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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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[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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[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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[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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[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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[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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[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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[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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[Cites] Leukemia. 2002 Sep;16(9):1818-26 [12200698.001]

[Cites] Leukemia. 2008 Nov;22(11):2029-40 [18685615.001]

[Cites] Genes Dev. 2003 Dec 15;17(24):3029-35 [14701873.001]

[Cites] Proc Natl Acad Sci U S A. 2004 May 18;101(20):7618-23 [15128949.001]

[Cites] Nature. 1994 Feb 17;367(6464):645-8 [7509044.001]

[Cites] EMBO J. 1994 Feb 15;13(4):928-33 [8112307.001]

[Cites] Nat Med. 1997 Jul;3(7):730-7 [9212098.001]

[Cites] Nature. 1999 Jul 29;400(6743):464-8 [10440377.001]

[Cites] Blood. 2006 Feb 1;107(3):1166-73 [16234360.001]

[Cites] Nature. 2006 Aug 17;442(7104):818-22 [16862118.001]

[Cites] Cancer Cell. 2006 Oct;10(4):257-68 [17045204.001]

[Cites] Science. 2007 Apr 27;316(5824):600-4 [17463288.001]

[Cites] Exp Hematol. 2007 May;35(5):782-92 [17577927.001]

[Cites] Exp Hematol. 2007 Oct;35(10):1538-49 [17889721.001]

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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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[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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[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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[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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[Cites] Blood. 1992 Oct 15;80(8):2066-73 [1327288.001]

[Cites] Leukemia. 2003 Aug;17(8):1538-43 [12886240.001]

[Cites] Blood. 1989 Nov 1;74(6):2096-102 [2553160.001]

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[CommentOn] Haematologica. 2009 Jul;94(7):919-27 [19454497.001]

(PMID = 19996120.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Comment; Letter

[Publication-country] Italy

[Chemical-registry-number] 0 / Antigens, CD34; EC 1.11.1.7 / Peroxidase

[Other-IDs] NLM/ PMC2791943

   

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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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[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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[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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[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

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(PMID = 17693199.001).

[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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[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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[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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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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[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

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(PMID = 18617064.001).

[ISSN] 1873-4456

[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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[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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[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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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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[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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[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

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(PMID = 20846093.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Letter; Research Support, Non-U.S. Gov't

[Publication-country] England

   

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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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[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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[Cites] Am J Surg Pathol. 1997 Sep;21(9):1037-46 [9298880.001]

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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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[Title] Lineage switch from precursor B cell acute lymphoblastic leukemia to acute monocytic leukemia at relapse.

A lineage switch in leukemia, in which the leukemic cell lineage at onset converts to another lineage at a later time, is an uncommon type of hybrid (mixed) leukemia regarded as a variation of bilineage leukemia.

We present a case of a 60-year-old female diagnosed with precursor B cell acute lymphoblastic leukemia (ALL), whose markers in flow cytometry shifted from their original status of CD19+, 22+, 79a+, 13+, HLA-DR+, and TdT+.

Residual disease was proved by biopsy and pathologically shown to have an immature phenotype of CD5+, CD10-, CD20-, CD79a- and myeloperoxidase negativity.

Two weeks after liver biopsy, blast cells progressively appeared in the peripheral blood; these cells had a monocytoid morphology and phenotype (CD13, 14) but were accompanied by myeloid (CD33) and lymphoid (CD2, 4, 20) cells.

This phenotypical conversion from B-ALL to hybrid leukemia featuring monocytoid characteristics is known as a lineage switch.

[MeSH-major] Leukemia, Biphenotypic, Acute / pathology. Leukemia, Monocytic, Acute / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

[MeSH-minor] Biomarkers, Tumor / blood. Bone Marrow / pathology. Cell Lineage. Female. Humans. Immunophenotyping. Middle Aged. Recurrence

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[Cites] Leukemia. 1995 Dec;9(12):2023-6 [8609712.001]

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(PMID = 20066454.001).

[ISSN] 1437-7772

[Journal-full-title] International journal of clinical oncology

[ISO-abbreviation] Int. J. Clin. Oncol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Biomarkers, Tumor

   

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[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

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[Cites] Blood. 1998 Jul 15;92(2):596-9 [9657760.001]

[Cites] Br J Haematol. 2005 Feb;128(4):548-51 [15686466.001]

[Cites] Ann Hematol. 2003 Apr;82(4):236-40 [12707727.001]

[Cites] Blood. 1986 Jan;67(1):1-11 [3079640.001]

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(PMID = 17483067.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] Japan

[Chemical-registry-number] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol

   

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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

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[Copyright] 2007 S. Karger AG, Basel

(PMID = 17804901.001).

[ISSN] 1421-9662

[Journal-full-title] Acta haematologica

[ISO-abbreviation] Acta Haematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

   

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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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[Cites] Blood. 2004 Jan 15;103(2):399-406 [14512321.001]

[Cites] Blood. 2003 Aug 1;102(3):981-6 [12649131.001]

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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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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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[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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[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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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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[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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[Cites] Blood. 2003 Jul 1;102(1):276-83 [12623848.001]

[Cites] Leukemia. 2003 Dec;17(12):2318-57 [14562125.001]

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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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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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[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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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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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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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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[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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[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

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(PMID = 15996732.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

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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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[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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[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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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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[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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[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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[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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[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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[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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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