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1. Abdallah E, Hajji Z, Mellal Z, Belmekki M, Bencherifa F, Berraho A: [Macular serous detachment revealing acute lymphoblastic leukemia]. J Fr Ophtalmol; 2005 Jan;28(1):39-44
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  • [Title] [Macular serous detachment revealing acute lymphoblastic leukemia].
  • BACKGROUND: Leukemias are a group of malignant diseases caused by immature hematopoietic cells proliferating in the blood marrow.
  • OBSERVATION: We report a case of a 42-year-old women presenting with loss of vision caused by serous macular detachment.
  • The investigations showed the diagnosis of acute lymphoblastic leukemia.
  • DISCUSSION: Ocular involvement is seen in 28%-80% of leukemia cases.
  • Serous detachment of the neuroepithelium is seldom reported, and can be the first symptom of the disease.
  • CONCLUSION: Ocular manifestations of leukemia are frequent but rarely reveal the disease.
  • However, the diagnosis of leukemia should be considered in case of pigmentary epithelium involvement.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Retinal Detachment / etiology

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  • (PMID = 15767897.001).
  • [ISSN] 0181-5512
  • [Journal-full-title] Journal français d'ophtalmologie
  • [ISO-abbreviation] J Fr Ophtalmol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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2. Faber J, Gregory RI, Armstrong SA: Linking miRNA regulation to BCR-ABL expression: the next dimension. Cancer Cell; 2008 Jun;13(6):467-9
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  • The introduction of tyrosine kinase inhibitors in the treatment of BCR-ABL1-rearranged malignancies has revolutionized therapy, but the prognosis for acute leukemias remains suboptimal.
  • In this issue of Cancer Cell, Bueno et al. (2008) add a new dimension to the regulation of ABL1 expression.
  • The authors demonstrate that ABL1 is a direct target of miR-203, miR-203 is silenced by genetic and epigenetic mechanisms in hematopoietic malignancies expressing either ABL1 or BCR-ABL1, and restoration of miR-203 expression reduces ABL1 and BCR-ABL1 levels and inhibits cell proliferation.
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Cell Proliferation. Gene Expression Regulation, Leukemic. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphoma, T-Cell / genetics. Lymphoma, T-Cell / metabolism. Lymphoma, T-Cell / pathology. Mice. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Protein Kinase Inhibitors / therapeutic use. Up-Regulation

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  • [CommentOn] Cancer Cell. 2008 Jun;13(6):496-506 [18538733.001]
  • (PMID = 18538729.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / MicroRNAs; 0 / Protein Kinase Inhibitors; 0 / abl-bcr fusion protein, human; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
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3. Chowdhury T, Brady HJ: Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia. Blood Cells Mol Dis; 2008 Mar-Apr;40(2):192-9
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  • [Title] Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.
  • Translocations involving the Mixed Lineage Leukemia (MLL) gene at 11q23 are found in both acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but have different prognostic implications depending on the phenotype of the leukemia in de novo pediatric cases.
  • The use of DNA microarray analysis to distinguish a particular gene signature for MLL-rearranged leukemias is shedding light on the molecular mechanisms and potential therapeutic targets of these leukemias.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17905612.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 82
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4. Migkou M, Dimopoulos MA, Gavriatopoulou M, Terpos E: Applications of monoclonal antibodies for the treatment of hematological malignancies. Expert Opin Biol Ther; 2009 Feb;9(2):207-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The introduction of mAbs has changed the clinical approach to patients with lymphoma and leukemia.
  • RESULTS: Rituximab (anti-CD20) was the first mAb developed for the treatment of B-cell lymphomas.
  • Several randomized studies have demonstrated its efficacy in lymphomas and low toxicity profile; rituximab also has significant activity in chronic lymphocytic leukemia (CLL).
  • Alemtuzumab (anti-CD52) has shown efficacy in previously untreated or refractory CLL patients, while gemtuzumab ozogamicin (anti-CD33) appears to have significant activity in acute myeloid leukemias and myelodysplastic syndromes.
  • CONCLUSIONS: In the next few years, investigations will be concentrated on the improvement of the older mAbs, and the development of new mAbs, targeting molecules important for malignant cell cycle and survival in an attempt to further improve patient survival.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy

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  • (PMID = 19236251.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents
  • [Number-of-references] 107
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5. Lü SQ, Yang JM, Wang JM: [Effects of proteasome inhibitors on leukemias]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):896-900
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  • [Title] [Effects of proteasome inhibitors on leukemias].
  • A lot of studies on effects of proteasome inhibitors on leukemias, including plasma cell leukemia; chronic lymphocytic leukemia, adult T cell lymphoma/leukemia, chronic myeloid leukemia and acute myeloid leukemia, were reviewed in this article.

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  • (PMID = 17708829.001).
  • [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; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 27
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6. Diakos C, Zhong S, Xiao Y, Zhou M, Vasconcelos GM, Krapf G, Yeh RF, Zheng S, Kang M, Wiencke JK, Pombo-de-Oliveira MS, Panzer-Grümayer R, Wiemels JL: TEL-AML1 regulation of survivin and apoptosis via miRNA-494 and miRNA-320a. Blood; 2010 Dec 2;116(23):4885-93
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  • We explored the impact of TEL-AML1 (ETV6-RUNX1), the most common fusion protein in childhood leukemia, on miRNA expression and the leukemic phenotype.
  • These miRNAs blocked survivin expression and resulted in apoptosis in a similar manner as TEL-AML1 silencing by itself; this silencing was also shown to be Dicer-dependent. miRNAs-494 and -320a are expressed at lower levels in TEL-AML1+ leukemias compared with immunophenotype-matched nonTEL-AML1 acute lymphoblastic leukemia subtypes, and within TEL-AML1+ leukemias their expression is correlated to survivin levels.

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  • (PMID = 20807887.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA089032; United States / NCI NIH HHS / CA / R03-CA137829; United States / NCI NIH HHS / CA / R01 CA089032-06; United States / NCI NIH HHS / CA / R03 CA137829; United States / NCI NIH HHS / CA / R01-CA89032; United States / NCI NIH HHS / CA / CA137829-02; United States / NCI NIH HHS / CA / R03 CA137829-02; United States / NCI NIH HHS / CA / R01 CA089032-05; United States / NCI NIH HHS / CA / CA137829-01A1; United States / NCI NIH HHS / CA / R03 CA137829-01A1
  • [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 / BIRC5 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Inhibitor of Apoptosis Proteins; 0 / MicroRNAs; 0 / Microtubule-Associated Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / TEL-AML1 fusion protein
  • [Other-IDs] NLM/ PMC3265147
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7. Schwonzen M, Diehl V, Dellanna M, Staib P: Immunophenotyping of surface antigens in acute myeloid leukemia by flow cytometry after red blood cell lysis. Leuk Res; 2007 Jan;31(1):113-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotyping of surface antigens in acute myeloid leukemia by flow cytometry after red blood cell lysis.
  • Immunophenotyping of acute leukemia using flow cytometry after density gradient separation (dg-sep) of mononuclear cells is the international gold standard.
  • Both methods revealed congruent results in phenotyping of 26 cases of acute myeloid leukemias by testing CD4, CD7, CD11b, CD11c, CD13, CD14, CD15, CD33, CD34, CD65s, Glycophorin A and HLA-DR antigens.
  • [MeSH-major] Antigens, CD / analysis. Antigens, Surface / analysis. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 16730795.001).
  • [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 / Antigens, CD; 0 / Antigens, Surface; 0 / Glycophorin; 0 / HLA-DR Antigens
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8. Cairoli R, Beghini A, Grillo G, Nadali G, Elice F, Ripamonti CB, Colapietro P, Nichelatti M, Pezzetti L, Lunghi M, Cuneo A, Viola A, Ferrara F, Lazzarino M, Rodeghiero F, Pizzolo G, Larizza L, Morra E: Prognostic impact of c-KIT mutations in core binding factor leukemias: an Italian retrospective study. Blood; 2006 May 1;107(9):3463-8
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  • [Title] Prognostic impact of c-KIT mutations in core binding factor leukemias: an Italian retrospective study.
  • Distinct forms of tyrosine kinase domain (TKD), juxtamembrane domain, exon 8, and internal tandem duplication (ITD) mutations of c-KIT, were observed in about 46% of core binding factor leukemia (CBFL) patients.
  • In acute myeloid leukemia (AML) with t(8;21), the presence of c-KIT TKD mutation at codon 816 (TKD(816)) was associated with a high white blood cell count at diagnosis (median, 29.60 x 10(9)/L) and a higher incidence (33%) of extramedullary leukemia (EML) during the course of the disease.
  • [MeSH-major] Core Binding Factors / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Proto-Oncogene Proteins c-kit / genetics

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  • (PMID = 16384925.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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9. Ishii E, Oda M, Kinugawa N, Oda T, Takimoto T, Suzuki N, Kosaka Y, Ohara A, Ogawa A, Ishii M, Sakata N, Okamura T, Koike K, Kojima S, Horibe K, Mizutani S: Features and outcome of neonatal leukemia in Japan: experience of the Japan infant leukemia study group. Pediatr Blood Cancer; 2006 Sep;47(3):268-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Features and outcome of neonatal leukemia in Japan: experience of the Japan infant leukemia study group.
  • BACKGROUND: Neonatal leukemia characterized by early stem cell origin and extramedullary infiltration in the first 4 weeks of life is rare.
  • We analyzed the features and outcome of neonatal leukemia in Japan to establish an appropriate treatment strategy for this rare disorder.
  • PROCEDURE: Patients with infant leukemia registered and treated in the Japan Infant Leukemia Study between 1996 and 2001 were analyzed.
  • RESULTS: Among 162 infant leukemia patients, 11 exhibited neonatal leukemia; frequencies for all infant leukemias were 6.9% (8/116) for acute lymphoblastic leukemia (ALL) and 7.3% (3/41) for acute myeloid leukemia (AML).
  • Acute monoblastic leukemia was apparent in all three patients with AML (M5a in the FAB classification).
  • Four patients (one with AML, and three with ALL) have survived following stem cell transplantation (SCT); however, growth impairment related to SCT was observed in these patients.
  • CONCLUSIONS: These results suggest an improvement attributable to treatment of neonatal leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation
  • [MeSH-minor] Acute Disease. Female. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Japan / epidemiology. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Registries. Survival Rate. Treatment Outcome

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  • [CommentIn] Pediatr Blood Cancer. 2006 Sep;47(3):234-5 [16206196.001]
  • (PMID = 16333820.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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10. Miller AL, Komak S, Webb MS, Leiter EH, Thompson EB: Gene expression profiling of leukemic cells and primary thymocytes predicts a signature for apoptotic sensitivity to glucocorticoids. Cancer Cell Int; 2007 Nov 28;7:18
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  • By activating the glucocorticoid receptor (GR), GCs evoke apoptosis through transcriptional regulation of a complex, interactive gene network over a period of time preceding activation of the apoptotic enzymes.
  • Pediatric CD4+/CD8+ T-cell leukemia was represented by 3 CEM clones: two sensitive, CEM-C7-14 and CEM-C1-6, and one resistant, CEM-C1-15, to Dex.
  • GC-sensitive pediatric B-cell leukemia was represented by the SUP-B15 line and adult B-cell leukemia by RS4;11 cells.
  • Kasumi-1 cells gave an example of the rare Dex-sensitive acute myeloblastic leukemia (AML).
  • To test the generality of the correlations in malignant cell gene sets, we compared with GC effects on mouse non-transformed thymocytes.

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  • (PMID = 18045478.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA041407
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2228275
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11. Kojima K, Burks JK, Arts J, Andreeff M: The novel tryptamine derivative JNJ-26854165 induces wild-type p53- and E2F1-mediated apoptosis in acute myeloid and lymphoid leukemias. Mol Cancer Ther; 2010 Sep;9(9):2545-57
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  • [Title] The novel tryptamine derivative JNJ-26854165 induces wild-type p53- and E2F1-mediated apoptosis in acute myeloid and lymphoid leukemias.
  • The development of small-molecule activators of p53 is currently focused on malignancies containing a wild-type p53 genotype, which is present in most leukemias.
  • Here, we report the effects of JNJ-26854165 in acute leukemias.
  • JNJ-26854165 treatment induced p53-mediated apoptosis in acute leukemia cells with wild-type p53, in which p53 rapidly drives transcription-independent apoptosis followed by activation of a transcription-dependent pathway.
  • Apoptotic activity of JNJ-26854165 against primary acute leukemia cells was maintained in leukemia/stroma cocultures, unlike doxorubicin, which has reduced cytrotoxicity in coculture systems.
  • Our data suggest that JNJ-26854165 may provide a novel therapeutic approach for the treatment of acute leukemias.
  • [MeSH-major] Apoptosis / drug effects. E2F1 Transcription Factor / metabolism. Genes, p53. Leukemia, Myeloid, Acute / drug therapy. Tryptamines / pharmacology
  • [MeSH-minor] Cell Line, Tumor. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Transfection

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  • (PMID = 20736344.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA89346; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA089346-03; United States / NCI NIH HHS / CA / CA49639; United States / NCI NIH HHS / CA / P01 CA049639-09A19007; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA055164-09; United States / NCI NIH HHS / CA / R01 CA089346; United States / NCI NIH HHS / CA / P30 CA016672-22S29015; United States / NCI NIH HHS / CA / P01 CA055164-08; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / P01 CA049639; 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 / E2F1 Transcription Factor; 0 / Tryptamines
  • [Other-IDs] NLM/ NIHMS231527; NLM/ PMC2949269
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12. Zwaan MC, Reinhardt D, Hitzler J, Vyas P: Acute leukemias in children with Down syndrome. Pediatr Clin North Am; 2008 Feb;55(1):53-70, x
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  • [Title] Acute leukemias in children with Down syndrome.
  • Children with Down syndrome have an increased risk for developing both acute myeloid as well as lymphoblastic leukemia.
  • These leukemias differ in presenting characteristics and underlying biology when compared with leukemias occurring in non-Down syndrome children.
  • Myeloid leukemia in children with Down syndrome is preceded by a preleukemic clone (transient leukemia or transient myeloproliferative disorder), which may disappear spontaneously, but may also need treatment in case of severe symptoms.
  • Twenty percent of children with transient leukemia subsequently develop myeloid leukemia.
  • This transition offers a unique model to study the stepwise development of leukemia, and of gene dosage effects mediated by aneuploidy.
  • [MeSH-major] Down Syndrome / complications. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Disease Progression. Humans. Infant. Infant, Newborn. Mutation

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  • (PMID = 18242315.001).
  • [ISSN] 0031-3955
  • [Journal-full-title] Pediatric clinics of North America
  • [ISO-abbreviation] Pediatr. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 83
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13. Radomska HS, Bassères DS, Zheng R, Zhang P, Dayaram T, Yamamoto Y, Sternberg DW, Lokker N, Giese NA, Bohlander SK, Schnittger S, Delmotte MH, Davis RJ, Small D, Hiddemann W, Gilliland DG, Tenen DG: Block of C/EBP alpha function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations. J Exp Med; 2006 Feb 20;203(2):371-81
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  • [Title] Block of C/EBP alpha function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations.
  • Mutations constitutively activating FLT3 kinase are detected in approximately 30% of acute myelogenous leukemia (AML) patients and affect downstream pathways such as extracellular signal-regulated kinase (ERK)1/2.
  • In contrast, there was no effect when serine 21 was mutated to aspartate (S21D), which mimics phosphorylation of C/EBPalpha.
  • Thus, our results suggest that therapies targeting the MEK/ERK cascade or development of protein therapies based on transduction of constitutively active C/EBPalpha may prove effective in treatment of FLT3 mutant leukemias resistant to the FLT3 inhibitor therapies.


14. Pratz KW, Cho E, Levis MJ, Karp JE, Gore SD, McDevitt M, Stine A, Zhao M, Baker SD, Carducci MA, Wright JJ, Rudek MA, Smith BD: A pharmacodynamic study of sorafenib in patients with relapsed and refractory acute leukemias. Leukemia; 2010 Aug;24(8):1437-44
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  • [Title] A pharmacodynamic study of sorafenib in patients with relapsed and refractory acute leukemias.
  • We report the results of a phase I dose escalation trial of the multikinase inhibitor sorafenib in relapsed and refractory acute leukemia patients using an intermittent dosing regimen.
  • Fifteen patients with advanced leukemia (12 with acute myeloid leukemia, 2 with acute lymphoblastic leukemia, 1 with biphenotypic) and a median age of 63 (range 37-85) years were enrolled and treated on a dose escalation trial.
  • Out of 15 patients, 11 experienced stable disease as best response.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use

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  • (PMID = 20535150.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA128864; United States / NCI NIH HHS / CA / P30 CA006973-48; United States / NCRR NIH HHS / RR / UL1 RR025005; United States / NCI NIH HHS / CA / P30CA006973; United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCRR NIH HHS / RR / UL1 RR025005-04; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / P50 CA100632-06; United States / NCI NIH HHS / CA / R01 CA128864-04; United States / NCI NIH HHS / CA / U01 CA070095-17; United States / NCI NIH HHS / CA / U01CA70095
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ NIHMS201571; NLM/ PMC2921005
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15. Lu L, Zhang L, Xiao Z, Lu S, Yang R, Han ZC: Neuropilin-1 in acute myeloid leukemia: expression and role in proliferation and migration of leukemia cells. Leuk Lymphoma; 2008 Feb;49(2):331-8
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  • [Title] Neuropilin-1 in acute myeloid leukemia: expression and role in proliferation and migration of leukemia cells.
  • The role of NRP-1 in the growth and progression of leukemia is unknown.
  • Our results showed that NRP-1 mRNA was expressed in six of seven leukemic cell lines and primary leukemias derived from all 24 patients with acute myeloid leukemia (AML).
  • Reduced NRP-1 expression by RNA interference led to a decrease of VEGF-mediated mitogenic and migration responses in acute myeloid leukemic cell line HEL.
  • Our data demonstrated that a higher level of NRP-1 mRNA was expressed in leukemias and NRP-1 promoted proliferation and chemotaxis of leukemic cells in response to VEGF.
  • [MeSH-major] Cell Movement. Cell Proliferation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / pathology. Neuropilin-1 / analysis. Vascular Endothelial Growth Factor A / physiology
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Survival. Chemotaxis. Child. Female. Humans. Male. Middle Aged. RNA, Messenger / analysis. RNA, Small Interfering / pharmacology. Tumor Cells, Cultured

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  • (PMID = 18231921.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 144713-63-3 / Neuropilin-1
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16. Yamamoto JF, Goodman MT: Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002. Cancer Causes Control; 2008 May;19(4):379-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002.
  • OBJECTIVE: Efforts to prevent leukemia have been hampered by an inability to identify significant risk factors.
  • Exploring incidence patterns of leukemia subtypes by sex and race/ethnic group may generate new etiologic hypotheses and identify high-risk groups for further study.
  • METHODS: Data from the North American Association of Central Cancer Registries for 1997-2002 were used to assess patterns of leukemia incidence by subtype, sex, age, race and ethnicity.
  • RESULTS: A total of 144,559 leukemia cases were identified, including 66,067 (46%) acute and 71,860 (50%) chronic leukemias.
  • The highest rates of acute myeloid leukemia with and without maturation were observed in Asian-Pacific Islanders (API).
  • Hispanics had a higher incidence of acute lymphocytic leukemia, particularly in childhood, and promyelocytic leukemia than did non-Hispanics.
  • African-Americans had the highest rates of HTLV-1 positive adult T-cell leukemia/lymphoma.
  • A sharp increase in the incidence of chronic myeloid leukemia was observed for both APIs and Hispanics, 85 years and older.
  • CONCLUSION: Known risk factors are unlikely to explain the observed disparities in leukemia incidence.
  • Further studies of differences in environmental and genetic risk factors in these populations by specific leukemia subtype may provide clues to the etiologies of these malignancies.
  • [MeSH-major] Leukemia / ethnology

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  • (PMID = 18064533.001).
  • [ISSN] 0957-5243
  • [Journal-full-title] Cancer causes & control : CCC
  • [ISO-abbreviation] Cancer Causes Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
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17. Qi H, Xiao L, Lingyun W, Ying T, Yi-Zhi L, Shao-Xu Y, Quan P: Expression of type 1 insulin-like growth factor receptor in marrow nucleated cells in malignant hematological disorders: correlation with apoptosis. Ann Hematol; 2006 Feb;85(2):95-101
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  • To verify the expression of type 1 insulin-like growth factor receptor (IGF-IR) and its impact on hematopoietic cells apoptosis in myelodysplastic syndromes (MDS) and acute myeloid leukemias (AML), marrow samples from 16 patients with MDS and 16 patients with AML were examined along with 16 healthy donors as controls.
  • Immunocytochemical methods (alkaline phosphatase anti-alkaline phosphatase) and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (fluorescence) were used simultaneously on nucleated cell cytospins.
  • In MDS nucleated cells, IGF-IR showed stronger expression in refractory anemia with excess blasts (RAEB)/RAEB in transformation/chronic myelomonocytic leukemia subgroup when compared to RA/RA with ringed sideroblasts cases (64.1+/-3.2 vs 53.5+/-16.2%) (P>0.05).
  • When analyzed by groups, cell number with IGF-IR expression showed a negative correlation to apoptotic cells amount (r=-0.852; P<0.01) but positive correlation to their blast count (r=0.677; P<0.01).
  • In conclusion, overexpression of IGF-IR existed in hematopoietic cells in MDS and AML marrows, which appeared to be contributed to disease progress.
  • [MeSH-major] Apoptosis. Bone Marrow Cells / cytology. Gene Expression Regulation, Neoplastic. Hematologic Neoplasms / metabolism. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Receptor, IGF Type 1 / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Anemia / metabolism. Cell Transformation, Neoplastic. Child. Female. Humans. Male. Middle Aged


18. Zhang X, Huang H, Xu Z, Zhan R: 2-Methoxyestradiol blocks cell-cycle progression at the G2/M phase and induces apoptosis in human acute T lymphoblastic leukemia CEM cells. Acta Biochim Biophys Sin (Shanghai); 2010 Sep;42(9):615-22
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  • [Title] 2-Methoxyestradiol blocks cell-cycle progression at the G2/M phase and induces apoptosis in human acute T lymphoblastic leukemia CEM cells.
  • The current study sought to determine the mechanism of anti-cancer activity of 2-ME2 in human acute T lymphoblastic leukemia CEM cells.
  • Exposure to 2-ME2 led to G(2)/M phase cell-cycle arrest, which preceded apoptosis characterized by the appearance of a sub-G(1) cell population.
  • Moreover, the expression level of p21 protein was upregulated, whereas Bcl-2 and dysfunctional p53 protein were downregulated, which also contributed to 2-ME2-induced apoptosis.
  • Our findings revealed that 2-ME2 might be a potent natural candidate for chemotherapeutic treatment of human acute T lymphoblastic leukemia when the precise effects of 2-ME2 were investigated further in other T leukemia cell lines and in primary T-cell leukemias.
  • [MeSH-major] Apoptosis / drug effects. Cell Cycle / drug effects. Estradiol / analogs & derivatives
  • [MeSH-minor] Apoptosis Regulatory Proteins / genetics. Apoptosis Regulatory Proteins / metabolism. Blotting, Western. Cell Division / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Flow Cytometry. G2 Phase / drug effects. Gene Expression Regulation, Leukemic / drug effects. Humans. Membrane Potential, Mitochondrial / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tubulin Modulators / pharmacology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 20732853.001).
  • [ISSN] 1745-7270
  • [Journal-full-title] Acta biochimica et biophysica Sinica
  • [ISO-abbreviation] Acta Biochim. Biophys. Sin. (Shanghai)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tubulin Modulators; 0 / Tumor Suppressor Protein p53; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol
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19. Clappier E, Cuccuini W, Cayuela JM, Vecchione D, Baruchel A, Dombret H, Sigaux F, Soulier J: Cyclin D2 dysregulation by chromosomal translocations to TCR loci in T-cell acute lymphoblastic leukemias. Leukemia; 2006 Jan;20(1):82-6
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  • [Title] Cyclin D2 dysregulation by chromosomal translocations to TCR loci in T-cell acute lymphoblastic leukemias.
  • While the cyclin D1 and D3 genes (CCND1 and CCND3) are recurrently involved in genomic rearrangements, especially in B-cell lymphoid neoplasias, no clear involvement of the cyclin D2 gene (CCND2) has been reported to date.
  • Here, we identified chromosomal translocations targeting the CCND2 locus at 12p13, and the T-cell receptor beta (TCRB) or the TCRA/D loci in T-cell acute lymphoblastic leukemias (T-ALLs).
  • In order to evaluate dysregulation in T-ALL with respect to normal T-cell differentiation, we analyzed CCND2 expression in normal purified human thymic subpopulations.
  • CCND2 levels were downregulated through progression from the early stages of human T-cell differentiation, further suggesting that the massive and sustained expression in the CCND2-rearranged T-ALL cases was oncogenic.
  • This report is the first clear evidence of a direct involvement of cyclin D2 in human cancer due to recurrent somatic genetic alterations.
  • [MeSH-major] Chromosomes, Human, Pair 12 / genetics. Cyclins / biosynthesis. Cyclins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Antigen, T-Cell / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Cell Separation. Child. Cyclin D2. Cytogenetic Analysis. DNA Mutational Analysis. Gene Rearrangement. Humans

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  • (PMID = 16270038.001).
  • [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 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Receptors, Antigen, T-Cell
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20. Aikawa Y, Katsumoto T, Zhang P, Shima H, Shino M, Terui K, Ito E, Ohno H, Stanley ER, Singh H, Tenen DG, Kitabayashi I: PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2. Nat Med; 2010 May;16(5):580-5, 1p following 585
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  • [Title] PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2.
  • Leukemias and other cancers possess self-renewing stem cells that help to maintain the cancer.
  • Cancer stem cell eradication is thought to be crucial for successful anticancer therapy.
  • Using an acute myeloid leukemia (AML) model induced by the leukemia-associated monocytic leukemia zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation of leukemia stem cells.
  • Cells expressing high amounts of CSF1R (CSF1R(high) cells), but not those expressing low amounts of CSF1R (CSF1R(low) cells), showed potent leukemia-initiating activity.
  • Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2-induced leukemia.
  • Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1R(high) cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach.

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  • (PMID = 20418886.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA041456-24; United States / NCI NIH HHS / CA / R01 CA032551; United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / 5P30-CA13330; United States / NCI NIH HHS / CA / CA041456-24; United States / NCI NIH HHS / CA / R01-CA41456; United States / NCI NIH HHS / CA / CA32551; United States / NCI NIH HHS / CA / R01 CA041456; United States / NCI NIH HHS / CA / P30 CA013330; United States / NHLBI NIH HHS / HL / R01 HL112719
  • [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 / Colony-Stimulating Factors; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Proto-Oncogene Proteins; 0 / Receptors, Colony-Stimulating Factor; 0 / Recombinant Fusion Proteins; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS265702; NLM/ PMC3039870
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21. Chen E, Kwon YT, Lim MS, Dubé ID, Hough MR: Loss of Ubr1 promotes aneuploidy and accelerates B-cell lymphomagenesis in TLX1/HOX11-transgenic mice. Oncogene; 2006 Sep 21;25(42):5752-63
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  • [Title] Loss of Ubr1 promotes aneuploidy and accelerates B-cell lymphomagenesis in TLX1/HOX11-transgenic mice.
  • The TLX1/HOX11 homeobox gene was originally identified at the recurrent t(10;14)(q24;q11) translocation breakpoint, a chromosomal abnormality observed in 5-7% of T-cell acute lymphoblastic leukemias (T-ALLs).
  • Proviral insertional mutagenesis studies performed on transgenic mice ectopically expressing TLX1/HOX11 in B lymphocytes (IgHmu-HOX11(Tg) mice) revealed the Ubr1 gene locus as a frequent site of proviral insertion, concomitant with accelerated development of diffuse large B-cell lymphoma.
  • Loss or reduced levels of Ubr1 expression was associated with 5/14 spontaneous B-cell lymphomas in IgHmu-HOX11(Tg) mice and one of nine primary human T-ALLs.
  • IgHmu-HOX11(Tg)/Ubr1(-/-) mice exhibited a modest but statistically significant acceleration of disease onset relative to IgHmu-HOX11(Tg)/Ubr1(+/-) mice.
  • Moreover, micronucleus assays to detect for chromosome missegregation were conducted and revealed increased presence of micronuclei in IgHmu-HOX11(Tg)/Ubr1(-/-) primary B lymphocyte cultures, and in both TLX1/HOX11-overexpressing T cell lines and fibroblast cultures following transfection with short interfering RNAs (siRNAs) targeting Ubr1.
  • [MeSH-major] Homeodomain Proteins / genetics. Lymphoma, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Ubiquitin-Protein Ligases / deficiency
  • [MeSH-minor] Animals. Blotting, Southern. DNA Primers. Genome, Viral. Humans. Lymphocytes / physiology. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Micronucleus Tests. Mitosis. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 16862188.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM69482
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 143275-75-6 / TLX1 protein, human; EC 6.3.2.19 / UBR1 protein, mouse; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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22. Hsu KC, Gooley T, Malkki M, Pinto-Agnello C, Dupont B, Bignon JD, Bornhäuser M, Christiansen F, Gratwohl A, Morishima Y, Oudshoorn M, Ringden O, van Rood JJ, Petersdorf E, International Histocompatibility Working Group: KIR ligands and prediction of relapse after unrelated donor hematopoietic cell transplantation for hematologic malignancy. Biol Blood Marrow Transplant; 2006 Aug;12(8):828-36
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  • [Title] KIR ligands and prediction of relapse after unrelated donor hematopoietic cell transplantation for hematologic malignancy.
  • Recurrent malignancy remains a significant complication after allogeneic hematopoietic cell transplantation (HCT).
  • Efforts to decrease relapse have included donor lymphocyte infusion to stimulate donor anti-recipient T-cell allorecognition of major and minor histocompatibility differences.
  • Recently, alloreactive effects of donor natural killer cell-mediated inhibitory killer immunoglobulin-like receptor (KIR) recognition of recipient HLA-C and -B ligands have been described.
  • We examined KIR ligand effects on risk of relapse in 1770 patients undergoing myeloablative T-replete HCT from HLA-matched or -mismatched unrelated donors for the treatment of myeloid and lymphoid leukemias.
  • The decrease in hazard of relapse in patients with acute myelogenous leukemia was similar to that in patients with chronic myelogenous leukemia and acute lymphoblastic leukemia (P = .95).
  • Recipient homozygosity for HLA-B or -C epitopes that define KIR ligands is likely to be a predictive factor for leukemia relapse after myeloablative HCT from HLA-mismatched unrelated donors.
  • [MeSH-major] HLA-B Antigens / genetics. Hematologic Neoplasms / genetics. Hematopoietic Stem Cell Transplantation. Isoantigens / genetics. Living Donors. Lymphocyte Transfusion
  • [MeSH-minor] Disease-Free Survival. Epitopes / genetics. Epitopes / immunology. Female. Follow-Up Studies. HLA-C Antigens / genetics. HLA-C Antigens / immunology. Humans. Killer Cells, Natural / immunology. Ligands. Male. Receptors, Immunologic / agonists. Receptors, Immunologic / genetics. Receptors, Immunologic / immunology. Receptors, KIR. Recurrence. Risk Factors. Survival Rate. T-Lymphocytes / immunology. Transplantation, Homologous

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  • (PMID = 16864053.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA 023766; United States / NIAID NIH HHS / AI / U24 AI 49215; United States / NIAID NIH HHS / AI / U24 AI49213; United States / NIAID NIH HHS / AI / UO1 AI 069197
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes; 0 / HLA-B Antigens; 0 / HLA-Bw4 antigen; 0 / HLA-C Antigens; 0 / Isoantigens; 0 / Ligands; 0 / Receptors, Immunologic; 0 / Receptors, KIR
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23. Okuya M, Kurosawa H, Kikuchi J, Furukawa Y, Matsui H, Aki D, Matsunaga T, Inukai T, Goto H, Altura RA, Sugita K, Arisaka O, Look AT, Inaba T: Up-regulation of survivin by the E2A-HLF chimera is indispensable for the survival of t(17;19)-positive leukemia cells. J Biol Chem; 2010 Jan 15;285(3):1850-60
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  • [Title] Up-regulation of survivin by the E2A-HLF chimera is indispensable for the survival of t(17;19)-positive leukemia cells.
  • The E2A-HLF fusion transcription factor generated by t(17;19)(q22;p13) translocation is found in a small subset of pro-B cell acute lymphoblastic leukemias (ALLs) and promotes leukemogenesis by substituting for the antiapoptotic function of cytokines.
  • Forced expression of E2A-HLF in t(17;19)(-) leukemia cells up-regulated Survivin expression, suggesting that Survivin is a downstream target of E2A-HLF.
  • Analysis using a counterflow centrifugal elutriator revealed that t(17;19)+ ALL cells express Survivin throughout the cell cycle.
  • Reporter assays revealed that E2A-HLF induces survivin expression at the transcriptional level likely through indirect down-regulation of a cell cycle-dependent cis element in the promoter region.
  • Down-regulation of Survivin function by a dominant negative mutant of Survivin or reduction of Survivin expression induced massive apoptosis throughout the cell cycle in t(17;19)+ cells mainly through caspase-independent pathways involving translocation of apoptosis-inducing factor (AIF) from mitochondria to the nucleus.
  • These data indicated that reversal of AIF translocation by Survivin, which is induced by E2A-HLF throughout the cell cycle, is one of the key mechanisms in the protection of t(17;19)+ leukemia cells from apoptosis.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Basic-Leucine Zipper Transcription Factors / metabolism. Microtubule-Associated Proteins / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Recombinant Fusion Proteins / metabolism. Translocation, Genetic / genetics. Up-Regulation
  • [MeSH-minor] Animals. Apoptosis. Base Sequence. Caspases / metabolism. Cell Cycle / genetics. Cell Line, Tumor. Cell Survival / genetics. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 19 / genetics. Humans. Inhibitor of Apoptosis Proteins. Mice. Molecular Sequence Data. Mutation. Precursor Cells, B-Lymphoid / cytology. Precursor Cells, B-Lymphoid / metabolism. Promoter Regions, Genetic / genetics. Transcriptional Activation

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  • (PMID = 19887369.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Basic-Leucine Zipper Transcription Factors; 0 / HLF protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Recombinant Fusion Proteins; 0 / TCF3 protein, human; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC2804343
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24. Sadananda Adiga MN, Chandy S, Ramachandra N, Appaji L, Aruna Kumari BS, Ramaswamy G, Savithri HS, Krishnamoorthy L: Methylenetetrahydrofolate reductase gene polymorphisms and risk of acute lymphoblastic leukemia in children. Indian J Cancer; 2010 Jan-Mar;47(1):40-5
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  • [Title] Methylenetetrahydrofolate reductase gene polymorphisms and risk of acute lymphoblastic leukemia in children.
  • Leukemias are malignancies arising from rapidly proliferating hematopoietic cells having great requirement of DNA synthesis.
  • This case-control study was undertaken to analyze the association of the MTHFR gene polymorphisms 677 C"T and 1298 A"C and the risk of acute lymphoblastic leukemia in children.
  • MATERIALS AND METHODS: Eighty-six patients aged below 15 years with a confirmed diagnosis of acute lymphoblastic leukemia (ALL) and 99 matched controls were taken for this study.
  • [MeSH-major] Genetic Predisposition to Disease. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20071789.001).
  • [ISSN] 1998-4774
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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25. Hu J, Fang J, Dong Y, Chen SJ, Chen Z: Arsenic in cancer therapy. Anticancer Drugs; 2005 Feb;16(2):119-27
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  • Arsenic, a natural substance that has been used as a drug for over 2000 years, has been revived because of its remarkable therapeutic efficacy in patients with acute promyelocytic leukemia (APL).
  • Specific degradation of the leukemogenic PML-RARalpha fusion protein induced by arsenic leads to the differentiation of leukemia cells.
  • Preliminary in vitro studies have also extended the potential anti-cancer effect of arsenic to non-APL leukemias, lymphoid malignancies and other cancers.
  • In vitro and in vivo studies demonstrate that arsenic exerts a broad spectrum of anti-cancer effects by induction of apoptosis, inhibition of cell proliferation, anti-angiogenesis and possible immunomodulation.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Clinical Trials as Topic. Dose-Response Relationship, Drug. Humans. Leukemia / drug therapy. Lymphoma / drug therapy. Multiple Myeloma / drug therapy

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  • (PMID = 15655408.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals
  • [Number-of-references] 65
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26. Sollars VE, Pequignot E, Rothstein JL, Buchberg AM: Analysis of expansion of myeloid progenitors in mice to identify leukemic susceptibility genes. Mamm Genome; 2006 Aug;17(8):808-21
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  • The myeloid progenitor cell compartment (MPC) exhibits pronounced expansion in human myeloid leukemias.
  • It is becoming more apparent that progression of myelodysplastic syndromes and myeloproliferative diseases to acute myelogenous leukemia is the result of defects in progenitor cell maturation.
  • The MPC of bone marrow was analyzed in mice using a cell culture assay for measuring the relative frequency of proliferative myeloid progenitors.
  • Given the importance of this cell compartment in leukemia progression and the soon to be released genomic sequence of 15 mouse strains, these differences may provide a valuable tool for research into leukemia.
  • [MeSH-major] Cell Proliferation. Genetic Predisposition to Disease. Leukemia / genetics. Myeloid Progenitor Cells / metabolism
  • [MeSH-minor] Animals. Bone Marrow / growth & development. Cell Size. Chromosomes, Mammalian. Cytokines / metabolism. Flow Cytometry. Linkage Disequilibrium. Male. Mice. Mice, Inbred Strains. Stem Cells

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  • [ISSN] 0938-8990
  • [Journal-full-title] Mammalian genome : official journal of the International Mammalian Genome Society
  • [ISO-abbreviation] Mamm. Genome
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32-CA09678
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines
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27. Catalina P, Bueno C, Montes R, Nieto A, Ligero G, Sanchez L, Jara M, Rasillo A, Orfao A, Cigudosa J, Hovatta O, Greaves M, Menendez P: Genetic stability of human embryonic stem cells: A first-step toward the development of potential hESC-based systems for modeling childhood leukemia. Leuk Res; 2009 Jul;33(7):980-90
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  • [Title] Genetic stability of human embryonic stem cells: A first-step toward the development of potential hESC-based systems for modeling childhood leukemia.
  • Of interest, are the human childhood acute leukemias harboring specific fusion oncogenes such as MLL-AF4, TEL-AML1 or BCR-ABL wherein clinically significant manifestations arise in utero.
  • The mechanisms of transformation are not amenable to analysis with patient samples and, many mouse models for pediatric leukemias have fallen short in illuminating the human disease because they do not recapitulate key aspects of the actual disease, suggesting that the mouse models are missing essential components of oncogenesis present in the human embryo.
  • Prior to using hESCs as a tentative system for modeling leukemia, robust studies aimed at demonstrating their genetic stability are required; otherwise, cooperating mutations already present could prime hESCs susceptible to transformation.
  • This data should encourage stem cell researchers to implement robust cytogenetic tools when assessing hESC genetic stability, in order to detect tiny but relevant biological functional or structural chromosome abnormalities and, paves the way for generating fusion oncogene-expressing transgenic hESCs as a human-specific system for studying the early in utero events leading to normal hematopoietic specification versus childhood leukemic transformation.
  • [MeSH-major] Cell Differentiation / genetics. Cell Lineage / genetics. Disease Models, Animal. Embryo, Mammalian / cytology. Embryonic Stem Cells / physiology. Genomic Instability
  • [MeSH-minor] Acute Disease. Adult. Animals. Cells, Cultured. Child. Comparative Genomic Hybridization. Flow Cytometry. Humans. Immunoenzyme Techniques. Karyotyping. Leukemia / genetics. Male. Mice. Mice, SCID. Mutation / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-kit / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Spectral Karyotyping. fms-Like Tyrosine Kinase 3 / genetics


28. Jeeninga RE, Jan B, van den Berg H, Berkhout B: Construction of doxycyline-dependent mini-HIV-1 variants for the development of a virotherapy against leukemias. Retrovirology; 2006 Sep 27;3:64
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  • [Title] Construction of doxycyline-dependent mini-HIV-1 variants for the development of a virotherapy against leukemias.
  • T-cell acute lymphoblastic leukemia (T-ALL) is a high-risk type of blood-cell cancer.
  • We describe the improvement of a candidate therapeutic virus for virotherapy of leukemic cells.
  • Virotherapy is based on the exclusive replication of a virus in leukemic cells, leading to the selective removal of these malignant cells.
  • These minimized HIV-rtTA variants contain up to 7 deletions/inactivating mutations (TAR, Tat, vif, vpR, vpU, nef and U3) and replicate efficiently in the leukemic SupT1 T cell line, but do not replicate in normal peripheral blood mononuclear cells.
  • The therapeutic viruses use CD4 and CXCR4 for cell entry and could potentially be used against CXCR4 expressing malignancies such as T-lymphoblastic leukemia/lymphoma, NK leukemia and some myeloid leukemias.

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  • (PMID = 17005036.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] ENG
  • [Grant] United States / PHS HHS / / R21-A147017-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antigens, CD4; 0 / Gene Products, tat; 0 / Receptors, CXCR4; 0 / tat Gene Products, Human Immunodeficiency Virus; N12000U13O / Doxycycline
  • [Other-IDs] NLM/ PMC1592508
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29. Patel A, Dharmarajan V, Vought VE, Cosgrove MS: On the mechanism of multiple lysine methylation by the human mixed lineage leukemia protein-1 (MLL1) core complex. J Biol Chem; 2009 Sep 4;284(36):24242-56
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  • [Title] On the mechanism of multiple lysine methylation by the human mixed lineage leukemia protein-1 (MLL1) core complex.
  • The mixed lineage leukemia protein-1 (MLL1) is a member of the SET1 family of H3K4 methyltransferases and is frequently rearranged in acute leukemias.
  • Single turnover kinetic experiments reveal that the reaction leading to H3K4 dimethylation involves the transient accumulation of a monomethylated species, suggesting that the MLL1 core complex uses a non-processive mechanism to catalyze multiple lysine methylation.

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  • (PMID = 19556245.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA140522
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ASH2L protein, human; 0 / DNA-Binding Proteins; 0 / DPY30 protein, human; 0 / Histones; 0 / MLL protein, human; 0 / Multiprotein Complexes; 0 / Nuclear Proteins; 0 / RBP5 protein, human; 0 / Retinol-Binding Proteins, Cellular; 0 / Transcription Factors; 0 / WDR5 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; K3Z4F929H6 / Lysine
  • [Other-IDs] NLM/ PMC2782018
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30. Krug U, Yasmeen A, Beger C, Bäumer N, Dugas M, Berdel WE, Müller-Tidow C: Cyclin A1 regulates WT1 expression in acute myeloid leukemia cells. Int J Oncol; 2009 Jan;34(1):129-36
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  • [Title] Cyclin A1 regulates WT1 expression in acute myeloid leukemia cells.
  • Cyclin A1 is a cell cycle protein that is expressed in testes, brain and CD34-positive hematopoietic progenitor cells.
  • Cyclin A1 is overexpressed in a variety of myeloid leukemic cell lines and in myeloid leukemic blasts.
  • Transgenic cyclin A1 overexpressing mice develop acute myeloid leukemia with low frequency.
  • Repression of WT1 expression was confirmed on the mRNA and protein level.
  • In addition, overexpression of the WT1-/+ isoform induced a G1 cell cycle arrest which was abrogated upon cotransfection with cyclin A1.
  • This study identified WT1 as a repressed target of cyclin A1 and suggests that the suppression of WT1 in cyclin A1-overexpressing leukemias might play a role in the growth and suppression of apoptosis in these leukemic cells.
  • [MeSH-minor] Animals. Blotting, Western. Bone Marrow / metabolism. Cell Line, Tumor. Colony-Forming Units Assay. Cyclin A1. G1 Phase / physiology. Gene Expression Profiling. Humans. Mice. Mice, Knockout. Oligonucleotide Array Sequence Analysis. Protein Isoforms. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection. U937 Cells / metabolism

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  • (PMID = 19082485.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / CCNA1 protein, human; 0 / Ccna1 protein, mouse; 0 / Cyclin A; 0 / Cyclin A1; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / WT1 Proteins
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31. Yee KW, Hagey A, Verstovsek S, Cortes J, Garcia-Manero G, O'Brien SM, Faderl S, Thomas D, Wierda W, Kornblau S, Ferrajoli A, Albitar M, McKeegan E, Grimm DR, Mueller T, Holley-Shanks RR, Sahelijo L, Gordon GB, Kantarjian HM, Giles FJ: Phase 1 study of ABT-751, a novel microtubule inhibitor, in patients with refractory hematologic malignancies. Clin Cancer Res; 2005 Sep 15;11(18):6615-24
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  • A phase 1 study was conducted to determine the maximum tolerated dose and toxicities of ABT-751 in patients with advanced myelodysplastic syndrome and relapsed or refractory acute leukemias.
  • RESULTS: Dose-limiting toxicity consisted of ileus in one patient at 200 mg/m(2), with a subsequent patient developing grade 2 constipation at the same dose level.
  • One patient with relapsed acute myelogenous leukemia achieved a complete remission that was sustained for 2 months.
  • Four other patients had transient hematologic improvements, consisting of a decrease in peripheral blood blasts and improvements in platelet counts.
  • CONCLUSION: Further assessment of ABT-751, especially in combination with other agents, in patients with acute leukemias is warranted.
  • [MeSH-minor] Acute Disease. Adult. Aged. Antigens, CD / analysis. Antigens, CD146. Antigens, CD31 / analysis. Antigens, CD45 / analysis. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Constipation / chemically induced. Diarrhea / chemically induced. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Endothelial Cells / chemistry. Female. Glycoproteins / analysis. Humans. Leukemia / blood. Leukemia / drug therapy. Leukemia / genetics. Male. Microtubules / metabolism. Middle Aged. Mutation. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / genetics. Nausea / chemically induced. Neoplasm Recurrence, Local. Neoplastic Cells, Circulating / chemistry. Neural Cell Adhesion Molecules / analysis. Peptides / analysis. Treatment Outcome. Tubulin / genetics. Vomiting / chemically induced

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  • (PMID = 16166440.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABT751; 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD146; 0 / Antigens, CD31; 0 / Antineoplastic Agents; 0 / Glycoproteins; 0 / Neural Cell Adhesion Molecules; 0 / Peptides; 0 / Sulfonamides; 0 / Tubulin; EC 3.1.3.48 / Antigens, CD45
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32. Fiegl M, Samudio I, Clise-Dwyer K, Burks JK, Mnjoyan Z, Andreeff M: CXCR4 expression and biologic activity in acute myeloid leukemia are dependent on oxygen partial pressure. Blood; 2009 Feb 12;113(7):1504-12
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  • [Title] CXCR4 expression and biologic activity in acute myeloid leukemia are dependent on oxygen partial pressure.
  • In acute myeloid leukemia (AML), elevated expression of CXCR4 has been shown to correlate with shortened survival.
  • At this pO(2), CXCR4 surface and total expression were up-regulated within 10 hours in leukemic cell lines and patient samples as shown by Western blotting, fluorescence-activated cell sorting, and microscopy.
  • Given the importance of CXCR4 in cell signaling, survival, and adhesion in leukemia, the results suggest that pO(2) be considered a critical variable in conducting and interpreting studies of CXCR4 expression and regulation in leukemias.

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  • (PMID = 18957686.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P01 CA55164
  • [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 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Receptors, CXCR4; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ PMC2644078
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33. Invernizzi R, Travaglino E, Benatti C, Malcovati L, Della Porta M, Cazzola M, Ascari E: Survivin expression, apoptosis and proliferation in chronic myelomonocytic leukemia. Eur J Haematol; 2006 Jun;76(6):494-501
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  • [Title] Survivin expression, apoptosis and proliferation in chronic myelomonocytic leukemia.
  • We analyzed the expression of the inhibitor of apoptosis survivin by immunocytochemistry in bone marrow cells from patients with chronic myelomonocytic leukemia (CMML) to evaluate possible abnormalities in comparison with other myelodysplastic (MDS) and myeloproliferative syndromes, and to investigate a possible correlation between survivin expression and altered apoptosis or proliferation, or relevant laboratory and clinical findings.
  • Thirty-four patients with CMML [18 MDS-CMML and 16 myeloproliferative disorder (MPD)-CMML], 90 with MDS, 41 with acute myeloid leukemia (AML), 19 with chronic MPD and 25 control subjects were studied.
  • In CMML and MDS apoptosis was significantly higher compared to normal controls and all other subtypes of leukemias (P < 0.0001).
  • In CMML there was no correlation between survivin expression and blast cell percentage, apoptosis or proliferation, FAB or WHO subgroup.
  • Survivin overexpression, by disrupting the balance between cell proliferation/differentiation and apoptosis, may play an important role in its pathophysiology.
  • [MeSH-major] Leukemia, Myelomonocytic, Chronic / pathology. Microtubule-Associated Proteins / physiology. Neoplasm Proteins / physiology
  • [MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis. Cell Division. Disease Progression. Female. Humans. Inhibitor of Apoptosis Proteins. Leukemia, Myeloid / classification. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / pathology. Male. Middle Aged. Myelodysplastic Syndromes / metabolism. Myelodysplastic Syndromes / pathology

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  • (PMID = 16529600.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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34. Zhang W, Konopleva M, Ruvolo VR, McQueen T, Evans RL, Bornmann WG, McCubrey J, Cortes J, Andreeff M: Sorafenib induces apoptosis of AML cells via Bim-mediated activation of the intrinsic apoptotic pathway. Leukemia; 2008 Apr;22(4):808-18
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  • Raf/MEK/Erk signaling is activated in the majority of acute myeloid leukemias (AMLs), providing rationale for targeting this pathway with therapeutic intent.
  • Our studies demonstrated that sorafenib significantly inhibited the phosphorylation levels of Raf downstream target proteins MEK1/2 and Erk, induced apoptosis and inhibited colony formation in AML cell lines and in primary AML samples.
  • Combination of sorafenib with cytarabine or the novel small molecule Bcl-2 inhibitor ABT-737 synergistically induced cell death in AML cell lines.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis Regulatory Proteins / metabolism. Benzenesulfonates / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Membrane Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Pyridines / pharmacology. Signal Transduction / drug effects
  • [MeSH-minor] Cell Line. Drug Synergism. Humans. Mitochondria / metabolism. Niacinamide / analogs & derivatives. Phenylurea Compounds

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  • (PMID = 18200035.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA55164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Benzenesulfonates; 0 / Membrane Proteins; 0 / Phenylurea Compounds; 0 / Proto-Oncogene Proteins; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib
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35. Wananukul S, Nuchprayoon I, Siripanich H: Mucocutaneous findings in febrile neutropenic children with acute leukemias. J Med Assoc Thai; 2005 Jun;88(6):817-23
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  • [Title] Mucocutaneous findings in febrile neutropenic children with acute leukemias.
  • Febrile neutropenia is common in children with leukemia.
  • The authors prospectively examined children with fever with neutropenia in acute leukemia, aged 1-15 years, who were admitted to the Department of Pediatrics, King Chulalongkorn Memorial Hospital, between September 2000 and August 2001.
  • The prevalence of infection was found in severe neutropenia (absolute neutrophil count, ANC less than 500 cell/cu mm), moderate neutropenia (ANC, 500-1000 cell/cu mm) and mild neutropenia (ANC, 1001-1500 cell/cu mm) was 72%, 9% and 5%, respectively.
  • Daily physical examination of skin and mucous membrane are suggested for proper and prompt diagnosis and treatment of febrile neutropenic children with acute leukemia to reduce mortality and morbidity in these patients.
  • A Guideline for the use of antimicrobial agents in neutropenic patients with acute leukemia is proposed In conclusion, infection was commonly found in severe neutropenia.
  • Mucocutaneous infection was the most common site of infection infebrile neutropenia in children with leukemia.
  • [MeSH-major] Fever. Neutropenia / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Skin Diseases / etiology

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  • (PMID = 16083222.001).
  • [ISSN] 0125-2208
  • [Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet
  • [ISO-abbreviation] J Med Assoc Thai
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Thailand
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36. Jeeninga RE, Jan B, van der Linden B, van den Berg H, Berkhout B: Construction of a minimal HIV-1 variant that selectively replicates in leukemic derived T-cell lines: towards a new virotherapy approach. Cancer Res; 2005 Apr 15;65(8):3347-55
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  • [Title] Construction of a minimal HIV-1 variant that selectively replicates in leukemic derived T-cell lines: towards a new virotherapy approach.
  • T-cell acute lymphoblastic leukemia is a high-risk type of blood-cell cancer.
  • We analyzed the possibility of developing virotherapy for T-cell acute lymphoblastic leukemia.
  • Virotherapy is based on the exclusive replication of a virus in leukemic cells, leading to the selective removal of these malignant cells.
  • This mini-HIV virus has five deletions (vif, vpR, vpU, nef, and U3) and replicated in the SupT1 cell line, but did not replicate in normal peripheral blood mononuclear cells.
  • The mini-HIV variant that uses CD4 and CXCR4 for cell entry could potentially be used against CXCR4-expressing malignancies such as T-lymphoblastic leukemia/lymphoma, natural killer leukemia, and some myeloid leukemias.
  • [MeSH-major] HIV-1 / physiology. Leukemia-Lymphoma, Adult T-Cell / therapy. Leukemia-Lymphoma, Adult T-Cell / virology. T-Lymphocytes / virology
  • [MeSH-minor] Antigens, CD4 / biosynthesis. Cell Line, Tumor. Female. Gene Deletion. Genes, nef / genetics. Genes, vif / genetics. Genes, vpr / genetics. Genes, vpu / genetics. HIV Long Terminal Repeat / genetics. Humans. Jurkat Cells. Receptors, CXCR4 / biosynthesis. Virus Replication

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  • (PMID = 15833868.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R21-AI47017-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Receptors, CXCR4
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37. Raponi S, De Propris MS, Wai H, Intoppa S, Elia L, Diverio D, Vitale A, Foà R, Guarini A: An accurate and rapid flow cytometric diagnosis of BCR-ABL positive acute lymphoblastic leukemia. Haematologica; 2009 Dec;94(12):1767-70
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  • [Title] An accurate and rapid flow cytometric diagnosis of BCR-ABL positive acute lymphoblastic leukemia.
  • Tyrosine kinase inhibitors have profoundly modified the treatment and prognosis of chronic myeloid leukemia and Ph(+) acute lymphoblastic leukemia.
  • A rapid and accurate detection of the BCR-ABL fusion protein is paramount today for an optimal management of Ph(+) acute lymphoblastic leukemia.
  • We have utilized a recently described and commercialized immunoassay that identifies qualitatively the presence of the BCR-ABL protein in leukemic cell lysates.
  • The assay was applied to 101 primary patient samples (94 acute leukemias and 7 chronic myeloid leukemia blast crisis) and the results of the immunoassay were concordant with those obtained by conventional molecular techniques.
  • This flow cytometric immunoassay has important implications for perfecting the management of Ph(+) acute lymphoblastic leukemia patients worldwide.
  • [MeSH-major] Flow Cytometry / methods. Fusion Proteins, bcr-abl / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 19608682.001).
  • [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] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ PMC2791932
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38. Kaufmann SH, Karp JE, Letendre L, Kottke TJ, Safgren S, Greer J, Gojo I, Atherton P, Svingen PA, Loegering DA, Litzow MR, Sloan JA, Reid JM, Ames MM, Adjei AA, Erlichman C: Phase I and pharmacologic study of infusional topotecan and Carboplatin in relapsed and refractory acute leukemia. Clin Cancer Res; 2005 Sep 15;11(18):6641-9
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  • [Title] Phase I and pharmacologic study of infusional topotecan and Carboplatin in relapsed and refractory acute leukemia.
  • PURPOSE: To assess the maximum tolerated dose, toxicities, pharmacokinetics, and antileukemic activity of topotecan and carboplatin in adults with recurrent or refractory acute leukemias.
  • Among 45 evaluable patients, there were 7 complete remissions, 2 partial remissions, 1 incomplete complete remission, and 1 reversion to chronic-phase chronic myelogenous leukemia.
  • Leukemic cell levels of topoisomerase I, checkpoint kinase 1, checkpoint kinase 2, and Mcl-1 correlated with proliferating cell nuclear antigen but not with response.
  • Responses seem to correlate with low pretreatment blast cell Bcl-2 expression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Bone Marrow Cells / drug effects. Bone Marrow Cells / metabolism. Carboplatin / administration & dosage. Carboplatin / adverse effects. Carboplatin / pharmacokinetics. Cell Cycle Proteins / metabolism. Combined Modality Therapy. DNA Topoisomerases, Type I / metabolism. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. HL-60 Cells. Hematopoietic Stem Cell Transplantation. Humans. Immunoblotting. Infusions, Intravenous. Male. Middle Aged. Neoplasm Recurrence, Local. Proliferating Cell Nuclear Antigen / metabolism. Topotecan / administration & dosage. Topotecan / adverse effects. Topotecan / pharmacokinetics. Treatment Outcome

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  • (PMID = 16166443.001).
  • [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 CA73709; United States / NCI NIH HHS / CA / U01 CA69854; United States / NCI NIH HHS / CA / U01 CA69912
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Proliferating Cell Nuclear Antigen; 7M7YKX2N15 / Topotecan; BG3F62OND5 / Carboplatin; EC 5.99.1.2 / DNA Topoisomerases, Type I
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39. Kurosu T, Ohki M, Wu N, Kagechika H, Miura O: Sorafenib induces apoptosis specifically in cells expressing BCR/ABL by inhibiting its kinase activity to activate the intrinsic mitochondrial pathway. Cancer Res; 2009 May 1;69(9):3927-36
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  • Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem.
  • Thus, sorafenib may provide an effective therapeutic measure to treat Ph+ leukemias, particularly those expressing the T315I mutant, which is totally resistant to imatinib and the second generation BCR/ABL inhibitors.
  • [MeSH-major] Apoptosis / drug effects. Benzenesulfonates / pharmacology. Fusion Proteins, bcr-abl / antagonists & inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mitochondria / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyridines / pharmacology

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  • (PMID = 19366808.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABT-737; 0 / Acetophenones; 0 / Benzamides; 0 / Benzenesulfonates; 0 / Benzopyrans; 0 / Biphenyl Compounds; 0 / Boronic Acids; 0 / Interleukin-3; 0 / Nitrophenols; 0 / Phenylurea Compounds; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrazines; 0 / Pyridines; 0 / Pyrimidines; 0 / Sulfonamides; 25X51I8RD4 / Niacinamide; 69G8BD63PP / Bortezomib; 8A1O1M485B / Imatinib Mesylate; 9ZOQ3TZI87 / sorafenib; E29LP3ZMUH / rottlerin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.22.- / Caspases
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40. Derwich K, Sedek L, Meyer C, Pieczonka A, Dawidowska M, Gaworczyk A, Wachowiak J, Konatkowska B, Witt M, Marschalek R, Szczepański T: Infant acute bilineal leukemia. Leuk Res; 2009 Jul;33(7):1005-8
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  • [Title] Infant acute bilineal leukemia.
  • Most cases of acute leukemia can be assigned to the myeloid, B or T lineage.
  • There are rare cases of acute leukemia, which cannot be clearly classified, because either blasts express antigens of more than one lineage (acute biphenotypic leukemias) or distinct blast populations of two lineages co-exist (acute bilineal leukemias, aBLL).
  • We present a 10-month-old infant with de novo aBLL, characterized by blasts of monocytic and B-cell precursor lineages.
  • Despite poor initial response, both to acute lymphoblastic leukemia (ALL) induction treatment and acute myeloid leukemia induction blocks, the child reached complete clinical remission with minimal residual disease negative status and was transplanted.
  • This case report illustrates that aBLL is a very aggressive type of acute leukemia that should be individually treated and monitored, particularly in children less than 1 year of age.
  • [MeSH-major] B-Lymphocytes / pathology. Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Cell Lineage. Hematopoietic Stem Cell Transplantation. Humans. Infant. Male. Remission Induction. Treatment Outcome

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  • (PMID = 19286255.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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41. Nakamura S, Okinaka K, Hirano I, Ono T, Sugimoto Y, Shigeno K, Fujisawa S, Shinjo K, Ohnishi K: KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells. Leuk Res; 2008 Sep;32(9):1358-65
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  • [Title] KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells.
  • The mRNA expressions of KIS were successfully reduced in all cell lines.
  • We showed that KIS protein directly interacted with p27(Kip1) protein, and reduction of KIS inhibited the S10 phosphorylation of p27(Kip1) in leukemia cells.
  • On these cells transfected with siRNA KIS, the inhibition of S10 phosphorylation of p27(Kip1) was strongly suppressed cell proliferation in a time-dependent manner.
  • These data demonstrated that the KIS activity was induced during G0/G1, and it promotes cell cycle progression by phosphorylation of S10 on p27(Kip1).
  • We showed that KIS mRNA expression was increased in primary leukemia specimens (acute myelogenous leukemia (AML); 37, myelodysplastic syndrome (MDS); 72, acute lymphoblastic leukemia (ALL); 23), and the mean ratios of KIS to G3PDH in AML, MDS and ALL specimens were 3.62+/-0.68, 3.27+/-0.73 and 3.17+/-0.58, respectively.
  • Moreover, we found that KIS protein was overexpressed in all 132 adults cases of various leukemias, including 37 AML (8 M1, 12 M2, 2 M3, 7 M4, 8 M5), 72 MDS (42 RAEB-I, 30 REAB-II) and 23 ALL (23 L2).
  • This study demonstrates that the elevated levels of KIS protein in leukemia cells promote the cell cycle progression in leukemia cells.
  • [MeSH-major] Cell Cycle / physiology. Cell Proliferation. Intracellular Signaling Peptides and Proteins / metabolism. Intracellular Signaling Peptides and Proteins / physiology. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Protein-Serine-Threonine Kinases / physiology

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  • (PMID = 18384876.001).
  • [ISSN] 0145-2126
  • [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 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / UHMK1 protein, human
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42. Kurosu T, Tsuji K, Kida A, Koyama T, Yamamoto M, Miura O: Rottlerin synergistically enhances imatinib-induced apoptosis of BCR/ABL-expressing cells through its mitochondrial uncoupling effect independent of protein kinase C-delta. Oncogene; 2007 May 10;26(21):2975-87
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  • Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myeloid leukemia (CML) and Philadelphia-chromosome positive acute lymphoblastic leukemia (ALL), relapse with emerging imatinib-resistance mutations in the BCR/ABL kinase domain poses a significant problem.
  • Rottlerin also enhanced the cytotoxic effect of imatinib in leukemic cells from patients with CML blast crisis and Ph-positive ALL or a cell line expressing the imatinib-resistant E255K BCR/ABL mutant.
  • The present study indicates that rottlerin synergistically enhances imatinib-induced apoptosis through its mitochondrial uncoupling effect independent of PKCdelta and may contribute to the development of new treatment strategy to overcome the imatinib resistance and to cure the BCR/ABL expressing leukemias.
  • [MeSH-minor] Animals. Benzamides. Drug Synergism. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. K562 Cells. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Erythroblastic, Acute / enzymology. Mice. Mitochondria / drug effects. Mitochondria / enzymology. Mitochondria / metabolism. Up-Regulation / drug effects

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  • (PMID = 17130834.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Acetophenones; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzopyrans; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Uncoupling Agents; 8A1O1M485B / Imatinib Mesylate; E29LP3ZMUH / rottlerin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.13 / Protein Kinase C-delta
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43. Alzani R, Pedrini O, Albanese C, Ceruti R, Casolaro A, Patton V, Colotta F, Rambaldi A, Introna M, Pesenti E, Ciomei M, Golay J: Therapeutic efficacy of the pan-cdk inhibitor PHA-793887 in vitro and in vivo in engraftment and high-burden leukemia models. Exp Hematol; 2010 Apr;38(4):259-269.e2
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  • [Title] Therapeutic efficacy of the pan-cdk inhibitor PHA-793887 in vitro and in vivo in engraftment and high-burden leukemia models.
  • MATERIALS AND METHODS: Thirteen leukemic cell lines bearing different cytogenetic abnormalities and normal hematopoietic cells were used in cytotoxicity and colony assays.
  • The drug activity at the molecular level was analyzed by Western blotting.
  • PHA-793887 was also tested in vivo in several leukemia xenograft models.
  • RESULTS: PHA-793887 was cytotoxic for leukemic cell lines in vitro, with IC(50) ranging from 0.3 to 7 microM (mean: 2.9 microM), regardless of any specific chromosomal aberration.
  • Interestingly, in colony assays PHA-793887 showed very high activity against leukemia cell lines, with an IC(50) <0.1 microM (mean: 0.08 microM), indicating that it has efficient and prolonged antiproliferative activity.
  • PHA-793887 induced cell-cycle arrest, inhibited Rb and nucleophosmin phosphorylation, and modulated cyclin E and cdc6 expression at low doses (0.2-1 microM) and induced apoptosis at the highest dose (5 microM).
  • It was also effective in vivo in both subcutaneous xenograft and primary leukemic disseminated models that better mimic naturally occurring human disease.
  • Interestingly, in one disseminated model derived from a relapsed Philadelphia-positive acute lymphoid leukemia patient, PHA-793887 showed strong therapeutic activity also when treatment was started after establishment of high disease burden.
  • CONCLUSIONS: We conclude that PHA-793887 has promising therapeutic activity against acute leukemias in vitro and in vivo.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cyclin-Dependent Kinases / antagonists & inhibitors. Leukemia / drug therapy
  • [MeSH-minor] Animals. Apoptosis. Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Disease Models, Animal. Drug Screening Assays, Antitumor. Humans. Immunohistochemistry. Inhibitory Concentration 50. Mice. Mice, SCID


44. Pichiorri F, Trapasso F, Palumbo T, Aqeilan RI, Drusco A, Blaser BW, Iliopoulos D, Caligiuri MA, Huebner K, Croce CM: Preclinical assessment of FHIT gene replacement therapy in human leukemia using a chimeric adenovirus, Ad5/F35. Clin Cancer Res; 2006 Jun 01;12(11 Pt 1):3494-501
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  • [Title] Preclinical assessment of FHIT gene replacement therapy in human leukemia using a chimeric adenovirus, Ad5/F35.
  • Adenovirus 5 (Ad5) virus or adeno-associated viral vectors have been used to study the tumor suppressor function of FHIT in solid tumors, but these tools have not been effective in leukemias.
  • EXPERIMENTAL DESIGN: Infection efficiency of Ad5/F35-FHIT and Ad5/F35-GFP viruses was tested in leukemia cell lines that lacked FHIT expression, and biological effects of successful infection were assessed.
  • An acute myelogenous leukemia, a chronic myelogenous leukemia, and four acute lymphoblastic leukemia human cell lines were examined as well as two EBV-transformed B lymphoblastoid cell lines that expressed endogenous FHIT.
  • RESULTS: Two of four acute lymphoblastic leukemia cell lines, Jurkat and MV4;11, which were efficiently infected with Ad5/F35-FHIT, underwent growth suppression and massive induction of apoptosis without apparent activation of caspase-8 or caspase-2 and late activation of caspase-3.
  • The two remaining infected acute lymphoblastic leukemia cell lines, Molt-3 and RS4;11, were apparently unaffected.
  • Restoration of FHIT expression in the chronic myelogenous leukemia K562 cell line and the acute myelogenous leukemia KG1a cell line also induced apoptosis but at later time points than seen in the acute lymphoblastic leukemia Jurkat and MV4;11 cell lines. I.v. injection of Ad5/F35-FHIT-infected Jurkat cells resulted in abrogation of tumorigenicity in the NOD/SCID xenogeneic engraftment model.
  • CONCLUSION: FHIT restoration in some FHIT-deficient leukemia cells induces both antiproliferative and proapoptotic effects involving the intrinsic caspase apoptotic pathway.
  • [MeSH-major] Acid Anhydride Hydrolases / genetics. Adenoviruses, Human / genetics. Gene Expression Regulation, Neoplastic / genetics. Genetic Therapy / methods. Leukemia / genetics. Neoplasm Proteins / genetics
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / genetics. Cell Cycle. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Drug Screening Assays, Antitumor. Enzyme Inhibitors / pharmacology. Gene Transfer Techniques. Genetic Vectors / genetics. Green Fluorescent Proteins / genetics. Humans. Kinetics. Mice. Mice, Inbred NOD. Mice, SCID. Structure-Activity Relationship. Transplantation, Heterologous. Xenograft Model Antitumor Assays

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  • [ErratumIn] Clin Cancer Res. 2016 Dec 15;22(24):6304 [27856602.001]
  • (PMID = 16740775.001).
  • [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 / CA56036; United States / NCI NIH HHS / CA / CA77738; United States / NCI NIH HHS / CA / CA78890; United States / NCI NIH HHS / CA / CA89341
  • [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 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / fragile histidine triad protein; 147336-22-9 / Green Fluorescent Proteins; EC 3.6.- / Acid Anhydride Hydrolases
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45. Haferlach T, Kohlmann A, Wieczorek L, Basso G, Kronnie GT, Béné MC, De Vos J, Hernández JM, Hofmann WK, Mills KI, Gilkes A, Chiaretti S, Shurtleff SA, Kipps TJ, Rassenti LZ, Yeoh AE, Papenhausen PR, Liu WM, Williams PM, Foà R: Clinical utility of microarray-based gene expression profiling in the diagnosis and subclassification of leukemia: report from the International Microarray Innovations in Leukemia Study Group. J Clin Oncol; 2010 May 20;28(15):2529-37
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  • [Title] Clinical utility of microarray-based gene expression profiling in the diagnosis and subclassification of leukemia: report from the International Microarray Innovations in Leukemia Study Group.
  • PURPOSE: The Microarray Innovations in Leukemia study assessed the clinical utility of gene expression profiling as a single test to subtype leukemias into conventional categories of myeloid and lymphoid malignancies.
  • An exploratory retrospective stage I study was designed for biomarker discovery and generated whole-genome expression profiles from 2,143 patients with leukemias and myelodysplastic syndromes.
  • In a second cohort of 1,152 prospectively collected patients, a classification scheme reached 95.6% median sensitivity and 99.8% median specificity for 14 standard subtypes of acute leukemia (eight acute lymphoblastic leukemia and six acute myeloid leukemia classes, n = 693).
  • Our comprehensive gene expression data set will be submitted to the public domain to foster research focusing on the molecular understanding of leukemias.
  • [MeSH-major] Leukemia / classification. Leukemia / genetics

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  • [CommentIn] Nat Rev Clin Oncol. 2010 Aug;7(8):422 [20700897.001]
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  • (PMID = 20406941.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / P01 CA081534
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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46. Parovichnikova EN, Savchenko VG, Verniuk MA, Vinogradova OA, Misiurin AV, Vorob'ev IA, Domracheva EV, Tikhonova LIu, Rukavitsyn OA, Rossiev VA, Kliasova GA, Turkina AG, Liubimova LS, Mendeleeva LP, Isaev VG: [Acute lymphoblastic leukemias with aberrations of BCR-ABL genes]. Ter Arkh; 2005;77(7):11-6
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  • [Title] [Acute lymphoblastic leukemias with aberrations of BCR-ABL genes].
  • AIM: To develop an original therapeutic strategy in Ph-positive acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16116902.001).
  • [ISSN] 0040-3660
  • [Journal-full-title] Terapevticheskiĭ arkhiv
  • [ISO-abbreviation] Ter. Arkh.
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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47. Kazemi T, Asgarian-Omran H, Memarian A, Shabani M, Sharifian RA, Vossough P, Ansaripour B, Rabbani H, Shokri F: Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia. Cancer Immunol Immunother; 2009 Jun;58(6):989-96
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  • [Title] Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia.
  • Recent studies have demonstrated expression of Fc receptor-like (FCRL) molecules, a newly identified family with preferential B-cell lineage expression, in some chronic B-cell leukemias with possible implication for classification and/or targeted immunotherapy.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cell Surface / genetics. Receptors, Fc / genetics. Receptors, Immunologic / genetics

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  • (PMID = 18802695.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / FCRL2 protein, human; 0 / FCRL4 protein, human; 0 / FCRL5 protein, human; 0 / FCRLA protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Fc; 0 / Receptors, Immunologic
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48. Fei F, Stoddart S, Groffen J, Heisterkamp N: Activity of the Aurora kinase inhibitor VX-680 against Bcr/Abl-positive acute lymphoblastic leukemias. Mol Cancer Ther; 2010 May;9(5):1318-27
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  • [Title] Activity of the Aurora kinase inhibitor VX-680 against Bcr/Abl-positive acute lymphoblastic leukemias.
  • The emergence of resistance to tyrosine kinase inhibitors due to point mutations in Bcr/Abl is a challenging problem for Philadelphia chromosome-positive (Ph-positive) acute lymphoblastic leukemia (ALL) patients, especially for those with the T315I mutation, against which neither nilotinib or dasatinib shows significant activity.

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  • (PMID = 20388735.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] None / None / / R01 CA090321-08S1; United States / NCI NIH HHS / CA / CA090321; United States / NCI NIH HHS / CA / R01 CA090321-08S1; United States / NCI NIH HHS / CA / R01 CA090321; United States / NCI NIH HHS / CA / R01 CA090321-08; None / None / / R01 CA090321-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 639089-54-6 / VX680; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ NIHMS185920; NLM/ PMC2868097
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49. Fu JF, Liang DC, Shih LY: Analysis of acute leukemias with MLL/ENL fusion transcripts: identification of two novel breakpoints in ENL. Am J Clin Pathol; 2007 Jan;127(1):24-30
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  • [Title] Analysis of acute leukemias with MLL/ENL fusion transcripts: identification of two novel breakpoints in ENL.
  • t(11;19)(q23;p13.3); is one of the common chromosomal translocations in acute leukemias involving MLL rearrangements.
  • In a study of acute leukemias, 148 patients were identified to have MLL rearrangements by Southern blot analysis.
  • Of 15 patients with MLL/ENL, 7 had precursor B-cell acute lymphoblastic leukemia, 4 had T-cell acute lymphoblastic leukemia, and 4 had acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Oncogene Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Child, Preschool. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

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  • (PMID = 17145626.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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50. Savani BN, Mielke S, Adams S, Uribe M, Rezvani K, Yong AS, Zeilah J, Kurlander R, Srinivasan R, Childs R, Hensel N, Barrett AJ: Rapid natural killer cell recovery determines outcome after T-cell-depleted HLA-identical stem cell transplantation in patients with myeloid leukemias but not with acute lymphoblastic leukemia. Leukemia; 2007 Oct;21(10):2145-52
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  • [Title] Rapid natural killer cell recovery determines outcome after T-cell-depleted HLA-identical stem cell transplantation in patients with myeloid leukemias but not with acute lymphoblastic leukemia.
  • Natural killer (NK) cells are the first lymphocytes to recover after allogeneic stem cell transplantation (SCT) and can exert powerful graft-versus-leukemia (GVL) effects determining transplant outcome.
  • Conditions governing NK cell alloreactivity and the role of NK recovery in sibling SCT are not well defined.
  • NK cells on day 30 post-transplant (NK30) were measured in 54 SCT recipients with leukemia and donor and recipient killer immunoglobulin-like receptor (KIR) genotype determined.
  • NK30 counts also correlated directly with the transplant CD34 cell dose and inversely with the CD3+ cell dose.
  • Patients with NK30 >150/microl had less relapse (HR 18.3, P=0.039), acute graft-versus-host disease (HR 3.2, P=0.03), non-relapse mortality (HR 10.7, P=0.028) and improved survival (HR 11.4, P=0.03).
  • Results suggest that T cell-depleted SCT might be improved and the GVL effect enhanced by selecting donors with favorable KIR genotype, and by optimizing CD34 and CD3 doses.
  • [MeSH-major] HLA Antigens / metabolism. Killer Cells, Natural / cytology. Leukemia, Myeloid / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Stem Cell Transplantation / methods. T-Lymphocytes / metabolism
  • [MeSH-minor] Adolescent. Adult. Antigens, CD3 / biosynthesis. Antigens, CD34 / biosynthesis. Child. Cohort Studies. Female. Genotype. Graft vs Leukemia Effect. Humans. Male. Middle Aged. Monomeric GTP-Binding Proteins / metabolism. Transplantation Conditioning. Transplantation, Homologous


51. Sancho JM, Morgades M, Arranz R, Fernández-Abellán P, Deben G, Alonso N, Blanes M, Rodríguez MJ, Nicolás C, Sánchez E, Fernández de Sevilla A, Conde E, Ribera JM, QUIT Study (PETHEMA, GELTAMO and GOTEL Groups): Practice of central nervous system prophylaxis and treatment in acute leukemias in Spain. Prospective registry study. Med Clin (Barc); 2008 Oct 4;131(11):401-5
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  • [Title] Practice of central nervous system prophylaxis and treatment in acute leukemias in Spain. Prospective registry study.
  • BACKGROUND AND OBJECTIVE: Central nervous system (CNS) involvement in patients diagnosed with acute leukemias (AL) is an uncommon complication with poor prognosis.
  • For acute lymphoblastic leukemia patients (n = 158), CNS therapy was given to 12 cases (10 at diagnosis and 2 at relapse) and consisted of triple intrathecal therapy (TIT, methotrexate, cytarabine and hydrocortisone) in 11 and liposomal depot cytarabine in one.
  • In acute myeloblastic leukemia patients (n = 107), CNS therapy was administered to 17 cases (9 at diagnosis and 8 at relapse).
  • [MeSH-major] Central Nervous System Neoplasms / prevention & control. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Registries

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  • (PMID = 18928719.001).
  • [ISSN] 0025-7753
  • [Journal-full-title] Medicina clínica
  • [ISO-abbreviation] Med Clin (Barc)
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antimetabolites, Antineoplastic; 0 / Liposomes; 04079A1RDZ / Cytarabine; WI4X0X7BPJ / Hydrocortisone; YL5FZ2Y5U1 / Methotrexate
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52. Yamane K, Kinsella TJ: Casein kinase 2 regulates both apoptosis and the cell cycle following DNA damage induced by 6-thioguanine. Clin Cancer Res; 2005 Mar 15;11(6):2355-63
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  • [Title] Casein kinase 2 regulates both apoptosis and the cell cycle following DNA damage induced by 6-thioguanine.
  • PURPOSE: The purine antimetabolite, 6-thioguanine (6-TG), is an effective drug in the management of acute leukemias.
  • Control and CK2 activity-reduced cells were cultured with 6-TG and assessed by flow cytometry to measure apoptosis and cell cycle profiles.
  • Additionally, transfection of Cdc2 with a mutation at Ser(39) to Ala, which is the CK2 phosphorylation site, partially inhibits cell cycle progression in G(1) to G(2) phase following 6-TG treatment.
  • [MeSH-major] Apoptosis / drug effects. Casein Kinase II / pharmacology. Caspases / metabolism. Cell Cycle / drug effects. DNA Damage / drug effects. Thioguanine / pharmacology

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  • (PMID = 15788687.001).
  • [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 / CA 84578; United States / NCI NIH HHS / CA / P30 CA 43703-12
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / RNA, Small Interfering; EC 2.7.11.1 / Casein Kinase II; EC 3.4.22.- / Caspases; FTK8U1GZNX / Thioguanine
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53. Kröger N, Bacher U, Bader P, Böttcher S, Borowitz MJ, Dreger P, Khouri I, Macapinlac HA, Olavarria E, Radich J, Stock W, Vose JM, Weisdorf D, Willasch A, Giralt S, Bishop MR, Wayne AS: NCI First International Workshop on the Biology, Prevention, and Treatment of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation: report from the Committee on Disease-Specific Methods and Strategies for Monitoring Relapse following Allogeneic Stem Cell Transplantation. Part I: Methods, acute leukemias, and myelodysplastic syndromes. Biol Blood Marrow Transplant; 2010 Sep;16(9):1187-211
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  • [Title] NCI First International Workshop on the Biology, Prevention, and Treatment of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation: report from the Committee on Disease-Specific Methods and Strategies for Monitoring Relapse following Allogeneic Stem Cell Transplantation. Part I: Methods, acute leukemias, and myelodysplastic syndromes.
  • Relapse has become the major cause of treatment failure after allogeneic stem cell transplantation.
  • To detect early relapse or minimal residual disease, sensitive methods such as molecular genetics, tumor-specific molecular primers, fluorescein in situ hybridization, and multiparameter flow cytometry (MFC) are commonly used after allogeneic stem cell transplantation to monitor patients, but not all of them are included in the commonly employed disease-specific response criteria.
  • Here, we summarize the current knowledge about the utilization of such sensitive monitoring techniques based on tumor-specific markers and donor cell chimerism and how these methods might augment the standard definitions of posttransplant remission, persistence, progression, relapse, and the prediction of relapse.
  • Critically important is the need for standardization of the different residual disease techniques and to assess the clinical relevance of minimal residual disease and chimerism surveillance in individual diseases, which in turn, must be followed by studies to assess the potential impact of specific interventional strategies.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia / therapy. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Acute Disease. Chimerism. Chromosome Banding. Disease Progression. Humans. Neoplasm Recurrence, Local / diagnosis. Transplantation Conditioning. Treatment Outcome

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  • [Copyright] Copyright (c) 2010 American Society for Blood and Marrow Transplantation. All rights reserved.
  • [ErratumIn] Biol Blood Marrow Transplant. 2010 Dec;16(12):1752. Macapintac, Homer [corrected to Macapinlac, Homer A]
  • (PMID = 20558311.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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54. Mahmoud LA, Shamaa SS, Salem MA, Aladle DA, Goda EF: A study for evaluation of different diagnostic approaches in acute leukemia in Egypt. Hematology; 2006 Apr;11(2):87-95
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  • [Title] A study for evaluation of different diagnostic approaches in acute leukemia in Egypt.
  • Cytomorphology, cytochemistry, immunophenotyping, in addition to cytogenetic and molecular analyses have specific roles in the diagnosis and management of acute leukemias.
  • This work was designed as a comparative study of different available methods for diagnosis of acute leukemia.
  • The study comprised 47 cases with acute leukemia (21 cases with ALL and 26 cases with AML).
  • The results of the study revealed that careful examination of Romanowsky-stained peripheral blood and BM films is fundamental in the diagnosis of acute leukemias, and when considered together with clinical and hematological features, indicates which of the more specialized techniques are most likely to be useful.
  • The major role of cytochemistry was in the diagnosis of AML, while the major role of immunophenotyping was in the diagnosis of acute leukemia, which is not obviously myeloid.
  • Apart from identification of chromosomal abnormalities unique to specific subtypes of leukemia, cytogenetic analysis had a salient impact on anticipating the prognosis and treatment outcome in acute leukemias.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 16753847.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers
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55. Lilljebjörn H, Soneson C, Andersson A, Heldrup J, Behrendtz M, Kawamata N, Ogawa S, Koeffler HP, Mitelman F, Johansson B, Fontes M, Fioretos T: The correlation pattern of acquired copy number changes in 164 ETV6/RUNX1-positive childhood acute lymphoblastic leukemias. Hum Mol Genet; 2010 Aug 15;19(16):3150-8
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  • [Title] The correlation pattern of acquired copy number changes in 164 ETV6/RUNX1-positive childhood acute lymphoblastic leukemias.
  • The ETV6/RUNX1 fusion gene, present in 25% of B-lineage childhood acute lymphoblastic leukemia (ALL), is thought to represent an initiating event, which requires additional genetic changes for leukemia development.
  • As previously demonstrated, alterations targeting genes involved in B-cell development were common (present in 28% of cases).

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  • (PMID = 20513752.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA026038-31; United States / NCI NIH HHS / CA / R01 CA026038-32; United States / NCI NIH HHS / CA / CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038; United States / NCI NIH HHS / CA / R01 CA026038-30A2
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
  • [Other-IDs] NLM/ PMC3146010
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56. Weir EG, Ali Ansari-Lari M, Batista DA, Griffin CA, Fuller S, Smith BD, Borowitz MJ: Acute bilineal leukemia: a rare disease with poor outcome. Leukemia; 2007 Nov;21(11):2264-70
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  • [Title] Acute bilineal leukemia: a rare disease with poor outcome.
  • Most cases of acute leukemia can be assigned to the myeloid, B or T lineage.
  • A subset of these, referred to as acute bilineal leukemias (aBLLs), is characterized by the presence of more than one population of blasts, each comprising a single lineage.
  • Of 16 patients with outcome data, only six achieved complete remission and only two remain free of disease 2.5 and 4.5 years after chemotherapy or stem cell transplantation. aBLL is a rare disease that combines B or T and myeloid blasts.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy

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  • (PMID = 17611554.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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57. Issa JP, Byrd JC: Decitabine in chronic leukemias. Semin Hematol; 2005 Jul;42(3 Suppl 2):S43-9
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  • [Title] Decitabine in chronic leukemias.
  • Indeed, promising clinical results have been observed in acute myeloid leukemia (AML) and the myelodysplastic syndromes (MDS).
  • Aberrant methylation has also been found in chronic leukemias, providing a rationale for investigating the use of decitabine in these diseases.
  • There is clear evidence of molecular (hypomethylation) as well as hematologic and cytogenetic responses to decitabine in chronic myelogenous leukemia of all phases, including in patients resistant to imatinib mesylate.
  • Clinical trials of decitabine in chronic lymphocytic leukemia are ongoing.
  • There are many unanswered questions regarding optimizing this treatment for chronic leukemias, but successful proof-of-concept studies for hypomethylating agents move us closer to approaches that may have a significant impact on patient outcomes.
  • [MeSH-major] Azacitidine / analogs & derivatives. Leukemia / drug therapy
  • [MeSH-minor] Chronic Disease. Combined Modality Therapy. Hematopoietic Stem Cell Transplantation. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy

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  • (PMID = 16015505.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  • [Number-of-references] 67
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58. Cony-Makhoul P, Bergeron A, Corm S, Dubruille V, Rea D, Rigal-Huguet F, Nicolini FE: [Guidelines for the management of dasatinib (Sprycel)-induced side effects in chronic myelogenous leukemia and Philadelphia positive acute lymphoblastic leukemias]. Bull Cancer; 2008 Sep;95(9):805-11
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  • [Title] [Guidelines for the management of dasatinib (Sprycel)-induced side effects in chronic myelogenous leukemia and Philadelphia positive acute lymphoblastic leukemias].
  • [Transliterated title] Recommandations pour la gestion des effets indésirables du traitement par dasatinib (Sprycel) au cours de la leucémie myéloïde chronique et des leucémies aiguës lymphoblastiques à chromosome Philadelphie.
  • Dasatinib (Sprycel) is a new-targeted therapy used since 2005 in the treatment of chronic myelogenous leukemia and de novo Philadelphia positive acute lymphoblastic leukaemia patients, intolerant or resistant to imatinib.
  • Despite its high efficacy in such patients in terms of hematologic, cytogenetic and molecular responses, the onset of frequent and sometimes serious side effects particularly in advanced phase patients, especially myelosuppressions and pleural effusions, may impair optimal administration of the drug.
  • Recently, dasatinib dose optimisation in chronic-phase has reduced the incidence of such adverse events without modification of the efficacy, however, their optimal overall management can efficiently reduce their severity and minimize their impact on disease response.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / adverse effects. Thiazoles / adverse effects


59. Zhang NN, Shen SH, Jiang LJ, Zhang W, Zhang HX, Sun YP, Li XY, Huang QH, Ge BX, Chen SJ, Wang ZG, Chen Z, Zhu J: RIG-I plays a critical role in negatively regulating granulocytic proliferation. Proc Natl Acad Sci U S A; 2008 Jul 29;105(30):10553-8
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  • However, we have found a significant RIG-I induction in a biological setting without active viral infection-namely, during RA-induced terminal granulocytic differentiation of acute myeloid leukemias.
  • Here, we present evidence that a significant Rig-I induction also occurs during normal myelopoiesis and that the disruption of the Rig-I gene in mice leads to the development of a progressive myeloproliferative disorder.
  • [MeSH-minor] Animals. Cell Differentiation. Cell Proliferation. Exons. Hematopoietic Stem Cells / cytology. Humans. Immunity, Innate. Mice. Mice, Knockout. Mice, Transgenic. Myeloid Cells / cytology. Myeloproliferative Disorders / metabolism

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  • (PMID = 18650396.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RARRES3 protein, human; 0 / Receptors, Retinoic Acid; EC 3.6.1.- / Ddx58 protein, mouse; EC 3.6.4.13 / DEAD-box RNA Helicases
  • [Other-IDs] NLM/ PMC2492484
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60. Kovacsovics T, Maziarz RT: Philadelphia chromosome-positive acute lymphoblastic leukemia: impact of imatinib treatment on remission induction and allogeneic stem cell transplantation. Curr Oncol Rep; 2006 Sep;8(5):343-51
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  • [Title] Philadelphia chromosome-positive acute lymphoblastic leukemia: impact of imatinib treatment on remission induction and allogeneic stem cell transplantation.
  • Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) has been associated with the worst patient survival rates of the various acute leukemias.
  • Hematopoietic stem cell transplantation has also integrated imatinib into its transplant strategies, with early data suggesting improved progression-free survival without clearly identifiable augmented toxicity.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Stem Cell Transplantation

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  • (PMID = 16901395.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 61
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61. Pabst T, Mueller BU: Transcriptional dysregulation during myeloid transformation in AML. Oncogene; 2007 Oct 15;26(47):6829-37
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  • The current paradigm on leukemogenesis indicates that leukemias are propagated by leukemic stem cells.
  • This concept is based on genomic mutations or functional dysregulation of transcription factors in malignant cells of patients with acute myeloid leukemia (AML).
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Myeloid Cells / pathology. Transcription, Genetic / physiology
  • [MeSH-minor] Acute Disease. Animals. Humans

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  • (PMID = 17934489.001).
  • [ISSN] 0950-9232
  • [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] 78
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62. Dou Y, Hess JL: Mechanisms of transcriptional regulation by MLL and its disruption in acute leukemia. Int J Hematol; 2008 Jan;87(1):10-8
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  • [Title] Mechanisms of transcriptional regulation by MLL and its disruption in acute leukemia.
  • Fusion of the mixed lineage leukemia protein (MLL) to one of over 50 different translocation partners converts it into a potent leukemogenic oncoprotein.
  • The resulting fusion proteins transform primarily through upregulation of A-cluster Hox genes, including Hoxa9 and the Hox cofactor Meis1.
  • Considerable progress has been made in delineating the differences between normal Hox gene regulation by MLL and deregulated transcription in MLL-induced leukemias.
  • [MeSH-major] Leukemia / genetics. Leukopoiesis / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Transcription, Genetic / genetics
  • [MeSH-minor] Animals. DNA Methylation. Disease Models, Animal. Histone-Lysine N-Methyltransferase. Homeodomain Proteins / genetics. Homeodomain Proteins / physiology. Humans. Mice. Mice, Knockout. Neoplasm Proteins / genetics. Neoplasm Proteins / physiology

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  • (PMID = 18224408.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Hoxa7 protein, mouse; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / myeloid ecotropic viral integration site 1 protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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63. Forestier E, Izraeli S, Beverloo B, Haas O, Pession A, Michalová K, Stark B, Harrison CJ, Teigler-Schlegel A, Johansson B: Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study. Blood; 2008 Feb 1;111(3):1575-83
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  • [Title] Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome: an iBFM-SG study.
  • Children with Down syndrome (DS) have a markedly increased risk of acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • To identify chromosomal changes cooperating with +21 that may provide information on the pathogenesis of these leukemias, we analyzed 215 DS-ALLs and 189 DS-AMLs.
  • Unlike previous smaller series, a significant proportion of DS-ALLs had the typical B-cell precursor ALL abnormalities high hyperdiploidy (HeH; 11%) and t(12;21)(p13;q22) (10%).
  • This series of DS leukemias-the largest to date-reveals that DS-ALL is a heterogeneous disorder that comprises both t(12;21) and HeH as well as DS-related abnormalities.
  • [MeSH-major] Down Syndrome / complications. Down Syndrome / genetics. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


64. Kraicheva I, Bogomilova A, Tsacheva I, Momekov G, Troev K: Synthesis, NMR characterization and in vitro antitumor evaluation of new aminophosphonic acid diesters. Eur J Med Chem; 2009 Aug;44(8):3363-7
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  • The compounds were tested for antiproliferative effects against 4 human leukemic cell lines, namely LAMA-84, K-562 (chronic myeloid leukemias), HL-60 (acute promyelocyte leukemia) and HL-60/Dox (multi-drug-resistant sub-line, characterized by overexpression of MRP-1 (ABC-C1)) and were found to exert concentration-dependent cytotoxic effects.
  • A representative aminophosphonate compound was shown to induce oligonucleosomal DNA fragmentation which implies that the induction of cell death through apoptosis plays an important role for its cytotoxicity mode of action.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic / drug effects. Humans. Inhibitory Concentration 50. Magnetic Resonance Spectroscopy. Multidrug Resistance-Associated Proteins / metabolism

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  • (PMID = 19361895.001).
  • [ISSN] 1768-3254
  • [Journal-full-title] European journal of medicinal chemistry
  • [ISO-abbreviation] Eur J Med Chem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Multidrug Resistance-Associated Proteins; 0 / Organophosphonates; 0 / multidrug resistance-associated protein 1
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65. Boublikova L, Kalinova M, Ryan J, Quinn F, O'Marcaigh A, Smith O, Browne P, Stary J, McCann SR, Trka J, Lawler M: Wilms' tumor gene 1 (WT1) expression in childhood acute lymphoblastic leukemia: a wide range of WT1 expression levels, its impact on prognosis and minimal residual disease monitoring. Leukemia; 2006 Feb;20(2):254-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Wilms' tumor gene 1 (WT1) expression in childhood acute lymphoblastic leukemia: a wide range of WT1 expression levels, its impact on prognosis and minimal residual disease monitoring.
  • Wilms' tumor gene 1 (WT1) is overexpressed in the majority (70-90%) of acute leukemias and has been identified as an independent adverse prognostic factor, a convenient minimal residual disease (MRD) marker and potential therapeutic target in acute leukemia.
  • We examined WT1 expression patterns in childhood acute lymphoblastic leukemia (ALL), where its clinical implication remains unclear.
  • In childhood B-cell precursor (BCP)-ALL, we detected a wide range of WT1 levels (5 logs) with a median WT1 expression close to that of normal BM.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Molecular Diagnostic Techniques / methods. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. WT1 Proteins / genetics


66. Godal R, Bachanova V, Gleason M, McCullar V, Yun GH, Cooley S, Verneris MR, McGlave PB, Miller JS: Natural killer cell killing of acute myelogenous leukemia and acute lymphoblastic leukemia blasts by killer cell immunoglobulin-like receptor-negative natural killer cells after NKG2A and LIR-1 blockade. Biol Blood Marrow Transplant; 2010 May;16(5):612-21
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  • [Title] Natural killer cell killing of acute myelogenous leukemia and acute lymphoblastic leukemia blasts by killer cell immunoglobulin-like receptor-negative natural killer cells after NKG2A and LIR-1 blockade.
  • Although the study of natural killer (NK) cell alloreactivity has been dominated by studies of killer cell immunoglobulin-like receptors (KIRs), we hypothesized that NKG2A and LIR-1, present on 53% +/- 13% and 36% +/- 18% of normal NK cells, respectively, play roles in the NK cell killing of primary leukemia targets.
  • KIR(-) cells, which compose nearly half of the circulating NK cell population, exhibit tolerance to primary leukemia targets, suggesting signaling through other inhibitory receptors.
  • Both acute myelogenous leukemia and acute lymphoblastic leukemia targets were rendered susceptible to lysis by fresh resting KIR(-) NK cells when inhibitory receptor-major histocompatibility class I interactions were blocked by pan-HLA antibodies, demonstrating that these cells are functionally competent.
  • Blockade of a single inhibitory receptor resulted in slightly increased killing, whereas combined LIR-1 and NKG2A blockade consistently resulted in increased NK cell cytotoxicity.
  • Together these results suggest that alloreactivity of a significant fraction of KIR(-) NK cells is mediated by NKG2A and LIR-1.
  • Thus strategies to interrupt NKG2A and LIR-1 in combination with anti-KIR blockade hold promise for exploiting NK cell therapy in acute leukemias.

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  • [Copyright] Copyright 2010 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved.
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  • (PMID = 20139023.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01-CA-111412; United States / NCI NIH HHS / CA / CA111412-01A1; United States / NCI NIH HHS / CA / P01 CA065493; United States / NCI NIH HHS / CA / CA065493-110010; United States / NCI NIH HHS / CA / P01 CA111412-01A1; United States / NCI NIH HHS / CA / P01 CA065493-110010; United States / NCI NIH HHS / CA / P01-CA-65493; United States / NCI NIH HHS / CA / P01 CA111412
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD; 0 / Histocompatibility Antigens Class I; 0 / KLRC1 protein, human; 0 / LILRB1 protein, human; 0 / NK Cell Lectin-Like Receptor Subfamily C; 0 / Receptors, Immunologic; 0 / Receptors, KIR
  • [Other-IDs] NLM/ NIHMS177123; NLM/ PMC2854246
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67. O'Neil J, Look AT: Mechanisms of transcription factor deregulation in lymphoid cell transformation. Oncogene; 2007 Oct 15;26(47):6838-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanisms of transcription factor deregulation in lymphoid cell transformation.
  • The most frequent targets of genetic alterations in human lymphoid leukemias are transcription factor genes with essential functions in blood cell development.
  • TAL1, LYL1, HOX11 and other transcription factors essential for normal hematopoiesis are often misexpressed in the thymus in T-cell acute lymphoblastic leukemia (T-ALL), leading to differentiation arrest and cell transformation.
  • The NOTCH1 gene, which is essential for key embryonic cell-fate decisions in multicellular organisms, was found to be activated by mutation in a large percentage of T-ALL patients.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Lymphocyte Subsets / metabolism. Lymphocyte Subsets / pathology. Transcription Factors / genetics

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  • (PMID = 17934490.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA109901
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Transcription Factors
  • [Number-of-references] 170
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68. Vempati S, Reindl C, Kaza SK, Kern R, Malamoussi T, Dugas M, Mellert G, Schnittger S, Hiddemann W, Spiekermann K: Arginine 595 is duplicated in patients with acute leukemias carrying internal tandem duplications of FLT3 and modulates its transforming potential. Blood; 2007 Jul 15;110(2):686-94
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  • [Title] Arginine 595 is duplicated in patients with acute leukemias carrying internal tandem duplications of FLT3 and modulates its transforming potential.
  • FLT3-internal tandem duplications (FLT3-ITDs) comprise a heterogeneous group of mutations in patients with acute leukemias that are prognostically important.
  • To characterize the mechanism of transformation by FLT3-ITDs, we sequenced the juxtamembrane region (JM) of FLT3 from 284 patients with acute leukemias.
  • [MeSH-major] Arginine. Leukemia / genetics. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Amino Acid Substitution. Cell Transformation, Neoplastic / genetics. Female. Gene Duplication. Humans. Male. Middle Aged. Mutagenesis. Sequence Deletion

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  • (PMID = 17387224.001).
  • [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] 94ZLA3W45F / Arginine; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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69. Takenokuchi M, Nakamachi Y, Yoneda K, Joo K, Kawano S, Tatsumi E, Saigo K, Kumagai S: Quantitative detection of PML-RARalpha fusion transcript by real-time PCR with a single primer pair. J Clin Lab Anal; 2009;23(4):223-30
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  • Quantitative detection of minimal residual disease has prognostic value for some leukemias.
  • Acute promyelocytic leukemia (APL) is characterized by the specific PML-RARalpha fusion gene from t(15;17).
  • [MeSH-major] Leukemia, Promyelocytic, Acute / genetics. Oncogene Proteins, Fusion / genetics. Receptors, Retinoic Acid / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods
  • [MeSH-minor] Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Line, Tumor. DNA Primers / genetics. Humans. Prognosis. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Neoplasm / analysis. Reproducibility of Results

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  • (PMID = 19623654.001).
  • [ISSN] 1098-2825
  • [Journal-full-title] Journal of clinical laboratory analysis
  • [ISO-abbreviation] J. Clin. Lab. Anal.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms; 0 / RNA, Neoplasm; 0 / Receptors, Retinoic Acid; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
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70. Zeng Z, Sarbassov dos D, Samudio IJ, Yee KW, Munsell MF, Ellen Jackson C, Giles FJ, Sabatini DM, Andreeff M, Konopleva M: Rapamycin derivatives reduce mTORC2 signaling and inhibit AKT activation in AML. Blood; 2007 Apr 15;109(8):3509-12
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  • We investigated the molecular effects of mTOR inhibition by the rapamycin derivatives (RDs) temsirolimus (CCI-779) and everolimus (RAD001) in acute myeloid leukemia (AML) cells.
  • Our study provides the first evidence that rapamycin derivatives inhibit AKT signaling in primary AML cells both in vitro and in vivo, and supports the therapeutic potential of mTOR inhibition strategies in leukemias.

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  • (PMID = 17179228.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 55164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA 49639; United States / NCI NIH HHS / CA / CA 16672; United States / NCI NIH HHS / CA / P01 CA049639; 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 / Adaptor Proteins, Signal Transducing; 0 / Carrier Proteins; 0 / Cyclin D; 0 / Cyclins; 0 / Glucose Transporter Type 1; 0 / Immunosuppressive Agents; 0 / Protein Kinase Inhibitors; 0 / Proteins; 0 / RICTOR protein, human; 0 / RNA, Messenger; 0 / RPTOR protein, human; 0 / SLC2A1 protein, human; 624KN6GM2T / temsirolimus; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC1852241
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71. Hassanein NM, Alcancia F, Perkinson KR, Buckley PJ, Lagoo AS: Distinct expression patterns of CD123 and CD34 on normal bone marrow B-cell precursors ("hematogones") and B lymphoblastic leukemia blasts. Am J Clin Pathol; 2009 Oct;132(4):573-80
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  • [Title] Distinct expression patterns of CD123 and CD34 on normal bone marrow B-cell precursors ("hematogones") and B lymphoblastic leukemia blasts.
  • We compared the expression of CD123, the alpha chain of the interleukin-3 receptor, on normal B-cell precursors in bone marrow ("hematogones") from 75 specimens and on leukemic blasts in 45 newly diagnosed B-acute lymphoblastic leukemias (B-ALL) cases.
  • [MeSH-major] Antigens, CD34 / genetics. Interleukin-3 Receptor alpha Subunit / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology

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  • (PMID = 19762535.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / IL3RA protein, human; 0 / Interleukin-3 Receptor alpha Subunit
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72. Chu SH, Small D: Mechanisms of resistance to FLT3 inhibitors. Drug Resist Updat; 2009 Feb-Apr;12(1-2):8-16
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  • The success of the small molecule tyrosine kinase receptor inhibitor (TKI) imatinib mesylate (Gleevec) in the treatment of chronic myeloid leukemia (CML) constitutes an eminent paradigm shift advocating the rational design of cancer therapeutics specifically targeting the transformation events that drive tumorigenicity.
  • In acute myeloid leukemias (AMLs), the most frequent identified transforming events are activating mutations in the FLT3 receptor tyrosine kinase that constitutively activate survival and proliferation pathways.

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  • (PMID = 19162530.001).
  • [ISSN] 1532-2084
  • [Journal-full-title] Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
  • [ISO-abbreviation] Drug Resist. Updat.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090668; United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P01 CA070970; United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / CA90668
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 119
  • [Other-IDs] NLM/ NIHMS787037; NLM/ PMC4891941
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73. Bartynski WS, Zeigler ZR, Shadduck RK, Lister J: Variable incidence of cyclosporine and FK-506 neurotoxicity in hematopoeitic malignancies and marrow conditions after allogeneic bone marrow transplantation. Neurocrit Care; 2005;3(1):33-45
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  • INTRODUCTION: This study examines whether malignant disease under treatment influences the incidence of cyclosporine or FK-506 neurotoxicity after myeloablative conditioning and allogeneic bone marrow transplantation (allo-BMT).
  • Underlying malignancy necessitating allo-BMT included leukemias (67%), lymphoma (10%), myelodysplastic syndrome (10%), and multiple myeloma (MM).
  • Frequency of neurotoxicity by disease was compared.
  • Other diseases demonstrated intermediate incidence, including acute leukemias (10%), myelodysplastic syndrome (6.4%), and chronic myelogenous leukemia (4.9%).
  • The variable susceptibility to the development of neurotoxicity in this population may depend on the interaction of host vasculature with disease specific factors.
  • [MeSH-minor] Graft vs Host Disease / diagnosis. Graft vs Host Disease / diagnostic imaging. Graft vs Host Disease / epidemiology. Graft vs Host Disease / prevention & control. Humans. Ischemic Preconditioning. Magnetic Resonance Imaging. Retrospective Studies. Tomography, X-Ray Computed

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  • (PMID = 16159093.001).
  • [ISSN] 1541-6933
  • [Journal-full-title] Neurocritical care
  • [ISO-abbreviation] Neurocrit Care
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 83HN0GTJ6D / Cyclosporine; 8N3DW7272P / Cyclophosphamide
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74. Wiemels JL, Kang M, Chang JS, Zheng L, Kouyoumji C, Zhang L, Smith MT, Scelo G, Metayer C, Buffler P, Wiencke JK: Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia. Blood Cells Mol Dis; 2010 Oct 15;45(3):186-91
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  • [Title] Backtracking RAS mutations in high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploidy is the single largest subtype of childhood acute lymphoblastic leukemia (ALL) and is defined by the presence of 51-68 chromosomes in a karyotype.
  • We screened for RAS mutations among 517 acute childhood leukemias (including 437 lymphocytic, of which 393 were B-cell subtypes) and found mutations in 30% of high hyperdiploids compared to only 10% of leukemias of other subtypes (P<0.0001).
  • While RAS mutations were previously associated with prior chemical exposures in childhood and adult leukemias, in this study RAS-mutated cases were not significantly associated with parental smoking when compared to study controls.
  • IGH rearrangements were backtracked in three RAS-positive patients (which were negative for KRAS mutation at birth) and found to be evident before birth, confirming a prenatal origin for the leukemia clone.
  • We posit a natural history for hyperdiploid leukemia in which prenatal mitotic catastrophe is followed by a postnatal RAS mutation to produce the leukemic cell phenotype.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20688547.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42-ES04705; United States / NCI NIH HHS / CA / R01 CA089032; United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NCI NIH HHS / CA / R25 CA112355; United States / NCI NIH HHS / CA / R25-CA112355; United States / NIEHS NIH HHS / ES / R01-ES09137; United States / NIEHS NIH HHS / ES / P01 ES018172; United States / NCI NIH HHS / CA / R01-CA089032; United States / NIEHS NIH HHS / ES / P01-ES018172; United States / NIEHS NIH HHS / ES / R01 ES009137
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS224426; NLM/ PMC2943008
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75. Inthal A, Krapf G, Beck D, Joas R, Kauer MO, Orel L, Fuka G, Mann G, Panzer-Grümayer ER: Role of the erythropoietin receptor in ETV6/RUNX1-positive acute lymphoblastic leukemia. Clin Cancer Res; 2008 Nov 15;14(22):7196-204
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  • [Title] Role of the erythropoietin receptor in ETV6/RUNX1-positive acute lymphoblastic leukemia.
  • PURPOSE: We explored the mechanisms leading to the distinct overexpression of EPOR as well as the effects of EPO signaling on ETV6/RUNX1-positive acute lymphoblastic leukemias.
  • EXPERIMENTAL DESIGN: ETV6/RUNX1-expressing model cell lines and leukemic cells were used for real-time PCR of EPOR expression.
  • Serum EPO levels and sequences of the EPOR (n = 53) as well as hemoglobin levels were taken from children with acute lymphoblastic leukemia enrolled in Austrian protocols.
  • Anemia, however, did not appear to influence EPOR expression on leukemic cells, although children with ETV6/RUNX1-positive leukemias had a lower median hemoglobin than controls.
  • Exposure to EPO increased proliferation and survival of ETV6/RUNX1-positive leukemias in vitro, whereas blocking its binding site did not alter cell survival.
  • CONCLUSIONS: Our data suggest that ETV6/RUNX1 leads to EPOR up-regulation and that activation by EPO might be of relevance to the biology of this leukemia subtype.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / metabolism. Oncogene Proteins, Fusion / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Erythropoietin / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Animals. Antineoplastic Agents, Hormonal / pharmacology. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Child. Erythropoietin / metabolism. Flow Cytometry. Humans. Prednisone / pharmacology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19010836.001).
  • [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] Austria / Austrian Science Fund FWF / / P 17551
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Erythropoietin; 0 / TEL-AML1 fusion protein; 11096-26-7 / Erythropoietin; VB0R961HZT / Prednisone
  • [Other-IDs] NLM/ EMS32871; NLM/ PMC4194425
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76. Rizack T, Mega A, Legare R, Castillo J: Management of hematological malignancies during pregnancy. Am J Hematol; 2009 Dec;84(12):830-41
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  • The purpose of this review is to evaluate the limited existing data and make useful suggestions in the management of acute and chronic leukemias, Hodgkin and non-Hodgkin lymphomas, plasma cell myeloma, and other hematological malignancies, such as myelodysplastic syndromes and hairy cell leukemia, during pregnancy.
  • [MeSH-minor] Abnormalities, Drug-Induced / etiology. Abnormalities, Drug-Induced / prevention & control. Abortion, Induced. Adult. Antiemetics / therapeutic use. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Antineoplastic Agents / contraindications. Antineoplastic Agents / therapeutic use. Cesarean Section. Clinical Protocols. Combined Modality Therapy. Disease Management. Female. Humans. Incidence. Infant, Newborn. Infant, Newborn, Diseases / chemically induced. Infant, Newborn, Diseases / prevention & control. Leukapheresis. Pregnancy. Pregnancy Outcome. Pregnancy Trimesters

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19844988.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiemetics; 0 / Antineoplastic Agents
  • [Number-of-references] 179
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77. Italiano A, Chambonniere ML, Attias R, Chibon F, Coindre JM, Pedeutour F: Monosomy 7 and absence of 12q amplification in two cases of spindle cell liposarcomas. Cancer Genet Cytogenet; 2008 Jul 15;184(2):99-104
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monosomy 7 and absence of 12q amplification in two cases of spindle cell liposarcomas.
  • Spindle cell liposarcoma (SCL) is a rare malignant adipose tissue tumor presently regarded as a variant of well-differentiated liposarcoma (WDLPS).
  • It has been described in myelodysplastic syndromes and acute myeloid or lymphoblastic leukemias, as well as in several benign or malignant solid tumors.

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  • (PMID = 18617058.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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78. Burmeister T, Meyer C, Thiel G, Reinhardt R, Thiel E, Marschalek R: A MLL-KIAA0284 fusion gene in a patient with secondary acute myeloid leukemia and t(11;14)(q23;q32). Blood Cells Mol Dis; 2008 Sep-Oct;41(2):210-4
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  • [Title] A MLL-KIAA0284 fusion gene in a patient with secondary acute myeloid leukemia and t(11;14)(q23;q32).
  • MLL aberrations are found in approximately 10% of acute leukemias.
  • More than 80 different MLL fusion genes have been cytogenetically described but a significant number of MLL fusion partners remain unidentified on the molecular level.
  • We describe here the case of a patient who developed secondary acute myeloid leukemia five years after the patient had received adjuvant radiochemotherapy because of breast cancer.
  • This therapy comprised 4 cycles epirubicin/cyclophosphamide, a mitoxantrone-based high-dose chemotherapy with autologous stem cell transplantation and a subsequent radiation.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 18640063.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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79. Geddes M, Kangarloo SB, Naveed F, Quinlan D, Chaudhry MA, Stewart D, Savoie ML, Bahlis NJ, Brown C, Storek J, Andersson BS, Russell JA: High busulfan exposure is associated with worse outcomes in a daily i.v. busulfan and fludarabine allogeneic transplant regimen. Biol Blood Marrow Transplant; 2008 Feb;14(2):220-8
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  • Low plasma busulfan (Bu) area under the concentration-time curve (AUC) is associated with graft failure and relapsed leukemias, and high AUC with toxicities when Bu is used orally or i.v.
  • 4 times daily combined with cyclophosphamide in myeloablative hematopoietic stem cell transplantation (SCT) conditioning regimens.
  • Total-body irradiation (TBI) 200 cGy x 2 was added for 51 patients with acute leukemias.
  • This effect was apparent in patients with standard-risk and high-risk disease, and persisted when potential confounders were considered (hazard ratio 3.2, 95% confidence interval 1.7-6.3).
  • [MeSH-major] Busulfan / administration & dosage. Busulfan / pharmacokinetics. Hematopoietic Stem Cell Transplantation / methods. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives

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  • (PMID = 18215782.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; G1LN9045DK / Busulfan; P2K93U8740 / fludarabine
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80. Song JH, Schnittke N, Zaat A, Walsh CS, Miller CW: FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias. Leuk Res; 2008 Nov;32(11):1751-5
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  • [Title] FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias.
  • Engineered FBXW7 null cells display cell cycle and chromosome stability defects.
  • Mutations of FBXW7 have been found in human colorectal, ovarian, endometrial tumors and T-cell acute lymphocytic leukemias.
  • Prompted by these findings we have examined acute myeloid leukemia, non-Hodgkin's lymphoma, T-cell acute lymphocytic leukemia, B-cell acute lymphocytic leukemia and adult T-cell leukemia DNA for mutations of the FBXW7 gene.
  • As expected, mutations were found in T-cell acute lymphocytic leukemias.
  • However mutations of FBXW7 were also found in four of 118 B-cell acute lymphocytic leukemias and one of 24 adult T-cell leukemia samples.
  • These observations suggest that disruption of FBXW7 has a role in several forms of lymphocytic leukemias and not exclusively T-cell acute lymphocytic leukemia.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Mutation / genetics. Ubiquitin-Protein Ligases / genetics

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  • (PMID = 18485478.001).
  • [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 / Cell Cycle Proteins; 0 / F-Box Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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81. Erkeland SJ, Palande KK, Valkhof M, Gits J, Danen-van Oorschot A, Touw IP: The gene encoding thioredoxin-interacting protein (TXNIP) is a frequent virus integration site in virus-induced mouse leukemia and is overexpressed in a subset of AML patients. Leuk Res; 2009 Oct;33(10):1367-71
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  • [Title] The gene encoding thioredoxin-interacting protein (TXNIP) is a frequent virus integration site in virus-induced mouse leukemia and is overexpressed in a subset of AML patients.
  • In a screen for novel disease genes in murine leukemia virus (MLV)-induced mouse leukemias, we identified Txnip as a frequent target for proviral integration.
  • These findings suggest that deregulated TXNIP expression contributes to MLV-induced murine leukemia as well as human AML.
  • [MeSH-major] Carrier Proteins / genetics. Gene Expression Regulation. Leukemia / genetics. Leukemia, Experimental / genetics. Leukemia, Myeloid, Acute / genetics. Thioredoxins / genetics. Virus Integration / genetics
  • [MeSH-minor] Animals. Blast Crisis / genetics. Blast Crisis / pathology. Cell Line. DNA Primers. Genes, Reporter. Humans. Leukemia Virus, Murine / genetics. Mice. Polymerase Chain Reaction. Promoter Regions, Genetic

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  • [CommentIn] Leuk Res. 2009 Oct;33(10):1297 [19560202.001]
  • (PMID = 19327827.001).
  • [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 / Carrier Proteins; 0 / DNA Primers; 0 / TXNIP protein, human; 0 / Txnip protein, mouse; 52500-60-4 / Thioredoxins
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82. Jourde-Chiche N, Dussol B, Daniel L: [Kidney involvement in hematologic malignancies. Diagnostic approach]. Rev Med Interne; 2010 Oct;31(10):685-96
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  • Various mechanisms could be implicated: deposits of immunoglobulin fractions or crystals, renal infiltration by malignant cells, urinary tract obstruction, paraneoplastic or storage glomerulopathies… Diagnostic strategy relies on the clinical presentation: acute renal failure, chronic kidney disease, glomerular proteinuria with or without nephrotic syndrome, tubular proteinuria, hydroelectrolytic disorders.
  • We propose diagnostic strategies of renal involvement in myeloma, Waldenström's disease, high grade lymphomas and acute leukemias, low grade lymphomas and chronic leukemias.
  • The adverse effects of treatments (chemotherapy, radiotherapy, stem cell graft …) are not addressed in this review.

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  • [Copyright] Copyright © 2010 Société nationale française de médecine interne (SNFMI). Published by Elsevier SAS. All rights reserved.
  • (PMID = 20483511.001).
  • [ISSN] 1768-3122
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
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83. Miyazaki K, Yamasaki N, Oda H, Kuwata T, Kanno Y, Miyazaki M, Komeno Y, Kitaura J, Honda Z, Warming S, Jenkins NA, Copeland NG, Kitamura T, Nakamura T, Honda H: Enhanced expression of p210BCR/ABL and aberrant expression of Zfp423/ZNF423 induce blast crisis of chronic myelogenous leukemia. Blood; 2009 May 7;113(19):4702-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Enhanced expression of p210BCR/ABL and aberrant expression of Zfp423/ZNF423 induce blast crisis of chronic myelogenous leukemia.
  • Chronic myelogenous leukemia (CML) is a hematopoietic disorder originating from p210BCR/ABL-transformed stem cells, which begins as indolent chronic phase (CP) but progresses into fatal blast crisis (BC).
  • To investigate molecular mechanism(s) underlying disease evolution, CML-exhibiting p210BCR/ABL transgenic mice were crossed with BXH2 mice that transmit a replication-competent retrovirus.
  • Whereas nontransgenic mice in the BXH2 background exclusively developed acute myeloid leukemia, p210BCR/ABL transgenic littermates developed nonmyeloid leukemias, in which inverse polymerase chain reaction detected 2 common viral integration sites (CISs).
  • The other was the 5' noncoding region of a transcription factor, Zfp423, which induced aberrant Zfp423 expression.
  • (1) introduction of Zfp423 in p210BCR/ABL transgenic bone marrow (BM) cells increased colony-forming ability, (2) suppression of ZNF423 (human homologue of Zfp423) in ZNF423-expressing, p210BCR/ABL-positive hematopoietic cells retarded cell growth, (3) mice that received a transplant of BM cells transduced with Zfp423 and p210BCR/ABL developed acute leukemia, and (4) expression of ZNF423 was found in human BCR/ABL-positive cell lines and CML BC samples.
  • [MeSH-major] B-Lymphocytes / pathology. Blast Crisis / genetics. DNA-Binding Proteins / physiology. Fusion Proteins, bcr-abl / physiology. Gene Expression Regulation, Leukemic. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Transcription Factors / physiology
  • [MeSH-minor] Animals. Blotting, Northern. Blotting, Southern. Blotting, Western. Bone Marrow Transplantation. Cell Proliferation. Colony-Forming Units Assay. Female. Flow Cytometry. Gene Rearrangement. Humans. Male. Mice. Mice, Knockout. Phenotype. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Retroviridae. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Zinc Fingers


84. Eguchi-Ishimae M, Eguchi M, Ishii E, Knight D, Sadakane Y, Isoyama K, Yabe H, Mizutani S, Greaves M: The association of a distinctive allele of NAD(P)H:quinone oxidoreductase with pediatric acute lymphoblastic leukemias with MLL fusion genes in Japan. Haematologica; 2005 Nov;90(11):1511-5
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  • [Title] The association of a distinctive allele of NAD(P)H:quinone oxidoreductase with pediatric acute lymphoblastic leukemias with MLL fusion genes in Japan.
  • Previous studies in Caucasian populations have provided evidence that a loss of function allele at nt 609 (C609T, Pro187Ser) is associated with increased risk of infant acute lymphoblastic leukemia (ALL) with MLL-AF4 fusion genes.
  • DESIGN AND METHODS: We genotyped 103 infants (<18 months) with ALL or acute myeloid leukemia (AML) in Japan and 185 controls for the frequency of allelic variation at nt 609 and 465 in NQO1 using standardized polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methodology.
  • [MeSH-major] Alleles. Asian Continental Ancestry Group / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. NAD(P)H Dehydrogenase (Quinone) / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16266898.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human
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85. Chen J, Jette C, Kanki JP, Aster JC, Look AT, Griffin JD: NOTCH1-induced T-cell leukemia in transgenic zebrafish. Leukemia; 2007 Mar;21(3):462-71
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  • [Title] NOTCH1-induced T-cell leukemia in transgenic zebrafish.
  • Activating mutations in the NOTCH1 gene have been found in about 60% of patients with T-cell acute lymphoblastic leukemia (T-ALL).
  • In order to study the molecular mechanisms by which altered Notch signaling induces leukemia, a zebrafish model of human NOTCH1-induced T-cell leukemia was generated.
  • Seven of sixteen mosaic fish developed a T-cell lymphoproliferative disease at about 5 months.
  • These neoplastic cells extensively invaded tissues throughout the fish and caused an aggressive and lethal leukemia when transplanted into irradiated recipient fish.
  • However, stable transgenic fish exhibited a longer latency for leukemia onset.
  • When the stable transgenic line was crossed with another line overexpressing the zebrafish bcl2 gene, the leukemia onset was dramatically accelerated, indicating synergy between the Notch pathway and the bcl2-mediated antiapoptotic pathway.
  • Reverse transcription-polymerase chain reaction analysis showed that Notch target genes such as her6 and her9 were highly expressed in NOTCH1-induced leukemias.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Leukemia-Lymphoma, Adult T-Cell / etiology. Proto-Oncogene Proteins c-bcl-2 / physiology. Receptor, Notch1 / physiology
  • [MeSH-minor] Animals. Animals, Genetically Modified. Apoptosis. Basic Helix-Loop-Helix Transcription Factors / physiology. Female. Gamma Rays. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor. Genes, bcl-2. Humans. Male. Mosaicism. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Neoplasm Proteins / physiology. Neoplasm Transplantation. Oncogenes. Radiation Chimera. Radiation Tolerance. Recombinant Fusion Proteins / physiology. Signal Transduction. Time Factors. Zebrafish. Zebrafish Proteins / physiology

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  • (PMID = 17252014.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-36167; United States / NCI NIH HHS / CA / CA-68484
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Her6 protein, zebrafish; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptor, Notch1; 0 / Recombinant Fusion Proteins; 0 / Zebrafish Proteins; 0 / her9 protein, zebrafish
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86. Passweg JR, Chalandon Y, Matthes T, Beris P, Aapro MS, Plan PA: [Acute leukemias]. Rev Med Suisse; 2008 May 21;4(158):1272-4, 1276-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute leukemias].
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 18616210.001).
  • [ISSN] 1660-9379
  • [Journal-full-title] Revue médicale suisse
  • [ISO-abbreviation] Rev Med Suisse
  • [Language] fre
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Number-of-references] 22
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87. Cerveira N, Meyer C, Santos J, Torres L, Lisboa S, Pinheiro M, Bizarro S, Correia C, Norton L, Marschalek R, Teixeira MR: A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia. BMC Cancer; 2010;10:518
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  • [Title] A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia.
  • BACKGROUND: Abnormalities of 11q23 involving the MLL gene are found in approximately 10% of human leukemias.
  • To date, nearly 100 different chromosome bands have been described in rearrangements involving 11q23 and 64 fusion genes have been cloned and characterized at the molecular level.
  • In this work we present the identification of a novel MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia.
  • METHODS: Cytogenetics, fluorescence in situ hybridization (FISH), molecular studies (RT-PCR and LDI-PCR), and bioinformatic sequence analysis were used to characterize the CT45A2 gene as novel MLL fusion partner in pediatric acute leukemia.
  • RNA analysis revealed the presence of a novel MLL-CT45A2 fusion transcript in which the first 9 exons of the MLL gene were fused in-frame to exon 2 of the CT45A2 gene, resulting in a spliced MLL fusion transcript with an intact open reading frame.
  • CONCLUSION: We have identified CT45A2 as a novel spliced MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia, as a result of a cryptic insertion of 11q23 in Xq26.3.
  • Since CT45A2 is the first Cancer/Testis antigen family gene found fused with MLL in acute leukemia, future studies addressing its biologic relevance for leukemogenesis are warranted.
  • [MeSH-major] Antigens, Neoplasm / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics