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1. Nakagawa Y, Hasegawa M, Kurata M, Yamamoto K, Abe S, Inoue M, Takemura T, Hirokawa K, Suzuki K, Kitagawa M: Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL). Am J Hematol; 2005 Mar;78(3):173-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL).
  • To determine the apoptosis-resistant mechanism in adult acute mixed lineage leukemia (AMLL) with biphenotypic blasts responsible for resistance against chemotherapy, the expression levels of IAP-family proteins in AMLL bone marrow cells were analyzed by quantitative RT-PCR.
  • These findings suggest that higher expression of various IAPs is associated with the chemotherapy-resistant nature of this specific type of leukemia.
  • [MeSH-major] Apoptosis. Biomarkers, Tumor / metabolism. Bone Marrow Cells / metabolism. Leukemia, Biphenotypic, Acute / metabolism. Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Flow Cytometry. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Inhibitor of Apoptosis Proteins. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Male. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / metabolism. Middle Aged. Neoplasm Proteins. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15726601.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [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 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proteins; 0 / RNA, Messenger
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2. Yin H, Glass J, Blanchard KL: MOZ-TIF2 repression of nuclear receptor-mediated transcription requires multiple domains in MOZ and in the CID domain of TIF2. Mol Cancer; 2007;6:51

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  • BACKGROUND: Fusion of the MOZ and TIF2 genes by an inv (8) (p11q13) translocation has been identified in patients with acute mixed-lineage leukemia.
  • Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response.
  • [MeSH-minor] Acute Disease. Blotting, Western. Carrier Proteins / genetics. Carrier Proteins / metabolism. Corticosterone. Genes, Reporter. Humans. Leukemia, Myeloid / genetics. Receptors, Androgen / genetics. Receptors, Estrogen / genetics

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  • (PMID = 17697320.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Androgen; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Estrogen; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human; W980KJ009P / Corticosterone
  • [Other-IDs] NLM/ PMC2048977
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3. Amakawa R, Hiramoto N, Kawano S, Hyo A, Nakamichi N, Tajima K, Ito T, Mori S, Kishimoto Y, Fukuhara S: Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia. J Clin Exp Hematop; 2010;50(1):51-8
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  • [Title] Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia.
  • We report a case of acute mixed-lineage leukemia, as seen in a 65 year-old female with MLL gene amplification and biallelic loss of wild type p53 gene.
  • The diagnosis was based on the findings that her bone marrow (BM) blasts expressed cytoplasmic CD3 (cyCD3), B-lineage antigens and myeloid antigens accompanied by clonal rearrangements of IgH gene.
  • Add (11q23) abnormality was found in sideline karyotypes as well as the stemline abnormality of dic(17;20) (p11;q11).
  • [MeSH-major] Gene Amplification. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

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  • (PMID = 20505276.001).
  • [ISSN] 1880-9952
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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4. Georgy M, Yonescu R, Griffin CA, Batista DA: Acute mixed lineage leukemia and a t(6;14)(q25;q32) in two adults. Cancer Genet Cytogenet; 2008 Aug;185(1):28-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute mixed lineage leukemia and a t(6;14)(q25;q32) in two adults.
  • Acute mixed lineage leukemia (AMLL) is a rare form of leukemia in which both myeloid and lymphoid markers are present.
  • Few chromosome abnormalities have been identified associated with this form of leukemia.
  • A translocation involving the long arms of chromosomes 6 and 14 was previously described in four young individuals with acute leukemia and in three of these cases the diagnosis was mixed lineage.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 6. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

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  • (PMID = 18656690.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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5. Liu HX, Cao XY, Tong CR, Wu T, Wang T, Fan QZ, Wu P, Zhang X, Cai P, Zhu P: [Major molecular response to imatinib in a patient with acute mixed lineage leukemia expressing a novel BCR/ABL transcript]. Zhonghua Yi Xue Za Zhi; 2009 Feb 3;89(4):220-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Major molecular response to imatinib in a patient with acute mixed lineage leukemia expressing a novel BCR/ABL transcript].
  • OBJECTIVE: To identify the novel BCR/ABL transcript in a patient with acute mixed lineage leukemia (AMLL), and to evaluate the imatinib treatment response by quantitatively monitoring the aberrant BCR/ABL.
  • Morphological analysis of the bone marrow showed the myeloid blast cells accounted for 66%, and immunophenotyping analysis showed 2 groups of aberrant blast cells: myeloid and B lineage.
  • Chemical therapy and bone marrow transplantation failed to control the disease, and a novel BCR/ABL transcript (GenBank: EF423615) was found by using several detection protocols.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Biphenotypic, Acute / drug therapy. Leukemia, Biphenotypic, Acute / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use

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  • (PMID = 19552835.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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6. Naghashpour M, Lancet J, Moscinski L, Zhang L: Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report. Am J Hematol; 2010 Jun;85(6):451-4
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  • [Title] Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report.
  • The majority of cases of acute leukemia belong to a specific lineage origin, either lymphoid or myeloid, and therefore are classified as acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML), based on morphologic features and cytochemical and immunophenotypic profile of the blast cells.
  • A minority of acute leukemias however, show no clear evidence of differentiation along a single lineage.
  • These are now classified under acute leukemias of ambiguous lineage by the most recent WHO classification and account for <4% of all cases of acute leukemia [1].
  • They include leukemias with no lineage specific antigens (acute undifferentiated leukemias) and those with blasts that express antigens of more than one lineage to such degree that it is not possible to assign the leukemia to any one particular lineage with certainty (mixed phenotype acute leukemias).
  • The latter can either be leukemias with two distinct populations of blasts, each expressing antigens of a different lineage (historically referred to as "bilineal" leukemias) or a single blast population expressing antigens of multiple lineages (historically referred to as "biphenotypic" acute leukemias) [2].
  • Acute leukemias of ambiguous lineage may harbor a variety of genetic lesions.
  • Those with t(9;22)(q34;q11) or translocations associated with mixed lineage leukemias (MLL) gene, i.e., t(11;V)(q23;V), occur frequently enough and are associated with distinct features, that are considered as separate entities according to the recent WHO classification.
  • Co-expression of myeloid and B-lymphoid antigens is most common in mixed phenotype acute leukemia (MPAL), followed by co-expression of myeloid and T-lymphoid antigens, accounting for 66-70% and 23-24% of MLLs, respectively.
  • Coexpression of B- and T-lineage associated antigens or antigens of all three lineages is exceedingly rare, accounting for <5% of MLLs [3,4].
  • The requirements for assigning more than one lineage to a single blast population has been established by current WHO classification [1].
  • [MeSH-major] Antigens, Neoplasm / blood. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Immunophenotyping. Leukemia / classification. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Bone Marrow / pathology. Cell Lineage. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 20513125.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / MLL-ENL oncoprotein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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7. Rubnitz JE, Onciu M, Pounds S, Shurtleff S, Cao X, Raimondi SC, Behm FG, Campana D, Razzouk BI, Ribeiro RC, Downing JR, Pui CH: Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital. Blood; 2009 May 21;113(21):5083-9
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  • [Title] Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital.
  • To characterize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the pathologic and clinical features, including response to therapy, of 35 patients with mixed-lineage leukemia.
  • The majority of cases (91%) had blasts cells that simultaneously expressed either T-lineage plus myeloid markers (T/myeloid, n = 20) or B-lineage plus myeloid markers (B/myeloid, n = 12).
  • Overall survival rates for the B/myeloid and T/myeloid subgroups were not significantly different from each other or from the rate for acute myeloid leukemia (AML) but were inferior to the outcome in children with acute lymphoblastic leukemia (ALL).
  • Analysis of gene-expression patterns identified a subset of biphenotypic leukemias that did not cluster with T-cell ALL, B-progenitor ALL, or AML.
  • We propose that treatment for biphenotypic leukemia begin with one course of AML-type induction therapy, with a provision for a switch to lymphoid-type induction therapy with a glucocorticoid, vincristine, and L-asparaginase if the patient responds poorly.
  • We also suggest that hematopoietic stem cell transplantation is often not required for cure of these patients.

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  • (PMID = 19131545.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2686179
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8. Xu B, Li L, Tang JH, Zhou SY: Detection of FLT3 gene and FLT3/ITD mutation by polymerase chain reaction-single-strand conformation polymorphism in patients with acute lymphoblastic leukemia. Di Yi Jun Yi Da Xue Xue Bao; 2005 Oct;25(10):1207-10
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  • [Title] Detection of FLT3 gene and FLT3/ITD mutation by polymerase chain reaction-single-strand conformation polymorphism in patients with acute lymphoblastic leukemia.
  • OBJECTIVE: To analyze Fms-like tyrosine kinase 3 (FLT3) gene and FLT3 internal tandem duplication (ITD) mutation in acute lymphoblastic leukemia (ALL) patients of different immunological subtypes.
  • The positivity rate of FLT3 gene in pre-pre B-lineage ALL, pre-B-ALL, B-lineage ALL and T-lineage ALL cases were 93.3% (14/15), 77.8% (14/18), 41.7% (5/12) and 28.6% (4/14), respectively.
  • Two cases (3.2%) were found to have FLT3/ITD mutation, which were also positive for myeloid antigen expression and diagnosed as acute mixed-lineage leukemia, showing leukocytosis and high percentage of bone marrow blast cells with poor prognosis.
  • CONCLUSIONS: FLT3 gene can be detected in both B-and T-lineage ALL patients, but more frequently in the former.
  • In B-lineage ALL patients, FLT3 gene is more frequent in cases with undifferentiated than those with differentiated blast cells.
  • FLT3/ITD is rarely detected in ALL patients and FLT3/ITD mutation detection might be helpful to identify the genotypes and evaluate the prognosis of acute leukemia.
  • [MeSH-major] Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor Protein-Tyrosine Kinases / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16234090.001).
  • [ISSN] 1000-2588
  • [Journal-full-title] Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA
  • [ISO-abbreviation] Di Yi Jun Yi Da Xue Xue Bao
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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9. Ning BT, Tang YM, Chen YH, Shen HQ, Qian BQ: Comparison between CD19 and CD20 expression patterns on acute leukemic cells. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2005 Dec;13(6):943-7
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  • [Title] Comparison between CD19 and CD20 expression patterns on acute leukemic cells.
  • In order to provide the evidences for CD19 as a better antibody targeting molecule for B lineage acute leukemias than CD20 through the multi-parameter flow-cytometry analysis of leukemia cells, the samples from 321 patients with acute leukemia (AL) were immunophenotyped by multi-color flow cytometry and CD45/SSC gating strategy followed by the analysis of CD19 and CD20 expression.
  • The results showed that the positive rate of CD19 (115/116, 99.1%) in 116 cases with B lineage acute lymphoblastic leukemia (B lineage ALL) was significantly higher than that of CD20 (33/116, 28.4%) (P < 0.01); in 17 patients with B lineage/Myeloid (B/My) acute mixed lineage leukemia (AMLL), the former positive rate (17/17, 100%) was also higher than the latter (5/17, 29.4%) (P < 0.01).
  • Both of the two antigens were negative in 29 patients with acute T lymphoblastic leukemia and 7 patients with T/My AMLL.
  • The positive rates of CD19 and CD20 in 152 patients with acute myeloid leukemia (AML) were 7.2% and 2.0%, respectively.
  • The difference of the fluorescence intensity between the two antigens on the cells from each patient with B lineage ALL or B/My AMLL was statistically significant (t = 20.68, P < 0.001).
  • The specificity of CD19 and CD20 in B lymphocytic lineage was 92.3% (132/143) and 92.7% (38/41), respectively, while the sensitivity was 99.2% (132/133) and 28.6% (38/133), respectively, the former sensitivity was significantly higher than the latter (chi(2) = 144.018, P = 0.001).
  • It is concluded that CD19 continuously and steadily express on almost all subtypes of B lineage leukemic cells with homogeneous pattern while only a small number of leukemias express CD20.
  • These indicate that CD19 may be a better antibody targeting molecule than CD20 for patients with B-lineage acute leukemia.

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  • (PMID = 16403255.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20
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10. Yamamoto K, Sada A, Kawano Y, Katayama Y, Shimoyama M, Matsui T: Therapy-related, mixed phenotype acute leukemia with t(1;21)(p36;q22) and RUNX1 rearrangement. Cancer Genet Cytogenet; 2010 Sep;201(2):122-7
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  • [Title] Therapy-related, mixed phenotype acute leukemia with t(1;21)(p36;q22) and RUNX1 rearrangement.
  • We describe here a new case of therapy-related acute leukemia with t(1;21)(p36;q22).
  • Immunophenotypic analyses revealed that blasts were positive for CD19, CD79a, and cytCD22, as well as MPO, CD13, and CD33, fulfilling the diagnostic criteria of mixed phenotype acute leukemia, B/myeloid.
  • The patient died of disease progression after 10 months.
  • Thus, acute leukemia with t(1;21) and RUNX1 rearrangement could be associated with B/myeloid mixed phenotype as well as previous topoisomerase II inhibitor therapy and poor prognoses.
  • [MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20682397.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human
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11. Ohe M, Hashino S: [Successful treatment with clarithromycin for Mixed phenotype acute leukemia, T/myeloid, NOS]. Rinsho Ketsueki; 2010 Apr;51(4):297-9
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  • [Title] [Successful treatment with clarithromycin for Mixed phenotype acute leukemia, T/myeloid, NOS].
  • The diagnosis was Mixed phenotype acute leukemia, T/myeloid, NOS.
  • This clinical course suggests CAM is effective for this leukemia.
  • [MeSH-major] Anti-Bacterial Agents / administration & dosage. Clarithromycin / administration & dosage. Leukemia / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Acute Disease. Aged. Drug Synergism. Drug Therapy, Combination. Female. Humans. Pneumonia, Bacterial / complications. Pneumonia, Bacterial / drug therapy. Prednisolone / administration & dosage

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  • (PMID = 20467229.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 9PHQ9Y1OLM / Prednisolone; H1250JIK0A / Clarithromycin
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12. Faderl S, Thomas DA, Gandhi V, Huang X, Borthakur G, O'Brien S, Ravandi F, Plunkett W, Bretz JL, Kantarjian HM: Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL). J Clin Oncol; 2009 May 20;27(15_suppl):7020

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  • [Title] Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL).
  • METHODS: Pts ≥ 21 years (yrs) with primary refractory or relapsed ALL, NYHA class < 3, and a cardiac ejection fraction ≥ 45% were eligible.
  • Twenty-one pts had pre-B ALL, 5 pts pre-T/T ALL, 1 pt mature B ALL, and 3 pts biphenotypic acute leukemias.

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  • (PMID = 27961382.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Li XL, Li R, Chen Y: [Clinical characteristics and immunophenotypes of mixed-lineage acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):636-9

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  • [Title] [Clinical characteristics and immunophenotypes of mixed-lineage acute leukemia].
  • The aim of study was to analyze the clinical, biological features, treatment outcome and prognosis of mixed-lineage acute leukemia (MAL).
  • 48 MAL patients diagnosed according to European Group of International Leukemia (EGIL) scoring system were retrospectively analyzed and the analysis results were compared with that from 68 cases of AML and 61 cases of ALL.
  • The results showed that the incidence of MAL in acute leukemia was 9.6%.
  • The median of white blood cell count in MAL was significantly higher than that of non-mixed-lineage cases (AML and ALL) observed during the same period (P < 0.05).
  • Coexpression of myeloid and B lymphoid antigens in MAL patients was predominant, its rate was 70.9%.
  • The coexpression rate of T lymphoid and myeloid antigens was 20.8%, coexpression of B, T lymphoid and myeloid antigens was 8.3%.
  • In MAL Ph chromosome abnormality incidence was 25% and was significantly higher than that in AML group (0%) (P < 0.01), but was not statistical defference with that in ALL group (16.7%) (P > 0.05).
  • It is concluded that MAL is supposed to be originated from stem cells, coexpression of lymphoid/myeloid antigens is the major feature of MAL which accompanies many poor prognosis factors and lower CR rate.

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  • (PMID = 17605883.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD34
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14. Takasaki H, Tachibana T, Tanaka M, Maruta A, Ishigatsubo Y, Kanamoari H: [Successful selection of chemotherapy based on cell surface antigens in a patient with mixed phenotype acute leukemia]. Rinsho Ketsueki; 2010 May;51(5):339-44
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  • [Title] [Successful selection of chemotherapy based on cell surface antigens in a patient with mixed phenotype acute leukemia].
  • The patient was diagnosed as having mixed phenotype acute leukemia, T/myeloid, NOS, according to the WHO classification.
  • After initial treatment, residual leukemic cells with CD13, CD33 and MPO were detected by FCM; therefore, he received re-induction chemotherapy for AML, and achieved CR.
  • Acute leukemia of ambiguous lineage is a relatively rare subtype in acute leukemia and standard chemotherapy has not been established.
  • [MeSH-major] Antigens, Surface. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia / drug therapy. Leukemia / immunology
  • [MeSH-minor] Acute Disease. Cyclophosphamide. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Humans. Male. Middle Aged. Prednisolone / administration & dosage. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 20534955.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, Surface; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; ZS7284E0ZP / Daunorubicin
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15. Mejstrikova E, Volejnikova J, Fronkova E, Zdrahalova K, Kalina T, Sterba J, Jabali Y, Mihal V, Blazek B, Cerna Z, Prochazkova D, Hak J, Zemanova Z, Jarosova M, Oltova A, Sedlacek P, Schwarz J, Zuna J, Trka J, Stary J, Hrusak O: Prognosis of children with mixed phenotype acute leukemia treated on the basis of consistent immunophenotypic criteria. Haematologica; 2010 Jun;95(6):928-35
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  • [Title] Prognosis of children with mixed phenotype acute leukemia treated on the basis of consistent immunophenotypic criteria.
  • BACKGROUND: Mixed phenotype acute leukemia (MPAL) represents a diagnostic and therapeutic dilemma.
  • The European Group for the Immunological Classification of Leukemias (EGIL) scoring system unambiguously defines MPAL expressing aberrant lineage markers.
  • DESIGN AND METHODS: Simple immunophenotypic criteria were used to classify all cases of childhood acute leukemia in order to provide therapy directed against acute lymphoblastic leukemia or acute myeloid leukemia.
  • Prognosis, genotype and immunoglobulin/T-cell receptor gene rearrangement status were analyzed.
  • RESULTS: The incidences of MPAL were 28/582 and 4/107 for children treated with acute lymphoblastic leukemia and acute myeloid leukemia regimens, respectively.
  • In immunophenotypic principal component analysis, MPAL treated as T-cell acute lymphoblastic leukemia clustered between cases of non-mixed T-cell acute lymphoblastic leukemia and acute myeloid leukemia, while other MPAL cases were included in the respective non-mixed B-cell progenitor acute lymphoblastic leukemia or acute myeloid leukemia clusters.
  • Analogously, immunoglobulin/T-cell receptor gene rearrangements followed the expected pattern in patients treated as having acute myeloid leukemia (non-rearranged, 4/4) or as having B-cell progenitor acute lymphoblastic leukemia (rearranged, 20/20), but were missing in 3/5 analyzed cases of MPAL treated as having T-cell acute lymphobastic leukemia.
  • In patients who received acute lymphoblastic leukemia treatment, the 5-year event-free survival of the MPAL cases was worse than that of the non-mixed cases (53+/-10% and 76+/-2% at 5 years, respectively, P=0.0075), with a more pronounced difference among B lineage cases.
  • The small numbers of MPAL cases treated as T-cell acute lymphoblastic leukemia or as acute myeloid leukemia hampered separate statistics.
  • CONCLUSIONS: Simple immunophenotypic criteria are useful for therapy decisions in MPAL.
  • In B lineage leukemia, MPAL confers poorer prognosis.
  • However, our data do not justify a preferential use of current acute myeloid leukemia-based therapy in MPAL.
  • [MeSH-major] Immunophenotyping. Leukemia / diagnosis. Leukemia / therapy. Phenotype
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Diagnosis, Differential. Follow-Up Studies. Humans. Infant. Infant, Newborn. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Prognosis. Receptors, Antigen, T-Cell / immunology

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  • (PMID = 20145275.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell
  • [Other-IDs] NLM/ PMC2878790
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16. Park J, Chae H, Kim M, Lim J, Kim Y, Lee J, Chung NG, Cho B, Kim HK, Lee S, Han K: [A study of mixed phenotype acute leukemia based on the 2008 World Health Organization classification]. Korean J Lab Med; 2010 Dec;30(6):525-32
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  • [Title] [A study of mixed phenotype acute leukemia based on the 2008 World Health Organization classification].
  • BACKGROUND: We evaluated the clinical significance of revised 2008 WHO classification needed to diagnose mixed phenotype acute leukemia (MPAL).
  • METHODS: A total of 22 MPAL patients, previously diagnosed by applying the scoring system of the European Group for Immunological Classification of Acute Leukemias (EGIL) were reclassified based on the 2008 WHO classification.
  • RESULTS: In 2008 WHO classification, the number of monoclonal antibodies (mAbs) required for assigning more than one lineage was markedly decreased, from 26 to 11, compared with that of EGIL.
  • Seventeen of the 22 MPAL patients were reclassified as MPAL with following details: 6 MPAL with t(9;22)(q34;q11.2); BCR-ABL1, 1 MPAL with t(v;11q23); MLL rearranged, 7 MPAL, B/Myeloid, not otherwise specified (NOS) and 3 MPAL, T/Myeloid, NOS.
  • Five patients were excluded from MPAL in the revised classification: 4 cytoplasmic myeloperoxidase (cMPO)-negative and 1 CD19-negative.
  • One patient with cCD79a, CD20, CD38, cMPO and CD15, whose diagnosis was reclassified from MPAL to AML has survived during the study period.
  • CONCLUSIONS: Because of decreased number of mAbs needed, it is possible that acute leukemia panel is designed to include all mAbs required to diagnose MPAL according to 2008 WHO classification.
  • When diagnosing MPAL, it is critical to figure out positivity in either cMPO or CD19, and AML expressing more than 2 lymphoid antigens are considered as MPAL.
  • [MeSH-major] Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal / immunology. Child. Chromosomes, Human. Female. Fusion Proteins, bcr-abl / metabolism. Humans. Infant. Male. Middle Aged. Phenotype. Philadelphia Chromosome. Survival Analysis. World Health Organization

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  • (PMID = 21157134.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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17. Shildkrot Y, Onciu M, Hoehn ME, Wilson MW: Mixed-phenotype acute leukemia relapse in the iris. J AAPOS; 2010 Oct;14(5):453-4
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  • [Title] Mixed-phenotype acute leukemia relapse in the iris.
  • Mixed-phenotype acute leukemia is a rare condition with no previously reported intraocular involvement.
  • We present clinical, radiologic, and cytologic findings of leukemic intraocular relapse in a 23-month-old girl, with lineage switch presenting as conjunctivitis after allogeneic bone marrow transplantation.

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  • [Copyright] Copyright © 2010 American Association for Pediatric Ophthalmology and Strabismus. Published by Mosby, Inc. All rights reserved.
  • (PMID = 20863726.001).
  • [ISSN] 1528-3933
  • [Journal-full-title] Journal of AAPOS : the official publication of the American Association for Pediatric Ophthalmology and Strabismus
  • [ISO-abbreviation] J AAPOS
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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18. Weinberg OK, Arber DA: Mixed-phenotype acute leukemia: historical overview and a new definition. Leukemia; 2010 Nov;24(11):1844-51
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  • [Title] Mixed-phenotype acute leukemia: historical overview and a new definition.
  • Acute leukemia with a mixed phenotype is a rare disease and comprises 2-5% of all acute leukemias.
  • These disorders have been known historically by a variety of names, such as mixed lineage leukemia, bilineal leukemia and biphenotypic leukemia, and the criteria for diagnosis have often been arbitrary.
  • The scoring criteria proposed by the European Group for the Immunological Characterization of Leukemias represented a major attempt to define this disorder.
  • However, the relative weight given to some markers and the lack of lineage specificity of most markers have raised questions regarding the significance of this approach.
  • In 2008, the World Health Organization classification of hematopoietic and lymphoid tumors proposed a simpler diagnostic algorithm, which relies on fewer and more lineage-specific markers to define mixed-phenotype acute leukemia (MPAL).
  • MPAL with t(9;22) and MLL rearrangement have been separated.
  • Several studies have suggested that patients with acute leukemia of mixed phenotype have a worse clinical outcome when compared with matched controls with acute myeloid leukemia or acute lymphoblastic leukemia.
  • Further studies are needed to confirm the significance of MPAL as currently defined, to determine a standardized treatment approach and to better understand the biological and clinical aspects of this disease.
  • [MeSH-major] Leukemia / genetics
  • [MeSH-minor] Acute Disease. Antigens, CD / analysis. Biomarkers, Tumor / analysis. Blast Crisis / pathology. Gene Rearrangement. Humans. Leukemia, B-Cell / classification. Leukemia, B-Cell / genetics. Leukemia, T-Cell / classification. Leukemia, T-Cell / genetics. Phenotype

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  • (PMID = 20844566.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor
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19. Lou Z, Zhang CC, Tirado CA, Slone T, Zheng J, Zaremba CM, Oliver D, Chen W: Infantile mixed phenotype acute leukemia (bilineal and biphenotypic) with t(10;11)(p12;q23);MLL-MLLT10. Leuk Res; 2010 Aug;34(8):1107-9
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  • [Title] Infantile mixed phenotype acute leukemia (bilineal and biphenotypic) with t(10;11)(p12;q23);MLL-MLLT10.
  • We report a case of a 6-month-old boy with a mixed phenotype acute leukemia (MPAL), bilineal and biphenotypic immunophenotype (B-lymphoid lineage and combined B-lymphoid and monocytic lineage) with t(10;11)(p12;q23);MLL-MLLT10.
  • He was treated with acute myeloid leukemia protocol and in complete remission at 7-month follow-up.
  • To the best of our knowledge, this is the first reported MLL-MLLT10 rearranged case presenting as MPAL in an infant.
  • From a clinical practice standpoint, this case illustrates the importance of detection of MLL rearrangement due to its prognostic implication and the effectiveness of flow cytometry immunophenotyping in diagnosing MPAL and monitoring minimal residual disease.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 11 / genetics. Leukemia, Biphenotypic, Acute / genetics. Leukemia, Monocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Flow Cytometry. Gene Rearrangement. Humans. Immunophenotyping. Infant. Karyotyping. Male. Neoplasm, Residual / genetics. Neoplasm, Residual / pathology. Neoplasm, Residual / therapy. Phenotype. Prognosis. Remission Induction

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20299091.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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20. Al-Seraihy AS, Owaidah TM, Ayas M, El-Solh H, Al-Mahr M, Al-Ahmari A, Belgaumi AF: Clinical characteristics and outcome of children with biphenotypic acute leukemia. Haematologica; 2009 Dec;94(12):1682-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical characteristics and outcome of children with biphenotypic acute leukemia.
  • BACKGROUND: Knowledge concerning the clinical and biological presentation, as well as the outcome of treatment, of biphenotypic acute leukemia in children is limited.
  • DESIGN AND METHODS: This retrospective review analyzes the clinical features and outcome of children with biphenotypic acute leukemia diagnosed and treated over an 8-year period.
  • According to the EGIL scoring system 24 (3.7%) of 633 patients with acute leukemia were classified as having biphenotypic acute leukemia.
  • The diagnostic work-up and results were reviewed specifically for this study in the light of the newly published WHO criteria for the diagnosis of leukemia of ambiguous lineage.
  • Based on these criteria, 11 (1.7%) patients were categorized according to the new nomenclature as having mixed phenotype acute leukemia.
  • The majority of the patients (58.3%) had a B-lymphoid/myeloid phenotype, followed by the T-lymphoid/myeloid phenotype.
  • The most frequent chromosomal abnormality involved the 14q32 locus.
  • Patients received therapy based on a treatment regimen for acute lymphocytic leukemia regimen, which included myeloid-effective agents.
  • The survival of those patients who underwent hematopoietic stem cell transplantation in first complete remission was not different from that of the patients who were treated with chemotherapy alone (overall survival: 70.1% versus 81.1%, respectively, p=0.39; event-free survival: 70.1% versus 76.2%, respectively, p=0.75).
  • The outcome of the 11 patients who were retrospectively classified as having mixed phenotype acute leukemia according to the new WHO criteria was excellent, with no relapses or deaths occurring among these patients.
  • CONCLUSIONS: An acute lymphocytic leukemia type of induction therapy, using agents that are active against lymphoid and myeloid leukemias, appears to be more effective in achieving and maintaining complete remissions regardless of whether the patients are classified according to EGIL criteria or the new WHO criteria.
  • Hematopoietic stem cell transplantation may not be necessary for all patients in first complete remission.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy
  • [MeSH-minor] Antigens, CD / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Flow Cytometry. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Outcome Assessment (Health Care) / methods. Remission Induction. Retrospective Studies

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  • (PMID = 19713227.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Other-IDs] NLM/ PMC2791935
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21. Desouki MM, Post GR, Cherry D, Lazarchick J: PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms. Clin Med Res; 2010 Jul;8(2):84-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms.
  • OBJECTIVE: Undifferentiated tumors and hematolymphoid neoplasms can be diagnostically challenging due to potential overlap of morphologic features and variant antigen expression.
  • PAX-5, a transcription factor expressed throughout B-cell maturation, is detected in most B-cell neoplasms including those that lack expression of mature B-cell markers, such as classical Hodgkin lymphoma (cHL), B-lymphoblastic leukemia and B-cell lymphomas following rituximab therapy.
  • The lack of PAX-5 expression in most CD30-positive non-hematopoietic malignancies (embryonal carcinoma and seminoma) and T-cell lymphomas, such as anaplastic large cell lymphoma (ALCL), suggests that the absence of PAX-5 may be used to confirm non-B-cell lineage.
  • DESIGN: Diagnostic lymph node, decalcified core bone marrow biopsies and tissue sections from 111 archived paraffin-embedded tissue blocks and a tissue lymphoma microarray were immunostained using a monoclonal antibody to PAX-5.
  • RESULTS: Nuclear PAX-5 immunoreactivity was detected in 88% (36/41) of Hodgkin lymphoma, all cases of diffuse large B-cell lymphoma (n=72), small B-cell lymphomas (n=5), B-lymphoblastic leukemia/lymphoma and mixed phenotype acute leukemia with B-cell lineage (n=5).
  • PAX-5 was not detected in ALCL (n=22), T-cell lymphoblastic leukemia/lymphoma, mixed phenotype acute leukemia with T-cell lineage (n=5), acute myeloid leukemia (n=4), carcinoid tumors with typical morphology (n=5), melanoma (n=3), and undifferentiated/metastatic tumors (n=8).
  • Non-neoplastic bone marrow sections showed scattered nuclear staining in small B-cell lymphocytes/hematogones.
  • CONCLUSION: Overall, our results demonstrate that including PAX-5 in a panel with other immunomarkers helps establish B-cell lineage and increases diagnostic yield.
  • [MeSH-major] B-Cell-Specific Activator Protein / analysis. Biomarkers, Tumor / analysis. Lymphoma / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Hodgkin Disease / diagnosis. Humans. Immunohistochemistry. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis

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  • (PMID = 20660931.001).
  • [ISSN] 1554-6179
  • [Journal-full-title] Clinical medicine & research
  • [ISO-abbreviation] Clin Med Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human
  • [Other-IDs] NLM/ PMC2910102
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22. Ru YX, Wang HJ, Yang BX, Liu JH, Li ZQ, Li CW, Wang JX, Mi YC: The ultrastructure of hybrid acute leukemia: a study of 15 cases. Ultrastruct Pathol; 2005 Sep-Oct;29(5):341-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The ultrastructure of hybrid acute leukemia: a study of 15 cases.
  • The objective of this study was to investigate the ultrastructural characteristics of hybrid acute leukemia (HAL).
  • By TEM, 5 out 15 cases of HAL were consistent with immunophenotyping (3 cases of biphenotypic type, and 2 cases of biclonal type with granulocytes and lymphocytes); 2 cases were suspected as HAL.
  • Most of the blast cells of biphenotypic HAL showed lymphoid features, except some cases containing MPO positive granules in blasts, while a few cases exhibited monocytic or nonspecific features.
  • TEM offers advantages in the diagnosis of biclonal type HAL and biphenotypic HAL positive for MPO.
  • However, it is difficult to differentiate MPO-negative cases of biphenotypic HAL from ALL and a few cases may be misinterpreted as M5 by TEM.
  • [MeSH-major] Granulocyte Precursor Cells / ultrastructure. Leukemia, Myeloid, Acute / diagnosis. Lymphocytes / ultrastructure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Child. Female. Humans. Immunophenotyping. Male. Microscopy, Electron, Transmission. Middle Aged. Peroxidase / metabolism. Phenotype

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  • (PMID = 16257860.001).
  • [ISSN] 0191-3123
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.11.1.7 / Peroxidase
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23. Kim MK, Mun YC, Seong CM, Chung WS, Huh J: [Variant Philadelphia chromosome identified by interphase fluorescence in situ hybridization (FISH) without evidence on G-banded karyotyping and metaphase FISH]. Korean J Lab Med; 2010 Dec;30(6):711-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A 52-year-old man was diagnosed with acute leukemia of mixed phenotype.
  • [MeSH-minor] Adult. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Humans. Interphase. Karyotyping. Leukemia / diagnosis. Leukemia / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Male. Metaphase. Middle Aged. Phenotype. Translocation, Genetic

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  • (PMID = 21157160.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
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24. Song MJ, Kim HJ, Ko YH, Kim SH: Discrepant immunophenotypic characteristics between the lymph node and bone marrow in two mixed-phenotype acute leukemia patients. Korean J Lab Med; 2009 Oct;29(5):396-401
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  • [Title] Discrepant immunophenotypic characteristics between the lymph node and bone marrow in two mixed-phenotype acute leukemia patients.
  • The immunophenotypic profile of hematological malignancies is usually consistent among different sites of involvement; this consistency allows reliable diagnosis from peripheral blood, bone marrow, or lymph node, especially in cases of acute leukemia.
  • Here, we report two Korean patients with acute leukemia where the results of immunophenotypic analysis of the bone marrow specimen were different from those of immunohistochemical studies of a biopsy sample of a cervical lymph node, particularly with respect to myeloperoxidase and CD3.
  • The clinical significance of the immunophenotypic disparity found in the patients still remains unknown; however, discrepancies between the different anatomic sites that are simultaneously involved can occur in a subset of leukemia patients.
  • Therefore, integration of all the relevant results, including those of the bone marrow studies, may be helpful for accurate diagnosis and selecting appropriate treatment modalities.
  • [MeSH-major] Bone Marrow / pathology. Immunophenotyping / methods. Leukemia / diagnosis. Lymph Nodes / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antigens, CD3 / metabolism. Female. Flow Cytometry. Humans. Male. Peroxidase / metabolism. Phenotype

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  • (PMID = 19893347.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD3; EC 1.11.1.7 / Peroxidase
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25. Carretta A, Ciriaco P, Melloni G, Bandiera A, Libretti L, Puglisi A, Giovanardi M, Zannini P: Surgical treatment of multiple primary adenocarcinomas of the lung. Thorac Cardiovasc Surg; 2009 Feb;57(1):30-4
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  • The aim of this study was to assess the results of surgical treatment of multiple primary adenocarcinomas of the lung (MPAL) analyzing the radiological and histological features.
  • METHODS: From 1988 to 2005, 26 patients underwent surgical treatment for MPAL at our department, for a total of 52 tumors.
  • RESULTS: Thirty-seven tumors were classified as solid, two as ground-glass opacities (GGO) and 13 as mixed solid/GGO tumors on the basis of CT scan evaluation.
  • CONCLUSIONS: Surgical treatment of MPAL is associated with favorable results.

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  • (PMID = 19169994.001).
  • [ISSN] 0171-6425
  • [Journal-full-title] The Thoracic and cardiovascular surgeon
  • [ISO-abbreviation] Thorac Cardiovasc Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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26. Jin ZX, Zhang SL, Wang XM, Bi SH, Xin M, Zhou JJ, Cui Q, Duan WX, Wang HB, Yi DH: The myocardial protective effects of a moderate-potassium adenosine-lidocaine cardioplegia in pediatric cardiac surgery. J Thorac Cardiovasc Surg; 2008 Dec;136(6):1450-5
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  • METHODS: One hundred thirty-four patients with congenital heart disease were randomly allocated to one of 3 groups according to the cardioplegia formula used: the high-potassium (HP) group (K(+), 20 mmol/L), 46 patients; the high-potassium adenosine-lidocaine (HPAL) group (K(+), 20 mmol/L; adenosine, 0.7 mmol/L; and lidocaine, 0.7 mmol/L), 44 patients; and the moderate-potassium adenosine-lidocaine (MPAL) group (K(+), 10 mmol/L; adenosine, 0.7 mmol/L; and lidocaine, 0.7 mmol/L), 44 patients.
  • RESULTS: At the end of cardiopulmonary bypass and modified ultrafiltration, the systolic and pulse pressures of the MPAL group were significantly increased compared with the respective values of the HP group.
  • At the time points of 1 to 12 hours after reperfusion, the levels of serum cardiac troponin I were significantly decreased in the MPAL group compared with those in the HP and HPAL groups.
  • CONCLUSIONS: The MPAL cardioplegia formula was associated with better myocardial protective effects.

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  • (PMID = 19114188.001).
  • [ISSN] 1097-685X
  • [Journal-full-title] The Journal of thoracic and cardiovascular surgery
  • [ISO-abbreviation] J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cardioplegic Solutions; 0 / Cardiotonic Agents; 98PI200987 / Lidocaine; K72T3FS567 / Adenosine; RWP5GA015D / Potassium
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27. Hu XX, Gong SL, Song XM, Chen L, Qiu HY, Gao L, Wang JM: [Report of a case of hybrid acute leukemia with t (12; 22) and literature review]. Zhonghua Xue Ye Xue Za Zhi; 2006 May;27(5):331-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Report of a case of hybrid acute leukemia with t (12; 22) and literature review].
  • OBJECTIVE: To report a hybrid acute leukemia (HAL) patient with t (12;.
  • Leukemia surface markers were detected by anti-biotin-biotin complex and monoclonal antibodies.
  • RESULTS: The clinical and hematological findings were compatible with the diagnosis of HAL.
  • Lymphoid and myeloid markers were positive on the leukemia cells.
  • 22) translocation is a rare chromosome abnormality in leukemia.
  • This translocation as a cytogenetic marker for poor-prognosis in leukemia needs to be further studied.
  • [MeSH-major] Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

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  • (PMID = 16875585.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 20
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28. Zhao XF, Gojo I, York T, Ning Y, Baer MR: Diagnosis of biphenotypic acute leukemia: a paradigmatic approach. Int J Clin Exp Pathol; 2009;3(1):75-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diagnosis of biphenotypic acute leukemia: a paradigmatic approach.
  • Biphenotypic acute leukemia (BAL), or acute leukemia with a single population of blasts coexpressing markers of two different lineages, is a rare clinical entity.
  • To define BAL, a scoring system was proposed by the European Group of Immunological Markers for Leukemias (EGIL) in 1995.
  • However, increasing evidence suggests that this system has limitations, as acknowledged by the 2008 World Health Organization (WHO) Classification of Tumors of Hematopoietic and Lymphoid Tissues.
  • We propose a new paradigmatic approach to defining BAL based on recent clinical studies of BAL and advances in immunologic marker definition and cytogenetics, and applied our new approach to 8 cases of "BAL" among a cohort of 742 new acute leukemias in our Cancer Center.
  • By our new criteria, 6 cases were reclassified as acute lymphoblastic leukemia (ALL), while only 2 were still classified as BAL.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged, 80 and over. Antigens, Neoplasm / analysis. Biomarkers, Tumor / genetics. Biomarkers, Tumor / immunology. Child. Female. Humans. Immunophenotyping. Male. Middle Aged. Phenotype. Retrospective Studies. World Health Organization. Young Adult

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  • (PMID = 19918331.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC2776262
  • [Keywords] NOTNLM ; ALL / AML / Biphenotypic acute leukemia / EGIL / classification
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29. Grembecka J, Belcher AM, Hartley T, Cierpicki T: Molecular basis of the mixed lineage leukemia-menin interaction: implications for targeting mixed lineage leukemias. J Biol Chem; 2010 Dec 24;285(52):40690-8
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  • [Title] Molecular basis of the mixed lineage leukemia-menin interaction: implications for targeting mixed lineage leukemias.
  • Chromosomal translocations targeting the mixed lineage leukemia (MLL) gene result in MLL fusion proteins that are found in aggressive human acute leukemias.
  • Disruption of MLL by such translocations leads to overexpression of Hox genes, resulting in a blockage of hematopoietic differentiation that ultimately leads to leukemia.
  • Altogether, our work establishes the molecular basis of the menin interaction with MLL and MLL fusion proteins and provides the necessary foundation for development of small molecule inhibitors targeting this interaction in leukemias with MLL translocations.
  • [MeSH-major] Myeloid-Lymphoid Leukemia Protein / chemistry. Proto-Oncogene Proteins / chemistry

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  • (PMID = 20961854.001).
  • [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 / MEN1 protein, human; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC3003368
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30. Vanura K, Vrsalovic MM, Le T, Marculescu R, Kusec R, Jäger U, Nadel B: V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2009 Aug;48(8):725-36
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  • [Title] V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia.
  • Translocations of proto-oncogenes to the B-cell or T-cell antigen receptor loci in acute T- or B-cell leukemia and lymphoma have been, in most cases, accredited to V(D)J or switch recombination depending on the location of the breakpoint at the receptor locus.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Recombination, Genetic. Translocation, Genetic. VDJ Recombinases / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cells, Cultured. DNA Breaks. DNA-Binding Proteins / genetics. Fibroblasts. Genes, T-Cell Receptor. Homeodomain Proteins / genetics. LIM Domain Proteins. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Metalloproteins / genetics. Mice. Receptors, Antigen, B-Cell / genetics. TCF Transcription Factors / genetics. Transcription Factor 7-Like 1 Protein

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  • (PMID = 19455608.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Receptors, Antigen, B-Cell; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Tlx1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.- / VDJ Recombinases
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31. He G, Wu D, Sun A, Xue Y, Jin Z, Qiu H, Tang X, Miao M, Fu Z, Ma X, Wang X, Chen Z, Ruan C: B-Lymphoid and myeloid lineages biphenotypic acute leukemia with t(8;21)(q22;q22). Int J Hematol; 2008 Mar;87(2):132-6
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  • [Title] B-Lymphoid and myeloid lineages biphenotypic acute leukemia with t(8;21)(q22;q22).
  • By analyzing the characteristics of morphology, immune phenotype, chromosome karyotype and clinical manifestations of six cases of B-lymphoid and myeloid lineages biphenotypic acute leukemia (BAL) with t(8;21)(q22;q22), a new subgroup of BAL was reported.
  • Immunophenotype revealed B-lymphoid and myeloid lineages positive, together with frequent and high expression of CD34 and CD33, and weak expression of HLA-DR.
  • Chemotherapy for myeloid and lymphoid leukemia simultaneously produced good response in the patients.
  • q22) might be a new subgroup of BAL, and it was suggested that the leukemia clone with t(8;21)(q22;q22) might have originated from an early phase of hematopoiesis, and AML1/ETO fusion gene might be related to differentiation of B lymphocyte.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic


32. Schimmer AD: Induction of apoptosis in lymphoid and myeloid leukemia. Curr Oncol Rep; 2006 Nov;8(6):430-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of apoptosis in lymphoid and myeloid leukemia.
  • Defects in the core machinery of the apoptosis pathway contribute to chemoresistance and poor outcomes in patients with acute leukemia.
  • This review highlights compounds that target the mitochondrial, death receptor, and convergence pathways of caspase activation that are being developed for the treatment of acute leukemia.
  • [MeSH-major] Apoptosis / physiology. Leukemia, Lymphoid / therapy. Leukemia, Myeloid / therapy

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  • (PMID = 17040621.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Receptors, Death Domain; EC 3.4.22.- / Caspases
  • [Number-of-references] 68
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33. Royer-Bégyn M, Teira P, Deybach JC, Mas E, Mazereeuw-Hautier J: [Porphyria cutanea tarda in a child undergoing bone marrow grafting]. Ann Dermatol Venereol; 2010 Oct;137(10):640-4
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  • [Transliterated title] Porphyrie cutanée tardive chez un enfant greffé de moelle.
  • His past medical history revealed acute biphenotypic leukaemia with complete remission after allogeneic hematopoietic stem cell transplantation (unrelated donor).
  • Complications of bone marrow transplant comprised anaemia (treated by blood transfusions), primary cytomegalovirus (CMV) infection, pulmonary aspergillosis and acute digestive graft-versus-host disease.
  • The diagnosis of type I sporadic PCT was based on high levels of porphyria and normal erythrocytic uroporphyrinogen decarboxylase activity.
  • The causative role of bone marrow transplantation in the development of PCT could be related to several triggering factors: primary CMV infection, hepatotoxic drugs, blood transfusion and possible chronic hepatic graft-versus-host disease.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Biphenotypic, Acute / therapy. Porphyria Cutanea Tarda / diagnosis. Porphyria Cutanea Tarda / therapy

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  • [Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.
  • (PMID = 20932445.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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34. Suh B, Song J, Kim J, Park TS, Choi JR: Constitutional pericentric inversion 9 in Korean patients with chronic myelogenous leukemia. Korean J Lab Med; 2010 Jun;30(3):218-23
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  • [Title] Constitutional pericentric inversion 9 in Korean patients with chronic myelogenous leukemia.
  • BACKGROUND: Although the pericentric inversion of chromosome 9, inv(9)(p11q13), is generally considered a normal variation, it is also associated with solid tumors and several hematologic malignancies such as biphenotypic acute leukemia, ALL, AML, and myeloproliferative neoplasms.
  • The purpose of this retrospective study was to investigate the frequency and clinical features of CML patients with concomitant inv(9) and t(9;22)(q34;q11.2) variation at our institution.
  • METHODS: We reviewed the bone marrow chromosome database entries between October 2006 and December 2008 to identify patients with concomitant inv(9) and t(9;22) variations.
  • RESULTS: Among the 51 CML patients, 4 (7.8%) had concomitant inv(9) and t(9;22) variations.
  • [MeSH-major] Asian Continental Ancestry Group / genetics. Chromosome Inversion. Chromosomes, Human, Pair 9. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20603579.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
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35. Cosgrove MS, Patel A: Mixed lineage leukemia: a structure-function perspective of the MLL1 protein. FEBS J; 2010 Apr;277(8):1832-42
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  • [Title] Mixed lineage leukemia: a structure-function perspective of the MLL1 protein.
  • Several acute lymphoblastic and myelogenous leukemias are correlated with alterations in the human mixed lineage leukemia protein-1 (MLL1) gene.
  • Despite the important biological role of SET1 family enzymes and their involvement in human leukemias, relatively little is understood about how these enzymes work.

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  • (PMID = 20236310.001).
  • [ISSN] 1742-4658
  • [Journal-full-title] The FEBS journal
  • [ISO-abbreviation] FEBS J.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA140522-02; United States / NCI NIH HHS / CA / R01 CA140522; United States / NCI NIH HHS / CA / R01 CA140522-02; United States / NCI NIH HHS / CA / R01CA140522
  • [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 / Histones; 0 / Ligands; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; K3Z4F929H6 / Lysine
  • [Number-of-references] 61
  • [Other-IDs] NLM/ NIHMS209384; NLM/ PMC2892832
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36. Bursen A, Schwabe K, Rüster B, Henschler R, Ruthardt M, Dingermann T, Marschalek R: The AF4.MLL fusion protein is capable of inducing ALL in mice without requirement of MLL.AF4. Blood; 2010 Apr 29;115(17):3570-9
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  • The chromosomal translocation t(4;11)(q21;q23) is the most frequent genetic aberration of the human MLL gene, resulting in high-risk acute lymphoblastic leukemia (ALL).
  • Recipients of AF4.MLL- or double-transduced LSPCs developed pro-B ALL, B/T biphenotypic acute leukemia, or mixed lineage leukemia.
  • Transplantation of MLL.AF4- or mock-transduced LSPCs did not result in disease development during an observation period of 13 months.
  • These findings indicate that the expression of the AF4.MLL fusion protein is capable of inducing acute lymphoblastic leukemia even in the absence of the MLL.AF4 fusion protein.
  • In view of recent findings, these results may imply that t(4;11) leukemia is based on 2 oncoproteins, providing an explanation for the very early onset of disease in humans.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Leukemic. Myeloid-Lymphoid Leukemia Protein / metabolism. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 20194896.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aff1 protein, mouse; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse
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37. Jin S, Zhao H, Yi Y, Nakata Y, Kalota A, Gewirtz AM: c-Myb binds MLL through menin in human leukemia cells and is an important driver of MLL-associated leukemogenesis. J Clin Invest; 2010 Feb;120(2):593-606
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] c-Myb binds MLL through menin in human leukemia cells and is an important driver of MLL-associated leukemogenesis.
  • Mixed-lineage leukemia (MLL) is a proto-oncogene frequently involved in chromosomal translocations associated with acute leukemia.
  • Recent data suggest that the MYB proto-oncogene, which is an important regulator of hematopoietic cell development, has a role in leukemogenesis driven by the MLL-ENL fusion protein, but exactly how is unclear.
  • Silencing MYB in human leukemic cell lines and primary patient material evoked a global decrease in H3K4 methylation, an unexpected decrease in HOXA9 and MEIS1 gene expression, and decreased MLL and menin occupancy in the HOXA9 gene locus.
  • The finding that c-Myb has the ability to direct epigenetic marks, along with its participation in an autoregulatory feedback loop with genes known to transform hematopoietic cells, lends mechanistic and translationally relevant insight into its role in MLL-associated leukemogenesis.
  • [MeSH-major] Leukemia / metabolism. Myeloid-Lymphoid Leukemia Protein / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-myb / metabolism

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  • (PMID = 20093773.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA072765; United States / NCI NIH HHS / CA / 2P01CA072765-11
  • [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 / DNA-Binding Proteins; 0 / Histones; 0 / Homeodomain Proteins; 0 / MEN1 protein, human; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myb; 0 / Recombinant Fusion Proteins; 0 / homeobox protein HOXA9; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC2810070
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38. Tashiro H, Mizutani-Noguchi M, Shirasaki R, Shirafuji N: Acute myelogenous leukemia cells with the MLL-ELL translocation convert morphologically and functionally into adherent myofibroblasts. Biochem Biophys Res Commun; 2010 Jan 1;391(1):592-7
MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

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  • [Title] Acute myelogenous leukemia cells with the MLL-ELL translocation convert morphologically and functionally into adherent myofibroblasts.
  • We show in this paper that non-adherent leukemia blasts can change into myofibroblasts.
  • When myeloblasts from two cases of acute myelogenous leukemia with a fusion product comprising mixed lineage leukemia and RNA polymerase II elongation factor, were cultured long term, their morphology changed to that of myofibroblasts with similar molecular characteristics to the parental myeloblasts.
  • The original leukemia blasts, when cultured on the leukemia blast-derived myofibroblasts, grew extensively.
  • Leukemia blasts can create their own microenvironment for proliferation.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Fibroblasts / pathology. Leukemia, Myeloid, Acute / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Myoblasts / pathology. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Cell Adhesion. Cell Line, Tumor. Humans. Karyotyping

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  • [Copyright] Copyright 2009 Elsevier Inc. All rights reserved.
  • (PMID = 19932689.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-ELL fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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39. Mohan AV, Ramnath VR, Patalas E, Attar EC: Non-specific interstitial pneumonia as the initial presentation of biphenotypic acute leukemia: a case report. Cases J; 2009;2:8217

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Non-specific interstitial pneumonia as the initial presentation of biphenotypic acute leukemia: a case report.
  • We present a 46-year-old woman with recent-onset rheumatologic illness who developed pulmonary symptoms as the presenting feature of biphenotypic acute leukaemia.
  • Corticosteroid therapy resulted in resolution of both her pulmonary and rheumatologic symptoms, and her pulmonary symptoms did not recur following treatment of her leukemia.

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  • [Other-IDs] NLM/ PMC2769415
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40. 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
The Lens. Cited by Patents in .

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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.

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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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41. Rudinskiy N, Grishchuk Y, Vaslin A, Puyal J, Delacourte A, Hirling H, Clarke PG, Luthi-Carter R: Calpain hydrolysis of alpha- and beta2-adaptins decreases clathrin-dependent endocytosis and may promote neurodegeneration. J Biol Chem; 2009 May 1;284(18):12447-58
Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

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  • Proteolysis of alpha- and beta2-adaptins, as well as the accessory clathrin adaptors epsin 1, adaptor protein 180, and the clathrin assembly lymphoid myeloid leukemia protein, was detected in brain tissues after experimentally induced ischemia and in cases of human Alzheimer disease.
  • [MeSH-major] Adaptor Protein Complex alpha Subunits / metabolism. Adaptor Protein Complex beta Subunits / metabolism. Alzheimer Disease / metabolism. Brain / metabolism. Calpain / metabolism. Clathrin / metabolism. Endocytosis. Neurons / metabolism
  • [MeSH-minor] Adaptor Proteins, Vesicular Transport. Animals. Brain Ischemia / genetics. Brain Ischemia / metabolism. Brain Ischemia / pathology. Calcium / metabolism. Cell Line. Cell Membrane / genetics. Cell Membrane / metabolism. Cell Membrane / pathology. Female. Glutamic Acid / metabolism. Humans. Hydrolysis. Male. Membrane Lipids / genetics. Membrane Lipids / metabolism. Monomeric Clathrin Assembly Proteins / genetics. Monomeric Clathrin Assembly Proteins / metabolism. Rats. Rats, Sprague-Dawley. Rats, Wistar

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  • (PMID = 19240038.001).
  • [ISSN] 0021-9258
  • [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 / Adaptor Protein Complex alpha Subunits; 0 / Adaptor Protein Complex beta Subunits; 0 / Adaptor Proteins, Vesicular Transport; 0 / Clathrin; 0 / Membrane Lipids; 0 / Monomeric Clathrin Assembly Proteins; 0 / PICALM protein, human; 0 / Picalm protein, rat; 0 / epsin; 3KX376GY7L / Glutamic Acid; EC 3.4.22.- / Calpain; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC2673311
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42. Liu B, Li R, Wu HJ, Chen Y: [Clinical study on prognosis of acute leukemia subtypes Ly + AML and My + ALL]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Apr;15(2):421-4
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  • [Title] [Clinical study on prognosis of acute leukemia subtypes Ly + AML and My + ALL].
  • The purpose of this study was to investigate the prognosis of acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL), lymphoid antigen-positive acute myeloid leukemia (Ly + AML), myeloid antigen-positive acute leukemia (My + ALL) and biphenotypic acute leukemia (BAL).
  • Immunophenotyping was performed on medullary specimens of 197 acute leukemia (AL) patients by using three-color flow cytometry analysis and CD45/SSC gating.
  • The results showed that in Ly + AML, CD7 was the most common (53.8%) as compared to other lymphoid markers, however, in My + ALL CD13 was the most common (47.2%) as compared to other myeloid markers.
  • It is concluded that since Ly + AML has lymphoid markers, and the prognosis of Ly + AML is worse than AML, the clinical therapy for Ly + AML should contain both AML and ALL.
  • Though My + ALL had myeloid markers, no significant difference was found between My + ALL and ALL, it might be supposed that their therapy could be the same.

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  • (PMID = 17493361.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, CD7; EC 3.4.11.2 / Antigens, CD13
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43. Eklund EA: The role of HOX genes in malignant myeloid disease. Curr Opin Hematol; 2007 Mar;14(2):85-9
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  • [Title] The role of HOX genes in malignant myeloid disease.
  • Recent studies indicate that a common characteristic of poor prognosis acute myeloid leukemia is dysregulated expression of a key group of these Hox proteins.
  • The purpose of this review is to outline recent progress in understanding the role that dysregulation of HOX-gene expression plays in the pathogenesis of myeloid leukemogenesis.
  • RECENT FINDINGS: A number of recent studies correlate increased expression of HOXA-genes with poor prognosis cytogenetics in acute myeloid leukemia and mixed lineage leukemia.
  • Many such studies also document co-overexpression of homeodomain proteins of the Meis and Pbx families in poor prognosis leukemia.
  • SUMMARY: These findings suggest that a key characteristic of poor prognosis acute myeloid leukemia is increased, differentiation-stage inappropriate expression of the Abd HoxA proteins and their DNA-binding partners.
  • Such results suggest that dysregulation of the 'Hox code' is important in the pathogenesis of myeloid malignancy.
  • [MeSH-major] Genes, Homeobox / physiology. Leukemia, Myeloid / genetics
  • [MeSH-minor] Chromosome Aberrations. Gene Expression Regulation, Leukemic. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein / physiology

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  • (PMID = 17255784.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [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
  • [Number-of-references] 44
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44. Okada Y, Jiang Q, Lemieux M, Jeannotte L, Su L, Zhang Y: Leukaemic transformation by CALM-AF10 involves upregulation of Hoxa5 by hDOT1L. Nat Cell Biol; 2006 Sep;8(9):1017-24
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  • Chromosomal translocation is a common cause of leukaemia and the most common chromosome translocations found in leukaemia patients involve the mixed lineage leukaemia (MLL) gene.
  • AF10 is one of more than 30 MLL fusion partners in leukaemia.
  • In addition to MLL, AF10 has also been reported to fuse to CALM (clathrin-assembly protein-like lymphoid-myeloid) in patients with T-cell acute lymphoblastic leukaemia (T-ALL) and acute myeloid leukaemia (AML).
  • Thus, our study establishes CALM-AF10 fusion as a cause of leukaemia and reveals that mistargeting of hDOT1L and upregulation of Hoxa5 through H3K79 methylation is the underlying mechanism behind leukaemia caused by CALM-AF10 fusion.

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  • [ErratumIn] Nat Cell Biol. 2006 Oct;8(10):1178
  • (PMID = 16921363.001).
  • [ISSN] 1465-7392
  • [Journal-full-title] Nature cell biology
  • [ISO-abbreviation] Nat. Cell Biol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI48407; United States / NIAID NIH HHS / AI / R56 AI048407; United States / NHLBI NIH HHS / HL / R21 HL072240; United States / NIAID NIH HHS / AI / R01 AI080432; United States / NIGMS NIH HHS / GM / R01 GM068804; United States / NIAID NIH HHS / AI / R01 AI077454; United States / NIGMS NIH HHS / GM / GM68804; United States / NHLBI NIH HHS / HL / HL72240; United States / NIAID NIH HHS / AI / R01 AI048407
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HOXA5 protein, human; 0 / Homeodomain Proteins; 0 / Hoxa5 protein, mouse; 0 / MLLT10 protein, human; 0 / Mllt10 protein, mouse; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Phosphoproteins; 0 / Transcription Factors; EC 2.1.1.- / DOT1L protein, human; EC 2.1.1.- / Methyltransferases
  • [Other-IDs] NLM/ NIHMS684864; NLM/ PMC4425349
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45. Stasik C, Ganguly S, Cunningham MT, Hagemeister S, Persons DL: Infant acute lymphoblastic leukemia with t(11;16)(q23;p13.3) and lineage switch into acute monoblastic leukemia. Cancer Genet Cytogenet; 2006 Jul 15;168(2):146-9
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  • [Title] Infant acute lymphoblastic leukemia with t(11;16)(q23;p13.3) and lineage switch into acute monoblastic leukemia.
  • Rearrangements of the mixed-lineage leukemia (MLL) gene have been associated with a poor prognosis in infant acute lymphoblastic leukemia (ALL).
  • Previously, MLL translocations involving the CREP-binding protein (CREBBP) gene at chromosome band 16p13.3 have primarily been reported in treatment-related acute myeloid leukemia, after chemotherapy for other primary malignancies using topoisomerase II inhibitors.
  • We report a case of de novo infant ALL with t(11;16)(q23;p13.3).
  • After chemotherapy, this patient developed an acute monoblastic leukemia (M5b) with retention of the t(11;16)(q23;p13.3), indicating that this is a lineage switch of the original leukemic clone.
  • [MeSH-major] Cell Lineage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 16 / genetics. Leukemia, Monocytic, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

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  • (PMID = 16843104.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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46. Piloto O, Nguyen B, Huso D, Kim KT, Li Y, Witte L, Hicklin DJ, Brown P, Small D: IMC-EB10, an anti-FLT3 monoclonal antibody, prolongs survival and reduces nonobese diabetic/severe combined immunodeficient engraftment of some acute lymphoblastic leukemia cell lines and primary leukemic samples. Cancer Res; 2006 May 1;66(9):4843-51
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  • [Title] IMC-EB10, an anti-FLT3 monoclonal antibody, prolongs survival and reduces nonobese diabetic/severe combined immunodeficient engraftment of some acute lymphoblastic leukemia cell lines and primary leukemic samples.
  • The class III receptor tyrosine kinase FLT3 is expressed on the blasts of >90% of patients with B-lineage acute lymphoblastic leukemias (ALL).
  • In addition, it is expressed at extremely high levels in ALL patients with mixed lineage leukemia rearrangements or hyperdiploidy and is sometimes mutated in these same patients.
  • In this report, we investigate the effects of treating ALL cell lines and primary samples with human anti-FLT3 monoclonal antibodies (mAb) capable of preventing binding of FLT3 ligand.
  • In vitro studies, examining the ability of two anti-FLT3 mAbs (IMC-EB10 and IMC-NC7) to affect FLT3 activation and downstream signaling in ALL cell lines and primary blasts, yielded variable results.
  • FLT3 phosphorylation was consistently inhibited by IMC-NC7 treatment, but in some cell lines, IMC-EB10 actually stimulated FLT3 activation, possibly as a result of antibody-mediated receptor dimerization.
  • Through antibody-dependent, cell-mediated cytotoxicity, such an antibody could still prove efficacious against leukemia cells in vivo.
  • In fact, IMC-EB10 treatment significantly prolonged survival and/or reduced engraftment of several ALL cell lines and primary ALL samples in nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice.
  • Moreover, fluorescence-activated cell sorting and PCR analysis of IMC-EB10-treated NOD/SCID mice surviving 150 days post-leukemic cell injection revealed that FLT3 immunotherapy reduced leukemic engraftment below the level of detection in these assays (<0.001%).
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. fms-Like Tyrosine Kinase 3 / immunology
  • [MeSH-minor] Animals. Cell Line, Tumor. Child. Cytotoxicity, Immunologic. Female. Humans. Immunization, Passive / methods. Killer Cells, Natural / immunology. Male. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Signal Transduction / drug effects

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  • (PMID = 16651440.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA62924; United States / NCI NIH HHS / CA / CA70970; United States / NCI NIH HHS / CA / CA90668; United States / NCRR NIH HHS / RR / RR00171
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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47. Xia ZB, Popovic R, Chen J, Theisler C, Stuart T, Santillan DA, Erfurth F, Diaz MO, Zeleznik-Le NJ: The MLL fusion gene, MLL-AF4, regulates cyclin-dependent kinase inhibitor CDKN1B (p27kip1) expression. Proc Natl Acad Sci U S A; 2005 Sep 27;102(39):14028-33
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  • MLL, involved in many chromosomal translocations associated with acute myeloid and lymphoid leukemia, has >50 known partner genes with which it is able to form in-frame fusions.
  • Characterizing important downstream target genes of MLL and of MLL fusion proteins may provide rational therapeutic strategies for the treatment of MLL-associated leukemia.
  • To this end, we developed inducible MLL-AF4 fusion cell lines in different backgrounds.
  • Overexpression of MLL-AF4 does not lead to increased proliferation in either cell line, but rather, cell growth was slowed compared with similar cell lines inducibly expressing truncated MLL.
  • We found that in the MLL-AF4-induced cell lines, the expression of the cyclin-dependent kinase inhibitor gene CDKN1B was dramatically changed at both the RNA and protein (p27kip1) levels.
  • Further, we confirmed CDKN1B promoter binding by ChIP in MLL-AF4 as well as in MLL-AF9 leukemia cell lines.
  • Our results suggest that CDKN1B is a downstream target of MLL and of MLL-AF4, and that, depending on the background cell type, MLL-AF4 inhibits or activates CDKN1B expression.
  • This finding may have implications in terms of leukemia stem cell resistance to chemotherapy in MLL-AF4 leukemias.

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  • (PMID = 16169901.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA40046; United States / NCI NIH HHS / CA / CA104300; United States / NCI NIH HHS / CA / P01 CA040046; United States / NCI NIH HHS / CA / CA78438; United States / NCI NIH HHS / CA / R01 CA104300; United States / NCI NIH HHS / CA / CA81269
  • [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 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC1236570
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48. Suzukawa K, Shimizu S, Nemoto N, Takei N, Taki T, Nagasawa T: Identification of a chromosomal breakpoint and detection of a novel form of an MLL-AF17 fusion transcript in acute monocytic leukemia with t(11;17)(q23;q21). Int J Hematol; 2005 Jul;82(1):38-41

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a chromosomal breakpoint and detection of a novel form of an MLL-AF17 fusion transcript in acute monocytic leukemia with t(11;17)(q23;q21).
  • More than 40 genes have been reported as translocation partners of the mixed lineage leukemia gene (MLL) in hematologic malignancies.
  • On the other hand, there is only 1 report of an MLL-AF17 fusion transcript in acute myeloid leukemia (AML).
  • Here we describe a 40-year-old man with a diagnosis of AML involving t(11;17)(q23;q21).
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. DNA-Binding Proteins / genetics. Leukemia, Monocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adult. Cell Transformation, Neoplastic / genetics. Chromosome Breakage. Histone-Lysine N-Methyltransferase. Humans. Leucine Zippers. Male. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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  • (PMID = 16105757.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / MLL-AF17 fusion protein, human; 0 / MLLT6 protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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49. Tenney K, Shilatifard A: A COMPASS in the voyage of defining the role of trithorax/MLL-containing complexes: linking leukemogensis to covalent modifications of chromatin. J Cell Biochem; 2005 Jun 1;95(3):429-36
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  • The trithorax-related mixed lineage leukemia (Mll) gene located on chromosome 11 is rearranged in a variety of aggressive human B and T lymphoid tumors as well as acute myeloid leukemia (AML) in both children and adults.
  • [MeSH-major] Chromatin / metabolism. DNA-Binding Proteins / metabolism. Leukemia / metabolism. Multiprotein Complexes / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Adult. Animals. Child. Histone-Lysine N-Methyltransferase. Humans. Methylation. Myeloid-Lymphoid Leukemia Protein. Proto-Oncogenes / genetics. Transcription, Genetic

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15786493.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / 1R01GM069905; United States / NCI NIH HHS / CA / 2R01CA089455
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Multiprotein Complexes; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 49
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50. Meyerholz A, Hinrichsen L, Groos S, Esk PC, Brandes G, Ungewickell EJ: Effect of clathrin assembly lymphoid myeloid leukemia protein depletion on clathrin coat formation. Traffic; 2005 Dec;6(12):1225-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of clathrin assembly lymphoid myeloid leukemia protein depletion on clathrin coat formation.
  • The endocytic accessory clathrin assembly lymphoid myeloid leukemia protein (CALM) is the ubiquitously expressed homolog of the neuron-specific protein AP180 that has been implicated in the retrieval of synaptic vesicle.
  • [MeSH-minor] Cell Membrane / metabolism. Coated Pits, Cell-Membrane / ultrastructure. Endosomes / metabolism. HeLa Cells. Humans. RNA Interference. Transcription Factor AP-2 / metabolism. trans-Golgi Network / metabolism


51. Imataki O, Ohnishi H, Yamaoka G, Arai T, Kitanaka A, Kubota Y, Kushida Y, Ishida T, Tanaka T: Lineage switch from precursor B cell acute lymphoblastic leukemia to acute monocytic leukemia at relapse. Int J Clin Oncol; 2010 Feb;15(1):112-5
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  • [Title] Lineage switch from precursor B cell acute lymphoblastic leukemia to acute monocytic leukemia at relapse.
  • A lineage switch in leukemia, in which the leukemic cell lineage at onset converts to another lineage at a later time, is an uncommon type of hybrid (mixed) leukemia regarded as a variation of bilineage leukemia.
  • We present a case of a 60-year-old female diagnosed with precursor B cell acute lymphoblastic leukemia (ALL), whose markers in flow cytometry shifted from their original status of CD19+, 22+, 79a+, 13+, HLA-DR+, and TdT+.
  • Residual disease was proved by biopsy and pathologically shown to have an immature phenotype of CD5+, CD10-, CD20-, CD79a- and myeloperoxidase negativity.
  • Two weeks after liver biopsy, blast cells progressively appeared in the peripheral blood; these cells had a monocytoid morphology and phenotype (CD13, 14) but were accompanied by myeloid (CD33) and lymphoid (CD2, 4, 20) cells.
  • This phenotypical conversion from B-ALL to hybrid leukemia featuring monocytoid characteristics is known as a lineage switch.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / pathology. Leukemia, Monocytic, Acute / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Biomarkers, Tumor / blood. Bone Marrow / pathology. Cell Lineage. Female. Humans. Immunophenotyping. Middle Aged. Recurrence

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  • [Cites] Leukemia. 1995 Dec;9(12):2023-6 [8609712.001]
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  • (PMID = 20066454.001).
  • [ISSN] 1437-7772
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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52. Coche D, Bergues B, Harrivel V, Guillaume N: [Biphenotypic acute leukaemia with Burkitt-like cytology]. Ann Biol Clin (Paris); 2009 Jul-Aug;67(4):437-40
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  • [Title] [Biphenotypic acute leukaemia with Burkitt-like cytology].
  • [Transliterated title] Leucémie aiguë biphénotypique avec aspect cytologique de type Burkitt.
  • Biphenotypic acute leukaemia (BAL) represents about 5% of adult acute leukaemia.
  • Based on a previously described scoring system, the European Group for Immunologic Classification of Leukaemia (EGIL) proposed a set of diagnostic criteria for BAL.
  • This scoring system is based on the number and degree of the specificity of several markers for myeloid or T/B lymphoid blasts.
  • Here, we report the case of a BAL with Burkitt-like cytology, corresponding to "the acute lymphoblastic leukaemia, Burkitt type" L3 for the FAB classification.
  • By flow cytometry, the blasts showed a positivity for B lymphoid cytoplasmic (CD79a and mu) and membrane (CD19, CD22, CD24, IgM) markers AND a positivity for the myeloid (CD13, CD33, CD65, CD15) markers.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / genetics

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  • (PMID = 19654084.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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53. Thavaraj V, Seth R: Prophylaxis of central nervous system leukemia: a case of chronic myeloid leukemia with lymphoid blast crisis treated with imatinib mesylate. World J Pediatr; 2008 May;4(2):145-7
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  • [Title] Prophylaxis of central nervous system leukemia: a case of chronic myeloid leukemia with lymphoid blast crisis treated with imatinib mesylate.
  • BACKGROUND: Chronic myeloid leukemia (CML) in blast crisis has a dismal prognosis.
  • METHODS: A child with CML in lymphoid blast crisis was diagnosed by complete hematological and bone marrow examination.
  • There was no central nervous system (CNS) leukemia at presentation.
  • Results of cerebrospinal fluid taken for cytopathology showed CNS leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy. Central Nervous System Neoplasms / prevention & control. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage
  • [MeSH-minor] Anti-Inflammatory Agents / administration & dosage. Benzamides. Blood Cell Count. Chemoprevention / methods. Child. Clinical Protocols. Cytarabine / administration & dosage. Drug Therapy, Combination. Female. Humans. Hydrocortisone / administration & dosage. Imatinib Mesylate. Injections, Spinal. Methotrexate / therapeutic use. Remission Induction

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  • (PMID = 18661773.001).
  • [ISSN] 1708-8569
  • [Journal-full-title] World journal of pediatrics : WJP
  • [ISO-abbreviation] World J Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate; WI4X0X7BPJ / Hydrocortisone; YL5FZ2Y5U1 / Methotrexate
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54. Aljurf M, Nassar A, Saleh AJ, Almhareb F, Alzahrani H, Walter C, Bakr M, Ahmed SO, Chaudhri N: Maternal acute lymphoctic leukemia with rearrangement of the mixed lineage leukemia gene occurring during pregnancy. Hematol Oncol Stem Cell Ther; 2009;2(3):399-402
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  • [Title] Maternal acute lymphoctic leukemia with rearrangement of the mixed lineage leukemia gene occurring during pregnancy.
  • Acute lymphoblastic leukemia (ALL) is a relatively rare disease during pregnancy, accounting for about 15% of all cases of pregnancy-associated leukemia.
  • Although mixed lineage leukemia gene (MLL) rearrangement is the dominant genetic aberration in infantile acute leukemia, the occurrence of MLL gene rearrangement in maternal ALL occurring during pregnancy has not been reported.
  • Out of 31 cases of maternal leukemia diagnosed during pregnancy at our institution, 5 were ALL cases.
  • We believe that the association of MLL gene rearrangement with maternal leukemia is biologically plausible and this observation needs to be validated in a larger cohort of pregnancy-associated maternal leukemia cases.
  • [MeSH-major] Gene Rearrangement. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Pregnancy Complications, Neoplastic
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Lineage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Combined Modality Therapy. Female. Gestational Age. Histone-Lysine N-Methyltransferase. Humans. Pregnancy. Prognosis. Stem Cell Transplantation. Translocation, Genetic. Young Adult

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  • (PMID = 20139053.001).
  • [ISSN] 1658-3876
  • [Journal-full-title] Hematology/oncology and stem cell therapy
  • [ISO-abbreviation] Hematol Oncol Stem Cell Ther
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Saudi Arabia
  • [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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55. Mulloy JC, Wunderlich M, Zheng Y, Wei J: Transforming human blood stem and progenitor cells: a new way forward in leukemia modeling. Cell Cycle; 2008 Nov 1;7(21):3314-9
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  • [Title] Transforming human blood stem and progenitor cells: a new way forward in leukemia modeling.
  • MLL-AF9 (MA9) is a leukemia fusion gene formed upon translocation of the AF9 gene on chromosome 9 and the MLL gene on chromosome 11.
  • MA9 is commonly found in acute myeloid leukemia (AML) and occasionally in acute lymphoid leukemia and is associated with intermediate to poor outcome.
  • We have recently described a model system whereby we expressed the MA9 fusion gene in human CD34(+) Umbilical Cord Blood (UCB) cells and showed that these cells transformed to acute myeloid or lymphoid leukemia when injected into immunodeficient mice.
  • The Mixed Lineage Leukemia (MLL) oncogenes are unique in this model system in that they promote full transformation of primary human blood cells, while all other leukemia-associated oncogenes tested thus far have induced only partial phenotypes.
  • Here we provide an update on the use of this system for modeling human leukemia and its potential application for therapeutic testing of novel compounds to treat the disease.

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  • (PMID = 18948748.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA118319; United States / NCI NIH HHS / CA / K01 CA090370; United States / NCRR NIH HHS / RR / M01 RR 08084; United States / NCRR NIH HHS / RR / M01 RR008084; United States / NCI NIH HHS / CA / CA118319-04; United States / NCI NIH HHS / CA / R01 CA118319-04; United States / NCI NIH HHS / CA / CA118319; United States / NCI NIH HHS / CA / CA90370
  • [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 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.6.5.2 / rac GTP-Binding Proteins
  • [Other-IDs] NLM/ NIHMS169825; NLM/ PMC2812025
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56. Ardianto B, Sugimoto T, Kawano S, Kasagi S, Jauharoh SN, Kurimoto C, Tatsumi E, Morikawa K, Kumagai S, Hayashi Y: The HPB-AML-I cell line possesses the properties of mesenchymal stem cells. J Exp Clin Cancer Res; 2010;29:163
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  • [Title] The HPB-AML-I cell line possesses the properties of mesenchymal stem cells.
  • BACKGROUND: In spite of its establishment from the peripheral blood of a case with acute myeloid leukemia (AML)-M1, HPB-AML-I shows plastic adherence with spindle-like morphology.
  • METHODS: To examine this possibility, we characterized HPB-AML-I by performing cytochemical, cytogenetic, and phenotypic analyses, induction of differentiation toward mesenchymal lineage cells, and mixed lymphocyte culture analysis.
  • Mixed lymphocyte culture demonstrated that CD3+ T-cell proliferation was suppressed in the presence of HPB-AML-I cells.
  • [MeSH-major] Cell Line, Tumor / cytology. Cell Line, Tumor / physiology. Mesenchymal Stromal Cells / cytology. Mesenchymal Stromal Cells / physiology. Neoplastic Stem Cells / cytology. Neoplastic Stem Cells / physiology
  • [MeSH-minor] Cell Differentiation / physiology. Cell Lineage. Humans

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  • (PMID = 21144016.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3016278
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57. Han TJ, Xu XP: [Advances of study on prognostic factors of molecular biology in acute myeloid leukemia with normal cytogenetics]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Aug;18(4):1063-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Advances of study on prognostic factors of molecular biology in acute myeloid leukemia with normal cytogenetics].
  • Acute myeloid leukemia (AML) is a group of diseases with a conspicuous heterogeneity.
  • However, with the foundation of available chromosome analysis, a large group of acute myeloid leukemia (AML) patients, 40% to 49% of adults and 25% of children had not been found abnormality of chromosome karyotype under microscope.
  • These so-called cytogenetically normal acute myeloid leukemia (CN-AML) patients have usually been classified in an intermediate-risk prognostic category.
  • The review focuses on research advances abroad in this field including gene mutations suggesting bad prognosis such as FMS-related tyrosine kinase 3 gene mutation, Baalc gene and ETS-related gene hyperexpression, Wilms' tumor gene mutation and other gene mutations as well as gene mutations suggesting good prognosis such as nucleophosmin gene mutation, mixed lineage leukemia-partial tandem duplication, CCAAT/enhancer-binding protein α gene mutation.

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  • (PMID = 20723330.001).
  • [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
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58. Mori T, Nishimura N, Hasegawa D, Kawasaki K, Kosaka Y, Uchide K, Yanai T, Hayakawa A, Takeshima Y, Nishio H, Matsuo M: Persistent detection of a novel MLL-SACM1L rearrangement in the absence of leukemia. Leuk Res; 2010 Oct;34(10):1398-401

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Persistent detection of a novel MLL-SACM1L rearrangement in the absence of leukemia.
  • Most chromosomal rearrangements including the mixed lineage leukemia (MLL) gene are manifested as leukemia and predict a poor prognosis.
  • Here we report a case of a 3-year old boy bearing a novel MLL-rearrangement with the suppressor of actin mutations 1-like (SACM1L) gene in the absence of leukemia.
  • Bone marrow cells harboring the MLL-SACM1L rearrangement appeared during chemotherapy for acute lymphoblastic leukemia with hyperdiploidy and were continuously detected over 7 years without clonal expansion.
  • [MeSH-major] Gene Rearrangement. Membrane Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20553989.001).
  • [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
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Membrane Proteins; 0 / SACM1L protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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59. Walter K, Cockerill PN, Barlow R, Clarke D, Hoogenkamp M, Follows GA, Richards SJ, Cullen MJ, Bonifer C, Tagoh H: Aberrant expression of CD19 in AML with t(8;21) involves a poised chromatin structure and PAX5. Oncogene; 2010 May 20;29(20):2927-37
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  • Correct hematopoietic differentiation requires the tightly regulated execution of lineage-specific and stage-restricted gene expression programs.
  • This process is disturbed in hematological malignancies that typically show incomplete differentiation but often also display a mixed lineage phenotype.
  • Co-expression of lymphoid and myeloid molecules is a well-known feature of acute myeloblastic leukemia (AML) with t(8;21).
  • These cells consistently express the B-cell-specific transcription factor PAX5, and the B-cell-specific cell surface protein CD19.
  • We show that CD19 chromatin exists in a poised configuration in myeloid progenitors and that this poised chromatin structure facilitates PAX5-dependent CD19 activation.
  • This study shows that expression of PAX5 in leukemic cells has functional consequences and points to an important role of a progenitor-specific chromatin configuration in myeloid leukemia.
  • [MeSH-major] Antigens, CD19 / genetics. B-Cell-Specific Activator Protein / genetics. Chromatin / chemistry. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 20208555.001).
  • [ISSN] 1476-5594
  • [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 / Antigens, CD19; 0 / B-Cell-Specific Activator Protein; 0 / Chromatin; 0 / PAX5 protein, human
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60. Lee SG, Park TS, Won SC, Song J, Lee KA, Choi JR, Marschalek R, Meyer C: Three-way translocation involving MLL, MLLT1, and a novel third partner, NRXN1, in a patient with acute lymphoblastic leukemia and t(2;19;11) (p12;p13.3;q23). Cancer Genet Cytogenet; 2010 Feb;197(1):32-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Three-way translocation involving MLL, MLLT1, and a novel third partner, NRXN1, in a patient with acute lymphoblastic leukemia and t(2;19;11) (p12;p13.3;q23).
  • Translocations involving mixed lineage leukemia (MLL) gene at 11q23 are associated with de novo acute leukemia as well as therapy-related acute leukemia.
  • More than 100 different translocations involving MLL have been described in acute leukemia, with more than 60 translocation partner genes characterized on the molecular level.
  • Here, we describe a novel three-way translocation of t(2;19;11)(p12;p13.3;q23) in a patient with acute lymphoblastic leukemia (ALL).
  • The apparent three-way translocation thus identified is noteworthy because few studies have reported complex rearrangements involving 11q23 and 19p13.3 in acute leukemias.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 19. Chromosomes, Human, Pair 2. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Nerve Tissue Proteins / genetics. Nuclear Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Base Sequence. Cell Adhesion Molecules, Neuronal. Child, Preschool. Female. Histone-Lysine N-Methyltransferase. Humans. Molecular Sequence Data

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20113834.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules, Neuronal; 0 / MLL protein, human; 0 / MLLT1 protein, human; 0 / NRXN1 protein, human; 0 / Neoplasm Proteins; 0 / Nerve Tissue 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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61. Doubek M, Folber F, Koristek Z, Brychtova Y, Krejci M, Tomiska M, Navratil M, Mikulasova P, Mayer J: Autologous hematopoietic stem cell transplantation in adult acute lymphoblastic leukemia: still not out of fashion. Ann Hematol; 2009 Sep;88(9):881-7
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  • [Title] Autologous hematopoietic stem cell transplantation in adult acute lymphoblastic leukemia: still not out of fashion.
  • The role of autologous hematopoietic stem cell transplantation (autoHSCT) in adult acute lymphoblastic leukemia (ALL) is still unclear.
  • We retrospectively analyzed the results of the autoHSCT and maintenance therapy, with oral 6-mercaptopurine and methotrexate, in comparison to conventional-dose chemotherapy in the consolidation treatment of adult ALL and lymphoblastic lymphoma (LBL).
  • Sixty consecutive adult patients (median age 35.2 years; range 17.3 to 70.7) with ALL (n = 52), LBL (n = 7), and acute biphenotypic leukemia (n = 1) were treated in our center from 1997 to 2007.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation, Autologous

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  • (PMID = 19172272.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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62. Widlak P, Garrard WT: Roles of the major apoptotic nuclease-DNA fragmentation factor-in biology and disease. Cell Mol Life Sci; 2009 Jan;66(2):263-74
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  • [Title] Roles of the major apoptotic nuclease-DNA fragmentation factor-in biology and disease.
  • Here we review the recent literature that has uncovered new insight into DFF's regulation, and both its positive and negative roles in human disease.
  • Cells from mice deficient in DFF still undergo apoptotic death without significant cell-autonomous DNA degradation.
  • Negative aspects of DFF expression include contributing to susceptibility to acquire systemic lupus erythematosus, to chromosomal translocations that result in mixed lineage leukemias, and in the possible spreading of oncogenes and HIV due to horizontal gene transfer.
  • [MeSH-minor] Animals. Enzyme Activation. Gene Transfer, Horizontal. Genetic Predisposition to Disease. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Lupus Erythematosus, Systemic / genetics. Mutation. Neoplasms / genetics. Neoplasms / metabolism. Protein Subunits / chemistry. Protein Subunits / genetics. Protein Subunits / metabolism

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  • (PMID = 18810317.001).
  • [ISSN] 1420-9071
  • [Journal-full-title] Cellular and molecular life sciences : CMLS
  • [ISO-abbreviation] Cell. Mol. Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Protein Subunits; EC 3.1.- / Deoxyribonucleases; EC 3.1.- / caspase-activated deoxyribonuclease
  • [Number-of-references] 118
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63. Gujral S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Jain H, Pais A, Amre Kadam PS, Banavali SD, Arora B, Kumar P, Hari Menon VG, Kurkure PA, Parikh PM, Mahadik S, Chogule AB, Shinde SC, Nair CN: Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India. Cytometry B Clin Cytom; 2009 May;76(3):199-205
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  • [Title] Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India.
  • BACKGROUND: To analyze the spectrum of various types and subtypes of acute leukemia.
  • METHODS: Two thousand five hundred and eleven consecutive new referral cases of acute leukemia (AL) were evaluated based on WHO classification.
  • RESULTS: It included 1,471 cases (58%) of acute lymphoblastic leukemia (ALL), 964 cases (38%) of acute myeloid leukemia (AML), 45 cases (1.8%) of chronic myelogenous leukemia in blast crisis (CMLBC), 37 cases (1.5%) of biphenotypic acute leukemia (BAL), 1 case of Triphenotypic AL, and 2 cases of acute undifferentiated leukemia (AUL).
  • Common subtypes of ALL were B-cell ALL (76%), which comprised of intermediate stage/CALLA positive (73%), early precursor/proBALL (3%).
  • T-cell ALL constituted 24% (351 cases) of ALL.
  • CMLBC was commonly of myeloid blast crisis subtype (40 cases).
  • CONCLUSION: B-cell ALL was the commonest subtype in children and AML in adults.
  • CD13 was most sensitive and CD117 most specific for determining myeloid lineage.
  • A minimal primary panel of nine antibodies consisting of three myeloid markers (CD13, CD33, and CD117), B-cell lymphoid marker (CD19), T-cell marker (CD7), with CD45, CD10, CD34, and HLADR could assign lineage to 92% of AL.
  • Cytogenetics findings lead to a change in the diagnostic subtype of myeloid malignancy in 38 (1.5%) cases.
  • [MeSH-major] Immunophenotyping. Leukemia / immunology. Leukemia / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Histocytochemistry. Humans. In Situ Hybridization. India. Infant. Infant, Newborn. Male. Middle Aged. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • [Copyright] (c) 2008 Clinical Cytometry Society.
  • (PMID = 18803279.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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64. Muntean AG, Giannola D, Udager AM, Hess JL: The PHD fingers of MLL block MLL fusion protein-mediated transformation. Blood; 2008 Dec 1;112(12):4690-3

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  • Chromosomal translocations involving the mixed lineage leukemia (MLL) gene are associated with aggressive acute lymphoid and myeloid leukemias.

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  • (PMID = 18796627.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / T32 HL007622; United States / NCI NIH HHS / CA / R01 CA078815; United States / NHLBI NIH HHS / HL / T32 HL07622; United States / NCI NIH HHS / CA / R01CA92251; United States / NCI NIH HHS / CA / R01 CA092251; United States / NCI NIH HHS / CA / R01CA78815
  • [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 / Homeodomain Proteins; 0 / MLL protein, human; 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC2597135
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65. 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.
  • 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] United States
  • [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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66. Faber J, Armstrong SA: Defining leukemia stem cells in MLL-translocated leukemias: implications for novel therapeutic strategies. Klin Padiatr; 2007 Nov-Dec;219(6):306-11
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  • [Title] Defining leukemia stem cells in MLL-translocated leukemias: implications for novel therapeutic strategies.
  • An important question in the development of novel, less toxic antileukemic strategies specifically targeting leukemia stem cells is how closely leukemia stem cells are related to normal hematopoietic stem cells.
  • It has been recently demonstrated that leukemia stem cells can be derived from different stages in normal hematopoiesis and have unique phenotypic and genetic features.
  • Introduction of Mixed-lineage leukemia ( MLL)-fusion oncoproteins, frequently found in infant leukemias and therapy-related leukemias, into differentiated hematopoietic progenitor cells results in the generation of leukemias with a high frequency of leukemia stem cells.
  • The progenitor-derived leukemia stem cells ectopically express a limited stem cell program while maintaining the global identity of differentiated myeloid cells.
  • Development of therapeutic strategies that specifically target the leukemia stem cell program while sparing normal hematopoietic stem cells may represent a novel therapeutic approach in human leukemias with high efficacy yet less side effects.
  • [MeSH-major] Leukemia / therapy. Leukemia, Biphenotypic, Acute. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplastic Stem Cells
  • [MeSH-minor] Child. Hematopoietic Stem Cells. Histone-Lysine N-Methyltransferase. Humans. Infant. Oncogene Proteins, Fusion. Phenotype

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  • (PMID = 18050039.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Germany
  • [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
  • [Number-of-references] 62
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67. Nishioka C, Ikezoe T, Yang J, Takeshita A, Taniguchi A, Komatsu N, Togitani K, Koeffler HP, Yokoyama A: Blockade of MEK/ERK signaling enhances sunitinib-induced growth inhibition and apoptosis of leukemia cells possessing activating mutations of the FLT3 gene. Leuk Res; 2008 Jun;32(6):865-72
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  • [Title] Blockade of MEK/ERK signaling enhances sunitinib-induced growth inhibition and apoptosis of leukemia cells possessing activating mutations of the FLT3 gene.
  • The FMS-like tyrosine kinase 3 (FLT3) is a cell surface receptor tyrosine kinase.
  • Activating mutations of this gene occur in nearly 30% of acute myelogenous leukemia (AML) patients.
  • In this study, we found that AZD6244 (ARRY-142886), a novel inhibitor of MEK1/2 kinases, effectively inhibited the proliferation of acute biphenotypic leukemia MV4-11 and acute monocytic leukemia MOLM13 cells.
  • Taken together, concomitant blockade of FLT3 and MEK signaling represents a promising treatment strategy for individuals with leukemia who possess activating mutations of FLT3.
  • [MeSH-major] Apoptosis / drug effects. Indoles / therapeutic use. Leukemia / pathology. MAP Kinase Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors. Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors. Mutation / genetics. Pyrroles / therapeutic use. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols. Benzimidazoles / therapeutic use. Cell Proliferation / drug effects. Female. Humans. Leukemia, Megakaryoblastic, Acute / drug therapy. Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Megakaryoblastic, Acute / pathology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Male. Middle Aged. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction / drug effects. Tumor Cells, Cultured

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  • (PMID = 17983653.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AZD 6244; 0 / Benzimidazoles; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 1
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68. 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.
  • It may also prove to have a useful role in both diagnosis and prognosis.
  • [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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69. Stieglmaier J, Bremer E, Kellner C, Liebig TM, ten Cate B, Peipp M, Schulze-Koops H, Pfeiffer M, Bühring HJ, Greil J, Oduncu F, Emmerich B, Fey GH, Helfrich W: Selective induction of apoptosis in leukemic B-lymphoid cells by a CD19-specific TRAIL fusion protein. Cancer Immunol Immunother; 2008 Feb;57(2):233-46
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  • [Title] Selective induction of apoptosis in leukemic B-lymphoid cells by a CD19-specific TRAIL fusion protein.
  • Although the treatment outcome of lymphoid malignancies has improved in recent years by the introduction of transplantation and antibody-based therapeutics, relapse remains a major problem.
  • Potent apoptosis was induced by scFvCD19:sTRAIL in several CD19-positive tumor cell lines, whereas normal blood cells remained unaffected.
  • In mixed culture experiments, selective binding of scFvCD19:sTRAIL to CD19-positive cells resulted in strong induction of apoptosis in CD19-negative bystander tumor cells.
  • Simultaneous treatment of CD19-positive cell lines with scFvCD19:sTRAIL and valproic acid (VPA) or Cyclosporin A induced strongly synergistic apoptosis.
  • Treatment of patient-derived acute B-lymphoblastic leukemia (B-ALL) and chronic B-lymphocytic leukemia (B-CLL) cells resulted in strong tumoricidal activity that was further enhanced by combination with VPA.
  • The pre-clinical data presented here warrant further investigation of scFvCD19:sTRAIL as a potential new therapeutic agent for CD19-positive B-lineage malignancies.
  • [MeSH-major] Antigens, CD19. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Leukemia, B-Cell / drug therapy. Recombinant Fusion Proteins / pharmacology. TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 17665197.001).
  • [ISSN] 0340-7004
  • [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 / Antigens, CD19; 0 / Antineoplastic Agents; 0 / Immunoglobulin Fragments; 0 / Recombinant Fusion Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 614OI1Z5WI / Valproic Acid; 83HN0GTJ6D / Cyclosporine
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70. Rice KL, Licht JD: HOX deregulation in acute myeloid leukemia. J Clin Invest; 2007 Apr;117(4):865-8
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  • [Title] HOX deregulation in acute myeloid leukemia.
  • The deregulation of homeobox (HOX) genes in acute myeloid leukemia (AML) and the potential for these master regulators to perturb normal hematopoiesis is well established.
  • To date, overexpression of HOX genes in AML has been attributed to specific chromosomal aberrations and abnormalities involving mixed-lineage leukemia (MLL), an upstream regulator of HOX genes.
  • The finding reported in this issue of the JCI by Scholl et al. that caudal-type homeobox transcription factor 2 (CDX2), which is capable of affecting HOX gene expression during embryogenesis, is overexpressed in 90% of patients with AML and induces a transplantable AML in murine models provides an alternative mechanism for HOX-induced leukemogenesis and yields important insights into the hierarchy of HOX gene regulation in AML (see the related article beginning on page 1037).
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics. Leukemia, Myeloid / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Animals. Disease Models, Animal. Genes, Homeobox. Humans. Mice. Transcription Factors / genetics

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  • (PMID = 17404613.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1838955
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71. Allen MD, Grummitt CG, Hilcenko C, Min SY, Tonkin LM, Johnson CM, Freund SM, Bycroft M, Warren AJ: Solution structure of the nonmethyl-CpG-binding CXXC domain of the leukaemia-associated MLL histone methyltransferase. EMBO J; 2006 Oct 04;25(19):4503-12
The Lens. Cited by Patents in .

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  • [Title] Solution structure of the nonmethyl-CpG-binding CXXC domain of the leukaemia-associated MLL histone methyltransferase.
  • The mixed-lineage leukaemia (MLL) CXXC domain selectively binds nonmethyl-CpG DNA, and is required for transformation by MLL fusion proteins that commonly arise from recurrent chromosomal translocations in infant and secondary treatment-related acute leukaemias.
  • These data provide a template for the design of specifically targeted therapeutics for poor prognosis MLL-associated leukaemias.
  • [MeSH-major] CpG Islands / genetics. Histone-Lysine N-Methyltransferase / chemistry. Leukemia / metabolism. Myeloid-Lymphoid Leukemia Protein / chemistry. Neoplasm Proteins / chemistry

  • MedlinePlus Health Information. consumer health - Leukemia.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 16990798.001).
  • [ISSN] 0261-4189
  • [Journal-full-title] The EMBO journal
  • [ISO-abbreviation] EMBO J.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105161083; United Kingdom / Medical Research Council / / MC/ U105459896
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Solutions; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 9007-49-2 / DNA; EC 2.1.1.- / Protein Methyltransferases; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC1589984
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72. Dorrance AM, Liu S, Yuan W, Becknell B, Arnoczky KJ, Guimond M, Strout MP, Feng L, Nakamura T, Yu L, Rush LJ, Weinstein M, Leone G, Wu L, Ferketich A, Whitman SP, Marcucci G, Caligiuri MA: Mll partial tandem duplication induces aberrant Hox expression in vivo via specific epigenetic alterations. J Clin Invest; 2006 Oct;116(10):2707-16
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  • We previously identified a rearrangement of mixed-lineage leukemia (MLL) gene (also known as ALL-1, HRX, and HTRX1), consisting of an in-frame partial tandem duplication (PTD) of exons 5 through 11 in the absence of a partner gene, occurring in approximately 4%-7% of patients with acute myeloid leukemia (AML) and normal cytogenetics, and associated with a poor prognosis.
  • The mechanism by which the MLL PTD contributes to aberrant hematopoiesis and/or leukemia is unknown.

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  • (PMID = 16981007.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / P30 AR050953-01; United States / NIAMS NIH HHS / AR / P30 AR050953; United States / NCI NIH HHS / CA / R01 CA89341; United States / NCI NIH HHS / CA / R01 CA089341; United States / NCI NIH HHS / CA / K01 CA96887; United States / NCI NIH HHS / CA / K01 CA096887; United States / NCI NIH HHS / CA / K08 CA089317
  • [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 / Histones; 0 / Homeodomain Proteins; 0 / Hoxa7 protein, mouse; 0 / Neoplasm Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 157907-48-7 / HoxA protein; 164384-16-1 / Hoxa10 protein, mouse; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse
  • [Other-IDs] NLM/ PMC1564428
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73. Sung PA, Libura J, Richardson C: Etoposide and illegitimate DNA double-strand break repair in the generation of MLL translocations: new insights and new questions. DNA Repair (Amst); 2006 Sep 8;5(9-10):1109-18
Hazardous Substances Data Bank. ETOPOSIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Faithful repair of chromosomal double-strand breaks (DSBs) is central to genome integrity and the suppression of genome rearrangements including translocations that are a hallmark of leukemia, lymphoma, and soft-tissue sarcomas [B.
  • Elliott, M. Jasin, Double-strand breaks and translocations in cancer, Cell. Mol. Life Sci.
  • Chemotherapy agents that target the essential cellular enzyme topoisomerase II (topo II) are known promoters of DSBs and are associated with therapy-related leukemias.
  • There is a clear clinical association between previous exposure to etoposide and therapy-related acute myeloid leukemia (t-AML) characterized by chromosomal rearrangements involving the mixed lineage leukemia (MLL) gene on chromosome band 11q23 [C.A.
  • Felix, Leukemias related to treatment with DNA topoisomerase II inhibitors, Med. Pediatr. Oncol.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Chromosome Breakage. DNA Damage. DNA Repair. Etoposide / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Topoisomerase II Inhibitors
  • [MeSH-minor] Chromosomes, Human, Pair 11. DNA Topoisomerases, Type II / genetics. Histone-Lysine N-Methyltransferase. Humans. Models, Genetic. Myeloid-Lymphoid Leukemia Protein. Sensitivity and Specificity

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
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  • (PMID = 16809075.001).
  • [ISSN] 1568-7864
  • [Journal-full-title] DNA repair
  • [ISO-abbreviation] DNA Repair (Amst.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / MLL protein, human; 0 / Topoisomerase II Inhibitors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 5.99.1.3 / DNA Topoisomerases, Type II
  • [Number-of-references] 94
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74. Hinrichsen L, Meyerholz A, Groos S, Ungewickell EJ: Bending a membrane: how clathrin affects budding. Proc Natl Acad Sci U S A; 2006 Jun 6;103(23):8715-20
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

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  • We have found that domains containing the adapter complex 2 (AP2)-coated vesicle adapter and the endocytic accessory proteins CALM (clathrin assembly lymphoid myeloid leukemia protein), epsin, and eps15/eps15R (EGF receptor pathway substrate 15-related) nevertheless persist at the plasma membrane.
  • [MeSH-major] Cell Membrane / metabolism. Cell Surface Extensions / metabolism. Clathrin / metabolism

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  • (PMID = 16735469.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Protein Complex 2; 0 / Adaptor Proteins, Vesicular Transport; 0 / Clathrin; 0 / epsin
  • [Other-IDs] NLM/ PMC1482644
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75. Golemović M, Sucić M, Zadro R, Mrsić S, Mikulić M, Labar B, Rajić LJ, Batinić D: IgH and TCRgamma gene rearrangements, cyclin A1 and HOXA9 gene expression in biphenotypic acute leukemias. Leuk Res; 2006 Feb;30(2):211-21
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IgH and TCRgamma gene rearrangements, cyclin A1 and HOXA9 gene expression in biphenotypic acute leukemias.
  • In this study we investigated IgH and TCRgamma gene rearrangements, cyclin A1 and HOXA9 gene expression as well as the in vitro growth of biphenotypic acute leukemia (BAL) blasts in relation to acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • This rare form of AL was identified in a total of 10 patients, comprising 4.3% of adult and 3.0% of pediatric patients with de novo AL referred to our institution during the 1999-2003 period.
  • Our results indicate that IgH and TCRgamma gene rearrangements correlated well with lymphoid BAL morphology, whereas the expression of cyclin A1 correlated with myeloid and undifferentiated BAL morphology.
  • Surprisingly, HOXA9 expression, a marker associated with myeloid cell lineage, showed no strong correlation with BAL morphology.
  • Finally, in vitro growth of blasts during a 7-day culture showed autonomous cell growth in 3/10 AML and 3/8 myeloid BAL samples tested, but not in any of the AL with lymphoid features.
  • Further studies are needed to confirm these findings and to extend research to a broader spectrum of cell markers.
  • [MeSH-major] Gene Rearrangement. Gene Rearrangement, T-Lymphocyte. Genes, T-Cell Receptor gamma. Homeodomain Proteins / genetics. Immunoglobulin Heavy Chains / genetics. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Proliferation. Child. Child, Preschool. Cyclin A / genetics. Cyclin A1. Female. Humans. Immunophenotyping. Male. Middle Aged

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  • (PMID = 16102826.001).
  • [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 / CCNA1 protein, human; 0 / Cyclin A; 0 / Cyclin A1; 0 / Homeodomain Proteins; 0 / Immunoglobulin Heavy Chains; 0 / homeobox protein HOXA9
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76. Zeiser R, Spyridonidis A, Wäsch R, Ihorst G, Grüllich C, Bertz H, Finke J: Evaluation of immunomodulatory treatment based on conventional and lineage-specific chimerism analysis in patients with myeloid malignancies after myeloablative allogeneic hematopoietic cell transplantation. Leukemia; 2005 May;19(5):814-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of immunomodulatory treatment based on conventional and lineage-specific chimerism analysis in patients with myeloid malignancies after myeloablative allogeneic hematopoietic cell transplantation.
  • Both conventional chimerism analysis (CCA) and lineage-specific chimerism analysis (LCA) have potential pitfalls as diagnostic means for the detection of minimal residual disease after allogeneic hematopoietic cell transplantation (aHCT).
  • A total of 168 individuals with acute myeloid leukemia (AML) (n = 137) and myelo dysplastic syndrome (n = 31) were investigated with CCA and LCA at mean intervals of 24 days (range: 11-116).
  • Of 32 patients, 10 who were offered donor lymphocyte infusions (DLI) treatment for increasing (n = 29) or stable (n = 3) mixed chimerism (MC) achieved at least transitory CC.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Immunotherapy, Adoptive / methods. Leukemia, Myeloid / therapy. Lymphocyte Transfusion / methods. Myelodysplastic Syndromes / therapy. Transplantation Chimera / immunology
  • [MeSH-minor] Cell Lineage / genetics. Follow-Up Studies. Humans. Recurrence. Remission Induction. Sensitivity and Specificity. Treatment Outcome

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  • (PMID = 15772700.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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77. Slany RK: The molecular biology of mixed lineage leukemia. Haematologica; 2009 Jul;94(7):984-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The molecular biology of mixed lineage leukemia.
  • Mixed lineage leukemia is a very aggressive blood cancer that predominantly occurs in pediatric patients.
  • In contrast to other types of childhood acute leukemias, mixed lineage leukemia presents with a dismal prognosis and despite the availability of advanced treatment methods cure rates have stagnated over the last years.
  • Mixed lineage leukemia is characterized by the presence of MLL fusion proteins that are the result of chromosomal translocations affecting the MLL gene at 11q23.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Child. Chromatin / chemistry. Chromatin / metabolism. DNA Methylation. Dimerization. Genes, Homeobox. Histone-Lysine N-Methyltransferase. Humans. Models, Biological. Myeloid-Lymphoid Leukemia Protein / genetics. Protein Structure, Tertiary. RNA Polymerase II / metabolism. Recombinant Fusion Proteins / chemistry. Time Factors. Transcription, Genetic

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  • (PMID = 19535349.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Chromatin; 0 / MLL protein, human; 0 / Recombinant Fusion Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.7.- / RNA Polymerase II
  • [Number-of-references] 122
  • [Other-IDs] NLM/ PMC2704309
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78. Sucić M, Batinić D, Zadro R, Mrsić S, Labar B: [Cytomorphology of acute mixed leukemia]. Acta Med Croatica; 2008 Oct;62(4):379-85

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Cytomorphology of acute mixed leukemia].
  • Biphenotypic acute leukemias (AL) with blasts expressing both myeloid and lymphoid antigens are grouped with undifferentiated AL and bilineal AL in the group of AL of ambiguous lineage.
  • Not all AL with myeloid and lymphoid antigens (ALMy+Ly) are true biphenotypic AL.
  • According to EGIL scoring system, true biphenotypic ALMy+Ly are those with a sum of antigens 2 or more points for both myeloid and lymphoid lineage or for B and T lineage.
  • The aim of this study was to compare cytomorphology and immunophenotype of AL to better understand the relation of certain AL morphology, immunophenotype, cytogenetics and molecular biology of biphenotypic AL.
  • PATIENTS AND METHODS: The study included a group of 169 AL patients treated from 1985 till 1991, and a group of 102 AL patients treated from 1993 till 1996 at Zagreb University Hospital Center.
  • RESULTS AND DISCUSSION: In the group of 169 adult AL patients, 116 were cytomorphologically classified as acute myeloblastic leukemias (AML), 35 as acute lymphoblastic leukemias (ALL) and 18 as acute undifferentiated leukemias (ANLM).
  • In 6 (3.4%) of 169 AL patients, blasts expressed both myeloid and lymphoid antigens.
  • In 64 patients cytomorphologically classified into AML subgroup out of 102 AL patients, there were 15 (14.7%/102; 23.4%/64) AML with lymphoid antigens (AMLLy+).
  • In 35 patients cytomorphologically diagnosed as ALL and 3 as ANLM out of 102 AL, there were 4 (3.9%/102; 10.5%/38) ALL with myeloid antigens (ALLMy+).
  • The incidence of mixed AL in 102 AL was more consistent with other studies, pointing to the necessity of myeloperoxidase (MPO), CD7 and TdT determination as part of standard immunophenotyping for better recognition of mixed AL.
  • In one ANLM,My+ out of 169 AL and also one ANLM,My+ out of 102 AL, blasts were cytomorphologically undifferentiated; in 3 ALLMy+ of 102 AL blasts expressed lymphoid morphology.
  • According to EGIL scoring system, among 15 AMLLy+ of 102 AL there were 4 true biphenotypic ALMy+Ly (1 M1, 2 M3, 1 M4), and in 4 ALMy+Ly with undifferentiated and lymphoid morphology there were 2 true biphenotypic AL (1 L2; 1 ANLM).
  • In 3 ALLB+T out of 35 ALL, one was interlineal biphenotypic AL.
  • These observations are consistent with other studies and WHO determinations indicating that the majority of true biphenotypic leukemias are associated with immature monoblastic or myeloid cytomorphology or with lymphoid or undifferentiated characteristics, but may also express any AML cytomorphology type.
  • Thus, there is no direct correlation of leukemic cell cytomorphology and biphenotypic AL immunophenotype.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / pathology
  • [MeSH-minor] Acute Disease. Humans. Immunophenotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19205415.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Croatia
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79. Mueller D, García-Cuéllar MP, Bach C, Buhl S, Maethner E, Slany RK: Misguided transcriptional elongation causes mixed lineage leukemia. PLoS Biol; 2009 Nov;7(11):e1000249
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Misguided transcriptional elongation causes mixed lineage leukemia.
  • Fusion proteins composed of the histone methyltransferase mixed-lineage leukemia (MLL) and a variety of unrelated fusion partners are highly leukemogenic.
  • Despite their prevalence, particularly in pediatric acute leukemia, many molecular details of their transforming mechanism are unknown.
  • Here, we provide mechanistic insight into the function of MLL fusions, demonstrating that they capture a transcriptional elongation complex that has been previously found associated with the eleven-nineteen leukemia protein (ENL).
  • [MeSH-major] Cell Transformation, Neoplastic. Gene Expression Regulation, Neoplastic. Leukemia / metabolism. Myeloid-Lymphoid Leukemia Protein / metabolism. Transcriptional Elongation Factors / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Chromatin Assembly and Disassembly. Cyclin-Dependent Kinase 9 / antagonists & inhibitors. Flavonoids. Histone-Lysine N-Methyltransferase. Humans. Mice. Mice, Inbred BALB C. Piperidines

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  • (PMID = 19956800.001).
  • [ISSN] 1545-7885
  • [Journal-full-title] PLoS biology
  • [ISO-abbreviation] PLoS Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ELL protein, human; 0 / Flavonoids; 0 / MLL protein, human; 0 / Piperidines; 0 / Transcriptional Elongation Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 45AD6X575G / alvocidib; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.11.22 / Cyclin-Dependent Kinase 9
  • [Other-IDs] NLM/ PMC2774266
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80. Rubnitz JE, Inaba H, Dahl G, Ribeiro RC, Bowman WP, Taub J, Pounds S, Razzouk BI, Lacayo NJ, Cao X, Meshinchi S, Degar B, Airewele G, Raimondi SC, Onciu M, Coustan-Smith E, Downing JR, Leung W, Pui CH, Campana D: Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial. Lancet Oncol; 2010 Jun;11(6):543-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial.
  • BACKGROUND: We sought to improve outcome in patients with childhood acute myeloid leukaemia (AML) by applying risk-directed therapy that was based on genetic abnormalities of the leukaemic cells and measurements of minimal residual disease (MRD) done by flow cytometry during treatment.
  • METHODS: From Oct 13, 2002, to June 19, 2008, 232 patients with de-novo AML (n=206), therapy-related or myelodysplasia-related AML (n=12), or mixed-lineage leukaemia (n=14) were enrolled at eight centres.
  • Induction 2 consisted of ADE with or without gemtuzumab ozogamicin (GO anti-CD33 monoclonal antibody); consolidation therapy included three additional courses of chemotherapy or haematopoietic stem-cell transplantation (HSCT).
  • Both MRD and genetic abnormalities at diagnosis were used to determine the final risk classification.
  • Other analyses were limited to the 216 patients with AML, excluding those with mixed-lineage leukaemia.
  • Induction failures included two deaths from toxic effects and ten cases of resistant leukaemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adolescent. Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Cytarabine / administration & dosage. Cytogenetic Analysis. Daunorubicin / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Flow Cytometry. Humans. Infant. Infant, Newborn. Male. Neoplasm, Residual. Remission Induction. Survival Rate. Young Adult

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 20451454.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00136084
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA115422; United States / NCI NIH HHS / CA / R01 CA115422-02
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 93NS566KF7 / gemtuzumab; ZS7284E0ZP / Daunorubicin; DAV regimen
  • [Other-IDs] NLM/ NIHMS319127; NLM/ PMC3171799
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81. Pieters R: Infant acute lymphoblastic leukemia: Lessons learned and future directions. Curr Hematol Malig Rep; 2009 Jul;4(3):167-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Infant acute lymphoblastic leukemia: Lessons learned and future directions.
  • Compared with acute lymphoblastic leukemia (ALL) in older children, ALL in infants has a dismal outcome because rearrangements of the mixed-lineage leukemia (MLL) gene occur in about 80% of these patients, leading to an aggressive type of leukemia.
  • [MeSH-major] Gene Rearrangement. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 20425430.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 52
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82. Lin C, Smith ER, Takahashi H, Lai KC, Martin-Brown S, Florens L, Washburn MP, Conaway JW, Conaway RC, Shilatifard A: AFF4, a component of the ELL/P-TEFb elongation complex and a shared subunit of MLL chimeras, can link transcription elongation to leukemia. Mol Cell; 2010 Feb 12;37(3):429-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AFF4, a component of the ELL/P-TEFb elongation complex and a shared subunit of MLL chimeras, can link transcription elongation to leukemia.
  • Chromosomal translocations involving the MLL gene are associated with infant acute lymphoblastic and mixed lineage leukemia.
  • There are a large number of translocation partners of MLL that share very little sequence or seemingly functional similarities; however, their translocations into MLL result in the pathogenesis of leukemia.
  • To define the molecular reason why these translocations result in the pathogenesis of leukemia, we purified several of the commonly occurring MLL chimeras.
  • Knockdown of AFF4 in leukemic cells shows reduction in MLL chimera target gene expression, suggesting that AFF4/SEC could be a key regulator in the pathogenesis of leukemia through many of the MLL partners.

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  • (PMID = 20159561.001).
  • [ISSN] 1097-4164
  • [Journal-full-title] Molecular cell
  • [ISO-abbreviation] Mol. Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA089455; United States / NIGMS NIH HHS / GM / GM041628-22; United States / NCI NIH HHS / CA / R01CA089455-10; United States / NIGMS NIH HHS / GM / R01 GM041628; United States / NCI NIH HHS / CA / CA089455-09; United States / NIGMS NIH HHS / GM / R01 GM041628-24; United States / NIGMS NIH HHS / GM / R37 GM041628-22; United States / NIGMS NIH HHS / GM / R37 GM041628; United States / NCI NIH HHS / CA / R01 CA150265; United States / NCI NIH HHS / CA / R01 CA089455-09; United States / NIGMS NIH HHS / GM / GM041628-24
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AFF4 protein, human; 0 / Drosophila Proteins; 0 / ELL protein, human; 0 / HSP70 Heat-Shock Proteins; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Repressor Proteins; 0 / Transcriptional Elongation Factors; 0 / homeobox protein HOXA9; 140441-81-2 / HOXA10 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.11.- / Positive Transcriptional Elongation Factor B
  • [Other-IDs] NLM/ NIHMS177069; NLM/ PMC2872029
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83. Bardini M, Spinelli R, Bungaro S, Mangano E, Corral L, Cifola I, Fazio G, Giordan M, Basso G, De Rossi G, Biondi A, Battaglia C, Cazzaniga G: DNA copy-number abnormalities do not occur in infant ALL with t(4;11)/MLL-AF4. Leukemia; 2010 Jan;24(1):169-76
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  • The pathogenesis of infant acute lymphoblastic leukemia (ALL) is still not well defined.
  • Short latency to leukemia and very high concordance rate for ALL in Mixed-Lineage Leukemia (MLL)-positive infant twins suggest that the MLL rearrangement itself could be sufficient for overt leukemia.
  • Attempts to generate a suitable mouse model for MLL-AF4-positive ALL did not thoroughly resolve the issue of whether cooperating mutations are required to reduce latency and to generate overt leukemia in vivo.
  • In contrast to pediatric, adolescent and adult ALL cases, the MLL rearrangement in infant ALL is associated with an exceptionally low frequency of copy-number abnormalities, thus confirming the unique nature of this disease.
  • By contrast, additional genetic aberrations are acquired at disease relapse.
  • It can be argued that the MLL rearrangement as a first hit, rather than inducing the acquisition of additional genetic lesions, has a major role to drive and hasten the onset of leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 4. Gene Dosage. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 19907438.001).
  • [ISSN] 1476-5551
  • [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 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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84. Bhojwani D, Howard SC, Pui CH: High-risk childhood acute lymphoblastic leukemia. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S222-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-risk childhood acute lymphoblastic leukemia.
  • Although most children with acute lymphoblastic leukemia (ALL) are cured, certain subsets have a high risk of relapse.
  • Though early treatment response can be assessed by the peripheral blast cell count after 1 week of single-agent glucocorticoid treatment or percent of bone marrow blasts by morphology after 1 or 2 weeks of multiagent induction treatment, determination of minimal residual disease by polymerase chain reaction (PCR) or flow cytometry after 2 to 6 weeks of induction is the most precise and useful measure.
  • Infants with mixed-lineage leukemia (MLL)-rearranged ALL comprise a very poor-risk group wherein further intensification of chemotherapy causes significant toxicity.
  • Hybrid protocols incorporating drugs effective for acute myeloid leukemia could improve survival, a strategy being tested in international trials.
  • New agents and methods to overcome resistance are under investigation, and allogeneic stem cell transplantation is recommended for certain subsets of patients, for example those with Ph+ and T-cell ALL with poor early response.
  • Genome-wide interrogation of leukemic cell genetic abnormalities and germline genetic variations promise to identify new molecular targets for therapy.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Glucocorticoids / therapeutic use. Humans. Infant. Neoplasm, Residual / drug therapy. Polymerase Chain Reaction. Recurrence. Remission Induction. Treatment Outcome

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  • (PMID = 19778845.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA021765-31; United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glucocorticoids
  • [Number-of-references] 92
  • [Other-IDs] NLM/ NIHMS163517; NLM/ PMC2814411
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85. Zangrando A, Dell'orto MC, Te Kronnie G, Basso G: MLL rearrangements in pediatric acute lymphoblastic and myeloblastic leukemias: MLL specific and lineage specific signatures. BMC Med Genomics; 2009;2:36
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  • [Title] MLL rearrangements in pediatric acute lymphoblastic and myeloblastic leukemias: MLL specific and lineage specific signatures.
  • BACKGROUND: The presence of MLL rearrangements in acute leukemia results in a complex number of biological modifications that still remain largely unexplained.
  • Armstrong et al. proposed MLL rearrangement positive ALL as a distinct subgroup, separated from acute lymphoblastic (ALL) and myeloblastic leukemia (AML), with a specific gene expression profile.
  • Here we show that MLL, from both ALL and AML origin, share a signature identified by a small set of genes suggesting a common genetic disregulation that could be at the basis of mixed lineage leukemia in both phenotypes.
  • RESULTS: We identified a MLL translocation-specific (379 probes) signature and a phenotype-specific (622 probes) signature which have been tested using unsupervised methods.
  • A final subset of 14 genes grants the characterization of acute leukemia patients with and without MLL rearrangements.
  • CONCLUSION: Our study demonstrated that a small subset of genes identifies MLL-specific rearrangements and clearly separates acute leukemia samples according to lineage origin.

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  • (PMID = 19549311.001).
  • [ISSN] 1755-8794
  • [Journal-full-title] BMC medical genomics
  • [ISO-abbreviation] BMC Med Genomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2709660
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86. Matsumoto Y, Taki T, Fujimoto Y, Taniguchi K, Shimizu D, Shimura K, Uchiyama H, Kuroda J, Nomura K, Inaba T, Shimazaki C, Horiike S, Taniwaki M: Monosomies 7p and 12p and FLT3 internal tandem duplication: possible markers for diagnosis of T/myeloid biphenotypic acute leukemia and its clonal evolution. Int J Hematol; 2009 Apr;89(3):352-8
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  • [Title] Monosomies 7p and 12p and FLT3 internal tandem duplication: possible markers for diagnosis of T/myeloid biphenotypic acute leukemia and its clonal evolution.
  • Biphenotypic acute leukemia co-expressing T-lymphoid and myeloid markers is rare, accounting for less than 1% of acute leukemias.
  • Recurrence of monosomies 7p and/or 12p in T/myeloid biphenotypic acute leukemia has been reported.
  • We treated a patient with T/myeloid biphenotypic acute leukemia showing clonal chromosomal and genetic abnormalities including dic(7;12)(p11;p11) and Fms-like tyrosine kinase 3 (FLT3)-internal tandem duplication.
  • Cytogenetic analysis of both bone marrow and lymph node cells disclosed that the patient's lymph node leukemia cells had chromosomal abnormalities in addition to dic(7;12).
  • Our findings suggest that the leukemia cells of systemic lymphadenopathy had evolved as secondary cells from marrow leukemia cells.
  • The patient was successfully treated with induction chemotherapy for acute myeloid leukemia followed by allogeneic bone marrow transplantation.
  • [MeSH-major] Biomarkers, Tumor / genetics. Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 7 / genetics. Gene Duplication. Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / enzymology. fms-Like Tyrosine Kinase 3 / metabolism

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  • (PMID = 19308660.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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87. de Jesus Marques-Salles T, Liehr T, Mkrtchyan H, Raimondi SC, Tavares de Souza M, de Figueiredo AF, Rouxinol S, Jordy Macedo FC, Abdelhay E, Santos N, Macedo Silva ML: A new chromosomal three-way rearrangement involving MLL masked by a t(9;19)(p11;p13) in an infant with acute myeloid leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):59-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new chromosomal three-way rearrangement involving MLL masked by a t(9;19)(p11;p13) in an infant with acute myeloid leukemia.
  • Infants diagnosed with acute myelogenous leukemia (AML) are likely to have subtypes M4 or M5 characterized by 11q23 abnormalities like a t(9;11)(p22;q23).
  • Detection of all possible types of chromosomal abnormalities, including mixed lineage leukemia (MLL) gene rearrangements at 11q23, is of importance for the identification of biological subgroups, which might differ in drug resistance and/or clinical outcome.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic / genetics

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  • (PMID = 19167614.001).
  • [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, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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88. Kakihana K, Ohashi K, Sakai F, Kamata N, Hosomi Y, Nishiwaki M, Yokoyama R, Kobayashi T, Yamashita T, Akiyama H, Sakamaki H: Leukemic infiltration of the lung following allogeneic hematopoietic stem cell transplantation. Int J Hematol; 2009 Jan;89(1):118-22
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  • [Title] Leukemic infiltration of the lung following allogeneic hematopoietic stem cell transplantation.
  • Pulmonary leukemic infiltration (PLI) is more common than generally recognized, but accurate antemortem diagnosis with pathological proof is rarely achieved.
  • We describe herein the clinical courses of two patients with PLI following hematopoietic stem cell transplantation (HSCT).
  • One case is a male patient with acute biphenotypic leukemia, and the other is a female patient with myelodysplastic syndrome.
  • Moreover, the former case presented PLI as the initial manifestation of relapsed leukemia and the latter was accompanied with the fungal pneumonia.
  • High-resolution computed tomography (HRCT) of the chest at onset of PLI showed diffuse small nodular lesions along peribronchovascular bundle, and diagnosis of leukemic infiltration was made based on pathological findings obtained from transbronchial lung biopsy.
  • Thus, radiological and pathological corroborating assessment was important to reach the correct diagnosis.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Leukemic Infiltration / diagnosis. Lung Neoplasms / etiology
  • [MeSH-minor] Adult. Female. Humans. Leukemia / pathology. Lung / pathology. Male. Middle Aged. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / etiology. Opportunistic Infections. Transplantation, Homologous

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  • (PMID = 19093164.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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89. Whelan JT, Ludwig DL, Bertrand FE: HoxA9 induces insulin-like growth factor-1 receptor expression in B-lineage acute lymphoblastic leukemia. Leukemia; 2008 Jun;22(6):1161-9
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  • [Title] HoxA9 induces insulin-like growth factor-1 receptor expression in B-lineage acute lymphoblastic leukemia.
  • Deregulation of Hox gene expression is frequently associated with acute leukemia.
  • HoxA9 is the most commonly overexpressed Hox gene in acute leukemia.
  • We have generated a conditional model of HoxA9 activity in the stromal cell dependent, HoxA9 negative, pre-B-cell line B-lineage-2 (BLIN-2).
  • Conditional HoxA9 activation in BLIN-2 resulted in increased proliferation in the presence and absence of stromal cell support.
  • IGF-1R expression correlated with endogenous HoxA9 expression in a small panel of mixed lineage leukemia (MLL)/AF4 cell lines. siRNA knockdown of endogenous HoxA9 expression in the MLL/AF4-positive cell line RS4;11 resulted in loss of IGF-1R expression.
  • These data indicate that HoxA9 overexpression induces IGF-1R expression and subsequently promotes leukemic cell growth.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / physiology. Homeodomain Proteins / physiology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, IGF Type 1 / genetics
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Blotting, Southern. Blotting, Western. Cell Proliferation. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunoprecipitation. Insulin-Like Growth Factor I / metabolism. Myeloid-Lymphoid Leukemia Protein / metabolism. Oncogene Proteins, Fusion / metabolism. Phosphorylation. Proto-Oncogene Proteins c-myc. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Retroviridae / genetics. Reverse Transcriptase Polymerase Chain Reaction. Stromal Cells / metabolism. Tumor Cells, Cultured

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  • (PMID = 18337761.001).
  • [ISSN] 1476-5551
  • [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 / Antibodies, Monoclonal; 0 / Homeodomain Proteins; 0 / MLL-AF4 fusion protein, human; 0 / MYC protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-myc; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / homeobox protein HOXA9; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 67763-96-6 / Insulin-Like Growth Factor I; EC 2.7.10.1 / Receptor, IGF Type 1
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90. Fender AB, Gust A, Wang N, Scott GA, Mercurio MG: Congenital leukemia cutis. Pediatr Dermatol; 2008 Jan-Feb;25(1):34-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Congenital leukemia cutis.
  • We describe a premature neonate who was born with pancytopenia and a single subcutaneous nodule on her right lower extremity.
  • Immunohistochemical stains and bone marrow examination confirmed a diagnosis of acute myelogenous leukemia.
  • A split in the mixed lineage leukemia gene was identified by fluorescence in situ hybridization.
  • As leukemia cutis more typically presents as multiple infiltrative papules, nodules, or plaques, we stress the importance of including leukemia in the differential diagnosis of a solitary nodule in a neonate.
  • [MeSH-major] Infant, Premature. Leukemia, Myeloid, Acute / congenital. Leukemia, Myeloid, Acute / pathology. Neoplasm Invasiveness / pathology. Skin Neoplasms / congenital. Skin Neoplasms / pathology
  • [MeSH-minor] Biopsy, Needle. Bone Marrow / pathology. Chromosome Aberrations. Chromosomes, Human, X. Cytogenetics / methods. Disease Progression. Fatal Outcome. Female. Humans. Immunohistochemistry. Infant, Newborn. Karyotyping. Risk Assessment

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  • (PMID = 18304150.001).
  • [ISSN] 1525-1470
  • [Journal-full-title] Pediatric dermatology
  • [ISO-abbreviation] Pediatr Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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91. Krivtsov AV, Armstrong SA: MLL translocations, histone modifications and leukaemia stem-cell development. Nat Rev Cancer; 2007 Nov;7(11):823-33
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  • [Title] MLL translocations, histone modifications and leukaemia stem-cell development.
  • Translocations that involve the mixed lineage leukaemia (MLL) gene identify a unique group of acute leukaemias, and often predict a poor prognosis.
  • A key feature of MLL fusion proteins is their ability to efficiently transform haematopoietic cells into leukaemia stem cells.
  • The link between a chromatin modulator and leukaemia stem cells provides support for epigenetic landscapes as an important part of leukaemia and normal stem-cell development.
  • [MeSH-major] Epigenesis, Genetic / physiology. Gene Expression Regulation. Histone-Lysine N-Methyltransferase / physiology. Histones / metabolism. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / physiology
  • [MeSH-minor] Adult. Animals. Cell Division / physiology. Cell Transformation, Neoplastic / genetics. Child. Chromatin / ultrastructure. Gene Expression Regulation, Developmental. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Humans. Infant. Methylation. Mice. Neoplastic Stem Cells / cytology. Oncogene Proteins, Fusion / chemistry. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / physiology. Prognosis. Protein Methyltransferases. Protein Processing, Post-Translational

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  • (PMID = 17957188.001).
  • [ISSN] 1474-1768
  • [Journal-full-title] Nature reviews. Cancer
  • [ISO-abbreviation] Nat. Rev. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromatin; 0 / Histones; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.- / Protein Methyltransferases; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse
  • [Number-of-references] 121
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92. Kuroda N, Mizobuchi M, Shimamura Y, Daibata M, Miyoshi I, Ohara M, Hirouchi T, Mizuno K, Lee GH: Bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of acute biphenotypic leukemia. APMIS; 2006 Dec;114(12):908-11
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  • [Title] Bridging necrosis and reticulin bridging fibrosis induced by intrahepatic involvement of acute biphenotypic leukemia.
  • A 47-year-old Japanese woman was diagnosed as having acute biphenotypic leukemia with association of t(9;22)(q34;q11).
  • In conclusion, extensive intrahepatic involvement by neoplastic cells in adult acute biphenotypic leukemia may cause the unusual "disorganized" hepatic fibrosis.
  • [MeSH-major] Leukemia, Myeloid, Acute / pathology. Liver Cirrhosis / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

  • Genetic Alliance. consumer health - Acute Biphenotypic Leukemia.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
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  • (PMID = 17207092.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / Reticulin; 0 / Transforming Growth Factor beta1; 0 / platelet-derived growth factor BB; 9007-34-5 / Collagen
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93. Matsuda K, Hidaka E, Ishida F, Yamauchi K, Makishima H, Ito T, Suzuki T, Imagawa E, Sano K, Katsuyama T, Ota H: A case of acute myelogenous leukemia with MLL-AF10 fusion caused by insertion of 5' MLL into 10p12, with concurrent 3' MLL deletion. Cancer Genet Cytogenet; 2006 Nov;171(1):24-30
Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of acute myelogenous leukemia with MLL-AF10 fusion caused by insertion of 5' MLL into 10p12, with concurrent 3' MLL deletion.
  • Structural abnormalities involving the mixed-lineage leukemia (MLL) gene on 11q23 ha