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1. Kong CT, Sham MH, So CW, Cheah KS, Chen SJ, Chan LC: The Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice. Leukemia; 2006 Oct;20(10):1829-39
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  • [Title] The Mll-Een knockin fusion gene enhances proliferation of myeloid progenitors derived from mouse embryonic stem cells and causes myeloid leukaemia in chimeric mice.
  • Rearrangement of the mixed lineage leukaemia (MLL) gene with extra eleven nineteen (EEN) was previously identified in an infant with acute myeloid leukaemia.
  • Using homologous recombination, we have created a mouse equivalent of the human MLL-EEN allele and showed that when Mll(Een/+) embryonic stem (ES) cells were induced to differentiate in vitro into haemopoietic cells, there was increased proliferation of myeloid progenitors with self-renewal property.
  • We also generated Mll(Een/+) chimeric mice, which developed leukaemia displaying enlarged livers, spleens, thymuses and lymph nodes owing to infiltration of Mll(Een/+)-expressing leukemic cells.
  • Immunophenotyping of cells from enlarged organs and bone marrow (BM) of the Mll(Een/+) chimeras revealed an accumulation of Mac-1+/Gr-1- immature myeloid cells and a reduction in normal B- and T-cell populations.
  • We observed differential regulation of Hox genes between myeloid cells derived from Mll(Een/+) ES cells and mouse BM leukemic cells which suggested different waves of Hox expression may be activated by MLL fusion proteins for initiation (in ES cells) and maintenance (in leukemic cells) of the disease.
  • We believe studies of MLL fusion proteins in ES cells combined with in vivo animal models offer new approaches to the dissection of molecular events in multistep pathogenesis of leukaemia.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology. Myeloid Cells / pathology. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Cell Division / physiology. Chimera. Disease Models, Animal. Female. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Genes, Homeobox / physiology. Humans. Infant. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Molecular Sequence Data. Translocation, Genetic

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  • (PMID = 16888613.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / SH3GL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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2. 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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3. 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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4. Zhao XF, Gojo I, York T, Ning Y, Baer MR: Diagnosis of biphenotypic acute leukemia: a paradigmatic approach. Int J Clin Exp Pathol; 2009;3(1):75-86
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  • [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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5. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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6. 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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7. Aljurf M, Nassar A, Saleh AJ, Almhareb F, Alzahrani H, Walter C, Bakr M, Ahmed SO, Chaudhri N: Maternal acute lymphoctic leukemia with rearrangement of the mixed lineage leukemia gene occurring during pregnancy. Hematol Oncol Stem Cell Ther; 2009;2(3):399-402
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  • [Title] Maternal acute lymphoctic leukemia with rearrangement of the mixed lineage leukemia gene occurring during pregnancy.
  • Acute lymphoblastic leukemia (ALL) is a relatively rare disease during pregnancy, accounting for about 15% of all cases of pregnancy-associated leukemia.
  • Although mixed lineage leukemia gene (MLL) rearrangement is the dominant genetic aberration in infantile acute leukemia, the occurrence of MLL gene rearrangement in maternal ALL occurring during pregnancy has not been reported.
  • Out of 31 cases of maternal leukemia diagnosed during pregnancy at our institution, 5 were ALL cases.
  • We believe that the association of MLL gene rearrangement with maternal leukemia is biologically plausible and this observation needs to be validated in a larger cohort of pregnancy-associated maternal leukemia cases.
  • [MeSH-major] Gene Rearrangement. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Pregnancy Complications, Neoplastic
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Lineage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Combined Modality Therapy. Female. Gestational Age. Histone-Lysine N-Methyltransferase. Humans. Pregnancy. Prognosis. Stem Cell Transplantation. Translocation, Genetic. Young Adult

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  • (PMID = 20139053.001).
  • [ISSN] 1658-3876
  • [Journal-full-title] Hematology/oncology and stem cell therapy
  • [ISO-abbreviation] Hematol Oncol Stem Cell Ther
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Saudi Arabia
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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8. Bhojwani D, Howard SC, Pui CH: High-risk childhood acute lymphoblastic leukemia. Clin Lymphoma Myeloma; 2009;9 Suppl 3:S222-30
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  • [Title] High-risk childhood acute lymphoblastic leukemia.
  • Although most children with acute lymphoblastic leukemia (ALL) are cured, certain subsets have a high risk of relapse.
  • Though early treatment response can be assessed by the peripheral blast cell count after 1 week of single-agent glucocorticoid treatment or percent of bone marrow blasts by morphology after 1 or 2 weeks of multiagent induction treatment, determination of minimal residual disease by polymerase chain reaction (PCR) or flow cytometry after 2 to 6 weeks of induction is the most precise and useful measure.
  • Infants with mixed-lineage leukemia (MLL)-rearranged ALL comprise a very poor-risk group wherein further intensification of chemotherapy causes significant toxicity.
  • Hybrid protocols incorporating drugs effective for acute myeloid leukemia could improve survival, a strategy being tested in international trials.
  • New agents and methods to overcome resistance are under investigation, and allogeneic stem cell transplantation is recommended for certain subsets of patients, for example those with Ph+ and T-cell ALL with poor early response.
  • Genome-wide interrogation of leukemic cell genetic abnormalities and germline genetic variations promise to identify new molecular targets for therapy.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Glucocorticoids / therapeutic use. Humans. Infant. Neoplasm, Residual / drug therapy. Polymerase Chain Reaction. Recurrence. Remission Induction. Treatment Outcome

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  • (PMID = 19778845.001).
  • [ISSN] 1938-0712
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA021765-31; United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Glucocorticoids
  • [Number-of-references] 92
  • [Other-IDs] NLM/ NIHMS163517; NLM/ PMC2814411
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9. Hatoum HA, Mahfouz RA, Otrock ZK, Hudaib AR, Taher AT, Shamseddine AI: Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report. Am J Hematol; 2007 Jan;82(1):69-72
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  • [Title] Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report.
  • The association of chronic lymphocytic leukemia (CLL) and acute leukemia, either lymphoid or myeloid is a rare event.
  • Our review of the medical literature revealed only 6 cases of CLL transformation to acute myeloid leukemia (AML) (M0, M1 and M2) with no other associated malignancy.
  • We report a similar case but with occurrence of AML-M4 associated with normal cytogenetic analysis and molecular testing but with positive T-cell receptor gamma gene rearrangement rather than the usual Vbeta rearrangement.
  • [MeSH-major] Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


10. Scolnik MP, Aranguren PN, Cuello MT, Palacios MF, Sanjurjo J, Giunta M, Bracco MM, Acevedo S: Biphenotypic acute leukemia with t(15;17). Leuk Lymphoma; 2005 Apr;46(4):607-10
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  • [Title] Biphenotypic acute leukemia with t(15;17).
  • Biphenotypic acute leukemias (BAL) represent 5% of all acute leukemias.
  • Immunophenotype revealed the compromise of myeloid and B-lymphoid lineages.
  • This report describes a BAL case with an unfrequent cytogenetic abnormality, and highlights the importance of correlating the results of multiple diagnostic methods in order to establish a correct diagnosis and treatment in BAL patients.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 15 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Child. Chromosome Aberrations. Chromosomes, Human, Pair 8 / genetics. Female. Flow Cytometry / methods. Gene Rearrangement. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence / methods. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Trisomy

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  • (PMID = 16019491.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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11. Mori T, Nishimura N, Hasegawa D, Kawasaki K, Kosaka Y, Uchide K, Yanai T, Hayakawa A, Takeshima Y, Nishio H, Matsuo M: Persistent detection of a novel MLL-SACM1L rearrangement in the absence of leukemia. Leuk Res; 2010 Oct;34(10):1398-401
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  • [Title] Persistent detection of a novel MLL-SACM1L rearrangement in the absence of leukemia.
  • Most chromosomal rearrangements including the mixed lineage leukemia (MLL) gene are manifested as leukemia and predict a poor prognosis.
  • Here we report a case of a 3-year old boy bearing a novel MLL-rearrangement with the suppressor of actin mutations 1-like (SACM1L) gene in the absence of leukemia.
  • Bone marrow cells harboring the MLL-SACM1L rearrangement appeared during chemotherapy for acute lymphoblastic leukemia with hyperdiploidy and were continuously detected over 7 years without clonal expansion.
  • [MeSH-major] Gene Rearrangement. Membrane Proteins / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20553989.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Membrane Proteins; 0 / SACM1L protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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12. Cheng F, Liu J, Zhou SH, Wang XN, Chew JF, Deng LW: RNA interference against mixed lineage leukemia 5 resulted in cell cycle arrest. Int J Biochem Cell Biol; 2008;40(11):2472-81
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  • [Title] RNA interference against mixed lineage leukemia 5 resulted in cell cycle arrest.
  • Mixed lineage leukemia 5 (MLL5) encodes a mammalian trithorax group (TrxG) protein located within chromosome band 7q22, which is a frequently deleted region found in acute myeloid malignancies.
  • Recently, the emerging roles of TrxG and PcG group proteins in cell cycle regulation have begun to be elucidated.
  • In this study, we demonstrated that the mammalian trxG protein MLL5 is involved in multiple cell cycle regulation.
  • Knockdown of MLL5 by small interfering RNA resulted in the retarded cell growth and attenuated intake of BrdU in multiple tumor and normal diploid cells.
  • The cell cycle arrest induced by knockdown of MLL5 took place at both the G1 and G2/M phases.
  • This growth-inhibitory effect and dual-phase arrest were also found in p53-knockout cell lines, suggesting that the transactivation activity of p53 was dispensable for the MLL5-knockdown-mediated cell cycle arrest.
  • In addition, up-regulation of cyclin-dependent kinase inhibitor p21 and de-phosphorylation of retinoblastoma protein were observed in all cell lines tested regardless of their p53 status.
  • These findings provide evidence that MLL5 might be an important cell cycle regulator, participating in cell cycle regulatory network machinery at multiple cell cycle stages.
  • [MeSH-major] Cell Cycle / physiology. DNA-Binding Proteins
  • [MeSH-minor] Animals. Cell Line. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Humans. RNA Interference. Retinoblastoma Protein / genetics. Retinoblastoma Protein / metabolism. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 18573682.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / MLL5 protein, human; 0 / Retinoblastoma Protein; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53
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13. 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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14. Buckley O, Reardon M: A young male with bone pain. Eur J Intern Med; 2005 Sep;16(5):366-8
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  • Bone marrow biopsy and peripheral blood film confirmed the diagnosis of an acute biphenotypic leukaemia.
  • This case report highlights the fact that bone pain associated with a normal peripheral blood count may be the presentation of an acute haematological disorder in both adults and children.

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  • (PMID = 16137555.001).
  • [ISSN] 0953-6205
  • [Journal-full-title] European journal of internal medicine
  • [ISO-abbreviation] Eur. J. Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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15. 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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16. Murase K, Iyama S, Sato T, Takimoto R, Kobune M, Kato J: [Therapeutic results in patients with biphenotypic acute leukemia at Sapporo Medical University Hospital]. Gan To Kagaku Ryoho; 2010 Oct;37(10):2011-3
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  • [Title] [Therapeutic results in patients with biphenotypic acute leukemia at Sapporo Medical University Hospital].
  • We reviewed the results of 6 patients with biphenotypic acute leukemia (BAL) which the diagnostic standard of the European Group for the Immunological Characterization of Leukemia (EGIL) at Sapporo Medical University Hospital between 2006 and 2008.
  • Among them, 4 were B lymphoid and myeloid, 2 were T lymphoid and myeloid, and one was T/B lymphoid.
  • Two of 4 patients did not attain complete remission, and two relapsed after first treatment with acute myeloblastic leukemia (AML) protocol.
  • On the other hand, two showed complete remission after the acute lymphoblastic leukemia (ALL) protocol.
  • One of 4 patients survived who had been treated with hematopoietic stem cell transplantation as a post-remission therapy.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / drug therapy

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  • (PMID = 20948276.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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17. Thavaraj V, Seth R: Prophylaxis of central nervous system leukemia: a case of chronic myeloid leukemia with lymphoid blast crisis treated with imatinib mesylate. World J Pediatr; 2008 May;4(2):145-7
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  • [Title] Prophylaxis of central nervous system leukemia: a case of chronic myeloid leukemia with lymphoid blast crisis treated with imatinib mesylate.
  • BACKGROUND: Chronic myeloid leukemia (CML) in blast crisis has a dismal prognosis.
  • METHODS: A child with CML in lymphoid blast crisis was diagnosed by complete hematological and bone marrow examination.
  • There was no central nervous system (CNS) leukemia at presentation.
  • Results of cerebrospinal fluid taken for cytopathology showed CNS leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blast Crisis / drug therapy. Central Nervous System Neoplasms / prevention & control. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage
  • [MeSH-minor] Anti-Inflammatory Agents / administration & dosage. Benzamides. Blood Cell Count. Chemoprevention / methods. Child. Clinical Protocols. Cytarabine / administration & dosage. Drug Therapy, Combination. Female. Humans. Hydrocortisone / administration & dosage. Imatinib Mesylate. Injections, Spinal. Methotrexate / therapeutic use. Remission Induction

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  • (PMID = 18661773.001).
  • [ISSN] 1708-8569
  • [Journal-full-title] World journal of pediatrics : WJP
  • [ISO-abbreviation] World J Pediatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 8A1O1M485B / Imatinib Mesylate; WI4X0X7BPJ / Hydrocortisone; YL5FZ2Y5U1 / Methotrexate
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18. Shen Q, Chen Z, Liu XP, Xing HY, Wang M, Wang JX: [Expression of PTEN mRNA in acute leukemia and its clinical significance]. Zhonghua Xue Ye Xue Za Zhi; 2005 Aug;26(8):493-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of PTEN mRNA in acute leukemia and its clinical significance].
  • OBJECTIVE: To explore PTEN gene expression and its clinical significance in acute leukemia.
  • METHODS: The expression levels of PTEN mRNA in 5 leukemia cell lines, 87 patients with acute leukemias (AL), including 59 acute myeloid leukemia (AML), 26 acute lymphoblastic leukemia (ALL), and 2 acute hybrid leukemia, 21 AL in complete remission (AL-CR), 31 chronic myelogenous leukemia (CML) and 14 normal controls were assayed by RT-PCR.
  • RESULTS: PTEN mRNA was detected in K562 cell line, but not in Kasumi-1, HL-60, U937, Nalm-6 cell lines.
  • The decreased level of PTEN mRNA had a positive correlation with poor-prognostic factors (high white blood cell count of > or = 20 x 10(9)/L and chromosome abnormality).
  • [MeSH-major] Leukemia / metabolism. PTEN Phosphohydrolase / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16383243.001).
  • [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 / RNA, Messenger; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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19. Unal S, Cetin M, Tuncer AM, Gümrük F, Yetgin S: The prognostic impact of myeloid antigen expression in pediatric acute lymphoblastic leukemia patients. Turk J Pediatr; 2008 Nov-Dec;50(6):533-6
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  • [Title] The prognostic impact of myeloid antigen expression in pediatric acute lymphoblastic leukemia patients.
  • The incidence of mixed-lineage leukemias in the pediatric age group was previously reported as 13.8% for myeloid antigen-positive ALL and 11.1% for lymphoid antigen-positive acute myeloid leukemia (AML).
  • Recent studies showed that extensive chemotherapy protocols overcome the risk of myeloid lineage.
  • Our study also supports most of the previous data and we postulate that myeloid antigen expression in pediatric ALL cases has insignificant effect on clinical presentation, relapse rates and survival.
  • Importantly, 54% of myeloid antigen-expressing ALL patients received high-risk treatment protocols for some other reasons and this may also have contributed to similar outcome in these patients to that observed in myeloid antigen-negative ALL patients.
  • [MeSH-major] Antigens, CD / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Antigens, Neoplasm / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 19227415.001).
  • [ISSN] 0041-4301
  • [Journal-full-title] The Turkish journal of pediatrics
  • [ISO-abbreviation] Turk. J. Pediatr.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antigens, Neoplasm
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20. 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
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  • [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
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2769415
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21. 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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22. Daser A, Rabbitts TH: The versatile mixed lineage leukaemia gene MLL and its many associations in leukaemogenesis. Semin Cancer Biol; 2005 Jun;15(3):175-88
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  • [Title] The versatile mixed lineage leukaemia gene MLL and its many associations in leukaemogenesis.
  • The marked association of abnormalities of chromosome 11 long arm, band q23, with human leukaemia led to the identification of the 11q23 gene called MLL (or HTRX, HRX, TRX1, ALL-1).
  • MLL can become fused with one of a remarkable panoply of genes from other chromosome locations in individual leukaemias, leading to either acute myeloid or lymphoid tumours (hence the name MLL for mixed lineage leukaemia).
  • The unusual finding that a single protein could be involved in both myeloid and lymphoid malignancies and that the truncated protein could do so as a fusion with very disparate partners has prompted studies to define the molecular role of MLL-fusions in leukaemogenesis and to the development of MLL-controlled mouse models of leukaemogenesis.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Leukemia / metabolism. Leukemia / pathology. Myeloid-Lymphoid Leukemia Protein / metabolism

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  • (PMID = 15826832.001).
  • [ISSN] 1044-579X
  • [Journal-full-title] Seminars in cancer biology
  • [ISO-abbreviation] Semin. Cancer Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Number-of-references] 123
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23. 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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24. 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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25. Tan S, Wang G, Peng M, Zhang X, Shen G, Jiang J, Chen F: Detection of myeloperoxidase activity in primary leukemic cells by an enhanced chemiluminescent assay for differentiation between acute lymphoblastic and non-lymphoblastic leukemia. Clin Chim Acta; 2009 May;403(1-2):216-8
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  • [Title] Detection of myeloperoxidase activity in primary leukemic cells by an enhanced chemiluminescent assay for differentiation between acute lymphoblastic and non-lymphoblastic leukemia.
  • BACKGROUND: Myeloperoxidase (MPO) plays a crucial role in the differentiation of acute lymphoblastic leukemia (ALL) and acute non-lymphoblastic leukemia (ANLL).
  • In this report, we proposed the application of the enhanced chemiluminescent (ECL) technique to the determination of MPO activity in blasts of acute leukemia (AL).
  • METHODS: Bone-marrow samples were obtained from 23 patients with AL (ALL, 5 cases; ANLL, 13 cases; AUL, 1 cases; mixed-lineage AL, 4 cases).
  • In addition, this technique was able to demonstrate MPO activity in 4 mixed-lineage AL cases which did not stain for MPO in cytochemistry preparations.
  • [MeSH-major] Leukemia, Myeloid, Acute / enzymology. Leukemia, Myeloid, Acute / pathology. Luminescent Measurements / methods. Peroxidase / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Diagnosis, Differential. Female. HL-60 Cells. Humans. Infant. Male. Middle Aged


26. Milne TA, Dou Y, Martin ME, Brock HW, Roeder RG, Hess JL: MLL associates specifically with a subset of transcriptionally active target genes. Proc Natl Acad Sci U S A; 2005 Oct 11;102(41):14765-70
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  • MLL (mixed-lineage leukemia) is a histone H3 Lys-4 specific methyltransferase that is a positive regulator of Hox expression.
  • MLL rearrangements and amplification are common in acute lymphoid and myeloid leukemias and myelodysplastic disorders and are associated with abnormal up-regulation of Hox gene expression.
  • [MeSH-major] Gene Expression Regulation. Genes, Homeobox / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. RNA Polymerase II / metabolism. Transcription, Genetic / genetics
  • [MeSH-minor] Animals. Cell Line. Chromatin Immunoprecipitation. Glutathione Transferase. Mice. Mice, Inbred C57BL. Polymerase Chain Reaction

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  • (PMID = 16199523.001).
  • [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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.5.1.18 / Glutathione Transferase; EC 2.7.7.- / RNA Polymerase II
  • [Other-IDs] NLM/ PMC1253553
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27. Shand JC, Jansson J, Hsu YC, Campbell A, Mullen CA: Differential gene expression in acute lymphoblastic leukemia cells surviving allogeneic transplant. Cancer Immunol Immunother; 2010 Nov;59(11):1633-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential gene expression in acute lymphoblastic leukemia cells surviving allogeneic transplant.
  • The effectiveness of allogeneic graft-versus-leukemia (GVL) activity in control of acute lymphoblastic leukemia is generally regarded as poor.
  • One possible factor is dynamic adaptation of the leukemia cell to the allogeneic environment.
  • This work tested the hypothesis that the pattern of gene expression in acute lymphoblastic leukemia cells in an allogeneic environment would differ from that in a non-allogeneic environment.
  • Expression microarray studies were performed in murine B lineage acute lymphoblastic leukemia cells recovered from mice that had undergone allogeneic MHC-matched but minor histocompatibility antigen mismatched transplants.
  • Several genes with known immune activities potentially relevant to leukemia survival (Ly6a/Sca-1, TRAIL and H2-T23) were examined in independent validation experiments.
  • Increased expression in vivo in allogeneic hosts was observed, and could be mimicked in vitro with soluble supernatants of mixed lymphocyte reactions or interferon-gamma.
  • The changes in gene expression were reversible when the leukemia cells were removed from the allogeneic environment.
  • These findings suggest that acute lymphoblastic leukemia cells respond to cytokines present after allogeneic transplantation and that these changes may reduce the effectiveness of GVL activity.
  • [MeSH-major] Biomarkers, Tumor / genetics. Bone Marrow Transplantation. Graft Survival / physiology. Graft vs Leukemia Effect / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20602231.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA10628
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Minor Histocompatibility Antigens; 0 / RNA, Messenger; 82115-62-6 / Interferon-gamma
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28. Zhang J, Mi YC, Wang Y, Lin D, Li W, Sun XM, Zhou K, Bian SG, Wang JX: [Study on the clinical characteristics of adult biphenotypic acute leukaemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):18-21
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  • [Title] [Study on the clinical characteristics of adult biphenotypic acute leukaemia].
  • OBJECTIVE: To analyze the clinical and biological characteristics and prognosis of adult biphenotypic acute leukaemia (BAL).
  • The chemotherapy regimens were accordingly for acute lymphoblastic leukaemia (ALL), acute myeloid leukaemia (AML) or for both ALL and AML.
  • (1) The incidence of BAL in acute leukaemias was 6.7%, with a male predominance and 52.3% of BAL patients had WBC > or = 30 x 10(9)/L and 16.9% WBC > or = 100 x 10(9)/L. (2) Percentages of coexpression of myeloid and B lymphoid antigens were 81.5%, of myeloid and T lymphoid antigens 10.8%, of myeloid, B- and T lymphoid antigens 4.6%, and of B and T lymphoid antigens 3.1%. (3) Normal and abnormal karyotypes accounted for 41.5% and 58.5%, respectively in 53 BAL patients with karyotype analysis.
  • (1) High white blood cell count and coexpression of myeloid/B lymphoid antigens are common in BAL. (2) Abnormal karyotypes and Ph (+) or bcr-abl( +) often happen. (3) The treatment outcome of BAL is poor.
  • [MeSH-major] Leukemia, Biphenotypic, Acute

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  • (PMID = 19563029.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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29. Faber J, Armstrong SA: Defining leukemia stem cells in MLL-translocated leukemias: implications for novel therapeutic strategies. Klin Padiatr; 2007 Nov-Dec;219(6):306-11
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  • [Title] Defining leukemia stem cells in MLL-translocated leukemias: implications for novel therapeutic strategies.
  • An important question in the development of novel, less toxic antileukemic strategies specifically targeting leukemia stem cells is how closely leukemia stem cells are related to normal hematopoietic stem cells.
  • It has been recently demonstrated that leukemia stem cells can be derived from different stages in normal hematopoiesis and have unique phenotypic and genetic features.
  • Introduction of Mixed-lineage leukemia ( MLL)-fusion oncoproteins, frequently found in infant leukemias and therapy-related leukemias, into differentiated hematopoietic progenitor cells results in the generation of leukemias with a high frequency of leukemia stem cells.
  • The progenitor-derived leukemia stem cells ectopically express a limited stem cell program while maintaining the global identity of differentiated myeloid cells.
  • Development of therapeutic strategies that specifically target the leukemia stem cell program while sparing normal hematopoietic stem cells may represent a novel therapeutic approach in human leukemias with high efficacy yet less side effects.
  • [MeSH-major] Leukemia / therapy. Leukemia, Biphenotypic, Acute. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplastic Stem Cells
  • [MeSH-minor] Child. Hematopoietic Stem Cells. Histone-Lysine N-Methyltransferase. Humans. Infant. Oncogene Proteins, Fusion. Phenotype

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  • (PMID = 18050039.001).
  • [ISSN] 0300-8630
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 62
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30. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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31. 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


32. Bursen A, Schwabe K, Rüster B, Henschler R, Ruthardt M, Dingermann T, Marschalek R: The AF4.MLL fusion protein is capable of inducing ALL in mice without requirement of MLL.AF4. Blood; 2010 Apr 29;115(17):3570-9
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  • The chromosomal translocation t(4;11)(q21;q23) is the most frequent genetic aberration of the human MLL gene, resulting in high-risk acute lymphoblastic leukemia (ALL).
  • Recipients of AF4.MLL- or double-transduced LSPCs developed pro-B ALL, B/T biphenotypic acute leukemia, or mixed lineage leukemia.
  • Transplantation of MLL.AF4- or mock-transduced LSPCs did not result in disease development during an observation period of 13 months.
  • These findings indicate that the expression of the AF4.MLL fusion protein is capable of inducing acute lymphoblastic leukemia even in the absence of the MLL.AF4 fusion protein.
  • In view of recent findings, these results may imply that t(4;11) leukemia is based on 2 oncoproteins, providing an explanation for the very early onset of disease in humans.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Leukemic. Myeloid-Lymphoid Leukemia Protein / metabolism. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 20194896.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aff1 protein, mouse; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse
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33. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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34. Liu Z, Liu XL, Du QF, Xu N, Zhong M, Song LL, Yi ZS, Liu QF, Meng FY, Zhou SY: [Clinical characteristics and outcomes of 59 patients with acute lymphoblastic leukemia positive for BCR/ABL]. Nan Fang Yi Ke Da Xue Xue Bao; 2009 Mar;29(3):512-5
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  • [Title] [Clinical characteristics and outcomes of 59 patients with acute lymphoblastic leukemia positive for BCR/ABL].
  • OBJECTIVE: To study the clinical characteristics and outcomes of BCR/ABL-positive acute lymphoblastic leukemia (BCR/ABL360888725-ALL) and screen the prognostic factors for BCR/ABL360888725-ALL.
  • METHODS: From January 2001 to May 2008, 59 patients (median age of 32 years ranging from 3 to 69 years) with the diagnosis of BCR/ABL360888725-ALL by fluorescence in situ hybridization received induction chemotherapy with VDLP-/+Ara-C regimen.
  • The patients who failed to respond to the chemotherapy received subsequent consolidation chemotherapy with imatinib (400-800 mg/day) (17 cases) or allogeneic hematopoietic stem cell transplantation (allo-HSCT) (16 cases).
  • In patients with peripheral white blood cell (WBC) count <30=10(9)/L, 30-99.9(9)/L and > or =100(9)/L, the CR rates were 75.0% (18/24), 56.3% (9/15) and 26.3% (5/19) (P=0.006), and the overall survival probability of 2 years ( OSs of 2-yrs) was 24.7%, 22.5% and 21.1%, respectively (P=0.180).
  • According to the FAB classification, 56 cases were divided into L1, L2 and biphenotypic acute leukemia (BAL) subgroups, and their CR rates were 66.7% (6/9), 63.2% (24/38) and 22.2% (2/9) (P=0.029), with OSs of 2-yrs of 22.2%, 27.0% and 22.0%, respectively (P=0.623).
  • In terms of immunophenotype grouping by EGIL, the patients with ALL, myeloid antigen-positive ALL and BAL had CR rates of 61.1% (11/18), 60.6% (20/33) and 12.5% (1/8) (P=0.039), and the OSs of 2-yrs of 22.7%, 21.0% and 18.8%, respectively (P=0.643).
  • In 55 patients with known karyotype, the CR rates were 71.4%(5/7), 70.8% (17/24) and 37.5% (9/24) in normal, sole t(9;22) abnormality, t(9;22) with additional abnormalities groups (P=0.046), with the OSs of 2-yrs of 42.9%, 34.0% and 7.3%, respectively (P=0.000).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Genes, abl / genetics. Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19304540.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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35. Gozzetti A, Calabrese S, Raspadori D, Crupi R, Tassi M, Bocchia M, Fabbri A, Lauria F: Concomitant t(4;11) and t(1;19) in a patient with biphenotypic acute leukemia. Cancer Genet Cytogenet; 2007 Aug;177(1):81-2
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  • [Title] Concomitant t(4;11) and t(1;19) in a patient with biphenotypic acute leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 4 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Banding. Fatal Outcome. Humans. Karyotyping. Male. Middle Aged. Phenotype


36. 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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37. 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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38. Kaltenbach S, Soler G, Barin C, Gervais C, Bernard OA, Penard-Lacronique V, Romana SP: NUP98-MLL fusion in human acute myeloblastic leukemia. Blood; 2010 Sep 30;116(13):2332-5
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  • [Title] NUP98-MLL fusion in human acute myeloblastic leukemia.
  • H3K4 (histone H3 lysine 4) methylation by the SET domain of the trithorax-group protein MLL (mixed-lineage leukemia) is important for the control of homeobox (HOX) gene expression during development.
  • MLL fusion proteins associated with human leukemia contain the menin interaction peptide and frequently recruit H3K79 (histone H3 lysine 79) methylation activity.
  • We have characterized a novel recurrent chromosomal aberration, inv(11)(p15q23), as an isolated chromosomal abnormality in 2 patients with acute myeloid leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics
  • [MeSH-minor] Adult. Aged. Base Sequence. Cell Transformation, Neoplastic / genetics. Chromosome Inversion. Chromosomes, Human, Pair 11 / genetics. DNA Primers / genetics. DNA, Neoplasm / genetics. Female. Gene Expression. Genes, Homeobox. Histone-Lysine N-Methyltransferase. Histones / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Oncogene Fusion. Proto-Oncogene Proteins / metabolism

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  • (PMID = 20558618.001).
  • [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 / DNA Primers; 0 / DNA, Neoplasm; 0 / Histones; 0 / Homeodomain Proteins; 0 / MEN1 protein, human; 0 / MLL protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 157907-48-7 / HoxA protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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39. 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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40. Cóser VM, Meyer C, Basegio R, Menezes J, Marschalek R, Pombo-de-Oliveira MS: Nebulette is the second member of the nebulin family fused to the MLL gene in infant leukemia. Cancer Genet Cytogenet; 2010 Apr 15;198(2):151-4
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  • [Title] Nebulette is the second member of the nebulin family fused to the MLL gene in infant leukemia.
  • Genetic aberrations involving the mixed lineage leukemia (MLL) gene are frequently diagnosed in infant acute lymphoblastic and acute myeloid leukemia.
  • More than 60 fusion partner genes have been described at the molecular level, 31 of which have been characterized solely in infant leukemia cases.
  • Here we describe a new MLL fusion partner gene, NEBL, which was identified in a case of acute myeloid leukemia in an infant.
  • [MeSH-major] Carrier Proteins / genetics. Cytoskeletal Proteins / genetics. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20362230.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Cytoskeletal Proteins; 0 / LIM Domain Proteins; 0 / MLL protein, human; 0 / Muscle Proteins; 0 / NEBL protein, human; 0 / Oncogene Proteins, Fusion; 0 / nebulin; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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41. Shimada A, Taki T, Tabuchi K, Taketani T, Hanada R, Tawa A, Tsuchida M, Horibe K, Tsukimoto I, Hayashi Y: Tandem duplications of MLL and FLT3 are correlated with poor prognoses in pediatric acute myeloid leukemia: a study of the Japanese childhood AML Cooperative Study Group. Pediatr Blood Cancer; 2008 Feb;50(2):264-9
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  • [Title] Tandem duplications of MLL and FLT3 are correlated with poor prognoses in pediatric acute myeloid leukemia: a study of the Japanese childhood AML Cooperative Study Group.
  • BACKGROUND: Mixed-lineage leukemia (MLL)-partial tandem duplication (PTD) is associated with poor prognosis in adult acute myeloid leukemia (AML), but its relationship to pediatric AML is unknown.
  • The differences between patients with and without MLL-PTD were significant for 3-year overall survival (OS) (56.3% vs. 83.2%, P = 0.018), disease-free survival (DFS) (41.7% vs. 69.6%, P = 0.010), and relapse rate (RR) (54.3% vs. 27.6%, P = 0.0085) of 135 AML patients excluding the FAB-M3 and DS patients.
  • [MeSH-major] Gene Duplication. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17763464.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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42. Wei J, Wunderlich M, Fox C, Alvarez S, Cigudosa JC, Wilhelm JS, Zheng Y, Cancelas JA, Gu Y, Jansen M, Dimartino JF, Mulloy JC: Microenvironment determines lineage fate in a human model of MLL-AF9 leukemia. Cancer Cell; 2008 Jun;13(6):483-95
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  • [Title] Microenvironment determines lineage fate in a human model of MLL-AF9 leukemia.
  • Faithful modeling of mixed-lineage leukemia in murine cells has been difficult to achieve.
  • We show that expression of MLL-AF9 in human CD34+ cells induces acute myeloid, lymphoid, or mixed-lineage leukemia in immunodeficient mice.
  • Some leukemia stem cells (LSC) were multipotent and could be lineage directed by altering either the growth factors or the recipient strain of mouse, highlighting the importance of microenvironmental cues.
  • Other LSC were strictly lineage committed, demonstrating the heterogeneity of the stem cell compartment in MLL disease.


43. Kim KE, Kim SH, Han JY: [Acute Monocytic Leukemia with t(11;17)(q23;q21) Involving a Rearrangement of Mixed Lineage Leukemia Gene.]. Korean J Lab Med; 2006 Oct;26(5):329-33
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  • [Title] [Acute Monocytic Leukemia with t(11;17)(q23;q21) Involving a Rearrangement of Mixed Lineage Leukemia Gene.].
  • A case of acute monocytic leukemia (AMoL) by French-American-British (FAB) classification in a 63-year-old male showed the abnormal karyotype 46,XY,t(11;17)(q23;q21), previously reported as a variant translocation in acute promyelocytic leukemia (APL).
  • Fluorescence in situ hybridization (FISH) analysis identified a mixed lineage leukemia (MLL) gene rearrangement, but not visible disruptions of promyelocytic leukemia (PML) or retinoic acid receptor alpha (RARA) genes.
  • Now, a few cases of AMoL with a similar translocation have been reported in the literature, and these cases emphasize the importance of cytogenetic and FISH studies in addition to morphology, cytochemistry, and immunophenotype in classifying acute myeloid leukemia (AML).

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  • (PMID = 18156746.001).
  • [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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44. 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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  • [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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45. Marques-Salles Tde J, Barros JE, Soares-Ventura EM, Cartaxo Muniz MT, Santos N, Ferreira da Silva E, Silva ML, Liehr T, Mkrtchyan H: Unusual childhood biphenotypic acute leukemia with a yet unreported t(3;13)(p25.1;q13). Leuk Res; 2010 Aug;34(8):e206-7
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  • [Title] Unusual childhood biphenotypic acute leukemia with a yet unreported t(3;13)(p25.1;q13).
  • [MeSH-major] Chromosomes, Human, Pair 13 / genetics. Chromosomes, Human, Pair 3 / genetics. Killer Cells, Natural / pathology. Leukemia, Myeloid, Acute / pathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic / genetics
  • [MeSH-minor] Adolescent. Humans. Male. Phenotype. Prognosis

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  • (PMID = 20338638.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
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46. 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
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  • [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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47. Jeha S, Kantarjian H: Clofarabine for the treatment of acute lymphoblastic leukemia. Expert Rev Anticancer Ther; 2007 Feb;7(2):113-8
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  • [Title] Clofarabine for the treatment of acute lymphoblastic leukemia.
  • A marked improvement in the outcome of patients with acute lymphoblastic leukemia has been achieved with chemotherapeutic agents developed between the 1950s and 1970s.
  • As the limits of optimizing the use of old drugs are reached, most adults with acute lymphoblastic leukemia still succumb to their disease and leukemia remains the leading cause of nonaccidental death in children.
  • Clofarabine, a next-generation deoxyadenosine analog, has demonstrated significant activity in children and adults with refractory lymphoid and myeloid leukemia in early clinical trials and was granted approval for use in children with acute lymphoblastic leukemia in second or higher relapse.
  • [MeSH-major] Adenine Nucleotides / therapeutic use. Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17288522.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
  • [Number-of-references] 36
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48. 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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  • 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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49. Zhang LJ, Lu XL, He J, Li Y: [Rearrangements of the mixed lineage leukemia gene in acute myeloid leukemia]. Zhonghua Yi Xue Za Zhi; 2006 Aug 29;86(32):2256-60
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  • [Title] [Rearrangements of the mixed lineage leukemia gene in acute myeloid leukemia].
  • OBJECTIVE: To study the frequency of mixed lineage leukemia (MLL) gene rearrangements in patients with acute myeloid leukemia (AML) and to determine the significance thereof.
  • METHODS: Conventional cytogenetics (CC) and karyotype analysis were conducted on the bone marrow cells from 58 patients with acute myelocytic leukemia (AML), 47 adults (aged 15 approximately 67) and 11 children (aged 1 approximately 14).
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 17064570.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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50. 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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51. Pullarkat V, Veliz L, Chang K, Mohrbacher A, Teotico AL, Forman SJ, Slovak ML: Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus. J Clin Pathol; 2007 May;60(5):562-4
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  • [Title] Therapy-related, mixed-lineage leukaemia translocation-positive, monoblastic myeloid sarcoma of the uterus.
  • Myeloid sarcomas are tumour masses of myeloid leukaemic cells at extramedullary sites.
  • These tumours can, on occasion, occur without concurrent or antecedent leukaemia.
  • Myeloid sarcomas have been described at unusual locations including the female genital tract.
  • An unusual case of therapy-related acute myeloid leukaemia (t-AML) presenting as isolated monoblastic myeloid sarcoma of the uterus in a patient who had received adjuvant chemotherapy for breast cancer is presented.
  • Fluorescence in situ hybridisation analysis performed on paraffin-wax-embedded tumour tissue revealed a mixed-lineage leukaemia (MLL) gene rearrangement, supporting the association of this malignancy with prior chemotherapy.
  • This case illustrates that t-AML can rarely present as isolated extramedullary tumours, and the detection of specific chromosomal abnormalities in these myeloid sarcomas can be useful for risk assessment and guiding definitive therapy.

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  • (PMID = 17513515.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA030206; United States / NCI NIH HHS / CA / 2 P01 CA030206-24A1; United States / NCI NIH HHS / CA / 5P30 CA33572
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1994540
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52. Shi M, Cui F, Li B, Li SY, Ma HJ: Mixed phenotype acute leukaemia with giant inclusions. Br J Haematol; 2010 Apr;149(1):2
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  • [Title] Mixed phenotype acute leukaemia with giant inclusions.
  • [MeSH-major] Inclusion Bodies / ultrastructure. Leukemia, Biphenotypic, Acute / pathology

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  • (PMID = 20015299.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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53. Pajuelo-Gámez JC, Cervera J, García-Casado Z, Mena-Durán AV, Valencia A, Barragán E, Such E, Bolufer P, Sanz MA: MLL amplification in acute myeloid leukemia. Cancer Genet Cytogenet; 2007 Apr 15;174(2):127-31
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  • [Title] MLL amplification in acute myeloid leukemia.
  • The chromosomal alterations at 11q23 that involve the mixed-lineage leukemia gene (MLL, HTRX1, HRX, ALL1) are one of the most common cytogenetic abnormalities in acute leukemia and have been associated with a poor prognosis.
  • [MeSH-major] Gene Amplification. Leukemia, Myeloid / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] Acute Disease. Aged. Aneuploidy. Base Sequence. Chromosome Banding. Chromosome Deletion. Female. Genome, Human. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Molecular Sequence Data. Nucleic Acid Hybridization / methods. Sequence Analysis, DNA

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  • (PMID = 17452254.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [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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54. Vega F, Medeiros LJ, Davuluri R, Cromwell CC, Alkan S, Abruzzo LV: t(8;13)-positive bilineal lymphomas: report of 6 cases. Am J Surg Pathol; 2008 Jan;32(1):14-20
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  • The 8p11 myeloproliferative syndrome (EMS) is a rare hematologic malignancy characterized by myeloid hyperplasia, eosinophilia, and precursor lymphoblastic lymphoma, associated with balanced translocations involving chromosome 8p11, most commonly t(8;13)(p11;q12).
  • Approximately 75% of EMS patients present with or develop precursor T-cell lymphoblastic lymphoma, and most subsequently develop acute myeloid leukemia.
  • Here we describe the morphologic and immunophenotypic features of 6 cases of t(8;13)-positive bilineal lymphoma of mixed T-cell and myeloid lineage, 5 in lymph nodes and 1 in breast.
  • Histologically, each tumor was composed of 2 distinct cellular components: small to medium-sized T cells with scant cytoplasm that resembled lymphoblasts, and larger immature-appearing cells with more abundant eosinophilic cytoplasm that resembled myeloblasts, a subset of which expressed myeloid antigens.
  • In all cases, the latter component tended to surround residual lymphoid follicles and/or blood vessels.
  • We believe that these bilineal neoplasms of mixed T-cell and myeloid lineages, which present as lymphoma, are analogous to bilineal leukemias.
  • They likely arise from an early hematopoietic cell with potential to differentiate along T-cell and myeloid pathways.
  • [MeSH-minor] Adolescent. Adult. Antigens, CD / metabolism. Cell Lineage. Child. Female. Granulocyte Precursor Cells / metabolism. Granulocyte Precursor Cells / pathology. Humans. Immunohistochemistry. Immunophenotyping. Lymphocytes / metabolism. Lymphocytes / pathology. Male. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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  • (PMID = 18162765.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD
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55. Bitoun E, Oliver PL, Davies KE: The mixed-lineage leukemia fusion partner AF4 stimulates RNA polymerase II transcriptional elongation and mediates coordinated chromatin remodeling. Hum Mol Genet; 2007 Jan 01;16(1):92-106
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  • [Title] The mixed-lineage leukemia fusion partner AF4 stimulates RNA polymerase II transcriptional elongation and mediates coordinated chromatin remodeling.
  • AF4 gene, frequently translocated with mixed-lineage leukemia (MLL) in childhood acute leukemia, encodes a putative transcriptional activator of the AF4/LAF4/FMR2 (ALF) protein family previously implicated in lymphopoiesis and Purkinje cell function in the cerebellum.
  • [MeSH-major] Chromatin Assembly and Disassembly. Leukemia / genetics. Nuclear Proteins / genetics. RNA Polymerase II / genetics. Transcription, Genetic
  • [MeSH-minor] Animals. Cell Line. DNA Polymerase II / metabolism. Down-Regulation. HeLa Cells. Humans. Methylation. Methyltransferases / metabolism. Mice. Models, Biological. Multiprotein Complexes / metabolism. Phosphorylation. Phosphotransferases / metabolism. Positive Transcriptional Elongation Factor B / metabolism. Proteasome Endopeptidase Complex / metabolism. Signal Transduction. Transcription Factors / metabolism. Transcriptional Activation. Transfection

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  • (PMID = 17135274.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137761449
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aff2 protein, mouse; 0 / Mllt10 protein, mouse; 0 / Mllt3 protein, mouse; 0 / Multiprotein Complexes; 0 / Nuclear Proteins; 0 / Transcription Factors; EC 2.1.1.- / Dot1l protein, mouse; EC 2.1.1.- / Methyltransferases; EC 2.7.- / Phosphotransferases; EC 2.7.11.- / Positive Transcriptional Elongation Factor B; EC 2.7.7.- / DNA Polymerase II; EC 2.7.7.- / RNA Polymerase II; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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56. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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57. Popovic R, Zeleznik-Le NJ: MLL: how complex does it get? J Cell Biochem; 2005 May 15;95(2):234-42
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  • The mixed lineage leukemia (MLL) gene encodes a very large nuclear protein homologous to Drosophila trithorax (trx).
  • MLL was identified as a common target of chromosomal translocations associated with human acute leukemias.
  • MLL gene rearrangements are found in leukemias with both lymphoid and myeloid phenotypes and are often associated with infant and secondary leukemias.
  • The immature phenotype of the leukemic blasts suggests an important role for MLL in the early stages of hematopoietic development.
  • [MeSH-minor] Animals. Gene Expression Regulation, Developmental / physiology. Genes, Homeobox. Histone-Lysine N-Methyltransferase. Humans. Leukemia, Lymphoid / genetics. Leukemia, Myeloid / genetics. Mice. Myeloid-Lymphoid Leukemia Protein. Phenotype

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  • (PMID = 15779005.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA40046
  • [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 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse
  • [Number-of-references] 49
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58. Dou Y, Hess JL: Mechanisms of transcriptional regulation by MLL and its disruption in acute leukemia. Int J Hematol; 2008 Jan;87(1):10-8
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  • [Title] Mechanisms of transcriptional regulation by MLL and its disruption in acute leukemia.
  • Fusion of the mixed lineage leukemia protein (MLL) to one of over 50 different translocation partners converts it into a potent leukemogenic oncoprotein.
  • Considerable progress has been made in delineating the differences between normal Hox gene regulation by MLL and deregulated transcription in MLL-induced leukemias.
  • [MeSH-major] Leukemia / genetics. Leukopoiesis / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Transcription, Genetic / genetics
  • [MeSH-minor] Animals. DNA Methylation. Disease Models, Animal. Histone-Lysine N-Methyltransferase. Homeodomain Proteins / genetics. Homeodomain Proteins / physiology. Humans. Mice. Mice, Knockout. Neoplasm Proteins / genetics. Neoplasm Proteins / physiology

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  • (PMID = 18224408.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Hoxa7 protein, mouse; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / myeloid ecotropic viral integration site 1 protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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59. 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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60. 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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61. Balgobind BV, Zwaan CM, Reinhardt D, Arentsen-Peters TJ, Hollink IH, de Haas V, Kaspers GJ, de Bont ES, Baruchel A, Stary J, Meyer C, Marschalek R, Creutzig U, den Boer ML, Pieters R, van den Heuvel-Eibrink MM: High BRE expression in pediatric MLL-rearranged AML is associated with favorable outcome. Leukemia; 2010 Dec;24(12):2048-55
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  • Translocations involving the mixed lineage leukemia (MLL) gene, localized at 11q23, frequently occur in pediatric acute myeloid leukemia (AML).
  • Forced expression of BRE did not result in altered cell proliferation, apoptosis or drug sensitivity, which could explain the favorable outcome.
  • [MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nerve Tissue Proteins / genetics

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  • (PMID = 20861917.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BRE protein, human; 0 / MLL protein, human; 0 / Nerve Tissue Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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62. 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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63. Di Croce L: Chromatin modifying activity of leukaemia associated fusion proteins. Hum Mol Genet; 2005 Apr 15;14 Spec No 1:R77-84
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  • [Title] Chromatin modifying activity of leukaemia associated fusion proteins.
  • The leukaemias, which are divided into chronic and acute forms, are malignant diseases of haematopoietic cells in which the proper balance between proliferation, differentiation and apoptosis is no longer operative.
  • Genes, such as those of mixed-lineage leukaemia, AML1 and retinoic acid receptor alpha, have been found to be aberrantly fused to different partners, which often encode transcription factors or other chromatin modifying enzymes, in numerous types of acute lymphoid and myeloid leukaemias.
  • These chimeric fusion oncoproteins, generated by reciprocal chromosomal translocations, are responsible for chromatin alterations on target genes whose expression is critical to stem cell development or lineage specification in haematopoiesis.
  • [MeSH-major] Chromatin / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Neoplastic. Leukemia / metabolism. Proto-Oncogene Proteins / metabolism. Receptors, Retinoic Acid / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Differentiation. Core Binding Factor Alpha 2 Subunit. DNA Methylation. Epigenesis, Genetic. Gene Silencing. Hematopoiesis. Humans. Models, Biological. Molecular Sequence Data. Oncogene Proteins, Fusion / chemistry

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  • (PMID = 15809276.001).
  • [ISSN] 0964-6906
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromatin; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Transcription Factors; 0 / retinoic acid receptor alpha
  • [Number-of-references] 64
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64. Fais F, Tenca C, Cimino G, Coletti V, Zanardi S, Bagnara D, Saverino D, Zarcone D, De Rossi G, Ciccone E, Grossi CE: CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis. Leukemia; 2005 Apr;19(4):551-6
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  • [Title] CD1d expression on B-precursor acute lymphoblastic leukemia subsets with poor prognosis.
  • Acute lymphoblastic leukemia (ALL) is the most frequent malignancy of childhood.
  • We investigated CD1d expression in 80 pediatric B-cell precursor (BCP) ALL cases defined according to immunophenotype, cytogenetic features and age at onset.
  • CD1d+ ALLs were significantly associated with infant leukemia, pro-B phenotype and mixed-lineage leukemia (MLL)/AF4 gene rearrangement.
  • [MeSH-major] Antigens, CD1 / metabolism. Hematopoietic Stem Cells / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Antigens, CD1d. B-Lymphocytes / cytology. Biomarkers, Tumor / metabolism. Cell Communication. Cell Line. Child. Galactosylceramides / metabolism. Humans. Infant. Killer Cells, Natural / cytology. Killer Cells, Natural / metabolism. Predictive Value of Tests. Prognosis. Survival Rate

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  • (PMID = 15744356.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD1; 0 / Antigens, CD1d; 0 / Biomarkers, Tumor; 0 / CD1D protein, human; 0 / Galactosylceramides; 0 / alpha-galactosylceramide
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65. 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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  • 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.

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  • (PMID = 18671852.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK058161; United States / NHLBI NIH HHS / HL / R01 HL079507; United States / NIDDK NIH HHS / DK / DK58161; United States / NHLBI NIH HHS / HL / HL079507
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CBFB protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / RUNX1 protein, human; 0 / Runx1 protein, mouse
  • [Other-IDs] NLM/ PMC2529319
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66. 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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67. 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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68. 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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69. Papenhausen PR, Griffin S, Tepperberg J: Oncogene amplification in transforming myelodysplasia. Exp Mol Pathol; 2005 Oct;79(2):168-75
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  • The MLL gene, located within band 11q23, has been shown to be involved in translocations with a large variety of reciprocal sites in both lymphoid and myeloid leukemia and has also been shown to undergo submicroscopic self-fusion/partial duplication.
  • The frequency and clinical correlations of MLL gene amplification in leukemia will need careful follow-up, since the frequently cryptic amplification described in these cases may not generally provoke confirmatory FISH studies.
  • A common cytogenetic profile of 5 q-, -17/17 p-, -18/18 q-, and a missing or abnormal chromosome 11, may help direct appropriate follow-up studies.
  • Both genes also show a high degree of diversity of pathogenic mechanisms of leukemia evolution, including numerous reciprocal fusion genes in transformation to either AML or ALL and gain of function amplification.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics

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  • (PMID = 16026782.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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70. Wu X, Hua X: Menin, histone h3 methyltransferases, and regulation of cell proliferation: current knowledge and perspective. Curr Mol Med; 2008 Dec;8(8):805-15
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  • [Title] Menin, histone h3 methyltransferases, and regulation of cell proliferation: current knowledge and perspective.
  • However, until recently little has been known as to how menin regulates cell proliferation.
  • Rapid research progress in the past several years suggests that menin represses proliferation of endocrine cells yet promotes proliferation in certain types of leukemia cells via interacting with various transcriptional regulators.
  • Menin interacts with histone H3 methyltransferases such as MLL (mixed lineage leukemia) protein.
  • Increasing evidence has linked the biological function of menin to epigenetic histone modifications, control of the pattern of gene expression, and regulation of cell proliferation in a cell type-specific manner.
  • In light of these recent findings, an emerging model suggests that menin is a crucial regulator of histone modifiers by acting as a scaffold protein to coordinate gene transcription and cell proliferation in a cell context-dependent manner.
  • This recent progress unravels the coordinating role of menin in epigenetics and regulation of cell cycle, providing novel insights into understanding regulation of beta cell functions and diabetes, as well as the development and therapy of endocrine tumors and leukemia.

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  • (PMID = 19075677.001).
  • [ISSN] 1566-5240
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA113962-02; United States / NCI NIH HHS / CA / CA113962-03; United States / NCI NIH HHS / CA / CA100912-04; United States / NCI NIH HHS / CA / R01 CA113962; United States / NCI NIH HHS / CA / R01 CA113962-03; United States / NCI NIH HHS / CA / R01 CA100912; United States / NCI NIH HHS / CA / R01 CA100912-04; United States / NCI NIH HHS / CA / CA100912-03; United States / NCI NIH HHS / CA / R01 CA100912-03; United States / NCI NIH HHS / CA / CA113962-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 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
  • [Number-of-references] 92
  • [Other-IDs] NLM/ NIHMS183824; NLM/ PMC2858577
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71. Lee JC, Yang S, Zou Y, Joseph L: Erythroid/B-cell biphenotypic acute leukemia first case report. Leukemia; 2009 Oct;23(10):1920-3
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  • [Title] Erythroid/B-cell biphenotypic acute leukemia first case report.
  • [MeSH-major] B-Lymphocytes / pathology. Erythroid Cells / pathology. Leukemia, Biphenotypic, Acute / pathology

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  • (PMID = 19458630.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD
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72. 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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73. Bardini M, Spinelli R, Bungaro S, Mangano E, Corral L, Cifola I, Fazio G, Giordan M, Basso G, De Rossi G, Biondi A, Battaglia C, Cazzaniga G: DNA copy-number abnormalities do not occur in infant ALL with t(4;11)/MLL-AF4. Leukemia; 2010 Jan;24(1):169-76
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  • The pathogenesis of infant acute lymphoblastic leukemia (ALL) is still not well defined.
  • Short latency to leukemia and very high concordance rate for ALL in Mixed-Lineage Leukemia (MLL)-positive infant twins suggest that the MLL rearrangement itself could be sufficient for overt leukemia.
  • Attempts to generate a suitable mouse model for MLL-AF4-positive ALL did not thoroughly resolve the issue of whether cooperating mutations are required to reduce latency and to generate overt leukemia in vivo.
  • In contrast to pediatric, adolescent and adult ALL cases, the MLL rearrangement in infant ALL is associated with an exceptionally low frequency of copy-number abnormalities, thus confirming the unique nature of this disease.
  • By contrast, additional genetic aberrations are acquired at disease relapse.
  • It can be argued that the MLL rearrangement as a first hit, rather than inducing the acquisition of additional genetic lesions, has a major role to drive and hasten the onset of leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 4. Gene Dosage. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 19907438.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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74. Rice KL, Licht JD: HOX deregulation in acute myeloid leukemia. J Clin Invest; 2007 Apr;117(4):865-8
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  • [Title] HOX deregulation in acute myeloid leukemia.
  • The deregulation of homeobox (HOX) genes in acute myeloid leukemia (AML) and the potential for these master regulators to perturb normal hematopoiesis is well established.
  • To date, overexpression of HOX genes in AML has been attributed to specific chromosomal aberrations and abnormalities involving mixed-lineage leukemia (MLL), an upstream regulator of HOX genes.
  • The finding reported in this issue of the JCI by Scholl et al. that caudal-type homeobox transcription factor 2 (CDX2), which is capable of affecting HOX gene expression during embryogenesis, is overexpressed in 90% of patients with AML and induces a transplantable AML in murine models provides an alternative mechanism for HOX-induced leukemogenesis and yields important insights into the hierarchy of HOX gene regulation in AML (see the related article beginning on page 1037).
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Homeodomain Proteins / genetics. Leukemia, Myeloid / genetics. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Animals. Disease Models, Animal. Genes, Homeobox. Humans. Mice. Transcription Factors / genetics

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  • (PMID = 17404613.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDX2 protein, human; 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC1838955
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75. Milne TA, Martin ME, Brock HW, Slany RK, Hess JL: Leukemogenic MLL fusion proteins bind across a broad region of the Hox a9 locus, promoting transcription and multiple histone modifications. Cancer Res; 2005 Dec 15;65(24):11367-74
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  • Chromosome translocations involving the mixed lineage leukemia gene MLL are associated with aggressive acute leukemias in both children and adults.
  • [MeSH-major] Homeodomain Proteins / metabolism. Myeloid-Lymphoid Leukemia Protein / metabolism. Oncogene Proteins, Fusion / metabolism. Transcription, Genetic

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  • (PMID = 16357144.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA78815; United States / NCI NIH HHS / CA / CA92251
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histones; 0 / Homeodomain Proteins; 0 / MLL-ENL oncoprotein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / homeobox protein HOXA9; 0 / myeloid ecotropic viral integration site 1 protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; K3Z4F929H6 / Lysine
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76. Stasik C, Ganguly S, Cunningham MT, Hagemeister S, Persons DL: Infant acute lymphoblastic leukemia with t(11;16)(q23;p13.3) and lineage switch into acute monoblastic leukemia. Cancer Genet Cytogenet; 2006 Jul 15;168(2):146-9
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  • [Title] Infant acute lymphoblastic leukemia with t(11;16)(q23;p13.3) and lineage switch into acute monoblastic leukemia.
  • Rearrangements of the mixed-lineage leukemia (MLL) gene have been associated with a poor prognosis in infant acute lymphoblastic leukemia (ALL).
  • Previously, MLL translocations involving the CREP-binding protein (CREBBP) gene at chromosome band 16p13.3 have primarily been reported in treatment-related acute myeloid leukemia, after chemotherapy for other primary malignancies using topoisomerase II inhibitors.
  • We report a case of de novo infant ALL with t(11;16)(q23;p13.3).
  • After chemotherapy, this patient developed an acute monoblastic leukemia (M5b) with retention of the t(11;16)(q23;p13.3), indicating that this is a lineage switch of the original leukemic clone.
  • [MeSH-major] Cell Lineage. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 16 / genetics. Leukemia, Monocytic, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

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  • (PMID = 16843104.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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77. Kozlov I, Beason K, Yu C, Hughson M: CD79a expression in acute myeloid leukemia t(8;21) and the importance of cytogenetics in the diagnosis of leukemias with immunophenotypic ambiguity. Cancer Genet Cytogenet; 2005 Nov;163(1):62-7
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  • [Title] CD79a expression in acute myeloid leukemia t(8;21) and the importance of cytogenetics in the diagnosis of leukemias with immunophenotypic ambiguity.
  • Acute leukemias that express antigens associated with more than one lineage have been classified as acute lymphocytic leukemia with myeloid markers, acute myeloid leukemia with lymphoid markers, or biphenotypic acute leukemia (BAL).
  • CD79a functions in and has a high degree of specificity for B-cell differentiation.
  • It has only recently begun to be reported in biphenotypic acute leukemias.
  • Cases of acute leukemia submitted to the flow cytometry laboratory were retrospectively reviewed beginning from the time analysis for cytoplasmic CD79a was added to leukemia and lymphoma panels.
  • The immunophenotyping met proposed scoring criteria for a diagnosis of BAL.
  • Nevertheless, the cytogenetic and FISH findings indicate that CD79a, despite its specificity for B-cell differentiation, represented the aberrant presence of a B-cell antigen in leukemias of distinct myeloid linage.
  • It is doubtful that, in this setting, CD79a expression should be considered a manifestation of lineage ambiguity.
  • [MeSH-major] Antigens, CD79 / genetics. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Leukemia, Myeloid / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / genetics. Antigens, CD / immunology. B-Lymphocytes / immunology. Blast Crisis. Bone Marrow Cells / pathology. Cytarabine / therapeutic use. Flow Cytometry. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. T-Lymphocytes / immunology

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  • [CommentIn] Cancer Genet Cytogenet. 2007 Apr 1;174(1):76-7 [17350472.001]
  • (PMID = 16271957.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD79; 04079A1RDZ / Cytarabine
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78. Takeda S, Chen DY, Westergard TD, Fisher JK, Rubens JA, Sasagawa S, Kan JT, Korsmeyer SJ, Cheng EH, Hsieh JJ: Proteolysis of MLL family proteins is essential for taspase1-orchestrated cell cycle progression. Genes Dev; 2006 Sep 1;20(17):2397-409
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  • [Title] Proteolysis of MLL family proteins is essential for taspase1-orchestrated cell cycle progression.
  • Taspase1 was identified as the threonine endopeptidase that cleaves mixed-lineage leukemia (MLL) for proper Hox gene expression in vitro.
  • Remarkably, our in vivo studies uncover an unexpected role of Taspase1 in the cell cycle.
  • Taspase1(-/-) mouse embryonic fibroblasts (MEFs) exhibit impaired proliferation, and acute deletion of Taspase1 leads to a marked reduction of thymocytes.
  • Lastly, Taspase1(-/-) cells are resistant to oncogenic transformation, and Taspase1 is overexpressed in many cancer cell lines.


79. Miyazawa Y, Irisawa H, Matsushima T, Mitsui T, Uchiumi H, Saitohi T, Handa H, Karasawa M, Murakami H, Tsukamoto N, Nojima Y: [Reversible posterior leukoencephalopathy syndrome probably caused by L-asparaginase]. Rinsho Ketsueki; 2006 Jun;47(6):531-5
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  • A 46-year-old male with refractory biphenotypic acute leukemia was treated with doxorubicin (days 1-3, 15-17), vincristine (days 1, 8, 15, 22), prednisolone (days 1-28), and L-asparaginase (L-ASP: days 15-28) as reinduction therapy.
  • [MeSH-major] Asparaginase / adverse effects. Brain / pathology. Brain Diseases / chemically induced. Brain Diseases / diagnosis
  • [MeSH-minor] Acute Disease. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Doxorubicin / administration & dosage. Humans. Hypertension / chemically induced. Leukemia / drug therapy. Male. Middle Aged. Prednisolone / administration & dosage. Seizures / chemically induced. Vincristine / administration & dosage

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  • (PMID = 16862982.001).
  • [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] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase
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80. Grembecka J, Belcher AM, Hartley T, Cierpicki T: Molecular basis of the mixed lineage leukemia-menin interaction: implications for targeting mixed lineage leukemias. J Biol Chem; 2010 Dec 24;285(52):40690-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular basis of the mixed lineage leukemia-menin interaction: implications for targeting mixed lineage leukemias.
  • Chromosomal translocations targeting the mixed lineage leukemia (MLL) gene result in MLL fusion proteins that are found in aggressive human acute leukemias.
  • Disruption of MLL by such translocations leads to overexpression of Hox genes, resulting in a blockage of hematopoietic differentiation that ultimately leads to leukemia.
  • Altogether, our work establishes the molecular basis of the menin interaction with MLL and MLL fusion proteins and provides the necessary foundation for development of small molecule inhibitors targeting this interaction in leukemias with MLL translocations.
  • [MeSH-major] Myeloid-Lymphoid Leukemia Protein / chemistry. Proto-Oncogene Proteins / chemistry

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  • (PMID = 20961854.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC3003368
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81. 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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82. Rubnitz JE, Inaba H, Dahl G, Ribeiro RC, Bowman WP, Taub J, Pounds S, Razzouk BI, Lacayo NJ, Cao X, Meshinchi S, Degar B, Airewele G, Raimondi SC, Onciu M, Coustan-Smith E, Downing JR, Leung W, Pui CH, Campana D: Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial. Lancet Oncol; 2010 Jun;11(6):543-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Minimal residual disease-directed therapy for childhood acute myeloid leukaemia: results of the AML02 multicentre trial.
  • BACKGROUND: We sought to improve outcome in patients with childhood acute myeloid leukaemia (AML) by applying risk-directed therapy that was based on genetic abnormalities of the leukaemic cells and measurements of minimal residual disease (MRD) done by flow cytometry during treatment.
  • METHODS: From Oct 13, 2002, to June 19, 2008, 232 patients with de-novo AML (n=206), therapy-related or myelodysplasia-related AML (n=12), or mixed-lineage leukaemia (n=14) were enrolled at eight centres.
  • Induction 2 consisted of ADE with or without gemtuzumab ozogamicin (GO anti-CD33 monoclonal antibody); consolidation therapy included three additional courses of chemotherapy or haematopoietic stem-cell transplantation (HSCT).
  • Both MRD and genetic abnormalities at diagnosis were used to determine the final risk classification.
  • Other analyses were limited to the 216 patients with AML, excluding those with mixed-lineage leukaemia.
  • Induction failures included two deaths from toxic effects and ten cases of resistant leukaemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Adolescent. Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Cytarabine / administration & dosage. Cytogenetic Analysis. Daunorubicin / administration & dosage. Disease-Free Survival. Etoposide / administration & dosage. Female. Flow Cytometry. Humans. Infant. Infant, Newborn. Male. Neoplasm, Residual. Remission Induction. Survival Rate. Young Adult

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 20451454.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00136084
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA115422; United States / NCI NIH HHS / CA / R01 CA115422-02
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 93NS566KF7 / gemtuzumab; ZS7284E0ZP / Daunorubicin; DAV regimen
  • [Other-IDs] NLM/ NIHMS319127; NLM/ PMC3171799
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83. Slany RK: The molecular biology of mixed lineage leukemia. Haematologica; 2009 Jul;94(7):984-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The molecular biology of mixed lineage leukemia.
  • Mixed lineage leukemia is a very aggressive blood cancer that predominantly occurs in pediatric patients.
  • In contrast to other types of childhood acute leukemias, mixed lineage leukemia presents with a dismal prognosis and despite the availability of advanced treatment methods cure rates have stagnated over the last years.
  • Mixed lineage leukemia is characterized by the presence of MLL fusion proteins that are the result of chromosomal translocations affecting the MLL gene at 11q23.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Child. Chromatin / chemistry. Chromatin / metabolism. DNA Methylation. Dimerization. Genes, Homeobox. Histone-Lysine N-Methyltransferase. Humans. Models, Biological. Myeloid-Lymphoid Leukemia Protein / genetics. Protein Structure, Tertiary. RNA Polymerase II / metabolism. Recombinant Fusion Proteins / chemistry. Time Factors. Transcription, Genetic