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1. 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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2. Bueno C, Montes R, Martín L, Prat I, Hernandez MC, Orfao A, Menendez P: NG2 antigen is expressed in CD34+ HPCs and plasmacytoid dendritic cell precursors: is NG2 expression in leukemia dependent on the target cell where leukemogenesis is triggered? Leukemia; 2008 Aug;22(8):1475-8
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  • [Title] NG2 antigen is expressed in CD34+ HPCs and plasmacytoid dendritic cell precursors: is NG2 expression in leukemia dependent on the target cell where leukemogenesis is triggered?
  • [MeSH-major] Antigens / immunology. Antigens, CD34 / immunology. Dendritic Cells / immunology. Leukemia, Biphenotypic, Acute / immunology. Proteoglycans / immunology
  • [MeSH-minor] Cell Line, Tumor. Flow Cytometry. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 18698324.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Editorial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens; 0 / Antigens, CD34; 0 / MLL protein, human; 0 / Proteoglycans; 0 / chondroitin sulfate proteoglycan 4; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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3. Alvarado Y, Welch MA, Swords R, Bruzzi J, Schlette E, Giles FJ: Nelarabine activity in acute biphenotypic leukemia. Leuk Res; 2007 Nov;31(11):1600-3
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  • [Title] Nelarabine activity in acute biphenotypic leukemia.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cyclophosphamide / administration & dosage. Dexamethasone / administration & dosage. Doxorubicin / administration & dosage. Flow Cytometry. Humans. Middle Aged. Phenotype. Vincristine / administration & dosage

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  • (PMID = 17512588.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 5J49Q6B70F / Vincristine; 60158CV180 / nelarabine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
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4. Tsutsumi Y, Tanaka J, Minami H, Musashi M, Fukushima A, Ehira N, Kanamori H, Yamato H, Sasaki J, Funaki C, Hasegawa S, Obara S, Ogura N, Asaka M, Imamura M, Masauzi N: Acute biphenotypic leukemia and an acquired X chromosome. Cancer Genet Cytogenet; 2005 Feb;157(1):94-5
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  • [Title] Acute biphenotypic leukemia and an acquired X chromosome.
  • [MeSH-major] Chromosomes, Human, X. Leukemia / genetics. Sex Chromosome Aberrations
  • [MeSH-minor] Acute Disease. Aged. Humans. Male

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  • (PMID = 15676158.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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5. Suh B, Song J, Kim J, Park TS, Choi JR: Constitutional pericentric inversion 9 in Korean patients with chronic myelogenous leukemia. Korean J Lab Med; 2010 Jun;30(3):218-23
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  • [Title] Constitutional pericentric inversion 9 in Korean patients with chronic myelogenous leukemia.
  • BACKGROUND: Although the pericentric inversion of chromosome 9, inv(9)(p11q13), is generally considered a normal variation, it is also associated with solid tumors and several hematologic malignancies such as biphenotypic acute leukemia, ALL, AML, and myeloproliferative neoplasms.
  • The purpose of this retrospective study was to investigate the frequency and clinical features of CML patients with concomitant inv(9) and t(9;22)(q34;q11.2) variation at our institution.
  • METHODS: We reviewed the bone marrow chromosome database entries between October 2006 and December 2008 to identify patients with concomitant inv(9) and t(9;22) variations.
  • RESULTS: Among the 51 CML patients, 4 (7.8%) had concomitant inv(9) and t(9;22) variations.
  • [MeSH-major] Asian Continental Ancestry Group / genetics. Chromosome Inversion. Chromosomes, Human, Pair 9. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20603579.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
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6. He GS, Zhang X, Wu DP, Sun AN, Jin ZM, Qiu HY, Miao M, Tang XW, Fu ZZ, Han Y: Outcomes of CAG regimen for refractory biphenotypic acute leukemia patients. Chin Med Sci J; 2009 Sep;24(3):178-81
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  • [Title] Outcomes of CAG regimen for refractory biphenotypic acute leukemia patients.
  • OBJECTIVE: To evaluated the efficiency of low-dose cytosine arabinoside plus aclarubicin with concurrent administration of granulocyte colony-stimulating factor (CAG) regimen for refractory biphenotypic acute leukemia (BAL).

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  • (PMID = 19848320.001).
  • [ISSN] 1001-9294
  • [Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih
  • [ISO-abbreviation] Chin. Med. Sci. J.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 74KXF8I502 / Aclarubicin
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7. Boatsman EE, Fu CH, Song SX, Moore TB: Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation. J Pediatr Hematol Oncol; 2010 Mar;32(2):e57-60
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  • [Title] Graft-versus-leukemia effect on infant lymphoblastic leukemia relapsed after sibling hematopoietic stem cell transplantation.
  • INTRODUCTION: Infant acute lymphoblastic leukemia (ALL) is considered a high-risk entity.
  • By morphology, infant ALL is classified as a lymphoid lineage leukemia; however, its physiologic behavior has brought many to consider it a pathologic hybrid between lymphoid leukemia and myeloid leukemias.
  • As such, standard of care currently employs the use of chemotherapeutic agents used commonly in ALL protocols and agents typically reserved for the treatment of myelogenous lineage leukemias.
  • The role of hematopoietic stem cell transplantation and graft-versus-leukemia effect in these patients has not been well studied.
  • CASE PRESENTATION: An earlier healthy 9-week-old Hispanic male diagnosed with precursor B-cell lymphoblastic leukemia was treated with protocol P9407 and matched sibling hematopoietic stem cell transplantation.
  • The sole antigraft-versus-host disease (GVHD) agent, cyclosporine, was discontinued.
  • He remains disease free more than 2 years posttransplant.
  • CONCLUSION: Traditionally, graft-versus-leukemia effect was thought to contribute therapeutically little to the treatment of ALL by hematopoietic stem cell transplantation (HSCT).
  • The effects of graft-versus-leukemia immunologic phenomenon in our patient with infant acute lymphoblastic leukemia underscore the potential that infant ALL may not be entirely the same biologic entity as standard pediatric ALL and may be more responsive than understood earlier.
  • Therapeutic response and appearance of GVHD after the withdrawal of immunosuppression in this patient provides evidence that graft-versus-leukemia effect may play a role in disease control in infant ALL after HSCT.
  • This suggests that other immunotherapeutic interventions in the context of relapse may offer potential clinical benefit in this disease.
  • [MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 20168246.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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8. Mulloy JC, Wunderlich M, Zheng Y, Wei J: Transforming human blood stem and progenitor cells: a new way forward in leukemia modeling. Cell Cycle; 2008 Nov 1;7(21):3314-9
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  • [Title] Transforming human blood stem and progenitor cells: a new way forward in leukemia modeling.
  • MLL-AF9 (MA9) is a leukemia fusion gene formed upon translocation of the AF9 gene on chromosome 9 and the MLL gene on chromosome 11.
  • MA9 is commonly found in acute myeloid leukemia (AML) and occasionally in acute lymphoid leukemia and is associated with intermediate to poor outcome.
  • We have recently described a model system whereby we expressed the MA9 fusion gene in human CD34(+) Umbilical Cord Blood (UCB) cells and showed that these cells transformed to acute myeloid or lymphoid leukemia when injected into immunodeficient mice.
  • The Mixed Lineage Leukemia (MLL) oncogenes are unique in this model system in that they promote full transformation of primary human blood cells, while all other leukemia-associated oncogenes tested thus far have induced only partial phenotypes.
  • Here we provide an update on the use of this system for modeling human leukemia and its potential application for therapeutic testing of novel compounds to treat the disease.

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  • (PMID = 18948748.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA118319; United States / NCI NIH HHS / CA / K01 CA090370; United States / NCRR NIH HHS / RR / M01 RR 08084; United States / NCRR NIH HHS / RR / M01 RR008084; United States / NCI NIH HHS / CA / CA118319-04; United States / NCI NIH HHS / CA / R01 CA118319-04; United States / NCI NIH HHS / CA / CA118319; United States / NCI NIH HHS / CA / CA90370
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.6.5.2 / rac GTP-Binding Proteins
  • [Other-IDs] NLM/ NIHMS169825; NLM/ PMC2812025
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9. Bastida Vilá P, Palacio García C, Solsona Riera M, Ortega Aramburu JJ, Sánchez de Toledo Codina J: [Minimal residual disease in acute lymphoblastic leukemia: a new concept of complete remission]. An Pediatr (Barc); 2005 Nov;63(5):390-5
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  • [Title] [Minimal residual disease in acute lymphoblastic leukemia: a new concept of complete remission].
  • [Transliterated title] Leucemia mínima residual: nuevo concepto de remisión completa.
  • INTRODUCTION: Early response to induction treatment is one of the most important prognostic factors in children with acute lymphoblastic leukemia (ALL).
  • More sensitive techniques are required to measure residual leukemia and establish a new definition of complete remission.
  • OBJECTIVE: To identify minimal residual disease (MRD) by immunological techniques and define its prognostic impact in children with ALL.
  • All the children achieved complete cytological remission (< 5 %) with the induction treatment and had at least one useful phenotype for follow-up: 11 % were T phenotype, one was biphenotypic and the remainder were B cell leukemias.
  • Elimination was slower in patients with a T phenotype and in high-risk patients according to the traditional classification.
  • [MeSH-major] Neoplasm, Residual / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 16266612.001).
  • [ISSN] 1695-4033
  • [Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)
  • [ISO-abbreviation] An Pediatr (Barc)
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
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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. Zheng C, Wu J, Liu X, Ding K, Cai X, Zhu W: What is the optimal treatment for biphenotypic acute leukemia? Haematologica; 2009 Dec;94(12):1778-80; author reply 1780
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  • [Title] What is the optimal treatment for biphenotypic acute leukemia?
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Biphenotypic, Acute / drug therapy

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  • (PMID = 19996120.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Letter
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  • [Chemical-registry-number] 0 / Antigens, CD34; EC 1.11.1.7 / Peroxidase
  • [Other-IDs] NLM/ PMC2791943
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12. Gerr H, Zimmermann M, Schrappe M, Dworzak M, Ludwig WD, Bradtke J, Moericke A, Schabath R, Creutzig U, Reinhardt D: Acute leukaemias of ambiguous lineage in children: characterization, prognosis and therapy recommendations. Br J Haematol; 2010 Apr;149(1):84-92
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  • [Title] Acute leukaemias of ambiguous lineage in children: characterization, prognosis and therapy recommendations.
  • Acute leukaemias of ambiguous lineage (ALAL) represent a rare type of leukaemia, expressing both myeloid and lymphoid markers.
  • This study retrospectively analyzed data from 92 children (biphenotypic n = 78, bilineal n = 6, lineage switch n = 8) with ALAL registered in the Berlin-Frankfürt-Münster (BFM) acute myeloid leukaemia (AML) and acute lymphoblastic leukaemia (ALL) studies between 1998 and 2006 (2.4% of all cases with acute leukaemia).
  • Our cohort of ALAL patients was characterized by comparatively high median age (8.9 years), high median white blood cell count (14.9 x 10(9)/l), as well as frequent hyperleucocytosis (18.5%) and central nervous system involvement (24.1%).
  • Our data suggest that an intensive therapy regimen including stem cell transplantation may be favourable for bilineal or lineage switch cases, whereas patients with ETV6/RUNX1 fusion, lymphoid morphology and patients with expression of cyCD22 and cyCD79a should be treated with an ALL-directed therapy.
  • [MeSH-major] Leukemia / diagnosis
  • [MeSH-minor] Acute Disease. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Chromosome Aberrations. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. Infant. Prognosis. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 20085575.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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13. Naghashpour M, Lancet J, Moscinski L, Zhang L: Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report. Am J Hematol; 2010 Jun;85(6):451-4
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  • [Title] Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report.
  • The majority of cases of acute leukemia belong to a specific lineage origin, either lymphoid or myeloid, and therefore are classified as acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML), based on morphologic features and cytochemical and immunophenotypic profile of the blast cells.
  • A minority of acute leukemias however, show no clear evidence of differentiation along a single lineage.
  • These are now classified under acute leukemias of ambiguous lineage by the most recent WHO classification and account for <4% of all cases of acute leukemia [1].
  • They include leukemias with no lineage specific antigens (acute undifferentiated leukemias) and those with blasts that express antigens of more than one lineage to such degree that it is not possible to assign the leukemia to any one particular lineage with certainty (mixed phenotype acute leukemias).
  • The latter can either be leukemias with two distinct populations of blasts, each expressing antigens of a different lineage (historically referred to as "bilineal" leukemias) or a single blast population expressing antigens of multiple lineages (historically referred to as "biphenotypic" acute leukemias) [2].
  • Acute leukemias of ambiguous lineage may harbor a variety of genetic lesions.
  • Those with t(9;22)(q34;q11) or translocations associated with mixed lineage leukemias (MLL) gene, i.e., t(11;V)(q23;V), occur frequently enough and are associated with distinct features, that are considered as separate entities according to the recent WHO classification.
  • Co-expression of myeloid and B-lymphoid antigens is most common in mixed phenotype acute leukemia (MPAL), followed by co-expression of myeloid and T-lymphoid antigens, accounting for 66-70% and 23-24% of MLLs, respectively.
  • Coexpression of B- and T-lineage associated antigens or antigens of all three lineages is exceedingly rare, accounting for <5% of MLLs [3,4].
  • The requirements for assigning more than one lineage to a single blast population has been established by current WHO classification [1].
  • [MeSH-major] Antigens, Neoplasm / blood. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Immunophenotyping. Leukemia / classification. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Bone Marrow / pathology. Cell Lineage. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics

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  • (PMID = 20513125.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / MLL-ENL oncoprotein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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14. Iacobucci I, Storlazzi CT, Cilloni D, Lonetti A, Ottaviani E, Soverini S, Astolfi A, Chiaretti S, Vitale A, Messa F, Impera L, Baldazzi C, D'Addabbo P, Papayannidis C, Lonoce A, Colarossi S, Vignetti M, Piccaluga PP, Paolini S, Russo D, Pane F, Saglio G, Baccarani M, Foà R, Martinelli G: Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto Acute Leukemia Working Party (GIMEMA AL WP). Blood; 2009 Sep 3;114(10):2159-67
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  • [Title] Identification and molecular characterization of recurrent genomic deletions on 7p12 in the IKZF1 gene in a large cohort of BCR-ABL1-positive acute lymphoblastic leukemia patients: on behalf of Gruppo Italiano Malattie Ematologiche dell'Adulto Acute Leukemia Working Party (GIMEMA AL WP).
  • The BCR-ABL1 fusion gene defines the subgroup of acute lymphoblastic leukemia (ALL) with the worst clinical prognosis.
  • The IKZF1 deletion also was identified in the progression of chronic myeloid leukemia to lymphoid blast crisis (66%) but never in myeloid blast crisis or chronic-phase chronic myeloid leukemia or in patients with acute myeloid leukemia.
  • [MeSH-major] Base Sequence / genetics. Chromosomes, Human, Pair 7 / genetics. Fusion Proteins, bcr-abl / genetics. Ikaros Transcription Factor / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion
  • [MeSH-minor] Adolescent. Adult. Aged. Blast Crisis / genetics. Blast Crisis / metabolism. Cell Line, Tumor. Codon, Initiator / genetics. Codon, Initiator / metabolism. Cohort Studies. Exons / genetics. Female. Gene Expression Regulation, Leukemic / genetics. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / metabolism. Male. Microarray Analysis. Middle Aged. Polymorphism, Single Nucleotide

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  • [ErratumIn] Blood. 2010 Sep 23;116(12):2196
  • (PMID = 19589926.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon, Initiator; 0 / IKZF1 protein, human; 148971-36-2 / Ikaros Transcription Factor; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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15. 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


16. 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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17. Weinberg OK, Arber DA: Mixed-phenotype acute leukemia: historical overview and a new definition. Leukemia; 2010 Nov;24(11):1844-51
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  • [Title] Mixed-phenotype acute leukemia: historical overview and a new definition.
  • Acute leukemia with a mixed phenotype is a rare disease and comprises 2-5% of all acute leukemias.
  • These disorders have been known historically by a variety of names, such as mixed lineage leukemia, bilineal leukemia and biphenotypic leukemia, and the criteria for diagnosis have often been arbitrary.
  • The scoring criteria proposed by the European Group for the Immunological Characterization of Leukemias represented a major attempt to define this disorder.
  • However, the relative weight given to some markers and the lack of lineage specificity of most markers have raised questions regarding the significance of this approach.
  • In 2008, the World Health Organization classification of hematopoietic and lymphoid tumors proposed a simpler diagnostic algorithm, which relies on fewer and more lineage-specific markers to define mixed-phenotype acute leukemia (MPAL).
  • Several studies have suggested that patients with acute leukemia of mixed phenotype have a worse clinical outcome when compared with matched controls with acute myeloid leukemia or acute lymphoblastic leukemia.
  • Further studies are needed to confirm the significance of MPAL as currently defined, to determine a standardized treatment approach and to better understand the biological and clinical aspects of this disease.
  • [MeSH-major] Leukemia / genetics
  • [MeSH-minor] Acute Disease. Antigens, CD / analysis. Biomarkers, Tumor / analysis. Blast Crisis / pathology. Gene Rearrangement. Humans. Leukemia, B-Cell / classification. Leukemia, B-Cell / genetics. Leukemia, T-Cell / classification. Leukemia, T-Cell / genetics. Phenotype

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  • (PMID = 20844566.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor
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18. Alsayed H, Owaidah T, Al Rawas F: Validation of a modified cryopreservation method for leukemic blasts for flow cytometry assessment. Hematol Oncol Stem Cell Ther; 2008 Apr-Jun;1(2):94-7
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  • BACKGROUND: Cryopreservation, a common method for storing human cells, has advantages when cells are used in retrospective studies of selected cell populations.
  • Frozen lymphocytes can be used for tissue typing, for monitoring cell-mediated immunity, and for various immunological tests.
  • Our report describes an efficient, simple and inexpensive method for cryopreservation of human acute leukemia cells.
  • METHODS: Leukemia cells from 20 newly diagnosed cases were frozen at -80 degrees C after cryopreservation with 5% dimethysulfoxide and then assayed by flow cytometry for antigen expression determined by monoclonal antibodies at different time intervals.
  • After 4 weeks, 91% of pre-B ALL, 88% of T-ALL, 100% of AML, and 100% of biphenotypic aliquots had viability over 75%.
  • CONCLUSION: We confirm that the method does not significantly alter the viability of cells and it preserved the antigenic expression of leukemia cells.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Cryopreservation / methods. Immunophenotyping / methods. Leukemia / diagnosis
  • [MeSH-minor] Cell Survival. Flow Cytometry. Humans

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  • (PMID = 20063537.001).
  • [ISSN] 1658-3876
  • [Journal-full-title] Hematology/oncology and stem cell therapy
  • [ISO-abbreviation] Hematol Oncol Stem Cell Ther
  • [Language] eng
  • [Publication-type] Journal Article; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm
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19. Lee HR, Kang SH, Kang HJ, Shin HY, Ahn HS, Kim HK, Park MH, Cho HI, Lee DS: Lineage switch from acute myeloid leukemia to biphenotypic acute leukemia with acquisition of Philadelphia chromosome. Cancer Genet Cytogenet; 2008 Jul 15;184(2):124-6
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  • [Title] Lineage switch from acute myeloid leukemia to biphenotypic acute leukemia with acquisition of Philadelphia chromosome.
  • [MeSH-major] Cell Lineage / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Leukemia, Myeloid, Acute / genetics. Philadelphia Chromosome
  • [MeSH-minor] Cell Transdifferentiation / genetics. Child. Disease Progression. Humans. Male. Phenotype


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

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  • (PMID = 18212483.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Lectins; EC 3.1.3.48 / Antigens, CD45
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21. 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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22. 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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23. Horton TM, Ames MM, Reid JM, Krailo MD, Pendergrass T, Mosher R, Reaman GH, Seibel NL, Children's Oncology Group: A Phase 1 and pharmacokinetic clinical trial of paclitaxel for the treatment of refractory leukemia in children: a Children's Oncology Group study. Pediatr Blood Cancer; 2008 Apr;50(4):788-92
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  • [Title] A Phase 1 and pharmacokinetic clinical trial of paclitaxel for the treatment of refractory leukemia in children: a Children's Oncology Group study.
  • BACKGROUND: This report summarizes a phase 1 study conducted by the Children's Cancer Group (CCG) to determine the maximum tolerated dose (MTD), dose-limiting toxicities (DLTs), pharmacokinetics, and anti-leukemia activity of paclitaxel in children with advanced stage leukemias.
  • Doses ranged from 250 to 500 mg/m(2) every 21 days in schedule A and 105 to 200 mg/m(2) weekly x 3 every 28 days in schedule B.
  • RESULTS: Sixty-three patients (median 10 years) with refractory or relapsed leukemia (ALL) (n = 39), acute myeloid leukemia (AML) (n = 19), biphenotypic (n = 4), and JCML (n = 1)) were enrolled.
  • Among 54 evaluable patients, there was one complete response (CR), three partial responses (PR), and five patients with stable disease (SD).

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 17668866.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA98543; United States / NCI NIH HHS / CA / K23 CA113775; United States / NCI NIH HHS / CA / U01 CA097452; United States / NCRR NIH HHS / RR / M01 RR000188; United States / NCI NIH HHS / CA / U01-CA97452; United States / NCI NIH HHS / CA / K23-CA113775; United States / NCI NIH HHS / CA / K12-CA90433; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCRR NIH HHS / RR / MO1 RR00108
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; P88XT4IS4D / Paclitaxel
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24. Formankova R, Sedlacek P, Keslová P, Sramkova L, Zizkova H, Stary J: Adoptive immunotherapy, chemotherapy, and second allogeneic transplant in the treatment of post-transplant relapse of acute leukemia in children: a single center experience. Leuk Lymphoma; 2010 Oct;51(10):1936-40
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  • [Title] Adoptive immunotherapy, chemotherapy, and second allogeneic transplant in the treatment of post-transplant relapse of acute leukemia in children: a single center experience.
  • [MeSH-major] Drug Therapy / methods. Hematopoietic Stem Cell Transplantation / methods. Immunotherapy, Adoptive / methods. Leukemia / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Humans. Leukemia, Biphenotypic, Acute / therapy. Leukemia, Myeloid / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Survival Analysis. Transplantation, Homologous. Treatment Outcome


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

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  • (PMID = 19308660.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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27. Imataki O, Ohnishi H, Yamaoka G, Arai T, Kitanaka A, Kubota Y, Kushida Y, Ishida T, Tanaka T: Lineage switch from precursor B cell acute lymphoblastic leukemia to acute monocytic leukemia at relapse. Int J Clin Oncol; 2010 Feb;15(1):112-5
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  • [Title] Lineage switch from precursor B cell acute lymphoblastic leukemia to acute monocytic leukemia at relapse.
  • A lineage switch in leukemia, in which the leukemic cell lineage at onset converts to another lineage at a later time, is an uncommon type of hybrid (mixed) leukemia regarded as a variation of bilineage leukemia.
  • We present a case of a 60-year-old female diagnosed with precursor B cell acute lymphoblastic leukemia (ALL), whose markers in flow cytometry shifted from their original status of CD19+, 22+, 79a+, 13+, HLA-DR+, and TdT+.
  • Residual disease was proved by biopsy and pathologically shown to have an immature phenotype of CD5+, CD10-, CD20-, CD79a- and myeloperoxidase negativity.
  • Two weeks after liver biopsy, blast cells progressively appeared in the peripheral blood; these cells had a monocytoid morphology and phenotype (CD13, 14) but were accompanied by myeloid (CD33) and lymphoid (CD2, 4, 20) cells.
  • This phenotypical conversion from B-ALL to hybrid leukemia featuring monocytoid characteristics is known as a lineage switch.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / pathology. Leukemia, Monocytic, Acute / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Biomarkers, Tumor / blood. Bone Marrow / pathology. Cell Lineage. Female. Humans. Immunophenotyping. Middle Aged. Recurrence

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  • (PMID = 20066454.001).
  • [ISSN] 1437-7772
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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28. Oka S, Yokote T, Akioka T, Hara S, Kobayashi K, Hirata Y, Hiraoka N, Tsuji M, Hanafusa T: Trisomy 21 as the sole acquired karyotypic abnormality in biphenotypic acute leukemia. Int J Hematol; 2007 Apr;85(3):270-2
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  • [Title] Trisomy 21 as the sole acquired karyotypic abnormality in biphenotypic acute leukemia.
  • [MeSH-major] Chromosome Aberrations. Down Syndrome / blood. Down Syndrome / pathology. Leukemia / genetics
  • [MeSH-minor] Acute Disease / classification. Acute Disease / therapy. Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Dexamethasone / therapeutic use. Doxorubicin / therapeutic use. Humans. Male. Treatment Outcome. Vincristine / therapeutic use


29. Ramamoorthy SK, Pandita R, Prakash A, Ramaswamy NV, Al Bahar S: Safety of imatinib in chronic myeloid leukemia in blastic crisis presenting as cholestatic jaundice. Acta Haematol; 2007;118(3):141-5
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  • [Title] Safety of imatinib in chronic myeloid leukemia in blastic crisis presenting as cholestatic jaundice.
  • Acute leukemia presenting as cholestatic jaundice is rare.
  • It can occur due to granulocytic sarcoma compressing the bile ducts in case of acute myeloid leukemia.
  • We report a case of chronic myeloid leukemia in lymphoid blast cell crisis presenting with severe cholestatic jaundice due to diffuse infiltration of the liver sinusoids with lymphoblasts.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / drug therapy. Jaundice, Obstructive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Liver Neoplasms / drug therapy. Piperazines / administration & dosage. Pyrimidines / administration & dosage
  • [MeSH-minor] Adult. Benzamides. Diagnosis, Differential. Drug-Related Side Effects and Adverse Reactions. Humans. Imatinib Mesylate. Male


30. Chou ST, Opalinska JB, Yao Y, Fernandes MA, Kalota A, Brooks JS, Choi JK, Gewirtz AM, Danet-Desnoyers GA, Nemiroff RL, Weiss MJ: Trisomy 21 enhances human fetal erythro-megakaryocytic development. Blood; 2008 Dec 1;112(12):4503-6
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  • Children with Down syndrome exhibit 2 related hematopoietic diseases: transient myeloproliferative disorder (TMD) and acute megakaryoblastic leukemia (AMKL).
  • Both exhibit clonal expansion of blasts with biphenotypic erythroid and megakaryocytic features and contain somatic GATA1 mutations.
  • Our findings indicate that trisomy 21 itself is associated with cell-autonomous expansion of erythro-megakaryocytic progenitors.

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  • (PMID = 18812473.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK061692; United States / NCRR NIH HHS / RR / UL1 RR024134; United States / NCRR NIH HHS / RR / UL1-RR-024134
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2597125
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31. Zekri AR, Ahmed H, Ismail M, El-Nashar AT, El-Mokadem T, Hassan A: Genetic profiling of non-Hodgkin's lymphoma with or without hepatitis C virus infection. Egypt J Immunol; 2010;17(2):81-90
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  • Hepatitis C virus (HCV) which is one of the endemic viral infections in Egypt is not only hepatotropic, but also a lymphotropic virus and has many extrahepatic manifestations as mixed cryoglobulinemia and non-Hodgkin's lymphoma.
  • We studied gene expression profile of 20 B-cell non-Hodgkin's lymphoma with HCV infection and 20 B-cell non-Hodgkin's lymphoma without HCV infection as a control group by c-DNA microarray.
  • Also, HCV was associated with overexpression of the genes related to myeloid/lymphoid leukemia and B lymphoma as MLLT3, BAL, influences the overexpression of transcription regulator genes as TATA box binding protein (TBP) and may influence the overexpression of some immunoglobulin genes as immunoglobulin superfamily containing leucine gene in B cells resulting in overproduction of immunoglobulins in B-lymphocyte disorders.

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  • (PMID = 23082489.001).
  • [ISSN] 1110-4902
  • [Journal-full-title] The Egyptian journal of immunology
  • [ISO-abbreviation] Egypt J Immunol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Immunoglobulins; 0 / MLLT3 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / PARP9 protein, human; 0 / TATA-Box Binding Protein; 0 / TBP protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP4 protein, human; EC 3.4.22.- / Caspases, Initiator; EC 3.4.22.36 / Caspase 1
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32. Teuffel O, Betts DR, Thali M, Eberle D, Meyer C, Schneider B, Marschalek R, Trakhtenbrot L, Amariglio N, Niggli FK, Schäfer BW: Clonal expansion of a new MLL rearrangement in the absence of leukemia. Blood; 2005 May 15;105(10):4151-2
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  • [Title] Clonal expansion of a new MLL rearrangement in the absence of leukemia.
  • [MeSH-major] Cell Lineage. Clone Cells / cytology. Clone Cells / metabolism. Leukemia, Biphenotypic, Acute / genetics. Leukemia, Myeloid / genetics. Leukemia, Myeloid / pathology
  • [MeSH-minor] Acute Disease. Bone Marrow Cells / metabolism. Child, Preschool. Female. Gene Expression Regulation, Neoplastic. Humans

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  • (PMID = 15867425.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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33. Sun JX, Zhang WG, Chen YX, Zhao WH, Tian W, Yang Y, Liu SH: Indoleamine 2, 3-dioxygenase expression in cells of human acute monocyte leukemia (M(5)) and acute lymphocyte leukemia and therapeutic effect of its inhibitor 1-methyl tryptophan. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Jun;15(3):478-82
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  • [Title] Indoleamine 2, 3-dioxygenase expression in cells of human acute monocyte leukemia (M(5)) and acute lymphocyte leukemia and therapeutic effect of its inhibitor 1-methyl tryptophan.
  • The objective of this study was to investigate the expression and function of indoleamine 2, 3-dioxygenase (IDO) in leukemia.
  • The IDO expressions in human acute monocyte leukemia (M(5)) and acute lymphocyte leukemia (ALL) were detected by immunofluorescence staining.
  • Constructed leukemia mouse model was used to observe whether the IDO inhibitor, 1-methyl tryptophan (1-MT), has any effect in treating leukemia.
  • After statistical test, IDO expression level in leukemia cells was significantly higher than that of normal mononuclear cells.
  • Some of the leukemia mice in the experimental group long-term survived without tumor (more than three months after vaccination).
  • It is concluded that human acute monocyte leukemia (M(5)) and acute lymphocyte leukemia (ALL) express IDO, and both can be treated by 1-MT in mice.

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  • (PMID = 17605849.001).
  • [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] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / 1-methyltryptophan; 0 / Indoleamine-Pyrrole 2,3,-Dioxygenase; 8DUH1N11BX / Tryptophan
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34. 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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35. Hayette S, Chabane K, Tchirkov A, Berger MG, Nicolini FE, Tournilhac O: Detection of twelve nucleotides insertion in the BCR-ABL kinase domain in an imatinib-resistant but dasatinib-sensitive patient with bi-phenotypic acute leukemia. Haematologica; 2009 Sep;94(9):1324-6
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  • [Title] Detection of twelve nucleotides insertion in the BCR-ABL kinase domain in an imatinib-resistant but dasatinib-sensitive patient with bi-phenotypic acute leukemia.
  • [MeSH-major] Base Sequence / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia, Biphenotypic, Acute / genetics. Piperazines / administration & dosage. Protein Kinase Inhibitors / administration & dosage. Protein-Tyrosine Kinases / genetics. Pyrimidines / administration & dosage. Sequence Deletion. Thiazoles / administration & dosage

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  • (PMID = 19734429.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ PMC2738731
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36. Andreeff M, Ruvolo V, Gadgil S, Zeng C, Coombes K, Chen W, Kornblau S, Barón AE, Drabkin HA: HOX expression patterns identify a common signature for favorable AML. Leukemia; 2008 Nov;22(11):2041-7
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  • Deregulated HOX expression, by chromosomal translocations and myeloid-lymphoid leukemia (MLL) rearrangements, is causal in some types of leukemia.
  • Using real-time reverse transcription-PCR, we examined the expression of 43 clustered HOX, polycomb, MLL and FLT3 genes in 119 newly diagnosed adult acute myeloid leukemias (AMLs) selected from all major cytogenetic groups.
  • We also observed that HOXA9 levels were significantly inversely correlated with survival and that BMI-1 was overexpressed in cases with 11q23 rearrangements, suggesting that p19(ARF) suppression may be involved in MLL-associated leukemia.
  • These results underscore the close relationship between HOX expression patterns and certain forms of AML and emphasize the need to determine whether these differences play a role in the disease process.

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  • (PMID = 18668134.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA97710; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA097710-04; United States / NCI NIH HHS / CA / R21 CA097710; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / R33 CA097710-04; United States / NCI NIH HHS / CA / R33 CA097710; United States / NCI NIH HHS / CA / P01 CA055164
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Polycomb-Group Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Repressor Proteins; 0 / myeloid ecotropic viral integration site 1 protein; 117896-08-9 / nucleophosmin; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 6.3.2.19 / Polycomb Repressive Complex 1
  • [Other-IDs] NLM/ NIHMS104075; NLM/ PMC2676170
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37. Ru YX, Wang HJ, Yang BX, Liu JH, Li ZQ, Li CW, Wang JX, Mi YC: The ultrastructure of hybrid acute leukemia: a study of 15 cases. Ultrastruct Pathol; 2005 Sep-Oct;29(5):341-7
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  • [Title] The ultrastructure of hybrid acute leukemia: a study of 15 cases.
  • The objective of this study was to investigate the ultrastructural characteristics of hybrid acute leukemia (HAL).
  • By TEM, 5 out 15 cases of HAL were consistent with immunophenotyping (3 cases of biphenotypic type, and 2 cases of biclonal type with granulocytes and lymphocytes); 2 cases were suspected as HAL.
  • Most of the blast cells of biphenotypic HAL showed lymphoid features, except some cases containing MPO positive granules in blasts, while a few cases exhibited monocytic or nonspecific features.
  • TEM offers advantages in the diagnosis of biclonal type HAL and biphenotypic HAL positive for MPO.
  • However, it is difficult to differentiate MPO-negative cases of biphenotypic HAL from ALL and a few cases may be misinterpreted as M5 by TEM.
  • [MeSH-major] Granulocyte Precursor Cells / ultrastructure. Leukemia, Myeloid, Acute / diagnosis. Lymphocytes / ultrastructure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 16257860.001).
  • [ISSN] 0191-3123
  • [Journal-full-title] Ultrastructural pathology
  • [ISO-abbreviation] Ultrastruct Pathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.11.1.7 / Peroxidase
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38. Ikezoe T, Nishioka C, Tasaka T, Yang Y, Komatsu N, Togitani K, Koeffler HP, Taguchi H: The antitumor effects of sunitinib (formerly SU11248) against a variety of human hematologic malignancies: enhancement of growth inhibition via inhibition of mammalian target of rapamycin signaling. Mol Cancer Ther; 2006 Oct;5(10):2522-30
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  • We studied antitumor effects of receptor tyrosine kinase inhibitor sunitinib (formerly SU11248) against a variety of hematologic malignancies including the following leukemias: eosinophilic (EOL-1), acute myeloid (THP-1, U937, Kasumi-1), biphenotypic (MV4-11), acute lymphoblastic (NALL-1, Jurkat, BALL-2, PALL-1, PALL-2), blast crisis of chronic myeloid (KU812, Kcl-22, K562), and adult T-cell (MT-1, MT-2, MT-4), as well as non-Hodgkin's lymphoma (KS-1, Dauji, Akata) and multiple myeloma (U266).
  • Thymidine uptake studies showed that sunitinib was active against EOL-1, MV4-11, and Kasumi-1 cells, which possessed activating mutations of the PDGFRalpha, FLT-3, and c-KIT genes, respectively, with IC(50)s of <30 nmol/L.
  • In addition, sunitinib inhibited the proliferation of freshly isolated leukemia cells from patients possessing mutations in FLT3 gene.
  • Interestingly, rapamycin analogue RAD001 enhanced the ability of sunitinib to inhibit the proliferation of leukemia cells and down-regulate levels of mammalian target of rapamycin effectors p70 S6 kinase and eukaryotic initiation factor 4E-binding protein 1 in these cells.
  • Taken together, sunitinib may be useful for treatment of individuals with leukemias possessing activation mutation of tyrosine kinase, and the combination of sunitinib and RAD001 represents a promising novel treatment strategy.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / antagonists & inhibitors. Adaptor Proteins, Signal Transducing / biosynthesis. Apoptosis. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Synergism. Everolimus. Humans. Leukemia / metabolism. Leukemia / pathology. Mutation. Phosphoproteins / antagonists & inhibitors. Phosphoproteins / biosynthesis. Receptor Protein-Tyrosine Kinases / genetics. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Ribosomal Protein S6 Kinases, 70-kDa / biosynthesis. Signal Transduction. Sirolimus / analogs & derivatives. Sirolimus / pharmacology. TOR Serine-Threonine Kinases

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  • (PMID = 17041096.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / EIF4EBP1 protein, human; 0 / Indoles; 0 / Phosphoproteins; 0 / Pyrroles; 0 / sunitinib; 9HW64Q8G6G / Everolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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39. Park AH, Muntz HR, Smith ME, Afify Z, Pysher T, Pavia A: Pediatric invasive fungal rhinosinusitis in immunocompromised children with cancer. Otolaryngol Head Neck Surg; 2005 Sep;133(3):411-6
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  • RESULTS: Seventeen consecutive pediatric immunocompromised patients with hematologic and lymphoid neoplasms underwent nasal endoscopy and biopsy for possible FS.
  • Eight patients had acute myelogenous leukemia (AML); 6 patients had acute lymphoblastic leukemia (ALL); 1 patient had Burkitt's lymphoma, 1 patient had undifferentiated leukemia; and 1 patient had biphenotypic acute leukemia.

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  • (PMID = 16143192.001).
  • [ISSN] 0194-5998
  • [Journal-full-title] Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
  • [ISO-abbreviation] Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Márkász L, Hajas G, Kiss A, Lontay B, Rajnavölgyi E, Erdodi F, Oláh E: Granulocyte colony stimulating factor increases drug resistance of leukaemic blast cells to daunorubicin. Pathol Oncol Res; 2008 Sep;14(3):285-92
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  • Acute leukaemia is known as the most common cancer in childhood.
  • The clinical use of Granulocyte Colony Stimulating Factor (G-CSF) has become widespread to minimize chemotherapy-induced myelosuppression and febrile neutropenia in childhood solid tumors, acute lymphoid leukaemia (ALL) and in several trials with AML.
  • In case of ALL this seems to be reasonable because, due to the absence of G-CSF receptor (G-CSFR) on the surface of normal lymphoid cells, G-CSF does not have any influence on the pathways of proliferation and differentiation of lymphoid lineage cells.
  • It has been suggested, however, that ALL blasts with B or T cell surface antigens as well as biphenotypic leukaemia cells express G-CSFR, and they are able to respond to exogenously added G-CSF with proliferation.
  • In this study we investigated how G-CSF might influence the sensitivity of leukemic cells to daunorubicin induced cell death using MTT assay, flow cytometry and Western blot analysis.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Daunorubicin / therapeutic use. Drug Resistance, Neoplasm / drug effects. Granulocyte Colony-Stimulating Factor / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Myeloid Cells / drug effects
  • [MeSH-minor] Cell Line, Tumor. Chemotherapy, Adjuvant. Dose-Response Relationship, Drug. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptors, Granulocyte Colony-Stimulating Factor / drug effects

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  • (PMID = 18493867.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor; ZS7284E0ZP / Daunorubicin
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41. 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

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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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42. Wang L, Lin D, Zhang X, Chen S, Wang M, Wang J: Analysis of FLT3 internal tandem duplication and D835 mutations in Chinese acute leukemia patients. Leuk Res; 2005 Dec;29(12):1393-8
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  • [Title] Analysis of FLT3 internal tandem duplication and D835 mutations in Chinese acute leukemia patients.
  • Genomic aberrations of Fms-like tyrosine kinase 3 (FLT3), including internal tandem duplication (ITD) and point mutations, have been demonstrated in 25-30% of adults acute myeloid leukemia (AML) and are markers of poor prognosis.
  • FLT3/ITD and D835 mutations were analyzed in 194 Chinese patients with acute leukemia and myelodysplastic syndromes (MDS) by polymerase chain reaction (PCR).
  • However, neither aberrations was found in 25 patients with acute lymphoblastic leukemia (ALL), 2 acute hybrid leukemia, 17 MDS and 7 chronic myeloid leukemia in blast crisis (CML-BC).
  • [MeSH-major] Leukemia / genetics. Mutation, Missense. Tandem Repeat Sequences. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Amino Acid Sequence. Asian Continental Ancestry Group / genetics. DNA Mutational Analysis. Female. Humans. Leukocytosis. Male. Middle Aged. Molecular Sequence Data. Myelodysplastic Syndromes / genetics. Prognosis. Remission Induction


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

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  • (PMID = 17515381.001).
  • [ISSN] 1546-3141
  • [Journal-full-title] AJR. American journal of roentgenology
  • [ISO-abbreviation] AJR Am J Roentgenol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media
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44. Ono R, Nakajima H, Ozaki K, Kumagai H, Kawashima T, Taki T, Kitamura T, Hayashi Y, Nosaka T: Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-lineage leukemogenesis. J Clin Invest; 2005 Apr;115(4):919-29
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  • [Title] Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-lineage leukemogenesis.
  • The mechanisms by which mixed-lineage leukemia (MLL) fusion products resulting from in utero translocations in 11q23 contribute to leukemogenesis and infant acute leukemia remain elusive.
  • It is still controversial whether the MLL fusion protein is sufficient to induce acute leukemia without additional genetic alterations, although carcinogenesis in general is known to result from more than 1 genetic disorder accumulating during a lifetime.
  • MLL-SEPT6 induced myeloproliferative disease with long latency in mice, but not acute leukemia, implying that secondary genotoxic events are required to develop leukemia.
  • We developed in vitro and in vivo model systems of leukemogenesis by MLL fusion proteins, where activated FMS-like receptor tyrosine kinase 3 (FLT3) together with MLL-SEPT6 not only transformed hematopoietic progenitors in vitro but also induced acute biphenotypic or myeloid leukemia with short latency in vivo.
  • [MeSH-major] Cell Transformation, Neoplastic. DNA-Binding Proteins. GTP-Binding Proteins. Leukemia, Myeloid, Acute / metabolism. Oncogene Proteins, Fusion. Proto-Oncogene Proteins / metabolism. Proto-Oncogenes. Receptor Protein-Tyrosine Kinases / metabolism. Recombinant Fusion Proteins. Transcription Factors
  • [MeSH-minor] Animals. Cell Transplantation. Cells, Cultured. Cytoskeletal Proteins. DNA Damage. Dimerization. Enzyme Activation. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. Histone-Lysine N-Methyltransferase. Humans. Infant. Liver / pathology. Liver / physiology. Mice. Mice, Inbred C57BL. Myeloid-Lymphoid Leukemia Protein. Protein Structure, Tertiary. Septins. Spleen / pathology. Spleen / physiology. fms-Like Tyrosine Kinase 3

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  • (PMID = 15761502.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Recombinant Fusion Proteins; 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; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Flt3 protein, mouse; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.1.- / GTP-Binding Proteins; EC 3.6.1.- / SEPT6 protein, human; EC 3.6.1.- / Septins
  • [Other-IDs] NLM/ PMC1062890
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45. Johny A, Song KW, Nantel SH, Lavoie JC, Toze CL, Hogge DE, Forrest DL, Sutherland HJ, Le A, Nitta JY, Barnett MJ, Smith CA, Shepherd JD, Nevill TJ: Early stem cell transplantation for refractory acute leukemia after salvage therapy with high-dose etoposide and cyclophosphamide. Biol Blood Marrow Transplant; 2006 Apr;12(4):480-9
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  • [Title] Early stem cell transplantation for refractory acute leukemia after salvage therapy with high-dose etoposide and cyclophosphamide.
  • Primary refractory acute leukemia (AL) has a poor prognosis, although some patients can be salvaged with allogeneic stem cell transplantation (SCT).
  • Forty-two patients had acute myelogenous leukemia (AML), 13 patients had acute lymphoblastic leukemia (ALL), and 4 patients had acute biphenotypic leukemia.
  • CR1 rates were similar in AML (54%) and ALL/acute biphenotypic leukemia (67%; P = .52), and analysis of baseline characteristics did not reveal any predictors of response to VP/Cy.
  • [MeSH-major] Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Cyclophosphamide / administration & dosage. Etoposide / administration & dosage. Leukemia / mortality. Salvage Therapy / mortality. Stem Cell Transplantation
  • [MeSH-minor] Adolescent. Adult. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Middle Aged. Remission Induction. Retrospective Studies. Survival Rate

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  • (PMID = 16545732.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide
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46. Hager JL, Mir MR, Hsu S: Candida krusei fungemia in an immunocompromised patient. Dermatol Online J; 2010;16(4):5
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  • We present a case of a patient with acute lymphoblastic leukemia who, despite being treated prophylactically with fluconazole, developed disseminated C. krusei.
  • [MeSH-major] Candidiasis, Cutaneous / diagnosis. Candidiasis, Cutaneous / immunology. Fungemia / diagnosis. Fungemia / immunology. Immunocompromised Host. Leukemia, Biphenotypic, Acute / complications

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  • (PMID = 20409412.001).
  • [ISSN] 1087-2108
  • [Journal-full-title] Dermatology online journal
  • [ISO-abbreviation] Dermatol. Online J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 8VZV102JFY / Fluconazole
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47. Kobayashi K, Ogasawara M, Kiyama Y, Miyazono T, Kagawa K, Imai K, Hirano T, Kobayashi N, Tanimoto M, Kasai M: Successful voriconazole treatment of invasive pulmonary aspergillosis in a patient with acute biphenotypic leukemia. Acta Med Okayama; 2009 Aug;63(4):213-6
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  • [Title] Successful voriconazole treatment of invasive pulmonary aspergillosis in a patient with acute biphenotypic leukemia.
  • A 23-year old woman with acute biphenotypic leukemia (ABL) complained of chest pain with cough, high fever and hemoptysis during induction chemotherapy, although she had been treated with anti-biotics and micafungin.
  • We made a clinical diagnosis of invasive pulmonary aspergillosis (IPA) based on a consolidation in the right upper lung field on a chest radiograph as well as a high level of serum beta-D-glucan (with no evidence of tuberculosis and candidiasis).
  • Later, we discovered an air-crescent sign by CT scan that supported the diagnosis of IPA.
  • Serological tests and CT findings can aid in early diagnosis of IPA, which, along with treatment for IPA, will improve clinical outcomes.
  • [MeSH-major] Antifungal Agents / therapeutic use. Invasive Pulmonary Aspergillosis / drug therapy. Leukemia, Biphenotypic, Acute / complications. Pyrimidines / therapeutic use. Triazoles / therapeutic use

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  • (PMID = 19727206.001).
  • [ISSN] 0386-300X
  • [Journal-full-title] Acta medica Okayama
  • [ISO-abbreviation] Acta Med. Okayama
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Pyrimidines; 0 / Triazoles; JFU09I87TR / Voriconazole
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48. Sárová I, Brezinová J, Zemanová Z, Izáková S, Lizcová L, Malinová E, Berková A, Cermák J, Maaloufová J, Nováková L, Michalová K: Cytogenetic manifestation of chromosome 11 duplication/amplification in acute myeloid leukemia. Cancer Genet Cytogenet; 2010 Jun;199(2):121-7
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  • [Title] Cytogenetic manifestation of chromosome 11 duplication/amplification in acute myeloid leukemia.
  • Gene amplification is a frequent genetic abnormality in solid tumors, and many oncogenes are activated in this way.
  • In acute myeloid leukemia (AML), a frequent target of gene amplification is chromosome 11, particularly chromosome region 11q23, including the MLL (myeloid/lymphoid leukemia) gene.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Gene Amplification. Gene Duplication. Leukemia, Myeloid, Acute / genetics. Trisomy

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20471515.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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49. 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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50. Hur M, Park JY, Cho HC, Lee KM, Shin HY, Cho HI: Methylenetetrahydrofolate reductase A1298C genotypes are associated with the risks of acute lymphoblastic leukaemia and chronic myelogenous leukaemia in the Korean population. Clin Lab Haematol; 2006 Jun;28(3):154-9
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  • [Title] Methylenetetrahydrofolate reductase A1298C genotypes are associated with the risks of acute lymphoblastic leukaemia and chronic myelogenous leukaemia in the Korean population.
  • We investigated the association between MTHFR polymorphisms and the risks of acute and chronic leukaemias.
  • They were acute lymphoblastic leukaemia (ALL, n = 89), acute myeloid leukaemia (AML, n = 55), biphenotypic acute leukaemia (n = 12), chronic myelogenous leukaemia (CML, n = 40), and normal controls (n = 200).
  • C677T genotypes were not associated with the risk of each disease.
  • [MeSH-major] Folic Acid / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid, Acute / genetics. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Genetic / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16706930.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 935E97BOY8 / Folic Acid; EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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51. Vanura K, Vrsalovic MM, Le T, Marculescu R, Kusec R, Jäger U, Nadel B: V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2009 Aug;48(8):725-36
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  • [Title] V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia.
  • Translocations of proto-oncogenes to the B-cell or T-cell antigen receptor loci in acute T- or B-cell leukemia and lymphoma have been, in most cases, accredited to V(D)J or switch recombination depending on the location of the breakpoint at the receptor locus.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Recombination, Genetic. Translocation, Genetic. VDJ Recombinases / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cells, Cultured. DNA Breaks. DNA-Binding Proteins / genetics. Fibroblasts. Genes, T-Cell Receptor. Homeodomain Proteins / genetics. LIM Domain Proteins. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Metalloproteins / genetics. Mice. Receptors, Antigen, B-Cell / genetics. TCF Transcription Factors / genetics. Transcription Factor 7-Like 1 Protein

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  • (PMID = 19455608.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Receptors, Antigen, B-Cell; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Tlx1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.- / VDJ Recombinases
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52. Rudinskiy N, Grishchuk Y, Vaslin A, Puyal J, Delacourte A, Hirling H, Clarke PG, Luthi-Carter R: Calpain hydrolysis of alpha- and beta2-adaptins decreases clathrin-dependent endocytosis and may promote neurodegeneration. J Biol Chem; 2009 May 1;284(18):12447-58
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  • Proteolysis of alpha- and beta2-adaptins, as well as the accessory clathrin adaptors epsin 1, adaptor protein 180, and the clathrin assembly lymphoid myeloid leukemia protein, was detected in brain tissues after experimentally induced ischemia and in cases of human Alzheimer disease.
  • [MeSH-major] Adaptor Protein Complex alpha Subunits / metabolism. Adaptor Protein Complex beta Subunits / metabolism. Alzheimer Disease / metabolism. Brain / metabolism. Calpain / metabolism. Clathrin / metabolism. Endocytosis. Neurons / metabolism
  • [MeSH-minor] Adaptor Proteins, Vesicular Transport. Animals. Brain Ischemia / genetics. Brain Ischemia / metabolism. Brain Ischemia / pathology. Calcium / metabolism. Cell Line. Cell Membrane / genetics. Cell Membrane / metabolism. Cell Membrane / pathology. Female. Glutamic Acid / metabolism. Humans. Hydrolysis. Male. Membrane Lipids / genetics. Membrane Lipids / metabolism. Monomeric Clathrin Assembly Proteins / genetics. Monomeric Clathrin Assembly Proteins / metabolism. Rats. Rats, Sprague-Dawley. Rats, Wistar

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  • (PMID = 19240038.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Protein Complex alpha Subunits; 0 / Adaptor Protein Complex beta Subunits; 0 / Adaptor Proteins, Vesicular Transport; 0 / Clathrin; 0 / Membrane Lipids; 0 / Monomeric Clathrin Assembly Proteins; 0 / PICALM protein, human; 0 / Picalm protein, rat; 0 / epsin; 3KX376GY7L / Glutamic Acid; EC 3.4.22.- / Calpain; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC2673311
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53. Aribi A, Bueso-Ramos C, Estey E, Estrov Z, O'Brien S, Giles F, Faderl S, Thomas D, Kebriaei P, Garcia-Manero G, Pierce S, Cortes J, Kantarjian H, Ravandi F: Biphenotypic acute leukaemia: a case series. Br J Haematol; 2007 Jul;138(2):213-6
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  • [Title] Biphenotypic acute leukaemia: a case series.
  • Biphenotypic acute leukaemia (BAL) is a rare type of leukaemia.
  • Whether patients with BAL should be treated with regimens designed for acute myeloid leukaemia (AML), acute lymphocytic leukaemia (ALL) or both remain unclear.
  • Most patients co-expressed B-lymphoid and myeloid markers.
  • No specific chromosomal abnormality was identified.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Cytarabine / therapeutic use. Dexamethasone / therapeutic use. Doxorubicin / therapeutic use. Female. Humans. Immunophenotyping. Leukemia, Myeloid, Acute / drug therapy. Male. Methotrexate / therapeutic use. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Treatment Outcome. Vincristine / therapeutic use

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  • (PMID = 17593028.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; YL5FZ2Y5U1 / Methotrexate; HCVAD protocol
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54. Schimmer AD: Induction of apoptosis in lymphoid and myeloid leukemia. Curr Oncol Rep; 2006 Nov;8(6):430-6
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  • [Title] Induction of apoptosis in lymphoid and myeloid leukemia.
  • Defects in the core machinery of the apoptosis pathway contribute to chemoresistance and poor outcomes in patients with acute leukemia.
  • This review highlights compounds that target the mitochondrial, death receptor, and convergence pathways of caspase activation that are being developed for the treatment of acute leukemia.
  • [MeSH-major] Apoptosis / physiology. Leukemia, Lymphoid / therapy. Leukemia, Myeloid / therapy

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  • (PMID = 17040621.001).
  • [ISSN] 1523-3790
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Receptors, Death Domain; EC 3.4.22.- / Caspases
  • [Number-of-references] 68
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55. Park JA, Ghim TT, Bae Kw, Im HJ, Jang SS, Park CJ, Chi HS, Seo JJ: Stem cell transplant in the treatment of childhood biphenotypic acute leukemia. Pediatr Blood Cancer; 2009 Sep;53(3):444-52
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  • [Title] Stem cell transplant in the treatment of childhood biphenotypic acute leukemia.
  • BACKGROUND: Many studies have found that biphenotypic acute leukemia (BAL) is associated with a poor outcome.
  • RESULTS: BAL constituted 4.4% of all acute childhood leukemia cases.
  • In terms of immunophenotype, 14 patients had leukemia with myeloid plus B-lymphoid (M + B) marker, 7 with myeloid plus T-lymphoid (M + T) marker, and 4 with myeloid plus B-lymphoid and T-lymphoid (M + B + T) markers.
  • Hematopoietic stem cell transplantation (HSCT) did not improve either overall survival or event-free survival compared to chemotherapy alone (hazard ratio 0.98, 95% CI 0.35-2.76, P = 0.966; hazard ratio 1.07, 95% CI 0.41-2.78, P = 0.88).
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Biphenotypic, Acute / therapy

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  • (PMID = 19489056.001).
  • [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
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56. Nishioka C, Ikezoe T, Yang J, Takeuchi S, Koeffler HP, Yokoyama A: MS-275, a novel histone deacetylase inhibitor with selectivity against HDAC1, induces degradation of FLT3 via inhibition of chaperone function of heat shock protein 90 in AML cells. Leuk Res; 2008 Sep;32(9):1382-92
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  • This study explored the effect of MS-275, a novel histone deacetylase inhibitor (HDACI), against a variety of human leukemia cells with defined genetic alterations.
  • MS-275 profoundly induced growth arrest of acute myelogenous leukemia (AML) MOLM13 and biphenotypic leukemia MV4-11 cells, which possess internal tandem duplication mutation in the fms-like tyrosine kinase 3 (FLT3) gene (FLT3-ITD), with IC50s less than 1 microM, as measured by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay on day two of culture.
  • Moreover, we found that further inhibition of MEK/ERK signaling potentiated the action of MS-275 in leukemia cells.
  • Taken together, MS-275 may be useful for treatment of individuals with leukemia possessing activating mutation of FLT3 gene.
  • [MeSH-major] Benzamides / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Histone Deacetylase Inhibitors. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism. Pyridines / pharmacology. Signal Transduction / drug effects. fms-Like Tyrosine Kinase 3 / metabolism
  • [MeSH-minor] Acetylation. Blotting, Western. Cell Cycle / drug effects. Cell Proliferation / drug effects. Enzyme Inhibitors / pharmacology. Female. Flow Cytometry. Genotype. Histone Deacetylase 1. Histone Deacetylases / metabolism. Humans. Immunoprecipitation. MAP Kinase Kinase 1 / metabolism. Male. Middle Aged. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. STAT5 Transcription Factor / metabolism. Tumor Cells, Cultured

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  • (PMID = 18394702.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / HSP90 Heat-Shock Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyridines; 0 / STAT5 Transcription Factor; 1ZNY4FKK9H / entinostat; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylases
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57. 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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58. Kern W, Haferlach T: [Quantification of minimal residual disease by multiparameter flow cytometry in acute myeloid leukemia. From diagnosis to prognosis]. Med Klin (Munich); 2005 Jan 15;100(1):54-9
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  • [Title] [Quantification of minimal residual disease by multiparameter flow cytometry in acute myeloid leukemia. From diagnosis to prognosis].
  • Today, multiparameter flow cytometry allows the simultaneous assessment of up to five surface and cytoplasmic antigens in different cell populations from peripheral blood and bone marrow samples.
  • In the setting of diagnosing acute myeloid leukemias (AML) this method is used not only to subclassify AML and separate it from acute lymphoblastic and biphenotypic leukemias but also for the identification of leukemia-associated aberrant immunophenotypes (LAIPs).
  • Since these LAIPs are defined individually for each patient, leukemic bone marrow cells can be detected during the course of treatment using the LAIP allowing the quantification of minimal residual disease (MRD) which is not detectable by cytomorphology.
  • Due to its close correlation with the course of the disease and with the risk of relapse the MRD represents an important prognostic parameter which is increasingly used for stratification of therapy in clinical trials.
  • [MeSH-major] Flow Cytometry / methods. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis

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  • (PMID = 15654545.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Epitopes; EC 3.1.3.48 / Antigens, CD45
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59. 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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60. Manola KN, Georgakakos VN, Marinakis T, Stavropoulou C, Paterakis G, Anagnostopoulos NI, Pantelias GE, Sambani C: Translocation (X;12)(p11;p13) as a sole abnormality in biphenotypic acute leukemia. Cancer Genet Cytogenet; 2007 Mar;173(2):159-63
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  • [Title] Translocation (X;12)(p11;p13) as a sole abnormality in biphenotypic acute leukemia.
  • A reciprocal t(X;12)(p11;p13) was found as the sole clonal abnormality in biphenotypic leukemia with myeloid and B-lymphoid differentiation.
  • To our knowledge, this cytogenetic aberration has not been reported previously as a sole abnormality in hematological malignancies.
  • Its presence may suggest an important role in the pathogenesis of biphenotypic leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 12. Chromosomes, Human, X. Leukemia / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Chromosome Banding. Chromosome Painting. Female. Humans. Karyotyping. Lymphocytes / metabolism. Lymphocytes / pathology. Middle Aged. Myeloid Cells / metabolism. Myeloid Cells / pathology

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  • (PMID = 17321333.001).
  • [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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61. Fujiwara S, Yamashita Y, Choi YL, Watanabe H, Kurashina K, Soda M, Enomoto M, Hatanaka H, Takada S, Ozawa K, Mano H: Transforming activity of purinergic receptor P2Y, G protein coupled, 8 revealed by retroviral expression screening. Leuk Lymphoma; 2007 May;48(5):978-86
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  • Biphenotypic acute leukemia (BAL) is a relatively rare subtype of acute leukemia characterized by the presence of both myeloid and lymphoid cell surface antigens.
  • A variety of luciferase-based reporter assays revealed that P2RY8 increased both the trans-activation activities of CREB and Elk-1 as well as the transcriptional activities of the serum response element and enhancer-promoter fragments of the c-Fos and c-Myc genes.
  • Quantitation of P2RY8 mRNA in CD34(+) cells of bone marrow showed that P2RY8 expression is frequently increased in leukemia patients, especially in those with refractory disease.
  • Our data thus reveal an abundant expression of P2RY8 in leukemic cells and its unexpected role in the pathogenesis of acute leukemia.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia / genetics. Leukemia / metabolism. Receptors, Purinergic / physiology. Receptors, Purinergic P2 / metabolism. Receptors, Purinergic P2Y / metabolism. Receptors, Purinergic P2Y / physiology. Retroviridae / metabolism
  • [MeSH-minor] 3T3 Cells. Animals. Antigens, CD34 / biosynthesis. Bone Marrow Cells / metabolism. Cell Line, Tumor. DNA, Complementary / genetics. Gene Library. Humans. Mice. Mice, Nude. Transcription, Genetic

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  • (PMID = 17487742.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA, Complementary; 0 / P2RY8 protein, human; 0 / P2RY9 receptor, human; 0 / P2RY9 receptor, mouse; 0 / Receptors, Purinergic; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2Y
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62. Kim HR, Hong JH, Yoon CH, Lee SH, Park SH, Kim HY: Arthritis preceding acute biphenotypic leukemia. Clin Rheumatol; 2006 May;25(3):380-1
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  • [Title] Arthritis preceding acute biphenotypic leukemia.
  • [MeSH-major] Arthritis / etiology. Leukemia / complications
  • [MeSH-minor] Acute Disease. Adult. Ankle / pathology. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Antineoplastic Agents / therapeutic use. Female. Humans. Magnetic Resonance Imaging. Pain / drug therapy. Phenotype

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  • [Cites] Acta Haematol. 1999 Mar;101(1):1-6 [10085431.001]
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  • (PMID = 16220224.001).
  • [ISSN] 0770-3198
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents
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63. Hegedus CM, Gunn L, Skibola CF, Zhang L, Shiao R, Fu S, Dalmasso EA, Metayer C, Dahl GV, Buffler PA, Smith MT: Proteomic analysis of childhood leukemia. Leukemia; 2005 Oct;19(10):1713-8
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  • [Title] Proteomic analysis of childhood leukemia.
  • Childhood acute lymphoblastic and myeloid leukemias are stratified into molecular and cytogenetic subgroups important for prognosis and therapy.
  • Studies have shown that gene expression profiles can discriminate between leukemia subtypes.
  • Thus, proteome analysis similarly holds the potential for characterizing different subtypes of childhood leukemia.
  • We used surface-enhanced laser desorption/ionization time-of-flight mass spectrometry to analyze cell lysates from childhood leukemia cell lines as well as pretreatment leukemic bone marrow derived from childhood leukemia cases.
  • Comparison of the acute myeloid leukemia (AML) cell line, Kasumi, and the biphenotypic myelomonocytic cell line, MV4;11, with the acute lymphoblastic leukemia (ALL) cell lines, 697 and REH, revealed many differentially expressed proteins.
  • In particular, one 8.3 kDa protein has been identified as a C-terminal truncated ubiquitin.
  • Analysis of childhood leukemia bone marrow showed differentially expressed proteins between AML and ALL, including a similar peak at 8.3 kDa, as well as several proteins that differentiate between the ALL t(12;21) and hyperdiploid subtypes.
  • These results demonstrate the potential for proteome analysis to distinguish between various forms of childhood leukemia.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Leukemia, Myeloid / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proteomics
  • [MeSH-minor] Acute Disease. Adolescent. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Child. Humans. Peptide Mapping. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

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  • (PMID = 16136170.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES004705; United States / NIEHS NIH HHS / ES / P30 ES01896; United States / NIEHS NIH HHS / ES / P42ES04705; United States / NIEHS NIH HHS / ES / R01 ES09137
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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64. 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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65. Lotem J, Netanely D, Domany E, Sachs L: Human cancers overexpress genes that are specific to a variety of normal human tissues. Proc Natl Acad Sci U S A; 2005 Dec 20;102(51):18556-61
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  • We have analyzed gene expression data from three different kinds of samples: normal human tissues, human cancer cell lines, and leukemic cells from lymphoid and myeloid leukemia pediatric patients.
  • Analysis of the expression levels of these two groups of genes in the human cancer cell lines and leukemias identified genes that were highly expressed in cancer cells but not in their normal counterparts and, thus, were overexpressed in the cancers.
  • The different cancer cell lines and leukemias varied in the number and identity of these overexpressed genes.
  • [MeSH-minor] Adenocarcinoma / genetics. Cell Line. Cell Line, Tumor. Health. Humans. Leukemia / classification. Leukemia / genetics. Multigene Family / genetics

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  • (PMID = 16339305.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1317977
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66. 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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67. Amakawa R, Hiramoto N, Kawano S, Hyo A, Nakamichi N, Tajima K, Ito T, Mori S, Kishimoto Y, Fukuhara S: Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia. J Clin Exp Hematop; 2010;50(1):51-8
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  • [Title] Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia.
  • We report a case of acute mixed-lineage leukemia, as seen in a 65 year-old female with MLL gene amplification and biallelic loss of wild type p53 gene.
  • The diagnosis was based on the findings that her bone marrow (BM) blasts expressed cytoplasmic CD3 (cyCD3), B-lineage antigens and myeloid antigens accompanied by clonal rearrangements of IgH gene.
  • Add (11q23) abnormality was found in sideline karyotypes as well as the stemline abnormality of dic(17;20) (p11;q11).
  • [MeSH-major] Gene Amplification. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

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  • (PMID = 20505276.001).
  • [ISSN] 1880-9952
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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68. Costantini AS, Benvenuti A, Vineis P, Kriebel D, Tumino R, Ramazzotti V, Rodella S, Stagnaro E, Crosignani P, Amadori D, Mirabelli D, Sommani L, Belletti I, Troschel L, Romeo L, Miceli G, Tozzi GA, Mendico I, Maltoni SA, Miligi L: Risk of leukemia and multiple myeloma associated with exposure to benzene and other organic solvents: evidence from the Italian Multicenter Case-control study. Am J Ind Med; 2008 Nov;51(11):803-11
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  • [Title] Risk of leukemia and multiple myeloma associated with exposure to benzene and other organic solvents: evidence from the Italian Multicenter Case-control study.
  • BACKGROUND: While there is a general consensus about the ability of benzene to induce acute myeloid leukemia (AML), its effects on chronic lymphoid leukemia and multiple myeloma (MM) are still under debate.
  • We conducted a population-based case-control study to evaluate the association between exposure to organic solvents and risk of myeloid and lymphoid leukemia and MM.
  • METHODS: Five hundred eighty-six cases of leukemia (and 1,278 population controls), 263 cases of MM (and 1,100 population controls) were collected.
  • There were elevated point estimates for the associations between medium/high benzene exposure and chronic lymphatic leukemia (OR = 1.8, 95% CI = 0.9-3.9) and MM (OR = 1.9, 95% CI = 0.9-3.9).
  • Risks of chronic lymphatic leukemia were somewhat elevated, albeit with wide confidence intervals, from medium/high exposure to xylene and toluene as well.
  • Our results support the association between benzene, xylene, and toluene and chronic lymphatic leukemia and between benzene and MM with longer latencies than have been observed for AML in other studies.
  • [MeSH-major] Benzene / adverse effects. Leukemia, Lymphoid / chemically induced. Multiple Myeloma / chemically induced. Occupational Exposure / adverse effects. Solvents / adverse effects


69. Rénard C, Girard S, Pracros JP, Dijoud F, André JM, Mialou V, Bertrand Y: [Granulocytic sarcoma, a diagnostic challenge: 3 pediatric cases]. Arch Pediatr; 2010 Feb;17(2):149-53
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  • [Transliterated title] Le sarcome granulocytaire, un diagnostic à connaître : à propos de 3 observations pédiatriques.
  • Granulocytic sarcoma (GS) is a rare extramedullary tumor frequently associated with acute myeloblastic leukemia (AML).
  • In all 3 cases, the diagnosis was delayed or initially missed.
  • Pathology and immunohistochemistry data identified the disease.
  • [MeSH-major] Facial Neoplasms / diagnosis. Intestinal Neoplasms / diagnosis. Intestine, Small. Leukemia, Myeloid, Acute / diagnosis. Neoplasms, Multiple Primary / diagnosis. Orbital Neoplasms / diagnosis. Sarcoma, Myeloid / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols. Biopsy. Bone Marrow / pathology. Bone Marrow Transplantation. Child, Preschool. Combined Modality Therapy. Diagnostic Errors. Female. Follow-Up Studies. Humans. Infant. Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / drug therapy. Leukemia, Biphenotypic, Acute / pathology. Male. Tomography, X-Ray Computed

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  • [Copyright] Copyright 2009 Elsevier Masson SAS. All rights reserved.
  • (PMID = 19945260.001).
  • [ISSN] 1769-664X
  • [Journal-full-title] Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
  • [ISO-abbreviation] Arch Pediatr
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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70. 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

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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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71. Harel A, Wu F, Mattson MP, Morris CM, Yao PJ: Evidence for CALM in directing VAMP2 trafficking. Traffic; 2008 Mar;9(3):417-29
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  • Clathrin assembly lymphoid myeloid leukemia protein (CALM) is a clathrin assembly protein with a domain structure similar to the neuron-specific assembly protein AP180.
  • Overexpression of CALM leads to the reduction of cell surface VAMP2, whereas knockdown of CALM by RNA interference results in the accumulation of surface VAMP2.
  • [MeSH-minor] Animals. Cell Line. Cell Membrane / metabolism. Endocytosis. Humans. Mutagenesis, Site-Directed. PC12 Cells. Protein Structure, Tertiary. Protein Transport. RNA Interference. RNA, Small Interfering / genetics. Rats. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Transfection. Transferrin / metabolism

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  • (PMID = 18182011.001).
  • [ISSN] 1398-9219
  • [Journal-full-title] Traffic (Copenhagen, Denmark)
  • [ISO-abbreviation] Traffic
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Monomeric Clathrin Assembly Proteins; 0 / PICALM protein, human; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / Transferrin; 0 / VAMP2 protein, human; 0 / Vesicle-Associated Membrane Protein 2
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72. 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

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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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73. 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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74. Pagano L, Caira M, Nosari A, Rossi G, Locatelli F, Viale P, Aversa F, Hema E-Chart Group Italy: Hema e-Chart: Italian Registry for prospective analysis of epidemiology, management and outcome of febrile events in patients with hematological malignancies. J Chemother; 2010 Feb;22(1):20-4
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  • A systematic approach that starts from the registration of new diagnosis and complete follow-up can be of help for the study of treatment and evolution of these complications.
  • Its aim is to improve the speed, quality and integration of information related to subjects with febrile event, ultimately resulting in improving patients' care.Patients included adults and children with acute and chronic myeloid or lymphoid leukemia, Hodgkin's and non-Hodgkin's lymphoma, myelodysplastic syndrome, or multiple myeloma.
  • The registry also included data regarding event onset in hematopoietic stem cell transplants (HSCTs).
  • [MeSH-minor] Hematopoietic Stem Cell Transplantation. Humans. Incidence. Italy. Prospective Studies

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  • (PMID = 20227988.001).
  • [ISSN] 1973-9478
  • [Journal-full-title] Journal of chemotherapy (Florence, Italy)
  • [ISO-abbreviation] J Chemother
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Investigator] Levis A; Leoni P; Liso V; Baccarani M; Cortellazzo S; Rossi G; Russo D; La Nasa G; Storti S; Giustolisi R; Morabito F; Cuneo A; Bosi A; Capalbo SF; Cascavilla N; Ghio R; Carella A; Brugiatelli M; Ciceri F; Martinelli G; Morra E; Pogliani E; Mettivier V; Carli M; Abbadessa V; Musso M; Aricò M; Lazzarino M; Visani G; Fioritoni G; Di Bartolomeo P; Vallisa D; Petrini M; Favre C; Olivieri A; Gugliotta L; Leone G; Amadori S; De Rossi G; De Fabritiis P; Majolino I; D'Arco A; Lauria F; Mazza P; Fagioli F; Gherlinzoni F; Chesesi T; Rodeghiero F
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75. Chatterjee T, Panigrahi I, Agrawal N, Naithani R, Mahapatra M, Pati HP, Wadhwa S, Saxena R: Cytochemical, immunophenotypic and ultrastructural characterization of acute leukemias: a prospective study of fifty cases: haematological malignancy. Hematology; 2006 Jun;11(3):147-51
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  • [Title] Cytochemical, immunophenotypic and ultrastructural characterization of acute leukemias: a prospective study of fifty cases: haematological malignancy.
  • Cytochemistry and immunophenotyping are established methods in the diagnosis of most leukemias but the role of electron microscopy in diagnosis, apart from understanding the cellular morphology is less studied.
  • We present here 50 cases of acute leukemias that were studied for morphology, conventional cytochemistry, immunophenotyping and transmission electron microscopy (TEM), including ultrastructural cytochemistry using myeloperoxidase (MPO) and platelet peroxidase activity.
  • TEM morphology using ultrastructural cytochemistry helped in definitive typing in one mixed lineage leukemia case, one AML-M5b, one AML-M6b and one microgranular variant of APML.
  • Thus, ultrastructural studies may be useful in accurate diagnosis of biphenotypic leukemia and further classification of acute leukemias.
  • Also, in cases with hypercellular marrow and with associated myelofibrosis, where the marrow aspirate gives low cell count, ultrastructural studies are a valuable aid to arriving at an accurate diagnosis.
  • [MeSH-major] Leukemia / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Antigens, CD / analysis. Antigens, Neoplasm / analysis. Child. Child, Preschool. Female. Humans. Immunophenotyping. Male. Microscopy, Electron. Middle Aged. Neoplasm Proteins / analysis. Neoplastic Stem Cells / chemistry. Neoplastic Stem Cells / ultrastructure. Peroxidase / analysis. Prospective Studies

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  • (PMID = 17325954.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Neoplasm Proteins; EC 1.11.1.7 / Peroxidase
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76. 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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77. Weir EG, Ali Ansari-Lari M, Batista DA, Griffin CA, Fuller S, Smith BD, Borowitz MJ: Acute bilineal leukemia: a rare disease with poor outcome. Leukemia; 2007 Nov;21(11):2264-70
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  • [Title] Acute bilineal leukemia: a rare disease with poor outcome.
  • Most cases of acute leukemia can be assigned to the myeloid, B or T lineage.
  • In a few cases, definitive assignment cannot be achieved because blasts express antigens of more than one lineage.
  • A subset of these, referred to as acute bilineal leukemias (aBLLs), is characterized by the presence of more than one population of blasts, each comprising a single lineage.
  • We identified 19 cases of aBLL, including 10 mixed T and myeloid (T-My) and nine mixed B and myeloid (B-My); no mixed B and T cases were identified.
  • Three of seven patients with B-My had a t(9;22)(q34q11.2), two had 11q23 translocations and one had del(9).
  • Of 16 patients with outcome data, only six achieved complete remission and only two remain free of disease 2.5 and 4.5 years after chemotherapy or stem cell transplantation. aBLL is a rare disease that combines B or T and myeloid blasts.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy

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  • (PMID = 17611554.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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78. Wang LH, Wang M, Zhou CL, Chen S, Zhang XW, Xing HY, Wang JX: [Detection of point mutation at second tyrosine kinase domain of FLT3 gene in acute myeloid leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2005 Jun;26(6):335-8
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  • [Title] [Detection of point mutation at second tyrosine kinase domain of FLT3 gene in acute myeloid leukemia].
  • OBJECTIVE: To evaluate the prevalence of a novel FLT3 activating mutation in tyrosine kinase domain (TDK) in acute leukemia patients and its clinical implication.
  • METHODS: Genomic DNA from bone marrow mononuclear cells of 143 cases of acute myeloid leukemia (AML), 25 acute lymphocytic leukemia (ALL), 2 acute hybrid leukemia (AHL), 17 myelodysplastic syndromes (MDS) and 7 chronic myelogenous leukemia in blast crisis (CML-BC) was screened by polymerase chain reaction (PCR) and gel electrophoresis for FLT3-TKD point mutations.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. fms-Like Tyrosine Kinase 3 / genetics


79. Goldstein BD: Benzene as a cause of lymphoproliferative disorders. Chem Biol Interact; 2010 Mar 19;184(1-2):147-50
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  • There is a long standing issue concerning the strength of evidence relating benzene to lymphocytic neoplasms.
  • Because benzene is a known cause of human acute myelogenous leukemia there has been little reason for organizations such as the International Agency for Research on Cancer (IARC) or the US National Toxicology Program (NTP) to perform standard hazard identification reviews of benzene as a possible cause of other cancers such as lymphomas.
  • There is also increasing evidence of a close relationship between lymphoid tumors and the types of myeloid tumors known to be caused by benzene.
  • This includes the not infrequent finding of biphenotypic lineage as well as the formation of lymphoid as well as myeloid leukemias following chemotherapy.
  • Studies of the mechanism of benzene toxicity are consistent with a relatively non-specific mechanism capable of producing multiple chromosomal changes, and there is evidence that the early hematopoietic stem cell, which is believed to be targeted by benzene in causing myeloid cancers, is also the progenitor of lymphocytic cell types.
  • Furthermore, the classification of lymphomas has evolved so that non-Hodgkin lymphoma now includes such formerly distinct disorders as chronic lymphocytic leukemia and multiple myeloma, and there is less of a distinction between leukemia and non-leukemia forms of lymphoma.

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  • [Copyright] Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20035727.001).
  • [ISSN] 1872-7786
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] J64922108F / Benzene
  • [Number-of-references] 54
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80. Al-Seraihy AS, Owaidah TM, Ayas M, El-Solh H, Al-Mahr M, Al-Ahmari A, Belgaumi AF: Clinical characteristics and outcome of children with biphenotypic acute leukemia. Haematologica; 2009 Dec;94(12):1682-90
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  • [Title] Clinical characteristics and outcome of children with biphenotypic acute leukemia.
  • BACKGROUND: Knowledge concerning the clinical and biological presentation, as well as the outcome of treatment, of biphenotypic acute leukemia in children is limited.
  • DESIGN AND METHODS: This retrospective review analyzes the clinical features and outcome of children with biphenotypic acute leukemia diagnosed and treated over an 8-year period.
  • According to the EGIL scoring system 24 (3.7%) of 633 patients with acute leukemia were classified as having biphenotypic acute leukemia.
  • The diagnostic work-up and results were reviewed specifically for this study in the light of the newly published WHO criteria for the diagnosis of leukemia of ambiguous lineage.
  • Based on these criteria, 11 (1.7%) patients were categorized according to the new nomenclature as having mixed phenotype acute leukemia.
  • The majority of the patients (58.3%) had a B-lymphoid/myeloid phenotype, followed by the T-lymphoid/myeloid phenotype.
  • The most frequent chromosomal abnormality involved the 14q32 locus.
  • Patients received therapy based on a treatment regimen for acute lymphocytic leukemia regimen, which included myeloid-effective agents.
  • The survival of those patients who underwent hematopoietic stem cell transplantation in first complete remission was not different from that of the patients who were treated with chemotherapy alone (overall survival: 70.1% versus 81.1%, respectively, p=0.39; event-free survival: 70.1% versus 76.2%, respectively, p=0.75).
  • The outcome of the 11 patients who were retrospectively classified as having mixed phenotype acute leukemia according to the new WHO criteria was excellent, with no relapses or deaths occurring among these patients.
  • CONCLUSIONS: An acute lymphocytic leukemia type of induction therapy, using agents that are active against lymphoid and myeloid leukemias, appears to be more effective in achieving and maintaining complete remissions regardless of whether the patients are classified according to EGIL criteria or the new WHO criteria.
  • Hematopoietic stem cell transplantation may not be necessary for all patients in first complete remission.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy
  • [MeSH-minor] Antigens, CD / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Flow Cytometry. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Outcome Assessment (Health Care) / methods. Remission Induction. Retrospective Studies

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  • (PMID = 19713227.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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81. 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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82. Pratz KW, Cho E, Levis MJ, Karp JE, Gore SD, McDevitt M, Stine A, Zhao M, Baker SD, Carducci MA, Wright JJ, Rudek MA, Smith BD: A pharmacodynamic study of sorafenib in patients with relapsed and refractory acute leukemias. Leukemia; 2010 Aug;24(8):1437-44
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  • [Title] A pharmacodynamic study of sorafenib in patients with relapsed and refractory acute leukemias.
  • We report the results of a phase I dose escalation trial of the multikinase inhibitor sorafenib in relapsed and refractory acute leukemia patients using an intermittent dosing regimen.
  • Fifteen patients with advanced leukemia (12 with acute myeloid leukemia, 2 with acute lymphoblastic leukemia, 1 with biphenotypic) and a median age of 63 (range 37-85) years were enrolled and treated on a dose escalation trial.
  • Out of 15 patients, 11 experienced stable disease as best response.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use

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  • (PMID = 20535150.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA128864; United States / NCI NIH HHS / CA / P30 CA006973-48; United States / NCRR NIH HHS / RR / UL1 RR025005; United States / NCI NIH HHS / CA / P30CA006973; United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCRR NIH HHS / RR / UL1 RR025005-04; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / P50 CA100632-06; United States / NCI NIH HHS / CA / R01 CA128864-04; United States / NCI NIH HHS / CA / U01 CA070095-17; United States / NCI NIH HHS / CA / U01CA70095
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ NIHMS201571; NLM/ PMC2921005
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83. Verheyden S, Demanet C: Susceptibility to myeloid and lymphoid leukemia is mediated by distinct inhibitory KIR-HLA ligand interactions. Leukemia; 2006 Aug;20(8):1437-8
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  • [Title] Susceptibility to myeloid and lymphoid leukemia is mediated by distinct inhibitory KIR-HLA ligand interactions.
  • [MeSH-major] HLA-B Antigens / physiology. HLA-C Antigens / physiology. Killer Cells, Natural / immunology. Leukemia, Lymphoid / immunology. Leukemia, Myeloid / immunology. Receptors, Immunologic / physiology. Tumor Escape

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  • (PMID = 16761016.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA-B Antigens; 0 / HLA-C Antigens; 0 / Receptors, Immunologic; 0 / Receptors, KIR
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84. Chen X, Zhang Y, Li Y, Lei P, Zhai Y, Liu L: Biphenotypic hematologic malignancy: a case report of the 8p11 myeloproliferative syndrome in a child. J Pediatr Hematol Oncol; 2010 Aug;32(6):501-3
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  • [Title] Biphenotypic hematologic malignancy: a case report of the 8p11 myeloproliferative syndrome in a child.
  • SUMMARY: The 8p11 myeloproliferative syndrome, also known as stem cell leukemia/lymphoma, is a rare, atypical, myeloproliferative disorder and lymphoid malignancy associated with chromosomal abnormalities involving the 8p11 chromosomal band.
  • Disease phenotypes associated with this translocation include poor prognosis and transformation to acute leukemia and non-Hodgkin lymphoma.
  • In common with a T-cell phenotype, obtaining and maintaining remission is difficult by conventional chemotherapy.
  • This study describes an illustrative case of 8p11 myeloproliferative syndrome/stem cell leukemia/lymphoma outlining its chief features and historical developments.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Cyclophosphamide / therapeutic use. Dexamethasone / therapeutic use. Doxorubicin / therapeutic use. Etoposide / therapeutic use. Humans. Male. Phenotype. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / physiopathology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / physiopathology. Prednisone / therapeutic use. Syndrome. Translocation, Genetic. Vincristine / therapeutic use

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  • (PMID = 20562652.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CVAD protocol; EPOCH protocol
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85. Steiner M, Attarbaschi A, Dworzak M, Strobl H, Pickl W, Kornmüller R, Haas O, Gadner H, Mann G, Austrian Berlin-Frankfurt-Münster Study Group: Cytochemically myeloperoxidase positive childhood acute leukemia with lymphoblastic morphology treated as lymphoblastic leukemia. J Pediatr Hematol Oncol; 2010 Jan;32(1):e4-7
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  • [Title] Cytochemically myeloperoxidase positive childhood acute leukemia with lymphoblastic morphology treated as lymphoblastic leukemia.
  • SUMMARY: Cytochemical myeloperoxidase (MPO) positivity represents the gold standard for discrimination between lymphatic and myeloid blasts.
  • Rarely, cytochemical MPO reaction may be positive in >or=3% of blasts with clear lymphoblastic morphology.
  • We present 5 patients with cytochemically MPO-positive acute leukemia classified as lymphoblastic by cytomorphology and lymphoblastic (n=3) or biphenotypic (n=2) by immunophenotyping, who entered first-line treatment for lymphoblastic leukemia.
  • The former 3 are in first remission and both with biphenotypic leukemia relapsed with acute myeloid leukemia.
  • The study primarily shows that cytochemical MPO expression in childhood acute leukemia revealing typical lymphoblastic morphology and phenotype does rarely exist.
  • Although a small number of patients studied, cytochemical MPO expression in acute leukemia does not seem to require myeloid leukemia treatment in case of otherwise lymphoblastic cytomorphology and phenotype.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Peroxidase / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


86. Georgy M, Yonescu R, Griffin CA, Batista DA: Acute mixed lineage leukemia and a t(6;14)(q25;q32) in two adults. Cancer Genet Cytogenet; 2008 Aug;185(1):28-31
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  • [Title] Acute mixed lineage leukemia and a t(6;14)(q25;q32) in two adults.
  • Acute mixed lineage leukemia (AMLL) is a rare form of leukemia in which both myeloid and lymphoid markers are present.
  • Few chromosome abnormalities have been identified associated with this form of leukemia.
  • A translocation involving the long arms of chromosomes 6 and 14 was previously described in four young individuals with acute leukemia and in three of these cases the diagnosis was mixed lineage.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 6. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

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  • (PMID = 18656690.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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87. El-Sissy A, El-Mashari M, Bassuni W, El-Swaayed A: Molecular detection of BCR/ABL fusion gene in Saudi acute lymphoblastic leukemia patients. J Egypt Natl Canc Inst; 2006 Jun;18(2):109-16
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  • [Title] Molecular detection of BCR/ABL fusion gene in Saudi acute lymphoblastic leukemia patients.
  • A fraction of acute lymphoblastic leukemia (ALL) cases carry the translocation t(9;22) (q34;q11.2) which juxtaposes the ABL proto-oncogene to the BCR gene generating a chimeric gene, BCR/ABL.
  • PATIENTS AND METHODS: Twenty newly diagnosed ALL patients, 16 adult and 4 paediatric cases, were included in the study, 11 cases (55%) were of precursor B phenotype, 8 cases (40%) belonged to T lineage, while one case was biphenotypic expressing mainly precursor B cell markers tether with CD13, CD33, CD117, Detection of BCR/ABL fusion gene was done using interphase FISH technique and was confirmed molecularly using the RT-PCR technique.
  • RESULTS: BCR/ABL fusion gene was negative in all the examined cases, yet abnormality involving 9q34, ABL gene, either by addition or deletion was detected in three cases (15%).
  • CONCLUSION: This may reflect the frequency of association of ABL gene and BCR gene abnormality in our cases, and that absence of fusion gene BCR/ABL does not exclude their role in the leukomogenic process, yet a larger study is required to confirm and detect the prevalence of these gene disturbances in ALL and their association.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 17496935.001).
  • [ISSN] 1110-0362
  • [Journal-full-title] Journal of the Egyptian National Cancer Institute
  • [ISO-abbreviation] J Egypt Natl Canc Inst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Antigens, Differentiation, B-Lymphocyte; 0 / RNA, Messenger; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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88. Jacobsohn DA, Hewlett B, Morgan E, Tse W, Duerst RE, Kletzel M: Favorable outcome for infant acute lymphoblastic leukemia after hematopoietic stem cell transplantation. Biol Blood Marrow Transplant; 2005 Dec;11(12):999-1005
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  • [Title] Favorable outcome for infant acute lymphoblastic leukemia after hematopoietic stem cell transplantation.
  • Infants with acute lymphoblastic leukemia (ALL) have a poor prognosis when treated with standard chemotherapy.
  • A subset of these infants, particularly those with mixed-lineage leukemia (MLL) rearrangements, has a high likelihood of relapse.
  • Hematopoietic stem cell transplantation (HSCT) performed early in first remission may improve outcome.
  • Six patients were < or =6 months of age at diagnosis, 11 had an initial white blood cell count of >50000/microL, and all patients with determinable cytogenetics had a high-risk karyotype [t(4:11) abnormality or other MLL rearrangement].
  • Two patients, 1 of whom had minimal residual disease at HSCT, died after relapse following HSCT.
  • Acute and chronic graft-versus-host disease were minimal in these patients.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Biphenotypic, Acute / therapy. Transplantation Conditioning
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Male. Recurrence. Remission Induction. Retrospective Studies. Risk Factors. Time Factors. Translocation, Genetic / genetics

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  • (PMID = 16338622.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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89. Bae SY, Yoon SY, Huh JH, Sung HJ, Choi IK: Hypereosinophilia in biphenotypic (B-cell/T-cell) acute lymphoblastic leukemia. Leuk Lymphoma; 2007 Jul;48(7):1417-9
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  • [Title] Hypereosinophilia in biphenotypic (B-cell/T-cell) acute lymphoblastic leukemia.
  • [MeSH-major] Hypereosinophilic Syndrome / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


90. Kiyomizu K, Yagi T, Yoshida H, Minami R, Tanimura A, Karasuno T, Hiraoka A: Fulminant septicemia of Bacillus cereus resistant to carbapenem in a patient with biphenotypic acute leukemia. J Infect Chemother; 2008 Oct;14(5):361-7
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  • [Title] Fulminant septicemia of Bacillus cereus resistant to carbapenem in a patient with biphenotypic acute leukemia.
  • A 33-year-old man was suffering from febrile neutropenia (FN) on day 15 after the start of remission-induction therapy for biphenotypic acute leukemia under gut decontamination with polymyxin B and nystatin.
  • If B. cereus resistant to carbapem increases, our method of gut decontamination with polymyxin B and nystatin may have to be changed to one containing a new quinolone for the prevention of septicemia.
  • [MeSH-major] Bacillus cereus / drug effects. Bacteremia / microbiology. Carbapenems / therapeutic use. Leukemia, Biphenotypic, Acute / complications
  • [MeSH-minor] Adult. Anti-Bacterial Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Stem / microbiology. Brain Stem / pathology. Fever / drug therapy. Gram-Positive Bacterial Infections / complications. Gram-Positive Bacterial Infections / diagnosis. Gram-Positive Bacterial Infections / drug therapy. Gram-Positive Bacterial Infections / pathology. Humans. Liver / microbiology. Liver / ultrastructure. Lung / microbiology. Lung / ultrastructure. Male. Microbial Sensitivity Tests. Neutropenia / drug therapy. Remission Induction. beta-Lactam Resistance

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  • (PMID = 18936889.001).
  • [ISSN] 1341-321X
  • [Journal-full-title] Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy
  • [ISO-abbreviation] J. Infect. Chemother.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Carbapenems
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91. Faber J, Armstrong SA: Mixed lineage leukemia translocations and a leukemia stem cell program. Cancer Res; 2007 Sep 15;67(18):8425-8
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  • [Title] Mixed lineage leukemia translocations and a leukemia stem cell program.
  • One possibility is that CSC arise from the stem cell counterparts in normal tissues.
  • In support of this idea, we showed recently that mixed lineage leukemia fusion oncoproteins can convert committed hematopoietic progenitors into leukemias, which include leukemia stem cells expressing a self-renewal associated program in the context of a differentiated myeloid cell.
  • [MeSH-major] Hematopoietic Stem Cells / pathology. Leukemia, Biphenotypic, Acute / pathology. Neoplastic Stem Cells / pathology
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Humans. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 17875678.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion
  • [Number-of-references] 24
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92. Naunheim MR, Nahed BV, Walcott BP, Kahle KT, Soupir CP, Cahill DP, Borges LF: Diagnosis of acute lymphoblastic leukemia from intracerebral hemorrhage and blast crisis. A case report and review of the literature. Clin Neurol Neurosurg; 2010 Sep;112(7):575-7
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  • [Title] Diagnosis of acute lymphoblastic leukemia from intracerebral hemorrhage and blast crisis. A case report and review of the literature.
  • Intracerebral hemorrhage (ICH) contributes significantly to the morbidity and mortality of patients suffering from acute leukemia.
  • While ICH is often identified in autopsy studies of leukemic patients, it is rare for ICH to be the presenting sign that ultimately leads to the diagnosis of leukemia.
  • We report a patient with previously undiagnosed acute precursor B-cell lymphoblastic leukemia (ALL) who presented with diffuse encephalopathy due to ICH in the setting of an acute blast crisis.
  • The diagnosis of ALL was initially suspected, because of the hyperleukocytosis observed on presentation, then confirmed with a bone marrow biopsy and flow cytometry study of the peripheral blood.
  • This case demonstrates that the presence of hyperleukocytosis in a patient with intracerebral hemorrhage should raise clinical suspicion for acute leukemia as the cause of the ICH.
  • [MeSH-major] Blast Crisis / diagnosis. Intracranial Hemorrhages / diagnosis. Leukemia, Biphenotypic, Acute / diagnosis
  • [MeSH-minor] Benzamides. Blood Cell Count. Diagnosis, Differential. Flow Cytometry. Humans. Imatinib Mesylate. In Situ Hybridization. Leukocyte Count. Male. Middle Aged. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Tomography, X-Ray Computed

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  • (PMID = 20493628.001).
  • [ISSN] 1872-6968
  • [Journal-full-title] Clinical neurology and neurosurgery
  • [ISO-abbreviation] Clin Neurol Neurosurg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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93. Aplan PD: Chromosomal translocations involving the MLL gene: molecular mechanisms. DNA Repair (Amst); 2006 Sep 8;5(9-10):1265-72
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  • Leukemias with MLL translocations have been the topic of intense interest because of the unusual, biphenotypic immunophenotype of these leukemias, because of the unique clinical presentation of some MLL translocations (infant leukemia and therapy-related leukemia), and because of the large number of different chromosomal loci that partner with MLL in these translocations.

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  • (PMID = 16797254.001).
  • [ISSN] 1568-7864
  • [Journal-full-title] DNA repair
  • [ISO-abbreviation] DNA Repair (Amst.)
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chromatin; 0 / MLL protein, human; 0 / Topoisomerase II Inhibitors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 71
  • [Other-IDs] NLM/ NIHMS13506; NLM/ PMC1635494
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94. Lou Z, Zhang CC, Tirado CA, Slone T, Zheng J, Zaremba CM, Oliver D, Chen W: Infantile mixed phenotype acute leukemia (bilineal and biphenotypic) with t(10;11)(p12;q23);MLL-MLLT10. Leuk Res; 2010 Aug;34(8):1107-9
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  • [Title] Infantile mixed phenotype acute leukemia (bilineal and biphenotypic) with t(10;11)(p12;q23);MLL-MLLT10.
  • We report a case of a 6-month-old boy with a mixed phenotype acute leukemia (MPAL), bilineal and biphenotypic immunophenotype (B-lymphoid lineage and combined B-lymphoid and monocytic lineage) with t(10;11)(p12;q23);MLL-MLLT10.
  • He was treated with acute myeloid leukemia protocol and in complete remission at 7-month follow-up.
  • 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

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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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95. Yao PJ, Petralia RS, Bushlin I, Wang Y, Furukawa K: Synaptic distribution of the endocytic accessory proteins AP180 and CALM. J Comp Neurol; 2005 Jan 3;481(1):58-69
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  • AP180 and clathrin assembly lymphoid myeloid leukemia protein (CALM) are clathrin accessory proteins that promote the formation of clathrin-coated vesicles.

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  • (PMID = 15558718.001).
  • [ISSN] 0021-9967
  • [Journal-full-title] The Journal of comparative neurology
  • [ISO-abbreviation] J. Comp. Neurol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Monomeric Clathrin Assembly Proteins; 0 / Picalm protein, rat; 0 / clathrin assembly protein AP180
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96. Gupta A, Modi CJ, Gujral S: Hemophagocytosis by leukemic cells in biphenotypic acute leukaemia: a rare case. Indian J Pathol Microbiol; 2010 Apr-Jun;53(2):370-1
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  • [Title] Hemophagocytosis by leukemic cells in biphenotypic acute leukaemia: a rare case.
  • [MeSH-major] Lymphocytes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 20551563.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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97. Gobbi G, Mirandola P, Malinverno C, Sponzilli I, Carubbi C, Ricci F, Binazzi R, Basso G, Giuliani-Piccari G, Ramazzotti G, Pasquantonio G, Cocco L, Vitale M: Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin. Int J Oncol; 2008 Aug;33(2):371-4
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  • [Title] Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin.
  • The B203.13 monoclonal antibody was developed by immunizing mice with the B/monocyte biphenotypic cell line B1b.
  • We tested this antibody as a marker of childhood B-acute lymphoblastic leukemia (B-ALL).
  • The CD10(+)/B203.13(+) phenotype was specific to B-ALL, since CD10(+)/CD20(+) cells from common acute lymphoblastic leukemia (c-ALL) did not express B203.13.
  • We concluded that the use of B203.13 in association with CD10 and CD20 provides meaningful information for distinguishing normal residual B-cells from leukemic B-lymphoblasts and that recurrence of a CD10(+)/B203.13(+) phenotype after transplantation may be a very early relapse indicator of early B-acute lymphoblastic leukemia.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18636158.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
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98. Jun KR, Jang S, Chi HS, Lee KH, Lee JH, Choi SJ, Seo JJ, Moon HN, Im HJ, Park CJ: Relationship between in vitro chemosensitivity assessed with MTT assay and clinical outcomes in 103 patients with acute leukemia. Korean J Lab Med; 2007 Apr;27(2):89-95
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  • [Title] Relationship between in vitro chemosensitivity assessed with MTT assay and clinical outcomes in 103 patients with acute leukemia.
  • METHODS: For MTT assay, we obtained bone marrow aspirates from 103 patients with acute leukemia at the time of initial diagnosis or relapse.
  • CONCLUSIONS: Although it does not provide the insight into the mechanisms that cause drug resistance, the MTT assay may be a useful tool in individually optimizing the chemotherapy of patients with acute leukemia.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18094557.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Coloring Agents; 0 / Tetrazolium Salts; 0 / Thiazoles; 04079A1RDZ / Cytarabine; 298-93-1 / thiazolyl blue; ZS7284E0ZP / Daunorubicin
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99. 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
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100. Cerveira N, Meyer C, Santos J, Torres L, Lisboa S, Pinheiro M, Bizarro S, Correia C, Norton L, Marschalek R, Teixeira MR: A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia. BMC Cancer; 2010;10:518
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  • [Title] A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia.
  • BACKGROUND: Abnormalities of 11q23 involving the MLL gene are found in approximately 10% of human leukemias.
  • In this work we present the identification of a novel MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia.
  • METHODS: Cytogenetics, fluorescence in situ hybridization (FISH), molecular studies (RT-PCR and LDI-PCR), and bioinformatic sequence analysis were used to characterize the CT45A2 gene as novel MLL fusion partner in pediatric acute leukemia.
  • CONCLUSION: We have identified CT45A2 as a novel spliced MLL fusion partner in a pediatric patient with de novo biphenotypic acute leukemia, as a result of a cryptic insertion of 11q23 in Xq26.3.
  • Since CT45A2 is the first Cancer/Testis antigen family gene found fused with MLL in acute leukemia, future studies addressing its biologic relevance for leukemogenesis are warranted.
  • [MeSH-major] Antigens, Neoplasm / genetics. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 20920256.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / CT45A1 protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2956734
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