation and its cooperative genetic events in Southeast Asian adult acute myeloid leukemia. Eur J Haematol; 2006 Jul;77(1):51-6
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  • [Title] Frequency of RAS gene mutation and its cooperative genetic events in Southeast Asian adult acute myeloid leukemia.
  • RAS gene as one of the most frequently mutated genes in acute myeloid leukemia (AML) has become an attractive target for molecular therapy.
  • The role of oncogenic RAS and its associated genetic events in AML are not yet defined.
  • We examined the frequency of RAS mutation in 239 Thai de novo adult AML patients using polymerase chain reaction-single-strand conformational polymorphism analysis.
  • Four patients had core-binding factor leukemia and four additional patients had coexisting FLT3 or AML1 mutation.
  • Future molecular-targeting approaches should take into account the multiple genetic events that coexist with RAS mutations in AML patients.
  • [MeSH-major] Leukemia, Myeloid / classification. Leukemia, Myeloid / genetics. Mutation. ras Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Asia, Southeastern / epidemiology. Codon. Core Binding Factor Alpha 2 Subunit / genetics. DNA Mutational Analysis. Female. Gene Frequency. Humans. Male. Molecular Epidemiology. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16573741.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Codon; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.5.2 / ras Proteins
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77. Yanada M, Suzuki M, Kawashima K, Kiyoi H, Kinoshita T, Emi N, Saito H, Naoe T: Long-term outcomes for unselected patients with acute myeloid leukemia categorized according to the World Health Organization classification: a single-center experience. Eur J Haematol; 2005 May;74(5):418-23
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  • [Title] Long-term outcomes for unselected patients with acute myeloid leukemia categorized according to the World Health Organization classification: a single-center experience.
  • The actual utility of a new classification system of acute myeloid leukemia (AML) recently introduced by the World Health Organization (WHO) has not been thoroughly investigated yet.
  • In this study, we evaluated long-term outcomes of unselected AML patients categorized according to the new WHO classification.
  • Between 1990 and 2002, 109 adult AML cases were referred to our hospital.
  • AML with recurrent genetic abnormalities accounted for 26%, AML with multilineage dysplasia for 29%, therapy-related AML for 13%, and AML not otherwise categorized for 32% of classifiable cases.
  • These results indicate that outcomes for AML patients appear to be distinguished on the basis of the WHO classification, but the prognostic significance of multilineage dysplasia and prior therapy is lost after adjusting for cytogenetic risk and age.
  • [MeSH-major] Leukemia, Myeloid / classification. Leukemia, Myeloid / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Humans. Middle Aged. Palliative Care. Retrospective Studies. Survival Analysis. Survivors. Treatment Outcome. World Health Organization

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  • (PMID = 15813916.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
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78. Becker PS, Kopecky KJ, Wilks AN, Chien S, Harlan JM, Willman CL, Petersdorf SH, Stirewalt DL, Papayannopoulou T, Appelbaum FR: Very late antigen-4 function of myeloblasts correlates with improved overall survival for patients with acute myeloid leukemia. Blood; 2009 Jan 22;113(4):866-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Very late antigen-4 function of myeloblasts correlates with improved overall survival for patients with acute myeloid leukemia.
  • Adhesion of acute myeloid leukemia (AML) blasts in the bone marrow microenvironment confers protection from chemotherapy-induced apoptosis.
  • To examine the relationship of functional expression of VLA-4 to prognosis in AML, we studied marrow samples from 175 adult AML patients who underwent induction chemotherapy with anthracycline and cytarabine on Southwest Oncology Group trials.
  • Adhesion and migratory properties of AML blasts thus appear to influence chemosensitivity and therefore may be therapeutic targets.
  • [MeSH-major] Granulocyte Precursor Cells / metabolism. Integrin alpha4beta1 / metabolism. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Cell Adhesion. Cell Line, Tumor. Cytokines / metabolism. Female. Fibronectins / metabolism. Gene Expression Regulation, Neoplastic / genetics. Humans. Male. Middle Aged. Peptide Fragments / metabolism. Protein Binding. Recombinant Proteins / metabolism. Survival Rate. Treatment Outcome. Vascular Cell Adhesion Molecule-1 / metabolism

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  • [Cites] Blood. 2001 Apr 1;97(7):2121-9 [11264180.001]
  • [Cites] Exp Hematol. 2001 Apr;29(4):448-57 [11301185.001]
  • [Cites] J Immunol. 2001 Sep 1;167(5):2824-30 [11509628.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1897-903 [11535527.001]
  • [Cites] Blood. 2001 Dec 1;98(12):3212-20 [11719356.001]
  • [Cites] Blood. 2002 Dec 1;100(12):3869-76 [12393614.001]
  • [Cites] Br J Haematol. 2003 Mar;120(5):782-6 [12614209.001]
  • [Cites] Br J Haematol. 2003 Aug;122(4):579-89 [12899713.001]
  • [Cites] Nat Med. 2003 Sep;9(9):1158-65 [12897778.001]
  • [Cites] J Biol Chem. 2003 Oct 3;278(40):38174-82 [12844491.001]
  • [Cites] Blood. 2004 Jul 15;104(2):550-7 [15054042.001]
  • [Cites] J Cell Biol. 1992 Jan;116(2):499-509 [1370496.001]
  • [Cites] Ann N Y Acad Sci. 1993 Mar 20;677:265-80 [8494214.001]
  • [Cites] Am J Clin Pathol. 1993 Nov;100(5):534-40 [8249893.001]
  • [Cites] Blood. 1996 Oct 15;88(8):2841-51 [8874180.001]
  • [Cites] Blood. 1997 May 1;89(9):3323-9 [9129038.001]
  • [Cites] Blood. 1998 May 15;91(10):3607-15 [9572995.001]
  • [Cites] Science. 1999 Feb 5;283(5403):845-8 [9933168.001]
  • [Cites] Exp Hematol. 1999 Mar;27(3):533-41 [10089917.001]
  • [Cites] Leukemia. 2005 Jan;19(1):57-63 [15510209.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6296-305 [16155012.001]
  • [Cites] Leuk Lymphoma. 2005 Dec;46(12):1679-87 [16263569.001]
  • [Cites] Oncogene. 2006 Jan 19;25(3):399-408 [16158049.001]
  • [Cites] Blood. 2006 May 1;107(9):3724-6 [16368883.001]
  • [Cites] Blood. 2006 May 1;107(9):3481-5 [16455952.001]
  • [Cites] Oncogene. 2006 May 25;25(22):3113-22 [16407823.001]
  • [Cites] Nat Med. 2006 Oct;12(10):1167-74 [16998484.001]
  • [Cites] Mol Cancer Ther. 2006 Dec;5(12):3113-21 [17172414.001]
  • [Cites] Blood. 2007 Jan 15;109(2):786-91 [16888090.001]
  • [Cites] Cancer. 2007 Mar 15;109(6):1152-6 [17315232.001]
  • [Cites] Am J Hematol. 2007 Dec;82(12):1056-62 [17696203.001]
  • [Cites] Blood. 2008 Jan 15;111(2):865-73 [17959854.001]
  • [Cites] Leukemia. 1996 Apr;10(4):682-6 [8618447.001]
  • (PMID = 18927435.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL058734
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cytokines; 0 / Fibronectins; 0 / Integrin alpha4beta1; 0 / Peptide Fragments; 0 / Recombinant Proteins; 0 / Vascular Cell Adhesion Molecule-1
  • [Other-IDs] NLM/ PMC2630271
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79. Buccisano F, Maurillo L, Gattei V, Del Poeta G, Del Principe MI, Cox MC, Panetta P, Consalvo MI, Mazzone C, Neri B, Ottaviani L, Fraboni D, Tamburini A, Lo-Coco F, Amadori S, Venditti A: The kinetics of reduction of minimal residual disease impacts on duration of response and survival of patients with acute myeloid leukemia. Leukemia; 2006 Oct;20(10):1783-9
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  • [Title] The kinetics of reduction of minimal residual disease impacts on duration of response and survival of patients with acute myeloid leukemia.
  • We assessed by multiparametric flow cytometry the levels of minimal residual disease (MRD) in 100 adult patients with acute myelogenous leukemia (AML) achieving complete remission after intensive chemotherapy.
  • (1) the threshold of 3.5 x 10(-4) is valid in discriminating risk categories in adult AML and (2) post-Cons MRD assessment is critical to predict disease outcome.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / pathology. Neoplasm, Residual / mortality. Neoplasm, Residual / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Disease-Free Survival. Female. Flow Cytometry. Humans. Immunophenotyping. Kinetics. Male. Middle Aged. Multivariate Analysis. Predictive Value of Tests. Prognosis. Remission Induction. Survival Analysis

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  • (PMID = 16838027.001).
  • [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
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80. Mele A, Leopardi G, Sparaventi G, Nicolini G, D'Adamo F, Guiducci B, Barulli S, Malerba L, Stramigioli S, Talevi N, Politi P, Isidori A, Malagola M, Piccaluga P, Visani G: Mini-ICE effectively mobilises peripheral blood stem cells after fludarabine-based regimens in acute myeloid leukaemia. Eur J Haematol; 2005 Apr;74(4):277-81
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  • [Title] Mini-ICE effectively mobilises peripheral blood stem cells after fludarabine-based regimens in acute myeloid leukaemia.
  • Fludarabine-based cycles severely impair mobilisation and collection of peripheral blood stem cells (PBSC) in acute myeloid leukaemia (AML).
  • In an effort of reversing this side-effect, we studied the action on mobilisation and collection of PBSC of a low-dose regimen: 5-d Mini-ICE (oral idarubicin and etoposide; subcutaneous cytosine arabinoside) administered after fludarabine-based regimens in seven adult AML patients.
  • We suggest that the Mini-ICE programme is feasible, well tolerated and effective in terms of PBSC mobilisation and collection in low-yield AML patients previously treated with fludarabine.
  • It is well known that a negative effect on stem cell mobilisation and harvest is observed not only after fludarabine administration in AML or low-grade lymphomas, but also after cycles based on different agents, such as thalidomide in multiple myeloma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cytarabine / administration & dosage. Etoposide / administration & dosage. Hematopoietic Stem Cell Mobilization / methods. Idarubicin / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / therapy. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives
  • [MeSH-minor] Adult. Female. Humans. Leukapheresis. Male. Middle Aged. Peripheral Blood Stem Cell Transplantation. Transplantation, Autologous

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  • [Copyright] Copyright 2005 Blackwell Munksgaard.
  • (PMID = 15777338.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin; ICE protocol 4
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81. Döhner K, Schlenk RF, Habdank M, Scholl C, Rücker FG, Corbacioglu A, Bullinger L, Fröhling S, Döhner H: Mutant nucleophosmin (NPM1) predicts favorable prognosis in younger adults with acute myeloid leukemia and normal cytogenetics: interaction with other gene mutations. Blood; 2005 Dec 1;106(12):3740-6
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  • [Title] Mutant nucleophosmin (NPM1) predicts favorable prognosis in younger adults with acute myeloid leukemia and normal cytogenetics: interaction with other gene mutations.
  • To assess the prognostic relevance of mutations in the NPM1 gene encoding a nucleocytoplasmic shuttle protein in younger adults with acute myeloid leukemia (AML) and normal cytogenetics, sequencing of NPM1 exon 12 was performed in diagnostic samples from 300 patients entered into 2 consecutive multicenter trials of the AML Study Group (AMLSG).
  • Multivariable analysis for OS revealed combined NPM1-mutated/FLT3 ITD-negative status, CEBPA mutation status, availability of a human leukocyte antigen (HLA)-compatible donor, secondary AML, and lactate dehydrogenase (LDH) as prognostic factors.
  • In conclusion, NPM1 mutations in the absence of FLT3 ITD define a distinct molecular and prognostic subclass of young-adult AML patients with normal cytogenetics.
  • [MeSH-major] Leukemia, Myeloid / genetics. Nuclear Proteins / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Amino Acid Sequence. Base Sequence. CCAAT-Binding Factor / genetics. Clinical Trials as Topic. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Mutation. Polymerase Chain Reaction. Prognosis. Survival Analysis. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16051734.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCAAT-Binding Factor; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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82. Shi HX, Jiang B, Qiu JY, Lu XJ, Fu JF, Wang DB, Lu DP: [Studies of treatment strategy and prognosis on acute myeloid leukemia with chromosome 8 and 21 translocation]. Zhonghua Xue Ye Xue Za Zhi; 2005 Aug;26(8):481-4
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  • [Title] [Studies of treatment strategy and prognosis on acute myeloid leukemia with chromosome 8 and 21 translocation].
  • OBJECTIVE: To investigate the relationship between the biological features and the treatment efficacy and prognosis in acute myeloid leukemia subtype M2 (AML-M2) patients with chromosome 8 and 21 translocation.
  • METHODS: By using Cox regression model and Kaplan-Meier analyses, prognostic factors in 54 cases of de novo adult AML with t(8;21) in our institute from 1990 to 2003 were retrospectively analyzed.
  • CONCLUSION: AML with t(8;21) is not a single defined AML subset, and patients with additional chromosome abnormalities have a worse prognosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Female. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Translocation, Genetic

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  • (PMID = 16383240.001).
  • [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
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83. Quentmeier H, Martelli MP, Dirks WG, Bolli N, Liso A, Macleod RA, Nicoletti I, Mannucci R, Pucciarini A, Bigerna B, Martelli MF, Mecucci C, Drexler HG, Falini B: Cell line OCI/AML3 bears exon-12 NPM gene mutation-A and cytoplasmic expression of nucleophosmin. Leukemia; 2005 Oct;19(10):1760-7
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  • We recently identified a new acute myeloid leukemia (AML) subtype characterized by mutations at exon-12 of the nucleophosmin (NPM) gene and aberrant cytoplasmic expression of NPM protein (NPMc+).
  • NPMc+ AML accounts for about 35% of adult AML and it is associated with normal karyotype, wide morphological spectrum, CD34-negativity, high frequency of FLT3-ITD mutations and good response to induction therapy.
  • In an attempt to identify a human cell line to serve as a model for the in vitro study of NPMc+ AML, we screened 79 myeloid cell lines for mutations at exon-12 of NPM.
  • This mutation corresponds to the type A, the NPM mutation most frequently observed in primary NPMc+ AML.
  • OCI/AML3 cells also displayed typical phenotypic features of NPMc+ AML, that is, expression of macrophage markers and lack of CD34, and the immunocytochemical hallmark of this leukemia subtype, that is, the aberrant cytoplasmic expression of NPM.
  • The OCI/AML3 cell line easily engrafts in NOD/SCID mice and maintains in the animals the typical features of NPMc+ AML, such as the NPM cytoplasmic expression.
  • For all these reasons, the OCI/AML3 cell line represents a remarkable tool for biomolecular studies of NPMc+ AML.
  • [MeSH-major] Exons / genetics. Gene Expression Regulation, Leukemic. Leukemia, Promyelocytic, Acute / genetics. Mutation / genetics. Nuclear Proteins / genetics

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  • (PMID = 16079892.001).
  • [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 / Antigens, CD34; 0 / Biomarkers; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
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84. Gil L, Styczynski J, Dytfeld D, Debski R, Kazmierczak M, Kolodziej B, Rafinska B, Kubicka M, Nowicki A, Komarnicki M, Wysocki M: Activity of bortezomib in adult de novo and relapsed acute myeloid leukemia. Anticancer Res; 2007 Nov-Dec;27(6B):4021-5
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  • [Title] Activity of bortezomib in adult de novo and relapsed acute myeloid leukemia.
  • AIM: The aim of the study was the analysis of in vitro drug resistance to bortezomib and other anticancer drugs in de novo and relapsed adult acute myeloid leukemia (AML).
  • PATIENTS AND METHODS: The leukemic cells of 46 adult patients with AML were tested for the in vitro drug resistance profile.
  • The group included 20 de novo and 26 relapsed AML patients, among whom, 12 relapsed after allogeneic hematopoietic stem cell transplantation (HSCT) and 4 after autologous HSCT.
  • RESULTS: No significant differences in drug resistance were found for all tested drugs between de novo and relapsed AML samples, while expression of PGP, MRP1 and LRP was higher in relapsed patients.
  • CONCLUSION: In vitro drug resistance in relapsed adult AML is comparable to that in de novo disease.
  • Activity in vitro of bortezomib might be a rationale for its use in refractory/relapsed AML adult patients.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Boronic Acids / pharmacology. Leukemia, Myeloid / drug therapy. Pyrazines / pharmacology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Bortezomib. Drug Resistance, Neoplasm. Female. Flow Cytometry. HL-60 Cells. Humans. Male. Middle Aged. Multidrug Resistance-Associated Proteins / biosynthesis. Multidrug Resistance-Associated Proteins / metabolism. P-Glycoprotein / biosynthesis. P-Glycoprotein / metabolism. Vault Ribonucleoprotein Particles / biosynthesis. Vault Ribonucleoprotein Particles / metabolism

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  • (PMID = 18225565.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / Pyrazines; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / multidrug resistance-associated protein 1; 69G8BD63PP / Bortezomib
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85. Schaich M, Soucek S, Thiede C, Ehninger G, Illmer T, SHG AML96 Study Group: MDR1 and MRP1 gene expression are independent predictors for treatment outcome in adult acute myeloid leukaemia. Br J Haematol; 2005 Feb;128(3):324-32
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  • [Title] MDR1 and MRP1 gene expression are independent predictors for treatment outcome in adult acute myeloid leukaemia.
  • The three major candidates accounting for the development of MDR in acute myeloid leukaemia (AML) are multi drug resistance gene (MDR1), multi drug resistance-related protein gene (MRP1) and lung resistance protein gene (LRP).
  • So far, the differential impact of resistance gene expression on treatment outcome in AML is not clear.
  • Therefore, we examined MDR1, MRP1 and LRP gene expression at diagnosis in 331 adult AML patients in the context of other known prognostic factors, such as age, disease status, cytogenetics and FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication mutational status.
  • LRP expression, however, had no impact on treatment outcome in AML.
  • Our study shows that resistance gene expression should be considered together with age, cytogenetics and FLT3 mutational status for risk-adapted treatment strategies in AML in the future.
  • [MeSH-major] Biomarkers, Tumor / genetics. Genes, MDR. Leukemia, Myeloid / genetics. Multidrug Resistance-Associated Proteins / genetics. Neoplasm Proteins / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Gene Expression. Humans. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Treatment Outcome

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  • (PMID = 15667534.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 0 / multidrug resistance-associated protein 1
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86. Sino-US Shanghai Leukemia Cooperative Group: [Distribution of WHO subtypes, initial treatment outcomes and prognosis study of 623 unselected adult patients with acute myeloid leukaemia in Shanghai.]. Zhonghua Xue Ye Xue Za Zhi; 2010 Feb;31(2):102-7
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  • [Title] [Distribution of WHO subtypes, initial treatment outcomes and prognosis study of 623 unselected adult patients with acute myeloid leukaemia in Shanghai.].
  • OBJECTIVE: To investigate the current status of acute myeloid leukemia (AML) treatment in Shanghai.
  • METHODS: From 2003 to 2007, a total of successive 623 patients with adult AML were diagnosed and classified according to WHO criteria.
  • Multilineage dysplasia in de novo AML was not an independent prognostic factor after adjusted by cytogenetics, age and WBC count.
  • CONCLUSIONS: The CR rate and survival of AML were improved in the past 20 years.
  • The short-term treatment outcome of AML was comparable to that in developed countries, while the long-term one was worse.
  • [MeSH-minor] Adult. China. Humans. Leukemia, Myeloid, Acute / drug therapy. Prognosis. Treatment Outcome

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  • (PMID = 20302797.001).
  • [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] 04079A1RDZ / Cytarabine
  • [Investigator] Wang XQ
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87. Faderl S, Verstovsek S, Cortes J, Ravandi F, Beran M, Garcia-Manero G, Ferrajoli A, Estrov Z, O'Brien S, Koller C, Giles FJ, Wierda W, Kwari M, Kantarjian HM: Clofarabine and cytarabine combination as induction therapy for acute myeloid leukemia (AML) in patients 50 years of age or older. Blood; 2006 Jul 1;108(1):45-51
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  • [Title] Clofarabine and cytarabine combination as induction therapy for acute myeloid leukemia (AML) in patients 50 years of age or older.
  • Outcome of patients with acute myeloid leukemia (AML) who are older than 60 years of age remains unsatisfactory, with low remission rates and poor overall survival.
  • We have previously established the activity of clofarabine plus cytarabine in AML relapse.
  • We have now conducted a phase 2 study of clofarabine plus cytarabine in patients aged 50 years or older with previously untreated AML.
  • Of 60 patients, 29 (48%) had secondary AML, 30 (50%) had abnormal karyotypes (monosomy 5 and/or 7 in 15 [25%]), and 11 (21%) showed FLT3 abnormalities.
  • Clofarabine plus cytarabine has activity in adult AML, achieving a good CR rate.
  • Modifications of this combination in AML therapy of older patients warrant further evaluation.
  • [MeSH-major] Adenine Nucleotides / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arabinonucleosides / administration & dosage. Cytarabine / administration & dosage. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Aged. Chromosome Aberrations. Drug Administration Schedule. Humans. Middle Aged. Remission Induction. Survival Rate. Treatment Outcome


88. Marzac C, Teyssandier I, Calendini O, Perrot JY, Faussat AM, Tang R, Casadevall N, Marie JP, Legrand O: Flt3 internal tandem duplication and P-glycoprotein functionality in 171 patients with acute myeloid leukemia. Clin Cancer Res; 2006 Dec 1;12(23):7018-24
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  • [Title] Flt3 internal tandem duplication and P-glycoprotein functionality in 171 patients with acute myeloid leukemia.
  • PURPOSE: Patients with adult acute myeloid leukemia (AML) with intermediate cytogenetics remain a heterogeneous group with highly variable individual prognoses.
  • We did a multivariate analysis on 171 patients with adult AML treated in the European Organization for Research and Treatment of Cancer protocols.
  • CONCLUSION: Flt3/ITD and Pgp activity are independent and additive prognostic factors which provide a powerful risk classification that can be routinely used to stratify the treatment of patients with intermediate cytogenetic AML.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. P-Glycoproteins / metabolism. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Cytogenetic Analysis. Follow-Up Studies. Humans. Middle Aged. Multivariate Analysis. Prognosis. Remission Induction. Risk Factors. Survival Rate. Tandem Repeat Sequences. Treatment Outcome

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  • (PMID = 17145823.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / P-Glycoproteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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89. Colovic N, Tosic N, Aveic S, Djuric M, Milic N, Bumbasirevic V, Colovic M, Pavlovic S: Importance of early detection and follow-up of FLT3 mutations in patients with acute myeloid leukemia. Ann Hematol; 2007 Oct;86(10):741-7
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  • [Title] Importance of early detection and follow-up of FLT3 mutations in patients with acute myeloid leukemia.
  • Mutations in the fms-like tyrosine kinase 3 (FLT3) gene, such as internal tandem duplication (FLT3/ITD) in the juxtamembrane domain and point mutations in the tyrosine kinase domain, are the most common abnormalities in acute myeloid leukemia (AML).
  • FLT3/ITD and FLT3/D835 mutations were analyzed in 113 Serbian adult AML patients using polymerase chain reaction.
  • The mutations occurred most frequently in M5 and M0 subtypes of AML.
  • However, changes in the pattern of FLT3/D835 mutations in initial and relapsed AML were observed.
  • Our results indicate an association of FLT3/ITD with the adverse outcome in AML patients treated with standard induction chemotherapy.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Point Mutation. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Disease-Free Survival. Female. Follow-Up Studies. Humans. Leukocyte Count. Male. Middle Aged. Recurrence. Risk Factors. Stem Cell Transplantation. Survival Rate. Transplantation, Homologous. Yugoslavia

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  • (PMID = 17579862.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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90. Beghini A, Bellini M, Magnani I, Colapietro P, Cairoli R, Morra E, Larizza L: STI 571 inhibition effect on KITAsn822Lys-mediated signal transduction cascade. Exp Hematol; 2005 Jun;33(6):682-8
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  • Gain-of-function KIT receptor mutations have been reported in adult AML patients, especially those with core binding factor leukemia (CBFL).
  • We have previously reported a new gain-of-function KIT(Asn822Lys) mutation that is constitutively expressed in the Kasumi-1 CBFL cell line, and has recently been described in two childhood AML patients.

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  • (PMID = 15911092.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 7006-34-0 / Asparagine; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; K3Z4F929H6 / Lysine
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91. Elghannam DM, Abousamra NK, Shahin DA, Goda EF, Azzam H, Azmy E, El-Din MS, El-Refaei MF: Prognostic implication of N-RAS gene mutations in Egyptian adult acute myeloid leukemia. Egypt J Immunol; 2009;16(1):9-15
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  • [Title] Prognostic implication of N-RAS gene mutations in Egyptian adult acute myeloid leukemia.
  • The pathogenesis of acute myeloid leukemia (AML) involves the cooperation of mutations promoting proliferation/survival and those impairing differentiation.
  • Point mutations of the N-RAS gene are the most frequent somatic mutations causing aberrant signal-transduction in acute myeloid leukemia (AML).
  • The aim of the present work is to study the frequency and prognostic significance of N-RAS gene mutations (N-RASmut) in de novo Egyptian adult AML.
  • Bone marrow specimens from 150 patients with de novo acute myeloid leukemia and controls were analyzed by genomic PCR-SSCP at codons 12, 13 (exon 1), and 61 (exon 2) for N-RAS mutations.
  • In 12.7% (19/150) AML cases, N-RAS gene mutations were found and were observed more frequently in the FAB subtype M4eo (P = 0.028) and with codon 12, 13 (14 of 19; 73.7%).
  • In conclusion, the frequency and spectrum of N-RAS gene mutation differ between biologically distinct subtypes of AML but do not significantly influence prognosis and clinical outcome in patients with AML.

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  • (PMID = 20726318.001).
  • [ISSN] 1110-4902
  • [Journal-full-title] The Egyptian journal of immunology
  • [ISO-abbreviation] Egypt J Immunol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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92. Aydin-Sayitoglu M, Hatirnaz O, Erensoy N, Ozbek U: Role of CYP2D6, CYP1A1, CYP2E1, GSTT1, and GSTM1 genes in the susceptibility to acute leukemias. Am J Hematol; 2006 Mar;81(3):162-70
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  • [Title] Role of CYP2D6, CYP1A1, CYP2E1, GSTT1, and GSTM1 genes in the susceptibility to acute leukemias.
  • Acute leukemias (ALs) are heterogeneous diseases.
  • Functional polymorphisms in the genes encoding detoxification enzymes cause inter-individual differences, which contribute to leukemia susceptibility.
  • The CYP2D6, CYP1A1, CYP2E1, GSTT1, and GSTM1 polymorphisms in ALL (n = 156) and AML (n = 94) patients and 140 healthy controls were genotyped by PCR and/or PCR-RFLP using blood or bone marrow samples.
  • Patients with ALL and AML had a higher prevalence of the GSTM1 deletions compared to controls but only the difference among adult AML patients (OR = 2.1, 95% CI = 1.0-4.2) was statistically significant.
  • The CYP2D6*3 variant allele frequency was lower in the overall acute leukemia patients (0.6%) compared to controls (P = 0.03).
  • CYP2D6*1/*3 genotype frequency also showed a protective association in AML patients (OR = 0.09, 95% CI = 0.01-1.7; P = 0.04).
  • We also found a risk association for CYP2E1*5 in ALL and AML (OR = 3.6, 95% CI = 1.4-9.4 and OR = 3.9, 95% CI = 1.4-10.5, respectively).
  • No association was found for the studied CYP2D6*4, CYP1A1*2A, and GSTT1"null" variants and the risk of acute leuke-mia (ALL or AML).
  • This case-control study suggests a contribution of CYP2E1, CYP2D6, and GSTM1 "null" variants to the development of acute leukemias.
  • [MeSH-major] Cytochrome P-450 CYP1A1 / genetics. Cytochrome P-450 CYP2D6 / genetics. Cytochrome P-450 CYP2E1 / genetics. Genetic Predisposition to Disease. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Aged. Alleles. Case-Control Studies. Female. Gene Deletion. Gene Frequency / genetics. Genotype. Humans. Male. Middle Aged. Point Mutation. Polymorphism, Restriction Fragment Length. Risk Factors

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  • (PMID = 16493615.001).
  • [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] EC 1.14.13.- / Cytochrome P-450 CYP2E1; EC 1.14.14.1 / Cytochrome P-450 CYP1A1; EC 1.14.14.1 / Cytochrome P-450 CYP2D6; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1
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93. El-Zawahry HM, Zeeneldin AA, Samra MA, Mattar MM, El-Gammal MM, Abd El-Samee A, Darwish T: Cost and outcome of treatment of adults with acute myeloid leukemia at the National Cancer Institute-Egypt. J Egypt Natl Canc Inst; 2007 Jun;19(2):106-13
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  • [Title] Cost and outcome of treatment of adults with acute myeloid leukemia at the National Cancer Institute-Egypt.
  • BACKGROUND: Despite important advances in the therapy of acute myeloid leukemia (AML), the majority of patients die of their disease, unless bone marrow transplantation (BMT) is done.
  • Infection and hemorrhage are still the major causes of mortality in AML patients.
  • PATIENTS AND METHODS: The aim of this study is to identify the outcome and costs of adult AML patients treated with conventional chemotherapy (CCT) at the National Cancer Institute (NCI), Cairo University during the time period from April 1999 to January 2002.
  • RESULTS: The median age of 82 identified AML patients was 34 years.
  • CONCLUSIONS: Outcome of patients with AML treated at NCI- Cairo University can be enhanced by improvement of supportive therapy; mainly infection control and expanding BMT programs to accommodate all eligible patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / economics
  • [MeSH-minor] Adolescent. Adult. Aged. Egypt. Female. Health Care Costs. Humans. Male. Middle Aged. Prognosis. Remission Induction. Retrospective Studies. Survival Rate. Treatment Outcome. Young Adult

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  • (PMID = 19034340.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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94. Faderl S, Ferrajoli A, Wierda W, Huang X, Verstovsek S, Ravandi F, Estrov Z, Borthakur G, Kwari M, Kantarjian HM: Clofarabine combinations as acute myeloid leukemia salvage therapy. Cancer; 2008 Oct 15;113(8):2090-6
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  • [Title] Clofarabine combinations as acute myeloid leukemia salvage therapy.
  • BACKGROUND: Outcome of patients with relapsed acute myeloid leukemia (AML) remains unsatisfactory.
  • Clofarabine is a nucleoside analog with activity in adult AML.
  • Combinations with cytarabine in AML are feasible and effective.
  • Idarubicin is another active AML drug, which has not yet been tested with clofarabine.
  • Patients with primary refractory or first-relapse AML were assigned to either clofarabine plus idarubicin (CI) if previously exposed to cytarabine with a response lasting <12 months, or clofarabine and idarubicin plus cytarabine (CIA) for responses > or = 12 months, or if never exposed to cytarabine.
  • [MeSH-major] Adenine Nucleotides / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Arabinonucleosides / administration & dosage. Cytarabine / administration & dosage. Idarubicin / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Salvage Therapy / methods
  • [MeSH-minor] Adult. Aged. Humans. Maximum Tolerated Dose. Middle Aged

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  • [Copyright] (c) 2008 American Cancer Society.
  • [CommentIn] Cancer. 2008 Oct 15;113(8):1995-8 [18780321.001]
  • (PMID = 18756533.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Arabinonucleosides; 04079A1RDZ / Cytarabine; 762RDY0Y2H / clofarabine; ZRP63D75JW / Idarubicin
  • [Other-IDs] NLM/ NIHMS593643; NLM/ PMC4163782
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95. Xu N, Liu XL, DU QF, Liu Z, Zhong M, Lin R, Song LL, Yi ZS, Meng FY, Zhou SY: [CD56 and CD11b antigen expressions in patients with acute monocytic leukemia and the clinical implications]. Nan Fang Yi Ke Da Xue Xue Bao; 2009 Aug;29(8):1605-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [CD56 and CD11b antigen expressions in patients with acute monocytic leukemia and the clinical implications].
  • OBJECTIVE: To investigate the expressions of cell surface differentiation antigen CD56 and CD11b antigen in acute monocytic leukemic (AML-M(5)) cells and their clinical significance.
  • METHODS: A total of 113 cases of de nove adult AML-M(5) were examined genetically and immunologically using G-banding technique, interphase fluorescence in situ hybridization (I-FISH) and flow cytometry immunophenotyping, and the results were analyzed in relation to their clinical data.
  • Compared with the patients positive for both CD56 and CD11b, those negative for both CD56 and CD11b showed increased peripheral blood white blood cell (WBC) count and also increased blast and progenitor cells in the bone marrow (P<0.05); the former patients often had karyotypic abnormalities, commonly involving 11q23 aberrations (P<0.05), whereas the latter patients presented more likely with extramedullary infiltration and refractory leukemia (P<0.01) with lowered complete remission rate and shortened median survival time (P<0.01).
  • CD56-positive patients were more likely to have karyotypic abnormalities and refractory leukemia than CD11b-postive patients (P<0.05), but the peripheral blood WBC counts, bone marrow blast and progenitor cells, extramedullary infiltration, complete remission rate or median survival time showed no significant differences between them (P>0.05).
  • CONCLUSION: AML-M(5) patients with CD56 positivity and high expression of CD11b often have aberrant karyotypes, commonly involving 11q23/MLL gene abnormality.
  • These patients frequently develop extramedullary infiltration and refractory leukemia often with poor prognosis.
  • [MeSH-major] Antigens, CD11b / metabolism. Antigens, CD56 / metabolism. Gene Expression Regulation. Leukemia, Monocytic, Acute / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Karyotyping. Leukocyte Count. Male. Middle Aged. Prognosis. Young Adult

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  • (PMID = 19726305.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Antigens, CD56
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96. Di Rocco A, Finolezzi E, Anaclerico B, Calabrese E, Levi A, Trasarti S, Tafuri A: [Therapeutic advances in neoplastic hematology: target therapy anti-CD33]. Clin Ter; 2005 Jul-Aug;156(4):183-6
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  • The CD33 antigen is present on 90% of acute myeloid leukemia blasts and is shared on normal hemopoietic cells only on the non stem dillerentiating fraction.
  • Gemtuzumab Ozogamicin (GO) is an engineered humanized antibody anti-CD33 conjugated with a potent intercalating agent, named calicheamicin, which is release only at intracellular level (lower pH), following a selective binding to CD33-positive cells, thus representing a promising approach for target anti-leukemia therapy.
  • GO was approved conditionally by the Federal Drug Administration in May 2000 as a single therapy for first recurrence of Acute Myeloid Leukemia (AML) in a subset of older patients.
  • Phase II trials have confirmed the activity and the efficacy of GO as single agent in the treatment of relapsed AML.
  • More recently, clinical trials on induction and post-remission treatment of adult AML have shown efficacy of GO in combination chemotherapy.
  • The strong and homogeneous CD33 expression in Acute Promyelocytic Leukemia (APL), have resulted in an effective treatment of this disease with GO used as salvage treatment, as well as innovative approach for molecular relapsed patients.
  • In conclusion, the extension of the approval in Italy to AML CD33+ in relapsed, regardless age limitation, along with the ongoing evaluation by the European EMEA, represent the basis for a large clinical application of GO in myeloid malignancies potentially extended to paediatric patients with AML and to ALL CD33+.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibiotics, Antineoplastic / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antigens, CD. Antigens, Differentiation, Myelomonocytic. Immunotoxins / therapeutic use. Leukemia, Myeloid / drug therapy. Leukemia, Promyelocytic, Acute / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Clinical Trials as Topic. Clinical Trials, Phase II as Topic. Enediynes. Humans. Middle Aged. Pilot Projects. Recurrence. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 16342520.001).
  • [ISSN] 0009-9074
  • [Journal-full-title] La Clinica terapeutica
  • [ISO-abbreviation] Clin Ter
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Enediynes; 0 / Immunotoxins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 108212-75-5 / calicheamicin gamma(1)I
  • [Number-of-references] 27
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97. Kuchenbauer F, Kern W, Schoch C, Kohlmann A, Hiddemann W, Haferlach T, Schnittger S: Detailed analysis of FLT3 expression levels in acute myeloid leukemia. Haematologica; 2005 Dec;90(12):1617-25
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  • [Title] Detailed analysis of FLT3 expression levels in acute myeloid leukemia.
  • BACKGROUND AND OBJECTIVES: FLT3 mutations are found in up to 30% of cases of acute myeloid leukemia (AML).
  • DESIGN AND METHODS: To further evaluate the role of FLT3 in AML we investigated FLT3 expression levels in 207 adult AML patients and 8 healthy donors by real-time polymerase chain reaction (PCR).
  • Independent analysis of FLT3 expression in cytogenetic AML subgroups showed the lowest levels in t(15;17) and the highest in the t(11q23) positive AML.
  • On the molecular level, no differences in FLT3 expression levels were detected between AML with and without any FLT3 mutation as well as for FAB M5 with or without MLL abnormalities (p=0.495).
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Myeloid / enzymology. Neoplasm Proteins / biosynthesis. fms-Like Tyrosine Kinase 3 / biosynthesis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Bone Marrow / pathology. Chromosome Aberrations. Disease-Free Survival. Enzyme Induction. Female. Gene Duplication. Humans. Karyotyping. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / pathology. Leukocyte Count. Life Tables. Male. Middle Aged. Polymerase Chain Reaction. Prognosis. Proportional Hazards Models. RNA, Messenger / biosynthesis. RNA, Messenger / metabolism. RNA, Neoplasm / biosynthesis. RNA, Neoplasm / metabolism. Survival Analysis. Tandem Repeat Sequences

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  • [CommentIn] Haematologica. 2005 Dec;90(12):1586 [16330422.001]
  • (PMID = 16330434.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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98. Flandrin P, Guyotat D, Duval A, Cornillon J, Tavernier E, Nadal N, Campos L: Significance of heat-shock protein (HSP) 90 expression in acute myeloid leukemia cells. Cell Stress Chaperones; 2008 Sep;13(3):357-64
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  • [Title] Significance of heat-shock protein (HSP) 90 expression in acute myeloid leukemia cells.
  • The objective of this study was to assess its expression in primary acute myeloid leukemia (AML) cells and to evaluate its biological and clinical significance.
  • Cells from 65 patients with newly diagnosed AML were studied.
  • Our study suggests that HSP90 is overexpressed in poor-prognosis AML cells and plays a role in cell survival and resistance to chemotherapy.
  • Targeted therapy with 17-AAG represents a promising antileukemic strategy in adult AML.
  • [MeSH-major] HSP90 Heat-Shock Proteins / metabolism. Leukemia, Myeloid, Acute / metabolism
  • [MeSH-minor] Adult. Aged. Antigens, CD34 / metabolism. Benzoquinones / pharmacology. Humans. Lactams, Macrocyclic / pharmacology. Middle Aged. Myeloid Cells / cytology. Myeloid Cells / drug effects. Myeloid Cells / metabolism. Statistics as Topic. Survival Rate

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  • [Cites] Annu Rev Genet. 1988;22:631-77 [2853609.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1438-40 [15175626.001]
  • [Cites] N Engl J Med. 1993 Mar 4;328(9):614-9 [8429853.001]
  • [Cites] Blood. 1993 Jun 1;81(11):3091-6 [7684624.001]
  • [Cites] J Biol Chem. 1993 Oct 15;268(29):21711-6 [8408024.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14536-41 [8962087.001]
  • [Cites] Leuk Lymphoma. 1997 Jan;24(3-4):221-8 [9156652.001]
  • [Cites] J Biol Chem. 1997 Sep 19;272(38):23843-50 [9295332.001]
  • [Cites] Cancer Chemother Pharmacol. 1998;42(4):273-9 [9744771.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1768-76 [15514006.001]
  • [Cites] J Clin Oncol. 2005 Feb 20;23(6):1078-87 [15718306.001]
  • [Cites] Blood. 2005 Jul 1;106(1):318-27 [15784732.001]
  • [Cites] Blood. 2005 Aug 1;106(3):1063-6 [15840695.001]
  • [Cites] Leuk Res. 2005 Sep;29(9):1049-58 [16038731.001]
  • [Cites] Leukemia. 2005 Jul;19(7):1198-206 [15902298.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2358-65 [16763210.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 26;97(20):10832-7 [10995457.001]
  • [Cites] Cancer Res. 2001 May 15;61(10):4003-9 [11358818.001]
  • [Cites] J Cell Biol. 2001 Jul 23;154(2):267-73 [11470816.001]
  • [Cites] J Biol Chem. 2002 Mar 22;277(12):10346-53 [11779851.001]
  • [Cites] Leukemia. 2002 Aug;16(8):1535-40 [12145695.001]
  • [Cites] J Biol Chem. 2002 Oct 11;277(41):38294-304 [12161444.001]
  • [Cites] J Biol Chem. 2002 Oct 18;277(42):39858-66 [12176997.001]
  • [Cites] Onkologie. 2002 Oct;25(5):466-73 [12415202.001]
  • [Cites] Exp Biol Med (Maywood). 2003 Feb;228(2):111-33 [12563018.001]
  • [Cites] Blood. 2003 Jul 1;102(1):269-75 [12623837.001]
  • [Cites] Blood. 2003 Aug 1;102(3):972-80 [12702506.001]
  • [Cites] Ann Oncol. 2003 Aug;14(8):1169-76 [12881371.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2198-204 [12791658.001]
  • [Cites] Cytometry A. 2003 Oct;55(2):61-70 [14505311.001]
  • [Cites] Nature. 2003 Sep 25;425(6956):407-10 [14508491.001]
  • [Cites] Clin Cancer Res. 2003 Oct 1;9(12):4483-93 [14555522.001]
  • [Cites] Cancer Res. 2003 Dec 1;63(23):8420-7 [14679005.001]
  • [Cites] Blood. 2004 Feb 1;103(3):1078-84 [14551138.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3645-52 [15150124.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]
  • [Cites] Cell Growth Differ. 2000 Jul;11(7):355-60 [10939589.001]
  • [Cites] Leuk Res. 1992 Jun-Jul;16(6-7):597-605 [1635378.001]
  • (PMID = 18386162.001).
  • [ISSN] 1355-8145
  • [Journal-full-title] Cell stress & chaperones
  • [ISO-abbreviation] Cell Stress Chaperones
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 4GY0AVT3L4 / tanespimycin
  • [Other-IDs] NLM/ PMC2673940
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99. McKoy JM, Angelotta C, Bennett CL, Tallman MS, Wadleigh M, Evens AM, Kuzel TM, Trifilio SM, Raisch DW, Kell J, DeAngelo DJ, Giles FJ: Gemtuzumab ozogamicin-associated sinusoidal obstructive syndrome (SOS): an overview from the research on adverse drug events and reports (RADAR) project. Leuk Res; 2007 May;31(5):599-604
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  • Gemtuzumab ozogamicin (GO) was approved for marketing in 2000 by the United States Food and Drug Administration (FDA) for older patients with relapsed acute myeloid leukemia (AML).
  • Among adult AML patients who received GO in clinical trials, SOS incidence was 3% at doses < or =6 mg/m(2) if administered as monotherapy or in combination with non-hepatotoxic agents versus 28% if administered with thioguanine and 15% when administered as monotherapy at a dose of 9 mg/m(2).
  • [MeSH-major] Aminoglycosides / adverse effects. Antibodies, Monoclonal / adverse effects. Antineoplastic Agents / adverse effects. Hepatic Veno-Occlusive Disease / chemically induced. Leukemia, Myeloid / drug therapy
  • [MeSH-minor] Acute Disease. Adverse Drug Reaction Reporting Systems. Antibodies, Monoclonal, Humanized. Clinical Trials, Phase II as Topic. Humans. Immunotoxins / adverse effects. Incidence. Prospective Studies. United States. United States Food and Drug Administration

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  • (PMID = 16959316.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Immunotoxins; 0 / gemtuzumab
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100. Iversen PO, Wiig H: Tumor necrosis factor alpha and adiponectin in bone marrow interstitial fluid from patients with acute myeloid leukemia inhibit normal hematopoiesis. Clin Cancer Res; 2005 Oct 1;11(19 Pt 1):6793-9
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  • [Title] Tumor necrosis factor alpha and adiponectin in bone marrow interstitial fluid from patients with acute myeloid leukemia inhibit normal hematopoiesis.
  • PURPOSE: Locally residing cytokines may inhibit bone marrow hematopoiesis in acute myeloid leukemia (AML).
  • Using a novel method to isolate bone marrow interstitial fluid, we examined if this fluid from 10 adult AML patients could affect normal bone marrow hematopoiesis.
  • RESULTS: Unlike plasma, AML-derived bone marrow interstitial fluid clearly repressed hematopoietic progenitor cell growth as determined by an in vitro colony assay, an effect that was lost after successful induction treatment.
  • Antibodies against tumor necrosis factor alpha (TNFalpha) and adiponectin abolished growth inhibition by bone marrow interstitial fluid, suggesting a mechanistic role of these cytokines in impairing normal hematopoiesis in AML.
  • Transcripts for TNFalpha, but not for adiponectin, were found in AML blast cells.
  • [MeSH-major] Adiponectin / physiology. Bone Marrow Cells / cytology. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / metabolism. Tumor Necrosis Factor-alpha / physiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD34 / biosynthesis. Biopsy. Bone Marrow / metabolism. Centrifugation. Cytokines / metabolism. Down-Regulation. Extracellular Fluid / metabolism. Female. Hematopoiesis. Hematopoietic Stem Cells / metabolism. Hematopoietic System. Humans. Male. Middle Aged. Neovascularization, Pathologic. Remission Induction. Time Factors

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • Genetic Alliance. consumer health - Bone marrow necrosis.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
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  • (PMID = 16203766.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Antigens, CD34; 0 / Cytokines; 0 / Tumor Necrosis Factor-alpha
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