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1. Bosch FJ, Badenhorst L, Le Roux JA, Louw VJ: Successful treatment of Chromobacterium violaceum sepsis in South Africa. J Med Microbiol; 2008 Oct;57(Pt 10):1293-5
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  • As far as could be ascertained, this infection has never been reported in a patient with leukaemia.
  • We describe what we believe to be the first such case of C. violaceum sepsis, in a 16-year-old female patient with acute biphenotypic leukaemia, which developed during the neutropenic phase after intensive chemotherapy.
  • [MeSH-minor] Adolescent. Antifungal Agents / pharmacology. Candidiasis / complications. Candidiasis / drug therapy. Female. Humans. Leukemia / complications. Neutropenia / complications. South Africa / epidemiology. Treatment Outcome

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  • (PMID = 18809561.001).
  • [ISSN] 0022-2615
  • [Journal-full-title] Journal of medical microbiology
  • [ISO-abbreviation] J. Med. Microbiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antifungal Agents
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2. 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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3. Amakawa R, Hiramoto N, Kawano S, Hyo A, Nakamichi N, Tajima K, Ito T, Mori S, Kishimoto Y, Fukuhara S: Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia. J Clin Exp Hematop; 2010;50(1):51-8
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  • [Title] Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia.
  • We report a case of acute mixed-lineage leukemia, as seen in a 65 year-old female with MLL gene amplification and biallelic loss of wild type p53 gene.
  • The diagnosis was based on the findings that her bone marrow (BM) blasts expressed cytoplasmic CD3 (cyCD3), B-lineage antigens and myeloid antigens accompanied by clonal rearrangements of IgH gene.
  • Add (11q23) abnormality was found in sideline karyotypes as well as the stemline abnormality of dic(17;20) (p11;q11).
  • [MeSH-major] Gene Amplification. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

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  • (PMID = 20505276.001).
  • [ISSN] 1880-9952
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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4. Xu XQ, Wang JM, Lü SQ, Chen L, Yang JM, Zhang WP, Song XM, Hou J, Ni X, Qiu HY: Clinical and biological characteristics of adult biphenotypic acute leukemia in comparison with that of acute myeloid leukemia and acute lymphoblastic leukemia: a case series of a Chinese population. Haematologica; 2009 Jul;94(7):919-27
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  • [Title] Clinical and biological characteristics of adult biphenotypic acute leukemia in comparison with that of acute myeloid leukemia and acute lymphoblastic leukemia: a case series of a Chinese population.
  • BACKGROUND: Biphenotypic acute leukemia is a rare disorder that is difficult to diagnose.
  • It displays features of both myeloid and lymphoid lineage.
  • There is still a lack of studies in biphenotypic acute leukemia in a Chinese population.
  • We present here a comprehensive investigation of the clinical and biological characteristics, and outcome of biphenotypic acute leukemia in our hospital in over a seven year period.
  • DESIGN AND METHODS: We retrospectively analyzed 452 adult acute leukemia patients diagnosed according to French-American-British (FAB) classification and biphenotypic acute leukemia diagnosed according to European Group for the Immunological Characterization of Leukemias (EGIL) classification, respectively.
  • Biological characteristics, response to treatment, and outcome were examined in biphenotypic acute leukemia patients and compared with that in acute myeloid leukemia and acute lymphoblastic leukemia patients with complete follow-up profiles diagnosed in the same period.
  • RESULTS: Of 452 acute leukemia patients, 21 cases (4.6%) were diagnosed as biphenotypic acute leukemia.
  • Among them, 14 (66.7%) were B lymphoid and myeloid, 5 (23.8%) were T lymphoid and myeloid, one (4.8%) was T/B lymphoid and one (4.8%) was trilineage differentiation.
  • When compared with acute myeloid leukemia and acute lymphoblastic leukemia, patients with biphenotypic acute leukemia showed significantly higher incidence of CD34 antigen expression, unfavorable karyotypes, and extramedullary infiltration (p<0.05).
  • In this cohort of patients with biphenotypic acute leukemia, t(9;22) was the most common abnormality in chromosome structure.
  • The median disease-free survival and overall survival in biphenotypic acute leukemia patients was five months and ten months, respectively, significantly shorter than those in acute myeloid leukemia and acute lymphoblastic leukemia patients (p<0.05).
  • CONCLUSIONS: The prognosis of biphenotypic acute leukemia patients is poor when compared with de novo acute myeloid leukemia or acute lymphoblastic leukemia.
  • Biphenotypic acute leukemia patients showed a much higher incidence of CD34 antigen expression, complex abnormal karyotype, extramedullary infiltration, relapse, and resistance to therapy after relapse.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


5. 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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6. Nakagawa Y, Hasegawa M, Kurata M, Yamamoto K, Abe S, Inoue M, Takemura T, Hirokawa K, Suzuki K, Kitagawa M: Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL). Am J Hematol; 2005 Mar;78(3):173-80
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  • [Title] Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL).
  • To determine the apoptosis-resistant mechanism in adult acute mixed lineage leukemia (AMLL) with biphenotypic blasts responsible for resistance against chemotherapy, the expression levels of IAP-family proteins in AMLL bone marrow cells were analyzed by quantitative RT-PCR.
  • These findings suggest that higher expression of various IAPs is associated with the chemotherapy-resistant nature of this specific type of leukemia.
  • [MeSH-major] Apoptosis. Biomarkers, Tumor / metabolism. Bone Marrow Cells / metabolism. Leukemia, Biphenotypic, Acute / metabolism. Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Flow Cytometry. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Inhibitor of Apoptosis Proteins. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Male. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / metabolism. Middle Aged. Neoplasm Proteins. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15726601.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proteins; 0 / RNA, Messenger
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7. 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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8. Haouas H, Haouas S, Uzan G, Hafsia A: Identification of new markers discriminating between myeloid and lymphoid acute leukemia. Hematology; 2010 Aug;15(4):193-203
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  • [Title] Identification of new markers discriminating between myeloid and lymphoid acute leukemia.
  • BACKGROUND: The heterogeneity of acute myeloid leukemia (AML) with respect to biology and clinical course resides in the fact that patients belonging to the same group show marked differences in their response to chemotherapy, necessitating a refinement of AML classification.
  • RESULTS: We have shown that two downregulated genes in AML, those encoding guanine nucleotide-binding protein gamma11 (GNG11) and amphiregulin (AREG), are also downregulated in B-lineage acute lymphoblastic leukemia (B-ALL) and T-lineage acute lymphoblastic leukemia (T-ALL) patients.
  • A second gene, that encoding ceruloplasmin (CP), is upregulated in AML but not in B-ALL and T-ALL.
  • Our study is the first to analyze these genes in AML, B-ALL, T-ALL and chronic leukemia (myeloid and lymphoid) patients by RT-PCR.
  • This rapid and sensitive method could be used to screen these genes in different types of leukemia.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Amphiregulin. Cell Line, Tumor. Ceruloplasmin / genetics. Ceruloplasmin / metabolism. Diagnosis, Differential. EGF Family of Proteins. Female. GTP-Binding Protein alpha Subunits, Gq-G11 / genetics. GTP-Binding Protein alpha Subunits, Gq-G11 / metabolism. Gene Expression Profiling. Glycoproteins / genetics. Glycoproteins / metabolism. Humans. Intercellular Signaling Peptides and Proteins / genetics. Intercellular Signaling Peptides and Proteins / metabolism. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 20670477.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AREG protein, human; 0 / Amphiregulin; 0 / Biomarkers, Tumor; 0 / EGF Family of Proteins; 0 / Glycoproteins; 0 / Intercellular Signaling Peptides and Proteins; EC 1.16.3.1 / Ceruloplasmin; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gq-G11
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9. Davis CC, Marti LC, Sempowski GD, Jeyaraj DA, Szabolcs P: Interleukin-7 permits Th1/Tc1 maturation and promotes ex vivo expansion of cord blood T cells: a critical step toward adoptive immunotherapy after cord blood transplantation. Cancer Res; 2010 Jul 1;70(13):5249-58
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  • Donor leukocyte infusions (DLI) in the allogeneic hematopoietic transplant setting can provide a clinically relevant boost of immunity to reduce opportunistic infections and to increase graft-versus-leukemia activity.
  • However, significant apoptosis occurs in proliferating T cells, diminishing the yield and skewing the CD4/CD8 ratio in the T-cell population, jeopardizing the potential efficacy of DLI.
  • Recognizing that infused T lymphocytes will need to meet microbial antigens in secondary lymphoid organs to generate effectors, we also show that expansion with IL-7 promotes the preservation of a polyclonal broad T-cell receptor repertoire and a surface phenotype that favors lymph node homing.
  • Expanded lymphocytes lack alloreactivity against recipient and other allogeneic cells, indicating a favorable safety profile from graft-versus-host disease.
  • Nevertheless, expanded T cells can be primed subsequently against lymphoid and myeloid leukemia cells to generate tumor-specific cytotoxic T cells.

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20530666.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL091749; United States / NHLBI NIH HHS / HL / 7R01HL091749; United States / NCI NIH HHS / CA / R01 CA132110; United States / NIAID NIH HHS / AI / UC6 AI058607; United States / NIAID NIH HHS / AI / P30 AI051445; United States / NHLBI NIH HHS / HL / R01 HL091749-04; United States / NCI NIH HHS / CA / R01-CA132110; United States / NCI NIH HHS / CA / R01 CA132110-03; United States / NCI NIH HHS / CA / CA132110-03; United States / NIAID NIH HHS / AI / UC6 AI58607; United States / NIAID NIH HHS / AI / P30 AI51445
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD137; 0 / Antigens, CD28; 0 / Antigens, CD3; 0 / Interleukin-7; 0 / Receptors, Antigen, T-Cell, alpha-beta; 126465-35-8 / Perforin; 147205-72-9 / CD40 Ligand
  • [Other-IDs] NLM/ NIHMS203765; NLM/ PMC2896454
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10. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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11. 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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12. Dixon N, Kishnani PS, Zimmerman S: Clinical manifestations of hematologic and oncologic disorders in patients with Down syndrome. Am J Med Genet C Semin Med Genet; 2006 Aug 15;142C(3):149-57
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  • Increased erythrocyte mean corpuscular volume (MCV) is frequently found among DS infants and remains elevated throughout life in two-thirds of patients, making interpretation of red cell indices for diagnosis of nutritional anemias or bone marrow failure disorders more challenging.
  • Transient myeloproliferative disorder (TMD) associated with pancytopenia, hepatosplenomegaly, and circulating immature WBCs, is found almost exclusively in DS infants with an incidence of approximately 10%.
  • Despite the high rate of spontaneous regression, TMD can be a preleukemic disorder in 20-30% of children with DS.
  • There is an increased risk of leukemia with an equal incidence of lymphoid and myeloid leukemia.
  • Acute megakaryocytic leukemia (AMKL) subtype is the most common form of acute myeloid leukemia (AML) in this setting, and is uncommon in children without DS.
  • Children with DS and leukemia are more sensitive to some chemotherapeutic agents such as methotrexate than other children which requires careful monitoring for toxicity.
  • Although the risk for leukemia is higher in individuals with DS, these patients have a lower risk of developing solid tumors, with the exception of germ cell tumors, and perhaps retinoblastoma and lymphoma.
  • [MeSH-major] Down Syndrome / complications. Hematologic Diseases / diagnosis. Hematologic Diseases / etiology. Neoplasms / diagnosis. Neoplasms / etiology
  • [MeSH-minor] Child. Female. Humans. Infant. Leukemia / diagnosis. Leukemia / etiology. Male. Myeloproliferative Disorders / diagnosis. Myeloproliferative Disorders / etiology

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  • (PMID = 17048354.001).
  • [ISSN] 1552-4868
  • [Journal-full-title] American journal of medical genetics. Part C, Seminars in medical genetics
  • [ISO-abbreviation] Am J Med Genet C Semin Med Genet
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 2T32 CA 09307
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 72
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13. 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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14. 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


15. 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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16. 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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17. 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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18. 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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19. 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


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

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  • (PMID = 20058478.001).
  • [ISSN] 1658-3876
  • [Journal-full-title] Hematology/oncology and stem cell therapy
  • [ISO-abbreviation] Hematol Oncol Stem Cell Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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22. 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
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  • [Language] eng
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23. 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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24. 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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25. 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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26. Kiratli H, Balci KE, Himmetoğlu C, Uner A: Isolated extraocular muscle involvement as the ophthalmic manifestation of leukaemia. Clin Exp Ophthalmol; 2009 Aug;37(6):609-13
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  • [Title] Isolated extraocular muscle involvement as the ophthalmic manifestation of leukaemia.
  • BACKGROUND: Clinical and imaging features of patients with orbital leukaemia primarily involving extraocular muscles were evaluated.
  • METHODS: This retrospective case series includes patients with leukaemia whose only ophthalmic manifestation was extraocular muscle enlargement.
  • Demographic data, clinical information on the systemic disease, prominent ocular signs and symptoms, computed tomography and magnetic resonance imaging characteristics, treatments applied and the outcomes were collected.
  • Acute myeloid leukaemia was the diagnosis in two patients, and chronic lymphocytic leukaemia, chronic myeloid leukaemia and biphenotypic acute leukaemia were found in one patient each, respectively.
  • Restricted ocular motility was the most common finding.
  • In one patient who had no prior history of leukaemia, an incisional biopsy established the diagnosis.
  • CONCLUSIONS: Leukaemic infiltration of extraocular muscles is a rare and late manifestation of the advanced disease associated with relapse and there seems to be a predilection for the lateral rectus muscle.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Leukemic Infiltration. Oculomotor Muscles / pathology. Orbital Neoplasms / diagnosis
  • [MeSH-minor] Child. Child, Preschool. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Ocular Motility Disorders / diagnosis. Prognosis. Retrospective Studies. Tomography, X-Ray Computed

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  • [CommentIn] Clin Exp Ophthalmol. 2010 Aug;38(6):651 [20553299.001]
  • (PMID = 19702712.001).
  • [ISSN] 1442-9071
  • [Journal-full-title] Clinical & experimental ophthalmology
  • [ISO-abbreviation] Clin. Experiment. Ophthalmol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
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27. Shankar DB, Cheng JC, Sakamoto KM: Role of cyclic AMP response element binding protein in human leukemias. Cancer; 2005 Nov 1;104(9):1819-24
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  • [Title] Role of cyclic AMP response element binding protein in human leukemias.
  • Acute myeloid leukemia (AML) in adults has a 20% 5-year disease-free survival despite treatment with aggressive cytotoxic chemotherapy.
  • Previous work from our laboratory demonstrated that the majority of patients with acute lymphoid and myeloid leukemia overexpress CREB in the bone marrow.
  • CREB overexpression is associated with poor initial outcome of clinical disease in AML patients.
  • CREB is a transcription factor that functions in glucose homeostasis, growth-factor-dependent cell survival, and memory.
  • To study its role in hematopoiesis, we overexpressed CREB in leukemia cell lines and in mice.
  • CREB overexpression resulted in increased survival and proliferation of myeloid cells and blast-transformation of bone marrow progenitor cells from transgenic mice expressing CREB in the myeloid lineage.
  • CREB transgenic mice also develop myeloproliferative disease after 1 year.
  • Thus, CREB acts as a protooncogene to regulate hematopoiesis and contributes to the leukemia phenotype.
  • Our results suggest that CREB-dependent pathways may serve as targets for directed therapies in leukemia in the future.
  • [MeSH-major] Cyclic AMP Response Element-Binding Protein / genetics. Leukemia / metabolism
  • [MeSH-minor] Acute Disease. Animals. Cell Line, Tumor. Cell Survival. Disease-Free Survival. Hematopoiesis / genetics. Humans. Mice. Mice, Transgenic. Mutation. Transcription Factors / genetics. Up-Regulation

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  • [Copyright] (c) 2005 American Cancer Society.
  • (PMID = 16196046.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16042; United States / NCI NIH HHS / CA / CA68221
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / Transcription Factors
  • [Number-of-references] 30
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28. Strick R, Zhang Y, Emmanuel N, Strissel PL: Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias. Hum Genet; 2006 Jun;119(5):479-95
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  • [Title] Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.
  • The t(9;22) BCR/ABL fusion is associated with over 90% of chronic myelogenous and 25% of acute lymphocytic leukemia.
  • Chromosome 11q23 translocations in acute myeloid and lymphoid leukemia cells demonstrate myeloid lymphoid leukemia (MLL) fusions with over 40 gene partners, like AF9 and AF4 on chromosomes 9 and 4, respectively.
  • Therapy-related leukemia is associated with the above gene rearrangements following the treatment with topoisomerase II (topo II) inhibitors.
  • In this report, using cell lines and primary cells, chromatin structural elements were analyzed in BCR, ABL and AF4 and, for comparison, in MLL2, which is a homolog to MLL, but not associated with chromosome translocations.
  • Although MLL2 was expressed in all cell lines tested, except for the presence of one DNAse I site in the promoter, no other structural elements were found in MLL2.
  • A NHR model presented demonstrates the importance of chromatin structure in chromosome translocations involved with leukemia.
  • [MeSH-major] Chromatin / chemistry. Chromosome Breakage. Chromosomes, Human / genetics. Leukemia / genetics. Leukemia / metabolism. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cells, Cultured. Chronic Disease. Humans. K562 Cells. Proto-Oncogene Proteins c-bcr / chemistry. Proto-Oncogene Proteins c-bcr / genetics. Recombination, Genetic

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  • (PMID = 16572268.001).
  • [ISSN] 0340-6717
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chromatin; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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29. 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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30. 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


31. 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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32. Rubnitz JE, Onciu M, Pounds S, Shurtleff S, Cao X, Raimondi SC, Behm FG, Campana D, Razzouk BI, Ribeiro RC, Downing JR, Pui CH: Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital. Blood; 2009 May 21;113(21):5083-9
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  • [Title] Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital.
  • To characterize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the pathologic and clinical features, including response to therapy, of 35 patients with mixed-lineage leukemia.
  • The majority of cases (91%) had blasts cells that simultaneously expressed either T-lineage plus myeloid markers (T/myeloid, n = 20) or B-lineage plus myeloid markers (B/myeloid, n = 12).
  • Overall survival rates for the B/myeloid and T/myeloid subgroups were not significantly different from each other or from the rate for acute myeloid leukemia (AML) but were inferior to the outcome in children with acute lymphoblastic leukemia (ALL).
  • Analysis of gene-expression patterns identified a subset of biphenotypic leukemias that did not cluster with T-cell ALL, B-progenitor ALL, or AML.
  • We propose that treatment for biphenotypic leukemia begin with one course of AML-type induction therapy, with a provision for a switch to lymphoid-type induction therapy with a glucocorticoid, vincristine, and L-asparaginase if the patient responds poorly.
  • We also suggest that hematopoietic stem cell transplantation is often not required for cure of these patients.

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  • (PMID = 19131545.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA-21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2686179
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33. Ara AI, Xia M, Ramani K, Mato JM, Lu SC: S-adenosylmethionine inhibits lipopolysaccharide-induced gene expression via modulation of histone methylation. Hepatology; 2008 May;47(5):1655-66
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  • We previously showed that S-adenosylmethionine (SAMe) and its metabolite methylthioadenosine (MTA) blocked lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNFalpha) expression in RAW (murine macrophage cell line) and Kupffer cells at the transcriptional level without affecting nuclear factor kappa B nuclear binding.
  • LPS increased the binding of histone methyltransferases Set1 and myeloid/lymphoid leukemia to these promoters, which was unaffected by SAMe or MTA.
  • Exogenous SAMe is unstable and converts spontaneously to MTA, which is stable and cell-permeant.

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  • (PMID = 18393372.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / T32 AA007578; None / None / / R01 AT001576-05; United States / NCCIH NIH HHS / AT / R01 AT001576-05; United States / NIAAA NIH HHS / AA / AA007578-07; United States / NIAAA NIH HHS / AA / AA12677; United States / NIDDK NIH HHS / DK / R01 DK051719-11; United States / NCCIH NIH HHS / AT / R01 AT001576; United States / NIDDK NIH HHS / DK / DK048522-139003; United States / NIDDK NIH HHS / DK / R01 DK051719; United States / NIAAA NIH HHS / AA / T32 AA07578; United States / NCCIH NIH HHS / AT / AT1576; United States / NIAAA NIH HHS / AA / T32 AA007578-07; United States / NIDDK NIH HHS / DK / DK48522; United States / NIAAA NIH HHS / AA / R01 AA013847; United States / NIAAA NIH HHS / AA / R01 AA012677; United States / NIDDK NIH HHS / DK / DK051719-11; United States / NIAAA NIH HHS / AA / R01 AA012677-05; United States / NIDDK NIH HHS / DK / DK51719; United States / NIAAA NIH HHS / AA / R01 AA013847-05; United States / NIDDK NIH HHS / DK / P30 DK048522; United States / NIAAA NIH HHS / AA / AA13847; United States / NIDDK NIH HHS / DK / P30 DK048522-139003; United States / NIAAA NIH HHS / AA / AA012677-05; United States / NIAAA NIH HHS / AA / AA013847-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chromatin; 0 / DNA Primers; 0 / Histones; 0 / Lipopolysaccharides; 0 / Tumor Necrosis Factor-alpha; 63231-63-0 / RNA; 7LP2MPO46S / S-Adenosylmethionine
  • [Other-IDs] NLM/ NIHMS49821; NLM/ PMC2408693
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34. Coche D, Bergues B, Harrivel V, Guillaume N: [Biphenotypic acute leukaemia with Burkitt-like cytology]. Ann Biol Clin (Paris); 2009 Jul-Aug;67(4):437-40
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  • [Title] [Biphenotypic acute leukaemia with Burkitt-like cytology].
  • [Transliterated title] Leucémie aiguë biphénotypique avec aspect cytologique de type Burkitt.
  • Biphenotypic acute leukaemia (BAL) represents about 5% of adult acute leukaemia.
  • Based on a previously described scoring system, the European Group for Immunologic Classification of Leukaemia (EGIL) proposed a set of diagnostic criteria for BAL.
  • This scoring system is based on the number and degree of the specificity of several markers for myeloid or T/B lymphoid blasts.
  • Here, we report the case of a BAL with Burkitt-like cytology, corresponding to "the acute lymphoblastic leukaemia, Burkitt type" L3 for the FAB classification.
  • By flow cytometry, the blasts showed a positivity for B lymphoid cytoplasmic (CD79a and mu) and membrane (CD19, CD22, CD24, IgM) markers AND a positivity for the myeloid (CD13, CD33, CD65, CD15) markers.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / genetics

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  • (PMID = 19654084.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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35. 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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36. 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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37. 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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  • [Cites] Leuk Lymphoma. 2002 Nov;43(11):2083-92 [12533032.001]
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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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38. 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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39. Huh JY, Chung S, Oh D, Kang MS, Eom HS, Cho EH, Han MH, Kong SY: Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature. Korean J Lab Med; 2010 Apr;30(2):117-21
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  • [Title] Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature.
  • The translocation t(10;11)(p13;q14q21) has been found to be recurrent in acute lymphoblastic and myeloid leukemias, and results in the fusion of the clathrin assembly lymphoid myeloid leukemia (CALM) gene with the AF10 gene; these genes are present on chromosomes 11 and 10, respectively.
  • Because the CALM-AF10 rearrangement is a rare chromosomal abnormality, it is not included in routine molecular tests for acute leukemia.
  • The first patient (case 1) was diagnosed with T-cell ALL, and the second patient (case 2) was diagnosed with AML.
  • Both patient samples showed expression of the homeobox A gene cluster and the histone methyltransferase hDOT1L, which suggests that they mediate leukemic transformation in CALM-AF10-positive and mixed-lineage leukemia-AF10-positive leukemias.
  • The first patient (case 1) relapsed after double-unit cord blood transplantation; there was no evidence of relapse in the second patient (case 2) after allogenic peripheral blood stem cell transplantation.
  • Since CALM-AF10- positive leukemias have been shown to have poor prognosis with conventional therapy, molecular tests for CALM-AF10 rearrangement would be necessary to detect minimal residual disease during follow-up.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Monomeric Clathrin Assembly Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow / pathology. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Cord Blood Stem Cell Transplantation. Female. Histone-Lysine N-Methyltransferase / genetics. Histone-Lysine N-Methyltransferase / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Recurrence. Translocation, Genetic

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  • (PMID = 20445327.001).
  • [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; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Transcription Factors; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 14
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40. Gujral S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Jain H, Pais A, Amre Kadam PS, Banavali SD, Arora B, Kumar P, Hari Menon VG, Kurkure PA, Parikh PM, Mahadik S, Chogule AB, Shinde SC, Nair CN: Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India. Cytometry B Clin Cytom; 2009 May;76(3):199-205
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  • [Title] Immunophenotypic profile of acute leukemia: critical analysis and insights gained at a tertiary care center in India.
  • BACKGROUND: To analyze the spectrum of various types and subtypes of acute leukemia.
  • METHODS: Two thousand five hundred and eleven consecutive new referral cases of acute leukemia (AL) were evaluated based on WHO classification.
  • RESULTS: It included 1,471 cases (58%) of acute lymphoblastic leukemia (ALL), 964 cases (38%) of acute myeloid leukemia (AML), 45 cases (1.8%) of chronic myelogenous leukemia in blast crisis (CMLBC), 37 cases (1.5%) of biphenotypic acute leukemia (BAL), 1 case of Triphenotypic AL, and 2 cases of acute undifferentiated leukemia (AUL).
  • Common subtypes of ALL were B-cell ALL (76%), which comprised of intermediate stage/CALLA positive (73%), early precursor/proBALL (3%).
  • T-cell ALL constituted 24% (351 cases) of ALL.
  • CMLBC was commonly of myeloid blast crisis subtype (40 cases).
  • CONCLUSION: B-cell ALL was the commonest subtype in children and AML in adults.
  • CD13 was most sensitive and CD117 most specific for determining myeloid lineage.
  • A minimal primary panel of nine antibodies consisting of three myeloid markers (CD13, CD33, and CD117), B-cell lymphoid marker (CD19), T-cell marker (CD7), with CD45, CD10, CD34, and HLADR could assign lineage to 92% of AL.
  • Cytogenetics findings lead to a change in the diagnostic subtype of myeloid malignancy in 38 (1.5%) cases.
  • [MeSH-major] Immunophenotyping. Leukemia / immunology. Leukemia / pathology
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Histocytochemistry. Humans. In Situ Hybridization. India. Infant. Infant, Newborn. Male. Middle Aged. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Young Adult

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  • [Copyright] (c) 2008 Clinical Cytometry Society.
  • (PMID = 18803279.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. 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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42. Lee JC, Yang S, Zou Y, Joseph L: Erythroid/B-cell biphenotypic acute leukemia first case report. Leukemia; 2009 Oct;23(10):1920-3
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  • [Title] Erythroid/B-cell biphenotypic acute leukemia first case report.
  • [MeSH-major] B-Lymphocytes / pathology. Erythroid Cells / pathology. Leukemia, Biphenotypic, Acute / pathology

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  • (PMID = 19458630.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD
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43. Papenhausen PR, Griffin S, Tepperberg J: Oncogene amplification in transforming myelodysplasia. Exp Mol Pathol; 2005 Oct;79(2):168-75
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  • The MLL gene, located within band 11q23, has been shown to be involved in translocations with a large variety of reciprocal sites in both lymphoid and myeloid leukemia and has also been shown to undergo submicroscopic self-fusion/partial duplication.
  • The frequency and clinical correlations of MLL gene amplification in leukemia will need careful follow-up, since the frequently cryptic amplification described in these cases may not generally provoke confirmatory FISH studies.
  • A common cytogenetic profile of 5 q-, -17/17 p-, -18/18 q-, and a missing or abnormal chromosome 11, may help direct appropriate follow-up studies.
  • Both genes also show a high degree of diversity of pathogenic mechanisms of leukemia evolution, including numerous reciprocal fusion genes in transformation to either AML or ALL and gain of function amplification.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics

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  • (PMID = 16026782.001).
  • [ISSN] 0014-4800
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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44. Zhang J, Mi YC, Wang Y, Lin D, Li W, Sun XM, Zhou K, Bian SG, Wang JX: [Study on the clinical characteristics of adult biphenotypic acute leukaemia]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):18-21
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  • [Title] [Study on the clinical characteristics of adult biphenotypic acute leukaemia].
  • OBJECTIVE: To analyze the clinical and biological characteristics and prognosis of adult biphenotypic acute leukaemia (BAL).
  • The chemotherapy regimens were accordingly for acute lymphoblastic leukaemia (ALL), acute myeloid leukaemia (AML) or for both ALL and AML.
  • (1) The incidence of BAL in acute leukaemias was 6.7%, with a male predominance and 52.3% of BAL patients had WBC > or = 30 x 10(9)/L and 16.9% WBC > or = 100 x 10(9)/L. (2) Percentages of coexpression of myeloid and B lymphoid antigens were 81.5%, of myeloid and T lymphoid antigens 10.8%, of myeloid, B- and T lymphoid antigens 4.6%, and of B and T lymphoid antigens 3.1%. (3) Normal and abnormal karyotypes accounted for 41.5% and 58.5%, respectively in 53 BAL patients with karyotype analysis.
  • (1) High white blood cell count and coexpression of myeloid/B lymphoid antigens are common in BAL. (2) Abnormal karyotypes and Ph (+) or bcr-abl( +) often happen. (3) The treatment outcome of BAL is poor.
  • [MeSH-major] Leukemia, Biphenotypic, Acute

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  • (PMID = 19563029.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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45. Kakihana K, Ohashi K, Sakai F, Kamata N, Hosomi Y, Nishiwaki M, Yokoyama R, Kobayashi T, Yamashita T, Akiyama H, Sakamaki H: Leukemic infiltration of the lung following allogeneic hematopoietic stem cell transplantation. Int J Hematol; 2009 Jan;89(1):118-22
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  • [Title] Leukemic infiltration of the lung following allogeneic hematopoietic stem cell transplantation.
  • Pulmonary leukemic infiltration (PLI) is more common than generally recognized, but accurate antemortem diagnosis with pathological proof is rarely achieved.
  • We describe herein the clinical courses of two patients with PLI following hematopoietic stem cell transplantation (HSCT).
  • One case is a male patient with acute biphenotypic leukemia, and the other is a female patient with myelodysplastic syndrome.
  • Moreover, the former case presented PLI as the initial manifestation of relapsed leukemia and the latter was accompanied with the fungal pneumonia.
  • High-resolution computed tomography (HRCT) of the chest at onset of PLI showed diffuse small nodular lesions along peribronchovascular bundle, and diagnosis of leukemic infiltration was made based on pathological findings obtained from transbronchial lung biopsy.
  • Thus, radiological and pathological corroborating assessment was important to reach the correct diagnosis.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Leukemic Infiltration / diagnosis. Lung Neoplasms / etiology
  • [MeSH-minor] Adult. Female. Humans. Leukemia / pathology. Lung / pathology. Male. Middle Aged. Myelodysplastic Syndromes / diagnosis. Myelodysplastic Syndromes / etiology. Opportunistic Infections. Transplantation, Homologous

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  • (PMID = 19093164.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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46. Liu Z, Liu XL, Du QF, Xu N, Zhong M, Song LL, Yi ZS, Liu QF, Meng FY, Zhou SY: [Clinical characteristics and outcomes of 59 patients with acute lymphoblastic leukemia positive for BCR/ABL]. Nan Fang Yi Ke Da Xue Xue Bao; 2009 Mar;29(3):512-5
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  • [Title] [Clinical characteristics and outcomes of 59 patients with acute lymphoblastic leukemia positive for BCR/ABL].
  • OBJECTIVE: To study the clinical characteristics and outcomes of BCR/ABL-positive acute lymphoblastic leukemia (BCR/ABL360888725-ALL) and screen the prognostic factors for BCR/ABL360888725-ALL.
  • METHODS: From January 2001 to May 2008, 59 patients (median age of 32 years ranging from 3 to 69 years) with the diagnosis of BCR/ABL360888725-ALL by fluorescence in situ hybridization received induction chemotherapy with VDLP-/+Ara-C regimen.
  • The patients who failed to respond to the chemotherapy received subsequent consolidation chemotherapy with imatinib (400-800 mg/day) (17 cases) or allogeneic hematopoietic stem cell transplantation (allo-HSCT) (16 cases).
  • In patients with peripheral white blood cell (WBC) count <30=10(9)/L, 30-99.9(9)/L and > or =100(9)/L, the CR rates were 75.0% (18/24), 56.3% (9/15) and 26.3% (5/19) (P=0.006), and the overall survival probability of 2 years ( OSs of 2-yrs) was 24.7%, 22.5% and 21.1%, respectively (P=0.180).
  • According to the FAB classification, 56 cases were divided into L1, L2 and biphenotypic acute leukemia (BAL) subgroups, and their CR rates were 66.7% (6/9), 63.2% (24/38) and 22.2% (2/9) (P=0.029), with OSs of 2-yrs of 22.2%, 27.0% and 22.0%, respectively (P=0.623).
  • In terms of immunophenotype grouping by EGIL, the patients with ALL, myeloid antigen-positive ALL and BAL had CR rates of 61.1% (11/18), 60.6% (20/33) and 12.5% (1/8) (P=0.039), and the OSs of 2-yrs of 22.7%, 21.0% and 18.8%, respectively (P=0.643).
  • In 55 patients with known karyotype, the CR rates were 71.4%(5/7), 70.8% (17/24) and 37.5% (9/24) in normal, sole t(9;22) abnormality, t(9;22) with additional abnormalities groups (P=0.046), with the OSs of 2-yrs of 42.9%, 34.0% and 7.3%, respectively (P=0.000).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Genes, abl / genetics. Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19304540.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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47. Nakada S, Katsuki Y, Imoto I, Yokoyama T, Nagasawa M, Inazawa J, Mizutani S: Early G2/M checkpoint failure as a molecular mechanism underlying etoposide-induced chromosomal aberrations. J Clin Invest; 2006 Jan;116(1):80-9
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  • Topoisomerase II (Topo II) inhibitors are cell cycle-specific DNA-damaging agents and often correlate with secondary leukemia with chromosomal translocations involving the mixed-lineage leukemia/myeloid lymphoid leukemia (MLL) gene on chromosome 11 band q23 (11q23).
  • [MeSH-major] Cell Cycle / physiology. Chromosome Aberrations / chemically induced. Etoposide / pharmacology. Myeloid-Lymphoid Leukemia Protein / genetics. Translocation, Genetic
  • [MeSH-minor] Bone Neoplasms. Cell Division. Cell Line. Cell Line, Tumor. Chromosome Banding. Chromosomes, Human, Pair 11. Cloning, Molecular. G2 Phase. Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Histone-Lysine N-Methyltransferase. Humans. Osteosarcoma

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  • (PMID = 16357944.001).
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6PLQ3CP4P3 / Etoposide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC1312016
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48. 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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49. Yin B, Delwel R, Valk PJ, Wallace MR, Loh ML, Shannon KM, Largaespada DA: A retroviral mutagenesis screen reveals strong cooperation between Bcl11a overexpression and loss of the Nf1 tumor suppressor gene. Blood; 2009 Jan 29;113(5):1075-85
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  • NF1 inactivation occurs in specific human cancers, including juvenile myelomonocytic leukemia, an aggressive myeloproliferative disorder of childhood.
  • However, evidence suggests that Nf1 loss alone does not cause leukemia.
  • We therefore hypothesized that inactivation of the Nf1 tumor suppressor gene requires cooperating mutations to cause acute leukemia.
  • One of these genes, Bcl11a, confers a growth advantage in cultured Nf1 mutant hematopoietic cells and causes early onset of leukemia of either myeloid or lymphoid lineage in mice when expressed in Nf1-deficient bone marrow.
  • Importantly, Bcl11a is expressed in human chronic myelomonocytic leukemia and juvenile myelomonocytic leukemia samples.
  • These findings suggest that deregulated Bcl11a cooperates with Nf1 in leukemogenesis, and a therapeutic strategy targeting the BCL11A pathway may prove beneficial in the treatment of leukemia.

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  • (PMID = 18948576.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084221; United States / NCI NIH HHS / CA / CA84221
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL11A protein, human; 0 / Bcl11a protein, mouse; 0 / CDKN1A protein, human; 0 / Carrier Proteins; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Neurofibromin 1; 0 / Nuclear Proteins
  • [Other-IDs] NLM/ PMC2635073
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50. Saitoh T, Matsushima T, Iriuchishima H, Yamane A, Irisawa H, Handa H, Tsukamoto N, Karasawa M, Nojima Y, Murakami H: Presentation of extramedullary Philadelphia chromosome-positive biphenotypic acute leukemia as testicular mass: Response to imatinib-combined chemotherapy. Leuk Lymphoma; 2006 Dec;47(12):2667-9
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  • [Title] Presentation of extramedullary Philadelphia chromosome-positive biphenotypic acute leukemia as testicular mass: Response to imatinib-combined chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Piperazines / pharmacology. Pyrimidines / pharmacology. Testicular Neoplasms / diagnosis
  • [MeSH-minor] Benzamides. Bone Marrow Cells / cytology. Flow Cytometry. Humans. Imatinib Mesylate. Male. Middle Aged. Philadelphia Chromosome. Stem Cell Transplantation. Transplantation, Homologous


51. 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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52. Yin H, Glass J, Blanchard KL: MOZ-TIF2 repression of nuclear receptor-mediated transcription requires multiple domains in MOZ and in the CID domain of TIF2. Mol Cancer; 2007;6:51
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  • BACKGROUND: Fusion of the MOZ and TIF2 genes by an inv (8) (p11q13) translocation has been identified in patients with acute mixed-lineage leukemia.
  • Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response.
  • [MeSH-minor] Acute Disease. Blotting, Western. Carrier Proteins / genetics. Carrier Proteins / metabolism. Corticosterone. Genes, Reporter. Humans. Leukemia, Myeloid / genetics. Receptors, Androgen / genetics. Receptors, Estrogen / genetics

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  • (PMID = 17697320.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Androgen; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Estrogen; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human; W980KJ009P / Corticosterone
  • [Other-IDs] NLM/ PMC2048977
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53. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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54. 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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55. 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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56. 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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57. 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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58. 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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59. 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


60. Schwartz CM, Cheng A, Mughal MR, Mattson MP, Yao PJ: Clathrin assembly proteins AP180 and CALM in the embryonic rat brain. J Comp Neurol; 2010 Sep 15;518(18):3803-18
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  • In this study, we focus on two closely related clathrin assembly proteins, AP180 and CALM (clathrin assembly lymphoid myeloid leukemia protein), in the developing embryonic rat brain.
  • [MeSH-minor] Animals. Cell Line. Clathrin / metabolism. Clathrin-Coated Vesicles / metabolism. Female. Neurons / cytology. Neurons / metabolism. Pregnancy. Rats. Stem Cells / cytology. Stem Cells / metabolism

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  • (PMID = 20653035.001).
  • [ISSN] 1096-9861
  • [Journal-full-title] The Journal of comparative neurology
  • [ISO-abbreviation] J. Comp. Neurol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 AG999999
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Clathrin; 0 / Monomeric Clathrin Assembly Proteins; 0 / Picalm protein, rat; 0 / clathrin assembly protein AP180
  • [Other-IDs] NLM/ NIHMS215726; NLM/ PMC2909614
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61. Serefhanoglu S, Buyukasik Y, Goker H, Sayinalp N, Ozcebe OI: Biphenotypic acute leukemia treated with acute myeloid leukemia regimens: a case series. J Natl Med Assoc; 2009 Mar;101(3):270-2
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  • [Title] Biphenotypic acute leukemia treated with acute myeloid leukemia regimens: a case series.
  • This study retrospectively analyzed 8 cases of biphenotypic acute leukemia (BAL) in respect of morphology, immune phenotype, karyotype, and clinical manifestations.
  • Six patients had myeloid plus T lymphoid, and 2 cases had myeloid plus B-lymphoid immune phenotypic markers.
  • Because selection of an antileukemic chemotherapy regimen for acute leukemia is largely based on whether a case is classified as myeloid or lymphoid, the presence of markers for both lineages may have important implications for treatment.
  • All of our patients were treated with regimens designed for acute myeloid leukemia (AML).
  • [MeSH-major] Leukemia, Biphenotypic, Acute / drug therapy
  • [MeSH-minor] Adult. Antibiotics, Antineoplastic / therapeutic use. Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Agents / therapeutic use. Biomarkers. Case-Control Studies. Cytarabine / therapeutic use. Female. Humans. Idarubicin / therapeutic use. Immunophenotyping. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / physiopathology. Male. Middle Aged. Mitoxantrone / therapeutic use. Retrospective Studies

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  • (PMID = 19331261.001).
  • [ISSN] 1943-4693
  • [Journal-full-title] Journal of the National Medical Association
  • [ISO-abbreviation] J Natl Med Assoc
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Biomarkers; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone; ZRP63D75JW / Idarubicin
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62. Guo Y, Chen YM, Zou Y, Chen XJ, Zhang L, Wang SC, Zhu XF: [Biologic features of 688 cases of childhood acute leukemia-a single centre retrospective study]. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Oct;11(10):793-6
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  • [Title] [Biologic features of 688 cases of childhood acute leukemia-a single centre retrospective study].
  • OBJECTIVE: To investigate the biologic features of childhood acute leukemia in the northern region of China through a small cohort study in a single center.
  • METHODS: The medical records of 688 children with acute leukemia (age< or =15 years) who were initially diagnosed at Blood Disease Hospital of Chinese Academy of Medical Sciences from October 2003 to June 2006 were retrospectively studied.
  • RESULTS: Four hundred children were diagnosed as acute lymphoblastic leukemia (ALL), with a peak incidence at ages of 1-4 years.
  • Two hundred and eighteen children were classified into B-cell ALL, and 34 into T-cell ALL.
  • E2A-PBX1 fusion gene was expressed in 3.9% of children with B-cell ALL.
  • Two hundred and twenty-two children were diagnosed as acute myeloid leukemia (AML), with a peak incidence at ages of 10-15 years.
  • Acute hybrid leukemia (AHL) was confirmed in 24 children (4.2%), with a median age of 9 years.
  • Seventy-four percent of the children with (AHL) had mainly CD13 and CD33 expression in myeloid antigen integral.
  • CONCLUSIONS: There are differences in the biologic features of childhood acute leukemia between the northern region of China and other regions and races, which suggests that there might be differences in the pathogenesis of childhood acute leukemia in different environmental exposures.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19849934.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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63. Xu B, Li L, Tang JH, Zhou SY: Detection of FLT3 gene and FLT3/ITD mutation by polymerase chain reaction-single-strand conformation polymorphism in patients with acute lymphoblastic leukemia. Di Yi Jun Yi Da Xue Xue Bao; 2005 Oct;25(10):1207-10
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  • [Title] Detection of FLT3 gene and FLT3/ITD mutation by polymerase chain reaction-single-strand conformation polymorphism in patients with acute lymphoblastic leukemia.
  • OBJECTIVE: To analyze Fms-like tyrosine kinase 3 (FLT3) gene and FLT3 internal tandem duplication (ITD) mutation in acute lymphoblastic leukemia (ALL) patients of different immunological subtypes.
  • The positivity rate of FLT3 gene in pre-pre B-lineage ALL, pre-B-ALL, B-lineage ALL and T-lineage ALL cases were 93.3% (14/15), 77.8% (14/18), 41.7% (5/12) and 28.6% (4/14), respectively.
  • Two cases (3.2%) were found to have FLT3/ITD mutation, which were also positive for myeloid antigen expression and diagnosed as acute mixed-lineage leukemia, showing leukocytosis and high percentage of bone marrow blast cells with poor prognosis.
  • CONCLUSIONS: FLT3 gene can be detected in both B-and T-lineage ALL patients, but more frequently in the former.
  • In B-lineage ALL patients, FLT3 gene is more frequent in cases with undifferentiated than those with differentiated blast cells.
  • FLT3/ITD is rarely detected in ALL patients and FLT3/ITD mutation detection might be helpful to identify the genotypes and evaluate the prognosis of acute leukemia.
  • [MeSH-major] Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor Protein-Tyrosine Kinases / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 16234090.001).
  • [ISSN] 1000-2588
  • [Journal-full-title] Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA
  • [ISO-abbreviation] Di Yi Jun Yi Da Xue Xue Bao
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
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64. 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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  • [ISO-abbreviation] Haematologica
  • [Language] eng
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  • [Other-IDs] NLM/ PMC2791943
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65. 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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66. Slany RK: The molecular biology of mixed lineage leukemia. Haematologica; 2009 Jul;94(7):984-93
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  • [Title] The molecular biology of mixed lineage leukemia.
  • Mixed lineage leukemia is a very aggressive blood cancer that predominantly occurs in pediatric patients.
  • In contrast to other types of childhood acute leukemias, mixed lineage leukemia presents with a dismal prognosis and despite the availability of advanced treatment methods cure rates have stagnated over the last years.
  • Mixed lineage leukemia is characterized by the presence of MLL fusion proteins that are the result of chromosomal translocations affecting the MLL gene at 11q23.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Child. Chromatin / chemistry. Chromatin / metabolism. DNA Methylation. Dimerization. Genes, Homeobox. Histone-Lysine N-Methyltransferase. Humans. Models, Biological. Myeloid-Lymphoid Leukemia Protein / genetics. Protein Structure, Tertiary. RNA Polymerase II / metabolism. Recombinant Fusion Proteins / chemistry. Time Factors. Transcription, Genetic

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  • (PMID = 19535349.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Chromatin; 0 / MLL protein, human; 0 / Recombinant Fusion Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.7.- / RNA Polymerase II
  • [Number-of-references] 122
  • [Other-IDs] NLM/ PMC2704309
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67. Jeha S, Kantarjian H: Clofarabine for the treatment of acute lymphoblastic leukemia. Expert Rev Anticancer Ther; 2007 Feb;7(2):113-8
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  • [Title] Clofarabine for the treatment of acute lymphoblastic leukemia.
  • A marked improvement in the outcome of patients with acute lymphoblastic leukemia has been achieved with chemotherapeutic agents developed between the 1950s and 1970s.
  • As the limits of optimizing the use of old drugs are reached, most adults with acute lymphoblastic leukemia still succumb to their disease and leukemia remains the leading cause of nonaccidental death in children.
  • Clofarabine, a next-generation deoxyadenosine analog, has demonstrated significant activity in children and adults with refractory lymphoid and myeloid leukemia in early clinical trials and was granted approval for use in children with acute lymphoblastic leukemia in second or higher relapse.
  • [MeSH-major] Adenine Nucleotides / therapeutic use. Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17288522.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
  • [Number-of-references] 36
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68. Kinjo K, Sandoval S, Sakamoto KM, Shankar DB: The role of CREB as a proto-oncogene in hematopoiesis. Cell Cycle; 2005 Sep;4(9):1134-5
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  • Cyclic-AMP response element binding protein (CREB) is a transcription factor that functions in glucose homeostasis, growth-factor- dependent cell survival, proliferation and memory.
  • Data from our laboratory shows that a majority of patients with acute lymphoid and myeloid leukemia overexpress CREB in the bone marrow.
  • CREB overexpression is associated with poor initial outcome of clinical disease in AML patients.
  • To study its role in hematopoiesis, we overexpressed CREB in leukemia cell lines and in mice.
  • CREB overexpression resulted in increased survival and proliferation of myeloid cells and blast-transformation of bone marrow progenitor cells from transgenic mice expressing CREB in the myeloid lineage.
  • CREB transgenic mice also develop myeloproliferative disease after one year.
  • Thus, CREB acts as a proto-oncogene to regulate hematopoiesis and contributes to the leukemia phenotype.
  • Our results suggest that CREB-dependent pathways may serve as targets for directed therapies in leukemia in the future.
  • [MeSH-minor] Animals. Bone Marrow Cells / metabolism. Cell Line, Tumor. Cell Proliferation. Cell Survival. Cell Transformation, Neoplastic. Gene Expression Regulation, Neoplastic. Glucose / metabolism. Granulocyte-Macrophage Colony-Stimulating Factor / metabolism. Humans. Leukemia, Myeloid, Acute / metabolism. Mice. Mice, Transgenic. Neoplasms / metabolism. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins / chemistry. Signal Transduction. Up-Regulation

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  • (PMID = 16096372.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclic AMP Response Element-Binding Protein; 0 / Proto-Oncogene Proteins; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; IY9XDZ35W2 / Glucose
  • [Number-of-references] 18
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69. 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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70. Hatoum HA, Mahfouz RA, Otrock ZK, Hudaib AR, Taher AT, Shamseddine AI: Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report. Am J Hematol; 2007 Jan;82(1):69-72
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  • [Title] Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report.
  • The association of chronic lymphocytic leukemia (CLL) and acute leukemia, either lymphoid or myeloid is a rare event.
  • Our review of the medical literature revealed only 6 cases of CLL transformation to acute myeloid leukemia (AML) (M0, M1 and M2) with no other associated malignancy.
  • We report a similar case but with occurrence of AML-M4 associated with normal cytogenetic analysis and molecular testing but with positive T-cell receptor gamma gene rearrangement rather than the usual Vbeta rearrangement.
  • [MeSH-major] Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


71. 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


72. Mandal C, Dutta A, Mallick A, Chandra S, Misra L, Sangwan RS, Mandal C: Withaferin A induces apoptosis by activating p38 mitogen-activated protein kinase signaling cascade in leukemic cells of lymphoid and myeloid origin through mitochondrial death cascade. Apoptosis; 2008 Dec;13(12):1450-64
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  • [Title] Withaferin A induces apoptosis by activating p38 mitogen-activated protein kinase signaling cascade in leukemic cells of lymphoid and myeloid origin through mitochondrial death cascade.
  • Here we demonstrate how WA exhibits a strong growth-inhibitory effect on several human leukemic cell lines and on primary cells from patients with lymphoblastic and myeloid leukemia in a dose-dependent manner, showing no toxicity on normal human lymphocytes and primitive hematopoietic progenitor cells.
  • WA-mediated decrease in cell viability was observed through apoptosis as demonstrated by externalization of phosphatidylserine, a time-dependent increase in Bax/Bcl-2 ratio; loss of mitochondrial transmembrane potential, cytochrome c release, caspases 9 and 3 activation; and accumulation of cells in sub-G0 region based on DNA fragmentation.
  • WA caused increased levels of Bax in response to MAPK signaling, which resulted in the initiation of mitochondrial death cascade, and therefore it holds promise as a new, alternative, inexpensive chemotherapeutic agent for the treatment of patients with leukemia of both lymphoid and myeloid origin.
  • [MeSH-major] Apoptosis / drug effects. Ergosterol / analogs & derivatives. Leukemia. MAP Kinase Signaling System / physiology. Mitochondria. Tumor Cells, Cultured / drug effects. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Animals. Caspase Inhibitors. Caspases / metabolism. Cell Survival / drug effects. Dose-Response Relationship, Drug. Enzyme Activation. Humans. Medicine, Traditional. Membrane Potential, Mitochondrial / drug effects. Mice. Molecular Structure. Plants, Medicinal / chemistry. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Withanolides. bcl-2-Associated X Protein / metabolism

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  • (PMID = 18987975.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caspase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Small Interfering; 0 / Withanolides; 0 / bcl-2-Associated X Protein; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases; L6DO3QW4K5 / withaferin A; Z30RAY509F / Ergosterol
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73. Hinrichsen L, Meyerholz A, Groos S, Ungewickell EJ: Bending a membrane: how clathrin affects budding. Proc Natl Acad Sci U S A; 2006 Jun 6;103(23):8715-20
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  • We have found that domains containing the adapter complex 2 (AP2)-coated vesicle adapter and the endocytic accessory proteins CALM (clathrin assembly lymphoid myeloid leukemia protein), epsin, and eps15/eps15R (EGF receptor pathway substrate 15-related) nevertheless persist at the plasma membrane.
  • [MeSH-major] Cell Membrane / metabolism. Cell Surface Extensions / metabolism. Clathrin / metabolism

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  • (PMID = 16735469.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Protein Complex 2; 0 / Adaptor Proteins, Vesicular Transport; 0 / Clathrin; 0 / epsin
  • [Other-IDs] NLM/ PMC1482644
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74. 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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  • (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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75. Watanabe-Okochi N, Kitaura J, Ono R, Harada H, Harada Y, Komeno Y, Nakajima H, Nosaka T, Inaba T, Kitamura T: AML1 mutations induced MDS and MDS/AML in a mouse BMT model. Blood; 2008 Apr 15;111(8):4297-308
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  • Myelodysplastic syndrome (MDS) is a hematopoietic stem-cell disorder characterized by trilineage dysplasia and susceptibility to acute myelogenous leukemia (AML).
  • Analysis of molecular basis of MDS has been hampered by the heterogeneity of the disease.
  • Interestingly, among integration sites identified, Evi1 seemed to collaborate with an AML1 mutant harboring a point mutation in the Runt homology domain (D171N) to induce MDS/AML with an identical phenotype characterized by marked hepatosplenomegaly, myeloid dysplasia, leukocytosis, and biphenotypic surface markers.
  • Collaboration between AML1-D171N and Evi1 was confirmed by a BMT model where coexpression of AML1-D171N and Evi1 induced acute leukemia of the same phenotype with much shorter latencies.
  • On the other hand, a C-terminal truncated AML1 mutant (S291fsX300) induced pancytopenia with erythroid dysplasia in transplanted mice, followed by progression to MDS-RAEB or MDS/AML.
  • Thus, we have developed a useful mouse model of MDS/AML that should help in the understanding of the molecular basis of MDS and the progression of MDS to overt leukemia.
  • [MeSH-major] Bone Marrow Transplantation. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Mutation / genetics. Myelodysplastic Syndromes / genetics
  • [MeSH-minor] Animals. Blood Cell Count. Cell Lineage. DNA-Binding Proteins / metabolism. Disease Models, Animal. Erythroid Cells / pathology. Humans. Leukocytosis / pathology. Leukopenia / pathology. Mice. Mice, Inbred C57BL. Mutant Proteins / metabolism. NIH 3T3 Cells. Neoplasm Invasiveness. Pancytopenia / pathology. Proto-Oncogenes. Spleen / pathology. Transcription Factors / metabolism. Transduction, Genetic


76. 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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77. 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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78. Owaidah TM, Al Beihany A, Iqbal MA, Elkum N, Roberts GT: Cytogenetics, molecular and ultrastructural characteristics of biphenotypic acute leukemia identified by the EGIL scoring system. Leukemia; 2006 Apr;20(4):620-6
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  • [Title] Cytogenetics, molecular and ultrastructural characteristics of biphenotypic acute leukemia identified by the EGIL scoring system.
  • Biphenotypic acute leukemia (BAL) is a rare, difficult to diagnose entity.
  • Its identification is important for risk stratification in acute leukemia (AL).
  • The scoring proposal of the European Group for the Classification of Acute Leukemia (EGIL) is useful for this purpose, but its performance against objective benchmarks is unclear.
  • Mixed, small and large blast cells predominated, with FAB M2 and L1 constituting the majority.
  • All patients were positive for myeloid (M) markers and either B cell (B) (17 or 74%) or T cell (T) (8 or 34%) markers with two exceptional patients demonstrating trilineage phenotype.
  • In six (26%) patients myeloid lineage commitment was also demonstrable by electron cytochemistry.
  • Abnormal findings were present in 19 (83%) patients by cytogenetics/FISH/molecular analysis as follows: t(9;22) (17%); MLL gene rearrangement (26%); deletion(6q) (13%); 12p11.2 (9%); numerical abnormalities (13%), and three (13%) new, previously unreported translocations t(X;6)(p22.3;q21); t(2;6)(q37;p21.3); and t(8;14)(p21;q32).
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human / genetics. Cytogenetic Analysis / methods. Leukemia / diagnosis. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Cell Lineage. Child. Child, Preschool. Cohort Studies. DNA Mutational Analysis. Female. Gene Rearrangement. Guidelines as Topic. Humans. In Situ Hybridization, Fluorescence / methods. In Vitro Techniques. Infant. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Phenotype. Risk Factors. Sensitivity and Specificity

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  • (PMID = 16437134.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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79. 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


80. 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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81. He G, Wu D, Sun A, Xue Y, Jin Z, Qiu H, Tang X, Miao M, Fu Z, Ma X, Wang X, Chen Z, Ruan C: B-Lymphoid and myeloid lineages biphenotypic acute leukemia with t(8;21)(q22;q22). Int J Hematol; 2008 Mar;87(2):132-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] B-Lymphoid and myeloid lineages biphenotypic acute leukemia with t(8;21)(q22;q22).
  • By analyzing the characteristics of morphology, immune phenotype, chromosome karyotype and clinical manifestations of six cases of B-lymphoid and myeloid lineages biphenotypic acute leukemia (BAL) with t(8;21)(q22;q22), a new subgroup of BAL was reported.
  • Immunophenotype revealed B-lymphoid and myeloid lineages positive, together with frequent and high expression of CD34 and CD33, and weak expression of HLA-DR.
  • Chemotherapy for myeloid and lymphoid leukemia simultaneously produced good response in the patients.
  • q22) might be a new subgroup of BAL, and it was suggested that the leukemia clone with t(8;21)(q22;q22) might have originated from an early phase of hematopoiesis, and AML1/ETO fusion gene might be related to differentiation of B lymphocyte.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic


82. Gujral S, Polampalli S, Badrinath Y, Kumar A, Subramanian PG, Raje G, Amare P, Arora B, Banavali SD, Nair CN: Clinico-hematological profile in biphenotypic acute leukemia. Indian J Cancer; 2009 Apr-Jun;46(2):160-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinico-hematological profile in biphenotypic acute leukemia.
  • BACKGROUND: We present a clinico-hematological profile and treatment outcome of Biphenotypic Acute Leukemia (BAL).
  • MATERIAL AND METHODS: Diagnosis was based on WHO classification, including clinical details, morphology, cytochemistry, immunophenotyping, and molecular genetics.
  • We included those cases, which fulfilled the European Group for the Immunological Characterization of Acute Leukemia's (EGIL's) scoring system criteria for the diagnosis of BAL, as per recommendation of the WHO classification.
  • B-Myeloid (14 cases) followed by T-Myeloid BAL (13 cases) were the commonest subtypes.
  • Polymorphous population of blasts (16 cases) was commonly associated with T-Myeloid BAL (10 cases).
  • BCR ABL fusion positivity was a common cytogenetic abnormality (seven cases).
  • CONCLUSIONS: Pediatric BAL and T-B lymphoid BAL have a better prognosis.
  • BCR-ABL expression is an important prognostic factor, as these cases will be labeled as Chronic myeloid leukemia (CML) in blast crisis with biphenotypic expression and treated accordingly.
  • [MeSH-major] Immunophenotyping. Leukemia, Biphenotypic, Acute / blood. Leukemia, Biphenotypic, Acute / diagnosis
  • [MeSH-minor] Adolescent. Adult. Case-Control Studies. Child. Child, Preschool. Disease Progression. Female. Hematologic Tests. Humans. Incidence. Male. Middle Aged. Phenotype. Retrospective Studies. Young Adult

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  • (PMID = 19346652.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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83. Van Etten RA: Aberrant cytokine signaling in leukemia. Oncogene; 2007 Oct 15;26(47):6738-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant cytokine signaling in leukemia.
  • Abnormalities of cytokine and growth factor signaling pathways are characteristic of all forms of leukemia: lymphoid and myeloid, acute and chronic.
  • In this review, our current knowledge of leukemic cell cytokine signaling will be summarized, and some speculations on the significance and implications of these insights will be advanced.
  • A better understanding of aberrant cytokine signaling in leukemia should provide additional targets for the rational therapy of these diseases.

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  • (PMID = 17934482.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090576; United States / NCI NIH HHS / CA / R01 CA105043; United States / NCI NIH HHS / CA / CA090576; United States / NCI NIH HHS / CA / CA105043
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 139
  • [Other-IDs] NLM/ NIHMS579951; NLM/ PMC4344827
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84. Han X, Bueso-Ramos CE: Precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma and acute biphenotypic leukemias. Am J Clin Pathol; 2007 Apr;127(4):528-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma and acute biphenotypic leukemias.
  • Session 4 of the 2005 Society of Hematopathology/European Association for Haematopathology Workshop focused on case presentations of precursor T-cell acute lymphoblastic leukemia/lymphoblastic lymphoma (pre-T ALL/LBL) and acute biphenotypic leukemia.
  • Acute biphenotypic leukemias are characterized by a sin