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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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2. 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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3. 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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4. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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5. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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6. 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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  • [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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7. 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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  • [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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8. 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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9. 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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10. 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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11. 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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12. 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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13. 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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14. 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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15. 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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16. 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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17. 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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18. 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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19. 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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  • [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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20. 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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  • [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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21. 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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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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  • 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. 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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26. 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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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. Schimmer AD: Induction of apoptosis in lymphoid and myeloid leukemia. Curr Oncol Rep; 2006 Nov;8(6):430-6
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  • [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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29. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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


30. 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
Genetic Alliance. consumer health - Acute Biphenotypic Leukemia.

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  • [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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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

  • Genetic Alliance. consumer health - Acute Biphenotypic Leukemia.
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  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
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  • (PMID = 18288568.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD79; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CD79A protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3
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32. 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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33. 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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34. 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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35. 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
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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

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  • 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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36. 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
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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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37. 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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  • [CommentIn] Lancet Oncol. 2010 Jun;11(6):502-3 [20522371.001]
  • (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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38. 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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39. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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40. Kinjo K, Sandoval S, Sakamoto KM, Shankar DB: The role of CREB as a proto-oncogene in hematopoiesis. Cell Cycle; 2005 Sep;4(9):1134-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cyclic-AMP response element binding protein (CREB) is a transcription factor that functions in glucose homeostasis, growth-factor- dependent cell survival, proliferation and memory.
  • Data from our laboratory shows that a majority of patients with acute lymphoid and myeloid leukemia overexpress CREB in the bone marrow.
  • CREB overexpression is associated with poor initial outcome of clinical disease in AML patients.
  • To study its role in hematopoiesis, we overexpressed CREB in leukemia cell lines and in mice.
  • CREB overexpression resulted in increased survival and proliferation of myeloid cells and blast-transformation of bone marrow progenitor cells from transgenic mice expressing CREB in the myeloid lineage.
  • CREB transgenic mice also develop myeloproliferative disease after one year.
  • Thus, CREB acts as a proto-oncogene to regulate hematopoiesis and contributes to the leukemia phenotype.
  • Our results suggest that CREB-dependent pathways may serve as targets for directed therapies in leukemia in the future.
  • [MeSH-minor] Animals. Bone Marrow Cells / metabolism. Cell Line, Tumor. Cell Proliferation. Cell Survival. Cell Transformation, Neoplastic. Gene Expression Regulation, Neoplastic. Glucose / metabolism. Granulocyte-Macrophage Colony-Stimulating Factor / metabolism. Humans. Leukemia, Myeloid, Acute / metabolism. Mice. Mice, Transgenic. Neoplasms / metabolism. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins / chemistry. Signal Transduction. Up-Regulation

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  • (PMID = 16096372.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / Proto-Oncogene Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; IY9XDZ35W2 / Glucose
  • [Number-of-references] 18
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41. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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42. 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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43. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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44. 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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  • (PMID = 19918465.001).
  • [ISSN] 1757-1626
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  • [ISO-abbreviation] Cases J
  • [Language] eng
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  • [Other-IDs] NLM/ PMC2769415
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45. 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 .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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46. 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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47. 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
The Lens. Cited by Patents in .

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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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48. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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49. 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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50. 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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51. 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
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  • [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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52. Kaćanski N, Konstantinidis N, Kolarović J, Slavković B, Vujić D: [Biphenotypic acute leukaemia: case reports of two paediatric patients]. Med Pregl; 2010 Nov-Dec;63(11-12):867-9
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  • [Title] [Biphenotypic acute leukaemia: case reports of two paediatric patients].
  • INTRODUCTION: Biphenotypic acute leukaemia is an uncommon type of leukaemia whose blasts co-express myeloid and B-or T-lymphoid antigens.
  • CASE REPORT: We describe two cases of paediatric patients with biphenotypic acute leukaemia.
  • A four-year-old female patient was found to have myeloid and B-lymphoid associated antigens in the same blast cells.
  • She was treated with combined acute myeloid leukaemia/acute lymphoblastic leukaemia induction therapy followed by autologous stem cell transplantation.
  • The patient died due to the complications of stem cell transplantation procedure.
  • Another patient was a 20-month-old girl with myeloid and T-lymphoid associated antigens in the blast cells and with normal karyotype.
  • She received acute myeloid leukaemia induction therapy.
  • DISCUSSION: Immunophenotype is essential to establish the diagnosis of biphenotypic acute leukaemia according to the scoring system adopted by the European Group of Immunological Classification of Leukaemia.
  • There is no agreement about uniformity in treatment for the patients with this type of leukaemia.
  • Biphenotypic acute leukaemia is a high risk leukaemia which requires a more intensive treatment.
  • CONCLUSION: Therapy for every patient with biphenotypic acute leukaemia should depend on their immunophenotype and gene rearrangement profiles.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy

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  • (PMID = 21553470.001).
  • [ISSN] 0025-8105
  • [Journal-full-title] Medicinski pregled
  • [ISO-abbreviation] Med. Pregl.
  • [Language] srp
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Serbia
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53. Boatsman EE, Fu CH, Song SX, Moore TB: Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation. J Pediatr Hematol Oncol; 2010 Mar;32(2):e57-60
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  • [Title] Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation.
  • INTRODUCTION: Infant acute lymphoblastic leukemia (ALL) is considered a high-risk entity.
  • By morphology, infant ALL is classified as a lymphoid lineage leukemia; however, its physiologic behavior has brought many to consider it a pathologic hybrid between lymphoid leukemia and myeloid leukemias.
  • As such, standard of care currently employs the use of chemotherapeutic agents used commonly in ALL protocols and agents typically reserved for the treatment of myelogenous lineage leukemias.
  • The role of hematopoietic stem cell transplantation and graft-versus-leukemia effect in these patients has not been well studied.
  • CASE PRESENTATION: An earlier healthy 9-week-old Hispanic male diagnosed with precursor B-cell lymphoblastic leukemia was treated with protocol P9407 and matched sibling hematopoietic stem cell transplantation.
  • The sole antigraft-versus-host disease (GVHD) agent, cyclosporine, was discontinued.
  • He remains disease free more than 2 years posttransplant.
  • CONCLUSION: Traditionally, graft-versus-leukemia effect was thought to contribute therapeutically little to the treatment of ALL by hematopoietic stem cell transplantation (HSCT).
  • The effects of graft-versus-leukemia immunologic phenomenon in our patient with infant acute lymphoblastic leukemia underscore the potential that infant ALL may not be entirely the same biologic entity as standard pediatric ALL and may be more responsive than understood earlier.
  • Therapeutic response and appearance of GVHD after the withdrawal of immunosuppression in this patient provides evidence that graft-versus-leukemia effect may play a role in disease control in infant ALL after HSCT.
  • This suggests that other immunotherapeutic interventions in the context of relapse may offer potential clinical benefit in this disease.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 20168246.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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54. Guo Y, Chen YM, Zou Y, Chen XJ, Zhang L, Wang SC, Zhu XF: [Biologic features of 688 cases of childhood acute leukemia-a single centre retrospective study]. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Oct;11(10):793-6
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  • [Title] [Biologic features of 688 cases of childhood acute leukemia-a single centre retrospective study].
  • OBJECTIVE: To investigate the biologic features of childhood acute leukemia in the northern region of China through a small cohort study in a single center.
  • METHODS: The medical records of 688 children with acute leukemia (age< or =15 years) who were initially diagnosed at Blood Disease Hospital of Chinese Academy of Medical Sciences from October 2003 to June 2006 were retrospectively studied.
  • RESULTS: Four hundred children were diagnosed as acute lymphoblastic leukemia (ALL), with a peak incidence at ages of 1-4 years.
  • Two hundred and eighteen children were classified into B-cell ALL, and 34 into T-cell ALL.
  • E2A-PBX1 fusion gene was expressed in 3.9% of children with B-cell ALL.
  • Two hundred and twenty-two children were diagnosed as acute myeloid leukemia (AML), with a peak incidence at ages of 10-15 years.
  • Acute hybrid leukemia (AHL) was confirmed in 24 children (4.2%), with a median age of 9 years.
  • Seventy-four percent of the children with (AHL) had mainly CD13 and CD33 expression in myeloid antigen integral.
  • CONCLUSIONS: There are differences in the biologic features of childhood acute leukemia between the northern region of China and other regions and races, which suggests that there might be differences in the pathogenesis of childhood acute leukemia in different environmental exposures.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19849934.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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55. Nishiuchi T, Ohnishi H, Kamada R, Kikuchi F, Shintani T, Waki F, Kitanaka A, Kubota Y, Tanaka T, Ishida T: Acute leukemia of ambiguous lineage, biphenotype, without CD34, TdT or TCR-rearrangement. Intern Med; 2009;48(16):1437-41

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  • [Title] Acute leukemia of ambiguous lineage, biphenotype, without CD34, TdT or TCR-rearrangement.
  • Biphenotypic acute leukemia (BAL) is a rare entity that comprises 0.5-3% of all acute leukemias and probably arises from multipotent progenitor cells.
  • We report the case of a 41-year-old man with BAL having myeloid and T-lymphoid lineage phenotypes.
  • This pattern is rarely encountered and suggests that the blast cells were possibly considered immature with aspects of differentiation indicating myeloid lineage, rather than T-lymphoid lineage.
  • [MeSH-major] Antigens, CD34 / genetics. Cell Lineage / genetics. DNA Nucleotidylexotransferase / genetics. Gene Rearrangement / genetics. Leukemia, Biphenotypic, Acute / genetics. Receptors, Antigen, T-Cell. Receptors, Antigen, T-Cell, alpha-beta / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics

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  • (PMID = 19687594.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; EC 2.7.7.31 / DNA Nucleotidylexotransferase
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56. Iacobucci I, Storlazzi CT, Cilloni D, Lonetti A, Ottaviani E, Soverini S, Astolfi A, Chiaretti S, Vitale A, Messa F, Impera L, Baldazzi C, D'Addabbo P, Papayannidis C, Lonoce A, Colarossi S, Vignetti M, Piccaluga PP, Paolini S, Russo D, Pane F, Saglio G, Baccarani M, Foà R, Martinelli G: Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto Acute Leukemia Working Party (GIMEMA AL WP). Blood; 2009 Sep 3;114(10):2159-67
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  • [Title] Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto Acute Leukemia Working Party (GIMEMA AL WP).
  • The BCR-ABL1 fusion gene defines the subgroup of acute lymphoblastic leukemia (ALL) with the worst clinical prognosis.
  • The IKZF1 deletion also was identified in the progression of chronic myeloid leukemia to lymphoid blast crisis (66%) but never in myeloid blast crisis or chronic-phase chronic myeloid leukemia or in patients with acute myeloid leukemia.
  • [MeSH-major] Base Sequence / genetics. Chromosomes, Human, Pair 7 / genetics. Fusion Proteins, bcr-abl / genetics. Ikaros Transcription Factor / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion
  • [MeSH-minor] Adolescent. Adult. Aged. Blast Crisis / genetics. Blast Crisis / metabolism. Cell Line, Tumor. Codon, Initiator / genetics. Codon, Initiator / metabolism. Cohort Studies. Exons / genetics. Female. Gene Expression Regulation, Leukemic / genetics. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Male. Microarray Analysis. Middle Aged. Polymorphism, Single Nucleotide

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  • [ErratumIn] Blood. 2010 Sep 23;116(12):2196
  • (PMID = 19589926.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Initiator; 0 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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57. Gujral S, Polampalli S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Amare P, Arora B, Banavali SD, Nair CN: Clinico-hematological profile in biphenotypic acute leukemia. Indian J Cancer; 2009 Apr-Jun;46(2):160-8
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  • [Title] Clinico-hematological profile in biphenotypic acute leukemia.
  • BACKGROUND: We present a clinico-hematological profile and treatment outcome of Biphenotypic Acute Leukemia (BAL).
  • MATERIAL AND METHODS: Diagnosis was based on WHO classification, including clinical details, morphology, cytochemistry, immunophenotyping, and molecular genetics.
  • We included those cases, which fulfilled the European Group for the Immunological Characterization of Acute Leukemia's (EGIL's) scoring system criteria for the diagnosis of BAL, as per recommendation of the WHO classification.
  • B-Myeloid (14 cases) followed by T-Myeloid BAL (13 cases) were the commonest subtypes.
  • Polymorphous population of blasts (16 cases) was commonly associated with T-Myeloid BAL (10 cases).
  • BCR ABL fusion positivity was a common cytogenetic abnormality (seven cases).
  • CONCLUSIONS: Pediatric BAL and T-B lymphoid BAL have a better prognosis.
  • BCR-ABL expression is an important prognostic factor, as these cases will be labeled as Chronic myeloid leukemia (CML) in blast crisis with biphenotypic expression and treated accordingly.
  • [MeSH-major] Immunophenotyping. Leukemia, Biphenotypic, Acute / blood. Leukemia, Biphenotypic, Acute / diagnosis
  • [MeSH-minor] Adolescent. Adult. Case-Control Studies. Child. Child, Preschool. Disease Progression. Female. Hematologic Tests. Humans. Incidence. Male. Middle Aged. Phenotype. Retrospective Studies. Young Adult

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  • (PMID = 19346652.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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58. Yin B, Delwel R, Valk PJ, Wallace MR, Loh ML, Shannon KM, Largaespada DA: A retroviral mutagenesis screen reveals strong cooperation between Bcl11a overexpression and loss of the Nf1 tumor suppressor gene. Blood; 2009 Jan 29;113(5):1075-85
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  • NF1 inactivation occurs in specific human cancers, including juvenile myelomonocytic leukemia, an aggressive myeloproliferative disorder of childhood.
  • However, evidence suggests that Nf1 loss alone does not cause leukemia.
  • We therefore hypothesized that inactivation of the Nf1 tumor suppressor gene requires cooperating mutations to cause acute leukemia.
  • One of these genes, Bcl11a, confers a growth advantage in cultured Nf1 mutant hematopoietic cells and causes early onset of leukemia of either myeloid or lymphoid lineage in mice when expressed in Nf1-deficient bone marrow.
  • Importantly, Bcl11a is expressed in human chronic myelomonocytic leukemia and juvenile myelomonocytic leukemia samples.
  • These findings suggest that deregulated Bcl11a cooperates with Nf1 in leukemogenesis, and a therapeutic strategy targeting the BCL11A pathway may prove beneficial in the treatment of leukemia.

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  • (PMID = 18948576.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / CA84221
  • [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 / BCL11A protein, human; 0 / Bcl11a protein, mouse; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Neurofibromin 1; 0 / Nuclear Proteins
  • [Other-IDs] NLM/ PMC2635073
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59. Forissier S, Razanajaona D, Ay AS, Martel S, Bartholin L, Rimokh R: AF10-dependent transcription is enhanced by its interaction with FLRG. Biol Cell; 2007 Oct;99(10):563-71
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

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  • RESULTS: In order to analyse the function of the nuclear form of FLRG, we performed a yeast two-hybrid screen, in which we identified AF10 [ALL1 (acute lymphoblastic leukaemia) fused gene from chromosome 10], a translocation partner of the MLL (mixed-lineage leukaemia) oncogene in human leukaemia, as a FLRG-interacting protein.

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  • (PMID = 17868029.001).
  • [ISSN] 1768-322X
  • [Journal-full-title] Biology of the cell
  • [ISO-abbreviation] Biol. Cell
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Follistatin-Related Proteins; 0 / MLLT10 protein, human; 0 / Protein Isoforms; 0 / Recombinant Fusion Proteins; 0 / Transcription Factors
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60. Dixon N, Kishnani PS, Zimmerman S: Clinical manifestations of hematologic and oncologic disorders in patients with Down syndrome. Am J Med Genet C Semin Med Genet; 2006 Aug 15;142C(3):149-57
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  • Increased erythrocyte mean corpuscular volume (MCV) is frequently found among DS infants and remains elevated throughout life in two-thirds of patients, making interpretation of red cell indices for diagnosis of nutritional anemias or bone marrow failure disorders more challenging.
  • Transient myeloproliferative disorder (TMD) associated with pancytopenia, hepatosplenomegaly, and circulating immature WBCs, is found almost exclusively in DS infants with an incidence of approximately 10%.
  • Despite the high rate of spontaneous regression, TMD can be a preleukemic disorder in 20-30% of children with DS.
  • There is an increased risk of leukemia with an equal incidence of lymphoid and myeloid leukemia.
  • Acute megakaryocytic leukemia (AMKL) subtype is the most common form of acute myeloid leukemia (AML) in this setting, and is uncommon in children without DS.
  • Children with DS and leukemia are more sensitive to some chemotherapeutic agents such as methotrexate than other children which requires careful monitoring for toxicity.
  • Although the risk for leukemia is higher in individuals with DS, these patients have a lower risk of developing solid tumors, with the exception of germ cell tumors, and perhaps retinoblastoma and lymphoma.
  • [MeSH-major] Down Syndrome / complications. Hematologic Diseases / diagnosis. Hematologic Diseases / etiology. Neoplasms / diagnosis. Neoplasms / etiology
  • [MeSH-minor] Child. Female. Humans. Infant. Leukemia / diagnosis. Leukemia / etiology. Male. Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / etiology

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  • (PMID = 17048354.001).
  • [ISSN] 1552-4868
  • [Journal-full-title] American journal of medical genetics. Part C, Seminars in medical genetics
  • [ISO-abbreviation] Am J Med Genet C Semin Med Genet
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 2T32 CA 09307
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 72
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61. Wong GC, Lee LH: Acute biphenotypic leukemia arising in a patient with essential thrombocythemia. Am J Hematol; 2006 Aug;81(8):624-6
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  • [Title] Acute biphenotypic leukemia arising in a patient with essential thrombocythemia.
  • Acute leukemia is an uncommon complication of patients with essential thrombocythemia (ET).
  • We describe a patient with ET, who transformed to acute biphenotypic leukemia 4 and 1/2 years after initial ET diagnosis.
  • Acute biphenotypic leukemia was confirmed on bone marrow studies and immunophenotyping.
  • Complete remission (CR) was achieved with induction chemotherapy for acute leukemia.
  • To our knowledge, this is a rare event of acute biphenotypic leukemic transformation of a patient with ET.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 20 / genetics. Leukemia / complications. Leukemia / genetics. Thrombocythemia, Essential / complications
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Cytogenetic Analysis. Female. Follow-Up Studies. Humans. Hydroxyurea / adverse effects. Hydroxyurea / therapeutic use. Middle Aged. Quinazolines / adverse effects. Quinazolines / therapeutic use. Remission Induction. Treatment Outcome

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  • (PMID = 16823822.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Quinazolines; 0 / anagrelide; X6Q56QN5QC / Hydroxyurea
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62. Shankar DB, Cheng JC, Sakamoto KM: Role of cyclic AMP response element binding protein in human leukemias. Cancer; 2005 Nov 1;104(9):1819-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of cyclic AMP response element binding protein in human leukemias.
  • Acute myeloid leukemia (AML) in adults has a 20% 5-year disease-free survival despite treatment with aggressive cytotoxic chemotherapy.
  • Previous work from our laboratory demonstrated that the majority of patients with acute lymphoid and myeloid leukemia overexpress CREB in the bone marrow.
  • CREB overexpression is associated with poor initial outcome of clinical disease in AML patients.
  • CREB is a transcription factor that functions in glucose homeostasis, growth-factor-dependent cell survival, and memory.
  • To study its role in hematopoiesis, we overexpressed CREB in leukemia cell lines and in mice.
  • CREB overexpression resulted in increased survival and proliferation of myeloid cells and blast-transformation of bone marrow progenitor cells from transgenic mice expressing CREB in the myeloid lineage.
  • CREB transgenic mice also develop myeloproliferative disease after 1 year.
  • Thus, CREB acts as a protooncogene to regulate hematopoiesis and contributes to the leukemia phenotype.
  • Our results suggest that CREB-dependent pathways may serve as targets for directed therapies in leukemia in the future.
  • [MeSH-major] Cyclic AMP Response Element-Binding Protein / genetics. Leukemia / metabolism
  • [MeSH-minor] Acute Disease. Animals. Cell Line, Tumor. Cell Survival. Disease-Free Survival. Hematopoiesis / genetics. Humans. Mice. Mice, Transgenic. Mutation. Transcription Factors / genetics. Up-Regulation

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  • [Copyright] (c) 2005 American Cancer Society.
  • (PMID = 16196046.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16042; United States / NCI NIH HHS / CA / CA68221
  • [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.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / Transcription Factors
  • [Number-of-references] 30
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63. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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64. 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] Japan
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65. 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
MedlinePlus Health Information. consumer health - Cirrhosis.

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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

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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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66. Rosenbluth MJ, Lam WA, Fletcher DA: Force microscopy of nonadherent cells: a comparison of leukemia cell deformability. Biophys J; 2006 Apr 15;90(8):2994-3003
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Force microscopy of nonadherent cells: a comparison of leukemia cell deformability.
  • We apply this technique to compare the deformability of human myeloid and lymphoid leukemia cells and neutrophils at low deformation rates, and we find that the cells are well described by an elastic model based on Hertzian mechanics.
  • Myeloid (HL60) cells were measured to be a factor of 18 times stiffer than lymphoid (Jurkat) cells and six times stiffer than human neutrophils on average (E(infinity) = 855 +/- 670 Pa for HL60 cells, E(infinity) = 48 +/- 35 Pa for Jurkat cells, E(infinity) = 156 +/- 87 for neutrophils, mean +/- SD).
  • This work demonstrates a simple method for extending AFM mechanical property measurements to nonadherent cells and characterizes properties of human leukemia cells that may contribute to leukostasis, a complication associated with acute leukemia.
  • [MeSH-major] Leukemia, Myeloid / pathology. Neutrophils / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Acute Disease. Cell Adhesion. Cell Line, Tumor. Cells, Cultured. Elasticity. Humans. Micromanipulation. Microscopy, Atomic Force. Models, Biological. Viscosity

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  • (PMID = 16443660.001).
  • [ISSN] 0006-3495
  • [Journal-full-title] Biophysical journal
  • [ISO-abbreviation] Biophys. J.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1414579
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67. 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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68. Zhao XC, Li CW, Dai Y, Liu XP, Qin S, Liu SH, Mi YC, Wang JX: [Combination of interphase- and metaphase-fluorescence in situ hybridization to identify 11q23/MLL abnormalities in acute leukemia patients]. Zhonghua Xue Ye Xue Za Zhi; 2006 Oct;27(10):682-6
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  • [Title] [Combination of interphase- and metaphase-fluorescence in situ hybridization to identify 11q23/MLL abnormalities in acute leukemia patients].
  • OBJECTIVE: To explore a rapid, sensitive and effective method for identifying 11 q23/MLL gene rearrangements and investigate the incidence and clinical features of adult acute leukemia (AL) patients with 11 q23/MLL abnormalities.
  • Furthermore by FISH assay II q23/MLL translocations were identified in one each patient with normal karyotype, with 11 q + and without overt 11 q23 abnormality.
  • AL patients with 11 q23/MLL abnormalities were frequently diagnosed as pro-B acute lymphoblastic leukemia (pro-B ALL) ,acute monocytic leukemia (AMoL) or biphenotypic acute leukemia (BAL).
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. In Situ Hybridization, Fluorescence / methods. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Child. Chromosome Deletion. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Interphase / genetics. Male. Metaphase / genetics. Middle Aged. Translocation, Genetic

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  • (PMID = 17343201.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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69. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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  • Hazardous Substances Data Bank. CYTARABINE .
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  • Hazardous Substances Data Bank. METHOTREXATE .
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70. Andreeff M, Ruvolo V, Gadgil S, Zeng C, Coombes K, Chen W, Kornblau S, Barón AE, Drabkin HA: HOX expression patterns identify a common signature for favorable AML. Leukemia; 2008 Nov;22(11):2041-7
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  • Deregulated HOX expression, by chromosomal translocations and myeloid-lymphoid leukemia (MLL) rearrangements, is causal in some types of leukemia.
  • Using real-time reverse transcription-PCR, we examined the expression of 43 clustered HOX, polycomb, MLL and FLT3 genes in 119 newly diagnosed adult acute myeloid leukemias (AMLs) selected from all major cytogenetic groups.
  • We also observed that HOXA9 levels were significantly inversely correlated with survival and that BMI-1 was overexpressed in cases with 11q23 rearrangements, suggesting that p19(ARF) suppression may be involved in MLL-associated leukemia.
  • These results underscore the close relationship between HOX expression patterns and certain forms of AML and emphasize the need to determine whether these differences play a role in the disease process.

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  • (PMID = 18668134.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA97710; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA097710-04; United States / NCI NIH HHS / CA / R21 CA097710; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / R33 CA097710-04; United States / NCI NIH HHS / CA / R33 CA097710; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Polycomb-Group Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Repressor Proteins; 0 / myeloid ecotropic viral integration site 1 protein; 117896-08-9 / nucleophosmin; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 6.3.2.19 / Polycomb Repressive Complex 1
  • [Other-IDs] NLM/ NIHMS104075; NLM/ PMC2676170
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71. Ara AI, Xia M, Ramani K, Mato JM, Lu SC: S-adenosylmethionine inhibits lipopolysaccharide-induced gene expression via modulation of histone methylation. Hepatology; 2008 May;47(5):1655-66
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  • We previously showed that S-adenosylmethionine (SAMe) and its metabolite methylthioadenosine (MTA) blocked lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNFalpha) expression in RAW (murine macrophage cell line) and Kupffer cells at the transcriptional level without affecting nuclear factor kappa B nuclear binding.
  • LPS increased the binding of histone methyltransferases Set1 and myeloid/lymphoid leukemia to these promoters, which was unaffected by SAMe or MTA.
  • Exogenous SAMe is unstable and converts spontaneously to MTA, which is stable and cell-permeant.

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  • (PMID = 18393372.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / T32 AA007578; None / None / / R01 AT001576-05; United States / NCCIH NIH HHS / AT / R01 AT001576-05; United States / NIAAA NIH HHS / AA / AA007578-07; United States / NIAAA NIH HHS / AA / AA12677; United States / NIDDK NIH HHS / DK / R01 DK051719-11; United States / NCCIH NIH HHS / AT / R01 AT001576; United States / NIDDK NIH HHS / DK / DK048522-139003; United States / NIDDK NIH HHS / DK / R01 DK051719; United States / NIAAA NIH HHS / AA / T32 AA07578; United States / NCCIH NIH HHS / AT / AT1576; United States / NIAAA NIH HHS / AA / T32 AA007578-07; United States / NIDDK NIH HHS / DK / DK48522; United States / NIAAA NIH HHS / AA / R01 AA013847; United States / NIAAA NIH HHS / AA / R01 AA012677; United States / NIDDK NIH HHS / DK / DK051719-11; United States / NIAAA NIH HHS / AA / R01 AA012677-05; United States / NIDDK NIH HHS / DK / DK51719; United States / NIAAA NIH HHS / AA / R01 AA013847-05; United States / NIDDK NIH HHS / DK / P30 DK048522; United States / NIAAA NIH HHS / AA / AA13847; United States / NIDDK NIH HHS / DK / P30 DK048522-139003; United States / NIAAA NIH HHS / AA / AA012677-05; United States / NIAAA NIH HHS / AA / AA013847-05
  • [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 / Chromatin; 0 / DNA Primers; 0 / Histones; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 63231-63-0 / RNA; 7LP2MPO46S / S-Adenosylmethionine
  • [Other-IDs] NLM/ NIHMS49821; NLM/ PMC2408693
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72. Cano F, Drynan LF, Pannell R, Rabbitts TH: Leukaemia lineage specification caused by cell-specific Mll-Enl translocations. Oncogene; 2008 Mar 20;27(13):1945-50
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  • [Title] Leukaemia lineage specification caused by cell-specific Mll-Enl translocations.
  • Chromosomal translocations involving the Mixed-Lineage Leukaemia (MLL) gene underlie many human leukaemias and MLL rearrangements are found in both acute myelogenous and acute lymphoblastic leukaemias.
  • To assess the functionally relevant haematopoietic cell contexts for MLL fusions to be tumorigenic, we have generated different lines of mice in which de novo Mll-associated translocations occur.
  • Translocations between Mll and Enl cause myeloid neoplasias, initiating in stem cells or progenitors while no tumours arose when the translocation was restricted to the B-cell compartment.
  • Despite the absence of tumorigenesis, Mll-Enl translocations did occur and Mll-Enl fusion mRNA was expressed in B-cell-restricted translocators.
  • [MeSH-major] B-Lymphocytes / pathology. Cell Lineage. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. T-Lymphocytes / pathology. Translocation, Genetic
  • [MeSH-minor] Animals. Antigens, CD19 / genetics. Antigens, CD19 / physiology. Cells, Cultured. Histone-Lysine N-Methyltransferase. Integrases / metabolism. Mice. Myeloid Progenitor Cells / cytology. Myeloid Progenitor Cells / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / physiology. Phenotype. Recombination, Genetic. Stem Cells / cytology. Stem Cells / metabolism

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  • (PMID = 17906700.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0600914; United Kingdom / Medical Research Council / / MC/ U105178807; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Mllt3 protein, mouse; 0 / Neoplasm 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; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases
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73. El-Ziny MA, Al-Tonbary YA, Salama OS, Bakr AA, Al-Marsafawy H, Elsharkawy AA: Low turnover bone disease in Egyptian children with acute leukemia. Hematology; 2005 Aug;10(4):327-33
Hazardous Substances Data Bank. CHOLECALCIFEROL .

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  • [Title] Low turnover bone disease in Egyptian children with acute leukemia.
  • The aim of this work was to study bone turnover markers, calcium homeostasis and bone mineral density (BMD) in children with acute leukemia at diagnosis, after induction chemotherapy, and during maintenance therapy to delineate abnormalities present.
  • After evaluation of L2-L4 BMD using dual-energy X-ray absorptiometry in patients with acute myeloid and lymphoid leukemia at presentation and after treatment, the results were compared to 352 healthy age- and sex-matched Egyptian controls.
  • Osteopenia was observed at diagnosis and during treatment in patients with acute leukemia.
  • At diagnosis osteopenia was observed in 27 patients (62.8%): 10 (23.3%) had non severe osteopenia and 17 (39.5%) had severe osteopenia.
  • Parathyroid hormone (PTH) (pg/ml) levels demonstrated non significant differences between children with acute leukemia at different stages of therapy and controls, while, 25 (OH) D3 (ng/ml) was significantly lower in acute leukemia patients at different stages of therapy compared to controls (p<0.001).
  • Osteocalcin (ng/ml) is significantly lower in patients at different stages of the disease compared to controls (p<0.001) but there was no significant difference between patients at different stages of therapy.
  • Deoxy-pyridoline cross links showed non-significant difference between the different types of acute leukemia and with controls.
  • Osteopenia is a significant problem in children with acute leukemia at presentation and after chemotherapy.
  • Osteopenia in acute leukemia appears to be of the low turnover type (decreased osteoblastic activity and decreased bone mineralization).
  • [MeSH-major] Bone Density. Bone Diseases, Metabolic / blood. Bone Remodeling. Leukemia / blood
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Cholecalciferol / blood. Egypt. Humans. Infant. Male. Osteoblasts / metabolism. Osteocalcin / blood. Parathyroid Hormone / blood

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  • (PMID = 16085546.001).
  • [ISSN] 1024-5332
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Parathyroid Hormone; 104982-03-8 / Osteocalcin; 1C6V77QF41 / Cholecalciferol
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74. Harel A, Wu F, Mattson MP, Morris CM, Yao PJ: Evidence for CALM in directing VAMP2 trafficking. Traffic; 2008 Mar;9(3):417-29
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

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  • Clathrin assembly lymphoid myeloid leukemia protein (CALM) is a clathrin assembly protein with a domain structure similar to the neuron-specific assembly protein AP180.
  • Overexpression of CALM leads to the reduction of cell surface VAMP2, whereas knockdown of CALM by RNA interference results in the accumulation of surface VAMP2.
  • [MeSH-minor] Animals. Cell Line. Cell Membrane / metabolism. Endocytosis. Humans. Mutagenesis, Site-Directed. PC12 Cells. Protein Structure, Tertiary. Protein Transport. RNA Interference. RNA, Small Interfering / genetics. Rats. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Transfection. Transferrin / metabolism

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  • (PMID = 18182011.001).
  • [ISSN] 1398-9219
  • [Journal-full-title] Traffic (Copenhagen, Denmark)
  • [ISO-abbreviation] Traffic
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Monomeric Clathrin Assembly Proteins; 0 / PICALM protein, human; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / Transferrin; 0 / VAMP2 protein, human; 0 / Vesicle-Associated Membrane Protein 2
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75. Schwartz CM, Cheng A, Mughal MR, Mattson MP, Yao PJ: Clathrin assembly proteins AP180 and CALM in the embryonic rat brain. J Comp Neurol; 2010 Sep 15;518(18):3803-18
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  • In this study, we focus on two closely related clathrin assembly proteins, AP180 and CALM (clathrin assembly lymphoid myeloid leukemia protein), in the developing embryonic rat brain.
  • [MeSH-minor] Animals. Cell Line. Clathrin / metabolism. Clathrin-Coated Vesicles / metabolism. Female. Neurons / cytology. Neurons / metabolism. Pregnancy. Rats. Stem Cells / cytology. Stem Cells / metabolism

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  • (PMID = 20653035.001).
  • [ISSN] 1096-9861
  • [Journal-full-title] The Journal of comparative neurology
  • [ISO-abbreviation] J. Comp. Neurol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 AG999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Clathrin; 0 / Monomeric Clathrin Assembly Proteins; 0 / Picalm protein, rat; 0 / clathrin assembly protein AP180
  • [Other-IDs] NLM/ NIHMS215726; NLM/ PMC2909614
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76. Slany RK: The molecular biology of mixed lineage leukemia. Haematologica; 2009 Jul;94(7):984-93
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 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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77. Pérez-Campos-Mayoral L, Ruiz-Argüelles A, Pérez-Romano B, Zenteno E, Hernández-Cruz P, Martínez-Cruz R, Martínez-Cruz M, Pina-Canseco S, Pérez-Campos E: Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia. Tohoku J Exp Med; 2008 Jan;214(1):11-6
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  • [Title] Potential use of the Macrobrachium rosenbergii lectin for diagnosis of T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia is the most common form of cancer in children.
  • Lectins are proteins or glycoproteins from plants or animals that recognize oligossacharides on the cell surface and have been used to characterize the structural changes of oligosaccharides in leukemias.
  • In this study, we used the lectin from the freshwater prawn Macrobrachium (M. rosenbergii), specific for acetyl groups in sialylated glycans, because increased sialylation of glycoproteins and glycolipids has been identified in lymphoblastic leukemias.
  • We compared the specificity of the M. rosenbergii lectin for lymphoblastic leukemias with the specificities of the lectins from Triticum vulgaris, Solanum tuberosum, Arachis hipogaea, and Phytolacca americana.
  • By morphologic and phenotype characterization with a panel of monoclonal antibodies, we identified four types of leukemias from 106 leukemia patients: 11 cases of T-cell acute lymphoblastic leukemia, 61 cases of B-cell acute lymphoblastic leukemia, 24 cases of acute myeloblastic leukemia, and 10 cases of acute biphenotypic leukemia.
  • As determined by cytofluorometric assays, nine of the eleven cases with T-cell acute lymphoblastic leukemia (8 +/- 3 years old) were specifically identified with the lectin from M. rosenbergii.
  • In contrast, only six cases of B-cell leukemia, one case of myeloblastic leukemia, and 2 cases of biphenotypic leukemia were identified with this M. rosenbergii lectin.
  • The other lectins tested showed no capacity to differentiate, in a significant manner, any of the four types of leukemias tested.
  • Thus, the lectin from M. rosenbergii could be considered a useful tool for the diagnosis and study of T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Lectins. Leukemia, Biphenotypic, Acute / diagnosis. Palaemonidae / chemistry
  • [MeSH-minor] Animals. Antibodies, Monoclonal. Antigens, CD45 / analysis. Antigens, Neoplasm / immunology. Child. Diagnosis, Differential. Flow Cytometry. Humans. Lymphocytes / drug effects. Lymphocytes / metabolism. Phenotype

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  • (PMID = 18212483.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Lectins; EC 3.1.3.48 / Antigens, CD45
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78. Fujiwara S, Yamashita Y, Choi YL, Watanabe H, Kurashina K, Soda M, Enomoto M, Hatanaka H, Takada S, Ozawa K, Mano H: Transforming activity of purinergic receptor P2Y, G protein coupled, 8 revealed by retroviral expression screening. Leuk Lymphoma; 2007 May;48(5):978-86
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  • Biphenotypic acute leukemia (BAL) is a relatively rare subtype of acute leukemia characterized by the presence of both myeloid and lymphoid cell surface antigens.
  • A variety of luciferase-based reporter assays revealed that P2RY8 increased both the trans-activation activities of CREB and Elk-1 as well as the transcriptional activities of the serum response element and enhancer-promoter fragments of the c-Fos and c-Myc genes.
  • Quantitation of P2RY8 mRNA in CD34(+) cells of bone marrow showed that P2RY8 expression is frequently increased in leukemia patients, especially in those with refractory disease.
  • Our data thus reveal an abundant expression of P2RY8 in leukemic cells and its unexpected role in the pathogenesis of acute leukemia.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia / genetics. Leukemia / metabolism. Receptors, Purinergic / physiology. Receptors, Purinergic P2 / metabolism. Receptors, Purinergic P2Y / metabolism. Receptors, Purinergic P2Y / physiology. Retroviridae / metabolism
  • [MeSH-minor] 3T3 Cells. Animals. Antigens, CD34 / biosynthesis. Bone Marrow Cells / metabolism. Cell Line, Tumor. DNA, Complementary / genetics. Gene Library. Humans. Mice. Mice, Nude. Transcription, Genetic

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  • (PMID = 17487742.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA, Complementary; 0 / P2RY8 protein, human; 0 / P2RY9 receptor, human; 0 / P2RY9 receptor, mouse; 0 / Receptors, Purinergic; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2Y
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79. Archangelo LF, Gläsner J, Krause A, Bohlander SK: The novel CALM interactor CATS influences the subcellular localization of the leukemogenic fusion protein CALM/AF10. Oncogene; 2006 Jul 6;25(29):4099-109
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  • The Clathrin Assembly Lymphoid Myeloid leukemia gene (CALM or PICALM) was first identified as the fusion partner of AF10 in the t(10;11)(p13;q14) translocation, which is observed in acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL) and malignant lymphoma.
  • Using the N-terminal half of CALM as a bait in a yeast two-hybrid screen, a novel protein named CATS (CALM interacting protein expressed in thymus and spleen) was identified.
  • [MeSH-major] Active Transport, Cell Nucleus. Carrier Proteins / metabolism. Cell Nucleolus / metabolism. Monomeric Clathrin Assembly Proteins / metabolism. Oncogene Proteins, Fusion / metabolism
  • [MeSH-minor] 3T3 Cells. Animals. Base Sequence. Cell Transformation, Neoplastic / genetics. Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 10 / metabolism. Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 13 / metabolism. Gene Expression Regulation / genetics. Humans. Mice. Molecular Sequence Data. Organ Specificity. Protein Binding / genetics. Translocation, Genetic / genetics

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  • (PMID = 16491119.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / Carrier Proteins; 0 / FAM64A protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human
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80. Liu Y, Tang SQ, Yang G, Feng C, Liu LZ, Lei Q: [Skin lesions and myelodysplastic syndrome as initial manifestations of biphenotypic acute leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Oct;15(5):961-6
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  • [Title] [Skin lesions and myelodysplastic syndrome as initial manifestations of biphenotypic acute leukemia].
  • The aim of this study was to investigate the clinical, pathological and biological features of biphenotypic acute leukemia.
  • The results showed that extramedullary skin lesions and myelodysplasia occurred before the onset of overt disease.
  • At the time of diagnosis, this case had more than 30% blasts in bone marrow with meningeal involvement.
  • Flow cytometry revealed the co-expression of myeloid antigens (cMPO, CD33 and CD117) and T-lymphoid antigens (cCD3, CD5, CD7, dual expression of CD4 and CD8).
  • All above-mentioned results led to the diagnosis of biphenotypic acute leukemia.
  • It is concluded that the biphenotypic acute leukemia is an uncommon type of leukemia which may be preceded by myelodysplastic syndrome and has aggressive clinical and biological behavior.
  • Immunophenotype, cytogenetics and molecular analysis can contribute to early diagnosis of BAL and evaluation of prognosis.

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  • (PMID = 17956670.001).
  • [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] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD43; 0 / CD99 protein, human; 0 / Cell Adhesion Molecules; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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81. Van Etten RA: Aberrant cytokine signaling in leukemia. Oncogene; 2007 Oct 15;26(47):6738-49
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  • [Title] Aberrant cytokine signaling in leukemia.
  • Abnormalities of cytokine and growth factor signaling pathways are characteristic of all forms of leukemia: lymphoid and myeloid, acute and chronic.
  • In this review, our current knowledge of leukemic cell cytokine signaling will be summarized, and some speculations on the significance and implications of these insights will be advanced.
  • A better understanding of aberrant cytokine signaling in leukemia should provide additional targets for the rational therapy of these diseases.

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  • (PMID = 17934482.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090576; United States / NCI NIH HHS / CA / R01 CA105043; United States / NCI NIH HHS / CA / CA090576; United States / NCI NIH HHS / CA / CA105043
  • [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 / Cytokines
  • [Number-of-references] 139
  • [Other-IDs] NLM/ NIHMS579951; NLM/ PMC4344827
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82. Liu H, Yu H, Jia HY, Zhang W, Guo CJ: [Detection of FLT3 gene mutation in hematologic malignancies and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):709-13
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  • To study the FLT3 gene expression and its internal tandem duplication in hematologic malignancies and its clinical significance, polymerase chain reaction (PCR) and DNA sequencing were used to detect the FLT3/ITD mutation in blast cells of bone marrow from 86 patients with hematologic malignancies, including 32 cases of acute myeoloid leukemia (AML), 18 cases of acute lymphoblastic leukemia (ALL), 2 cases of acute hybrid leukemia (AHL), 12 cases of myelodysplastic syndromes (MDS), 10 cases of chronic myelogenous leukemia (CML), 3 cases of non-Hodgkin's lymphoma (NHL) and 9 cases of multiple myeloma (MM).
  • FLT3/ITD was associated with a higher peripheral blood white cell count (p < 0.01), higher percentage of bone marrow blast cells (p < 0.01) and lower complete mission rate.
  • FLT3/ITD mutation is associated with higher peripheral blood white cell count, higher percentage of bone marrow blast cells and lower complete remission rate, FIT3/IID gene mutation may be used to predict prognosis of patients with AML.

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  • (PMID = 17708788.001).
  • [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] EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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83. Choi EK, Byun JH, Lee SJ, Jung SE, Park MS, Park SH, Lee MG: Imaging findings of leukemic involvement of the pancreaticobiliary system in adults. AJR Am J Roentgenol; 2007 Jun;188(6):1589-95
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  • CONCLUSION: Pancreatic myeloid and lymphoid leukemia show single or multiple mass lesions of homogeneous low attenuation and poor contrast enhancement on CT that is radiographically indistinguishable from that of pancreatic lymphoma.
  • [MeSH-major] Biliary Tract Neoplasms / radiography. Leukemia / radiography. Pancreatic Neoplasms / radiography. Radiographic Image Enhancement / methods

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  • (PMID = 17515381.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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84. Gluzman DF, Nadgornaya VA, Sklyarenko LM, Ivanovskaya TS, Poludnenko LY, Ukrainskaya NI: Immunocytochemical markers in acute leukaemias diagnosis. Exp Oncol; 2010 Sep;32(3):195-9
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  • [Title] Immunocytochemical markers in acute leukaemias diagnosis.
  • The study included 1742 patients with acute myeloblastic leukaemias (AML) and acute lymphoblastic leukaemias (ALL), Kyiv city residents and patients from 20 regions of Ukraine.
  • Bone marrow and blood smears were sent at diagnosis to Reference Center.
  • Immunocytochemical techniques (APAAP, LSAB) and broad panel of monoclonal antibodies (MoAbs) against lineage specific and differentiation antigens of leukocytes were employed for immunophenotyping of leukemic blast cells directly in blood and bone marrow smears.
  • Different types of AML were defined by the expression of the cell surface and cytoplasmic antigens.
  • Immunocytochemical study was required especially in diagnosing of AML with minimal differentiation, acute megakaryoblastic leukaemia, acute erythroid leukaemia and acute leukaemias of ambiguous lineage.
  • Acute lymphoblastic leukaemias was broadly classified into B-lineage and T-lineage ALL.
  • According to the degree of B-lymphoid differentiation of the blast cells four subtypes of B-lineage ALL were established.
  • T-lineage ALL observed in patients were also divided into four subtypes.
  • Immunocytochemical examination was required to diagnose AL of ambiguous lineage with no clear evidence of lineage differentiation (acute undifferentiated leukaemia) or those with blasts that express markers of more than one lineage (mixed phenotype acute leukaemias).
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / immunology. Humans. Immunohistochemistry. Immunophenotyping. Lymphocyte Subsets / immunology. Lymphocyte Subsets / pathology

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  • (PMID = 21403617.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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85. Mikulic M, Batinic D, Sucic M, Davidovic-Mrsic S, Dubravcic K, Nemet D, Serventi-Seiwerth R, Sertic D, Labar B: Biological features and outcome of biphenotypic acute leukemia: a case series. Hematol Oncol Stem Cell Ther; 2008 Oct-Dec;1(4):225-30
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  • [Title] Biological features and outcome of biphenotypic acute leukemia: a case series.
  • BACKGROUND: Biphenotypic acute leukemia (BAL) is a distinct entity that is immunophenotypically defined by the European Group for the Immunological Classification of Leukemia (EGIL) scoring system and accounts for less than 5% of all acute leukemia cases.
  • Since it is a rare and heterogeneous form of acute leukemia with an allegedly poor outcome, there is no consensus on the best treatment approach in these patients.
  • PATIENTS AND METHODS: Using the EGIL system, we identified 21 cases (3.9%) of BAL from 535 newly diagnosed acute leukemia patients in an 11-year period.
  • RESULTS: There were ten cases of myeloid+B-lymphoid leukemia, eight cases of myeloid+T-lymphoid, one case of B+T-lymphoid and two cases of trilineage (myeloid+B+T-lymphoid leukemia).
  • Patients that received acute lymphoblastic leukemia-oriented chemotherapy had a higher CR rate compared with those who received acute myeloid leukemia-oriented chemotherapy (100% vs. 60%, P = .007).
  • The white blood cell count at diagnosis was found to have statistically significant impact on survival.
  • CONCLUSION: Despite the progress in the treatment of acute leukemia, the prognosis of BAL remains poor and treatment protocols devised explicitly for this entity should be investigated in prospective collaborative studies.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / pathology. Leukemia, Biphenotypic, Acute / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Disease-Free Survival. Female. Humans. Immunophenotyping. Male. Middle Aged. Prognosis. Stem Cell Transplantation. Treatment Outcome. Young Adult

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  • (PMID = 20058478.001).
  • [ISSN] 1658-3876
  • [Journal-full-title] Hematology/oncology and stem cell therapy
  • [ISO-abbreviation] Hematol Oncol Stem Cell Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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86. Xu XQ, Wang JM, Lü SQ, Chen L, Yang JM, Zhang WP, Song XM, Hou J, Ni X, Qiu HY: Clinical and biological characteristics of adult biphenotypic acute leukemia in comparison with that of acute myeloid leukemia and acute lymphoblastic leukemia: a case series of a Chinese population. Haematologica; 2009 Jul;94(7):919-27
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  • [Title] Clinical and biological characteristics of adult biphenotypic acute leukemia in comparison with that of acute myeloid leukemia and acute lymphoblastic leukemia: a case series of a Chinese population.
  • BACKGROUND: Biphenotypic acute leukemia is a rare disorder that is difficult to diagnose.
  • It displays features of both myeloid and lymphoid lineage.
  • There is still a lack of studies in biphenotypic acute leukemia in a Chinese population.
  • We present here a comprehensive investigation of the clinical and biological characteristics, and outcome of biphenotypic acute leukemia in our hospital in over a seven year period.
  • DESIGN AND METHODS: We retrospectively analyzed 452 adult acute leukemia patients diagnosed according to French-American-British (FAB) classification and biphenotypic acute leukemia diagnosed according to European Group for the Immunological Characterization of Leukemias (EGIL) classification, respectively.
  • Biological characteristics, response to treatment, and outcome were examined in biphenotypic acute leukemia patients and compared with that in acute myeloid leukemia and acute lymphoblastic leukemia patients with complete follow-up profiles diagnosed in the same period.
  • RESULTS: Of 452 acute leukemia patients, 21 cases (4.6%) were diagnosed as biphenotypic acute leukemia.
  • Among them, 14 (66.7%) were B lymphoid and myeloid, 5 (23.8%) were T lymphoid and myeloid, one (4.8%) was T/B lymphoid and one (4.8%) was trilineage differentiation.
  • When compared with acute myeloid leukemia and acute lymphoblastic leukemia, patients with biphenotypic acute leukemia showed significantly higher incidence of CD34 antigen expression, unfavorable karyotypes, and extramedullary infiltration (p<0.05).
  • In this cohort of patients with biphenotypic acute leukemia, t(9;22) was the most common abnormality in chromosome structure.
  • The median disease-free survival and overall survival in biphenotypic acute leukemia patients was five months and ten months, respectively, significantly shorter than those in acute myeloid leukemia and acute lymphoblastic leukemia patients (p<0.05).
  • CONCLUSIONS: The prognosis of biphenotypic acute leukemia patients is poor when compared with de novo acute myeloid leukemia or acute lymphoblastic leukemia.
  • Biphenotypic acute leukemia patients showed a much higher incidence of CD34 antigen expression, complex abnormal karyotype, extramedullary infiltration, relapse, and resistance to therapy after relapse.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


87. Choi HW, Shin MG, Kim HJ, Lee IK, Yun JH, Kim HR, Kim YK, Yun HK, Cho D, Kee SJ, Shin JH, Suh SP, Ryang DW: [Biphenotypic Acute Leukemia with BCR-ABL mRNA Transcript b3a2 Type: A Case Report with Review of the Literature.]. Korean J Lab Med; 2006 Aug;26(4):249-54
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  • [Title] [Biphenotypic Acute Leukemia with BCR-ABL mRNA Transcript b3a2 Type: A Case Report with Review of the Literature.].
  • Biphenotypic acute leukemia (BAL) is a subtype of leukemia of ambiguous lineage in the World Health Organization classification system.

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  • (PMID = 18156734.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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88. Strick R, Zhang Y, Emmanuel N, Strissel PL: Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias. Hum Genet; 2006 Jun;119(5):479-95
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  • [Title] Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.
  • The t(9;22) BCR/ABL fusion is associated with over 90% of chronic myelogenous and 25% of acute lymphocytic leukemia.
  • Chromosome 11q23 translocations in acute myeloid and lymphoid leukemia cells demonstrate myeloid lymphoid leukemia (MLL) fusions with over 40 gene partners, like AF9 and AF4 on chromosomes 9 and 4, respectively.
  • Therapy-related leukemia is associated with the above gene rearrangements following the treatment with topoisomerase II (topo II) inhibitors.
  • In this report, using cell lines and primary cells, chromatin structural elements were analyzed in BCR, ABL and AF4 and, for comparison, in MLL2, which is a homolog to MLL, but not associated with chromosome translocations.
  • Although MLL2 was expressed in all cell lines tested, except for the presence of one DNAse I site in the promoter, no other structural elements were found in MLL2.
  • A NHR model presented demonstrates the importance of chromatin structure in chromosome translocations involved with leukemia.
  • [MeSH-major] Chromatin / chemistry. Chromosome Breakage. Chromosomes, Human / genetics. Leukemia / genetics. Leukemia / metabolism. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cells, Cultured. Chronic Disease. Humans. K562 Cells. Proto-Oncogene Proteins c-bcr / chemistry. Proto-Oncogene Proteins c-bcr / genetics. Recombination, Genetic

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  • (PMID = 16572268.001).
  • [ISSN] 0340-6717
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chromatin; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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89. Lotem J, Netanely D, Domany E, Sachs L: Human cancers overexpress genes that are specific to a variety of normal human tissues. Proc Natl Acad Sci U S A; 2005 Dec 20;102(51):18556-61
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  • We have analyzed gene expression data from three different kinds of samples: normal human tissues, human cancer cell lines, and leukemic cells from lymphoid and myeloid leukemia pediatric patients.
  • Analysis of the expression levels of these two groups of genes in the human cancer cell lines and leukemias identified genes that were highly expressed in cancer cells but not in their normal counterparts and, thus, were overexpressed in the cancers.
  • The different cancer cell lines and leukemias varied in the number and identity of these overexpressed genes.
  • [MeSH-minor] Adenocarcinoma / genetics. Cell Line. Cell Line, Tumor. Health. Humans. Leukemia / classification. Leukemia / genetics. Multigene Family / genetics

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  • (PMID = 16339305.001).
  • [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
  • [Other-IDs] NLM/ PMC1317977
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90. Beesley AH, Rampellini JL, Palmer ML, Heng JY, Samuels AL, Firth MJ, Ford J, Kees UR: Influence of wild-type MLL on glucocorticoid sensitivity and response to DNA-damage in pediatric acute lymphoblastic leukemia. Mol Cancer; 2010;9:284
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  • [Title] Influence of wild-type MLL on glucocorticoid sensitivity and response to DNA-damage in pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Rearrangement of the mixed-lineage leukemia gene (MLL) is found in 80% of infant acute lymphoblastic leukemia (ALL) and is associated with poor prognosis and resistance to glucocorticoids (GCs).
  • We have recently observed that GC resistance in T-ALL cell lines is associated with a proliferative metabolism and reduced expression of MLL.
  • RESULTS: Negative correlation of MLL expression with GC resistance in 15 T-ALL cell lines was confirmed by quantitative RT-PCR.
  • RNAi knockdown of MLL expression in T-ALL cell lines significantly increased resistance to dexamethasone and gamma irradiation indicating an important role for wild-type MLL in the control of cellular apoptosis.
  • [MeSH-major] DNA Damage / genetics. Drug Resistance, Neoplasm / genetics. Glucocorticoids / pharmacology. Lymphocytes / drug effects. Myeloid-Lymphoid Leukemia Protein / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. Oligonucleotide Array Sequence Analysis. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20979663.001).
  • [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 / Glucocorticoids; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2987983
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91. Haouas H, Haouas S, Uzan G, Hafsia A: Identification of new markers discriminating between myeloid and lymphoid acute leukemia. Hematology; 2010 Aug;15(4):193-203
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  • [Title] Identification of new markers discriminating between myeloid and lymphoid acute leukemia.
  • BACKGROUND: The heterogeneity of acute myeloid leukemia (AML) with respect to biology and clinical course resides in the fact that patients belonging to the same group show marked differences in their response to chemotherapy, necessitating a refinement of AML classification.
  • RESULTS: We have shown that two downregulated genes in AML, those encoding guanine nucleotide-binding protein gamma11 (GNG11) and amphiregulin (AREG), are also downregulated in B-lineage acute lymphoblastic leukemia (B-ALL) and T-lineage acute lymphoblastic leukemia (T-ALL) patients.
  • A second gene, that encoding ceruloplasmin (CP), is upregulated in AML but not in B-ALL and T-ALL.
  • Our study is the first to analyze these genes in AML, B-ALL, T-ALL and chronic leukemia (myeloid and lymphoid) patients by RT-PCR.
  • This rapid and sensitive method could be used to screen these genes in different types of leukemia.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Amphiregulin. Cell Line, Tumor. Ceruloplasmin / genetics. Ceruloplasmin / metabolism. Diagnosis, Differential. EGF Family of Proteins. Female. GTP-Binding Protein alpha Subunits, Gq-G11 / genetics. GTP-Binding Protein alpha Subunits, Gq-G11 / metabolism. Gene Expression Profiling. Glycoproteins / genetics. Glycoproteins / metabolism. Humans. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20670477.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AREG protein, human; 0 / Amphiregulin; 0 / Biomarkers, Tumor; 0 / EGF Family of Proteins; 0 / Glycoproteins; 0 / Intercellular Signaling Peptides and Proteins; EC 1.16.3.1 / Ceruloplasmin; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11
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92. Balgobind BV, Hollink IH, Reinhardt D, van Wering ER, de Graaf SS, Baruchel A, Stary J, Beverloo HB, de Greef GE, Pieters R, Zwaan CM, van den Heuvel-Eibrink MM: Low frequency of MLL-partial tandem duplications in paediatric acute myeloid leukaemia using MLPA as a novel DNA screenings technique. Eur J Cancer; 2010 Jul;46(10):1892-9
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  • [Title] Low frequency of MLL-partial tandem duplications in paediatric acute myeloid leukaemia using MLPA as a novel DNA screenings technique.
  • Mixed-lineage leukaemia (MLL)-partial tandem duplications (PTDs) are found in 3-5% of adult acute myeloid leukaemia (AML), and are associated with poor prognosis.
  • [MeSH-major] Gene Duplication. Genetic Testing / methods. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Tandem Repeat Sequences / genetics

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20233657.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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93. Serefhanoglu S, Buyukasik Y, Goker H, Sayinalp N, Ozcebe OI: Biphenotypic acute leukemia treated with acute myeloid leukemia regimens: a case series. J Natl Med Assoc; 2009 Mar;101(3):270-2
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  • [Title] Biphenotypic acute leukemia treated with acute myeloid leukemia regimens: a case series.
  • This study retrospectively analyzed 8 cases of biphenotypic acute leukemia (BAL) in respect of morphology, immune phenotype, karyotype, and clinical manifestations.
  • Six patients had myeloid plus T lymphoid, and 2 cases had myeloid plus B-lymphoid immune phenotypic markers.
  • Because selection of an antileukemic chemotherapy regimen for acute leukemia is largely based on whether a case is classified as myeloid or lymphoid, the presence of markers for both lineages may have important implications for treatment.
  • All of our patients were treated with regimens designed for acute myeloid leukemia (AML).
  • [MeSH-major] Leukemia, Biphenotypic, Acute / drug therapy
  • [MeSH-minor] Adult. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Agents / therapeutic use. Biomarkers. Case-Control Studies. Cytarabine / therapeutic use. Female. Humans. Idarubicin / therapeutic use. Immunophenotyping. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / physiopathology. Male. Middle Aged. Mitoxantrone / therapeutic use. Retrospective Studies

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  • (PMID = 19331261.001).
  • [ISSN] 1943-4693
  • [Journal-full-title] Journal of the National Medical Association
  • [ISO-abbreviation] J Natl Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Biomarkers; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin
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94. Xavier MO, Oliveira Fde M, Almeida Vd, Prolla G, Severo LC: Invasive Aspergillus flavus sinusitis: case report in a patient with biphenotypic acute leukemia. Rev Inst Med Trop Sao Paulo; 2009 Jan-Feb;51(1):57-8
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  • [Title] Invasive Aspergillus flavus sinusitis: case report in a patient with biphenotypic acute leukemia.
  • Here we report a case of invasive pansinusitis with proptosis of the right eye caused by Aspergillus flavus in an immunocompromised patient with acute biphenotypic leukemia without aggressive therapy response.
  • [MeSH-major] Aspergillosis / diagnosis. Aspergillus flavus / isolation & purification. Immunocompromised Host. Leukemia, Biphenotypic, Acute / immunology. Sinusitis / microbiology

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  • (PMID = 19229393.001).
  • [ISSN] 1678-9946
  • [Journal-full-title] Revista do Instituto de Medicina Tropical de São Paulo
  • [ISO-abbreviation] Rev. Inst. Med. Trop. Sao Paulo
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
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95. Michaud J, Simpson KM, Escher R, Buchet-Poyau K, Beissbarth T, Carmichael C, Ritchie ME, Schütz F, Cannon P, Liu M, Shen X, Ito Y, Raskind WH, Horwitz MS, Osato M, Turner DR, Speed TP, Kavallaris M, Smyth GK, Scott HS: Integrative analysis of RUNX1 downstream pathways and target genes. BMC Genomics; 2008 Jul 31;9:363
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The RUNX1 transcription factor gene is frequently mutated in sporadic myeloid and lymphoid leukemia through translocation, point mutation or amplification.
  • It is also responsible for a familial platelet disorder with predisposition to acute myeloid leukemia (FPD-AML).
  • The disruption of the largely unknown biological pathways controlled by RUNX1 is likely to be responsible for the development of leukemia.
  • We have used multiple microarray platforms and bioinformatic techniques to help identify these biological pathways to aid in the understanding of why RUNX1 mutations lead to leukemia.
  • 1) cell lines with RUNX1 mutations from FPD-AML patients, 2) over-expression of RUNX1 and CBFbeta, and 3) Runx1 knockout mouse embryos using either cDNA or Affymetrix microarrays.
  • A number of biological processes were identified among the differentially expressed genes and functional assays suggest that heterozygous RUNX1 point mutations in patients with FPD-AML impair cell proliferation, microtubule dynamics and possibly genetic stability.
  • CONCLUSION: This work is the first large-scale study attempting to identify the genetic networks regulated by RUNX1, a master regulator in the development of the hematopoietic system and leukemia.
  • The biological pathways and target genes controlled by RUNX1 will have considerable importance in disease progression in both familial and sporadic leukemia as well as therapeutic implications.