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[Title] [Childhood acute lymphoblastic leukemia in Norway 1992-2000].

BACKGROUND: Acute lymphoblastic leukemia is the most common malignancy in childhood.

Four of 6 infants with acute lymphoblastic leukemia and all 4 with mature B-cell leukemia are alive.

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

[MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Neoplasm Recurrence, Local. Norway / epidemiology. Risk Factors. Stem Cell Transplantation. Treatment Outcome

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(PMID = 17551551.001).

[ISSN] 0807-7096

[Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række

[ISO-abbreviation] Tidsskr. Nor. Laegeforen.

[Language] nor

[Publication-type] English Abstract; Journal Article

[Publication-country] Norway

   

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

[Title] Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32).

The BCR-ABL1 fusion kinase is frequently associated with chronic myeloid leukemia and B-cell acute lymphoblastic leukemia but is rare in T-cell acute lymphoblastic leukemia (T-ALL).

[MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 9. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Fusion Proteins, bcr-abl / chemistry. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, T-Cell / pathology. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

[MeSH-minor] Adolescent. Base Sequence. Benzamides. Blotting, Western. Cell Line. Cell Survival. DNA, Complementary / metabolism. DNA-Binding Proteins / metabolism. Female. Gene Deletion. Genes, abl. Humans. Imatinib Mesylate. In Situ Hybridization, Fluorescence. Karyotyping. Microtubules / metabolism. Milk Proteins / metabolism. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Models, Genetic. Molecular Sequence Data. Open Reading Frames. Phenotype. Phosphorylation. Piperazines / pharmacology. Polymerase Chain Reaction. Protein Kinase Inhibitors / pharmacology. Protein Structure, Tertiary. Protein-Tyrosine Kinases / metabolism. Pyrimidines / pharmacology. Recombinant Fusion Proteins / metabolism. Retroviridae. Reverse Transcriptase Polymerase Chain Reaction. STAT5 Transcription Factor. Signal Transduction. Time Factors. Trans-Activators / metabolism

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(PMID = 15713800.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Benzamides; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / EML1-ABL1 fusion protein, human; 0 / Milk Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Recombinant Fusion Proteins; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 0 / abl-bcr fusion protein, human; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3

   

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

[Title] Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia.

Previously, we reported that SALL4 was constitutively expressed in acute myeloid leukemia and SALL4 transgenic mice developed acute myeloid leukemia.

In this study, we aimed to survey SALL4 protein expression in benign and neoplastic hematopoietic tissues in addition to acute myeloid leukemia using immunostaining with a polyclonal anti-SALL4 antibody.

Reverse transcription-polymerase chain reaction was also performed to detect SALL4 mRNA expression on eight precursor B-cell lymphoblastic leukemia/lymphomas, 10 benign hematopoietic tissues, and seven hematopoietic cancer cell lines.

Of the benign tissues, SALL4 expression was detectable only in CD34+ hematopoietic stem/progenitor cells (2/2 at protein level, 3/3 at RNA level).

In neoplastic tissues, only precursor B-cell lymphoblastic leukemia/lymphomas had detectable SALL4 (12/16 at protein level, 7/8 at RNA level), similar to that observed in acute myeloid leukemia.

Of the seven cell lines examined, only those derived from acute myeloid leukemia and precursor B-cell lymphoblastic leukemia/lymphomas were positive.

The persistence of SALL4 expression in leukemic blasts in precursor B-cell lymphoblastic leukemia/lymphomas resembles to what we observed in acute myeloid leukemia, and correlates with the maturation arrest of these cells.

We have shown in our previous study that the constitutive expression of SALL4 in mice can lead to acute myeloid leukemia development.

The similar expression pattern of SALL4 in acute myeloid leukemia and B-cell lymphoblastic leukemia/lymphomas suggests that these two disease entities may share similar biological features and/or mechanisms of leukemogenesis.

More definite studies to investigate the role of SALL4 in the pathogenesis of B-cell lymphoblastic leukemia/lymphomas are needed in the future to address this question.

[MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma / genetics. Plasmacytoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics

[MeSH-minor] Antigens, CD34 / metabolism. Biomarkers, Tumor / metabolism. Cell Line, Tumor. Cell Separation. Flow Cytometry. Hematopoietic Stem Cells / metabolism. Hematopoietic Stem Cells / pathology. Humans. Immunoenzyme Techniques. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 16998462.001).

[ISSN] 0893-3952

[Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

[ISO-abbreviation] Mod. Pathol.

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / K08 DK063220

[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 / Antigens, CD34; 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / SALL4 protein, human; 0 / Transcription Factors

   

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

[Title] The chromosomal translocation (11;14) (p13; q11) in acute B-Cell lymphocytic leukemia.

BACKGROUND: Cytogenetic abnormalities are the most important independent prognostic factors of acute leukemia and imply the potential molecular mechanism of the disease.

Translocation (11;14)(p13;q11) has been predominantly found in T-cell acute lymphocytic leukemia (ALL) but is rare in B-cell ALL.

CASE REPORT: We present the case of a 30-year-old male patient, who presented with symptomatic anemia, thrombocytopenia and leukocytosis.

CONCLUSIONS: Translocation (11;14) (p13;q11) in B-cell ALL is rare, but it is worth exploring the molecular mechanisms and discovering the prognostic value in more B-cell ALL patients.

[MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 14 / genetics. Leukemia, B-Cell / genetics. Translocation, Genetic / genetics

[MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Chromosome Banding. Disease Progression. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Male. Prognosis. Remission Induction

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[Copyright] Copyright 2010 S. Karger AG, Basel.

(PMID = 20631486.001).

[ISSN] 1423-0240

[Journal-full-title] Onkologie

[ISO-abbreviation] Onkologie

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Switzerland

   

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

[Title] Attenuation of CXCR4 responses by CCL18 in acute lymphocytic leukemia B cells.

Elevated levels of CCL18 have been described in various diseases including childhood acute lymphocytic leukemia (ALL) but its functions remain poorly characterized.

CXCL12 is a pivotal chemokine for hematopoiesis and B cell homing processes.

We demonstrate that CCL18 interferes with CXCL12-mediated pre-B ALL cell activation.

CXCL12-induced calcium mobilization, chemotaxis, pseudo-emperipolesis and cellular proliferation could be significantly reduced by CCL18 in pre-B ALL cell lines.

[MeSH-major] Chemokines, CC / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology. Receptors, CXCR4 / metabolism. Signal Transduction

[MeSH-minor] Animals. Apoptosis. COS Cells. Calcium Signaling. Cell Line, Tumor. Cell Proliferation. Cercopithecus aethiops. Chemokine CXCL12 / metabolism. Chemotaxis, Leukocyte. Estradiol / metabolism. Estrogen Antagonists / pharmacology. Humans. Ligands. Lymphocyte Activation. Receptors, Estrogen. Receptors, G-Protein-Coupled / antagonists & inhibitors. Receptors, G-Protein-Coupled / genetics. Receptors, G-Protein-Coupled / metabolism. Recombinant Proteins / metabolism. Transfection

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[Copyright] © 2010 Wiley-Liss, Inc.

(PMID = 20568229.001).

[ISSN] 1097-4652

[Journal-full-title] Journal of cellular physiology

[ISO-abbreviation] J. Cell. Physiol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / CCL18 protein, human; 0 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CC; 0 / Estrogen Antagonists; 0 / GPER protein, human; 0 / Ligands; 0 / Receptors, CXCR4; 0 / Receptors, Estrogen; 0 / Receptors, G-Protein-Coupled; 0 / Recombinant Proteins; 4TI98Z838E / Estradiol

   

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

[Title] [Acute leukemia relapse of donor origin in two cases after haploidentical bone marrow transplantation].

To investigate the leukemia relapse of AL patients after HLA haploidentical bone marrow transplantation (HLA HBMT), 2 relapsed leukemia patients received HLA HBMT were studied, peripheral blood simples and bone marrow smear were examined, morphologic change of bone marrow cells was observed, while the HLA genotype and chromosome karyotye were analyzed by PCR and routine G-banding methods, respectively.

The results indicated that the two cases were diagnosed primarily as acute lymphocytic leukemia (common cell subtype) and acute megakaryocytic leukemia, in which chromosome abnormalities or activation of protooncogene in leukemic cells were observed.

The complete hematopuietie reconstitution of donor origin was obtained in these 2 cases after HLA HBMT, but the leukemic cells in these 2 leukemia patients were confirmed to be donor origin after relapse, their blood groups and HLA genotype were found to be originated from donor.

These 2 relapsed leukemia patients were diagnosed as acute lymphocytic leukemia (B cell subtype) and acute megakaryocytic leukemia.

It is suggested that high-dose of immunosuppressive agents used in transplantation may contribute to leukemia relapse of donor origin in these patients.

Abnormalities in hematopoietic microenvironment may be also involved in the leukemia development.

Donor-cell leukemia after allogeneic hematopoietic stem cell transplantation can be an ideal model to investigate the related events in human leukemogenesis.

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(PMID = 16638225.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / HLA Antigens

   

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

[Title] Self-renewal of acute lymphocytic leukemia cells is limited by the Hedgehog pathway inhibitors cyclopamine and IPI-926.

Recent data suggests that Hh signaling plays a role in normal B-cell development, and we hypothesized that Hh signaling may be important in precursor B-cell acute lymphocytic leukemia (B-ALL).

We found that the expression of Hh pathway components was common in human B-ALL cell lines and clinical samples.

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(PMID = 21203400.001).

[ISSN] 1932-6203

[Journal-full-title] PloS one

[ISO-abbreviation] PLoS ONE

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / R01 HL075826; United States / NCI NIH HHS / CA / P01 CA015396; United States / NCI NIH HHS / CA / R01 CA127574; United States / NCI NIH HHS / CA / R01CA127574; United States / NCI NIH HHS / CA / R01 CA127574-05; United States / NHLBI NIH HHS / HL / HL83077; United States / NHLBI NIH HHS / HL / HL75826; United States / NHLBI NIH HHS / HL / R01 HL083077; United States / NHLBI NIH HHS / HL / T32 HL086345; United States / NCI NIH HHS / CA / P01CA15396

[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 / Antigens, CD19; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Hedgehog Proteins; 0 / IPI-926; 0 / Receptors, G-Protein-Coupled; 0 / SMO protein, human; 0 / Veratrum Alkaloids; EC 1.2.1.3 / Aldehyde Dehydrogenase; ZH658AJ192 / cyclopamine

[Other-IDs] NLM/ PMC3011010

   

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

[Title] zeta-Crystallin is a bcl-2 mRNA binding protein involved in bcl-2 overexpression in T-cell acute lymphocytic leukemia.

The human antiapoptotic bcl-2 gene has been discovered in t(14;18) B-cell leukemias/lymphomas because of its overexpression caused at a transcriptional control level by the bcl-2/IgH fusion gene.

An increased Bcl-2 level observed in normal phytohemagglutinin (PHA)-activated T lymphocytes, acute lymphatic leukemia (ALL) T-cell lines, and T cells of patients with leukemia in comparison with normal non-PHA-activated T lymphocytes was concomitant with an increase in zeta-crystallin level.

The specific association of zeta-crystallin with the bcl-2 ARE was significantly enhanced in T cells of patients with ALL, which accounts for the higher stability of bcl-2 mRNA and suggests a possible contribution of zeta-crystallin to bcl-2 overexpression occurring in this leukemia.

[MeSH-major] 3' Untranslated Regions / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / metabolism. zeta-Crystallins / metabolism

[MeSH-minor] Blotting, Western. Cytoplasm / drug effects. Cytoplasm / metabolism. Female. Gene Expression Regulation. Humans. Immunoprecipitation. Male. Middle Aged. Phytohemagglutinins. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization. T-Lymphocytes / drug effects. T-Lymphocytes / pathology

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(PMID = 20103721.001).

[ISSN] 1530-6860

[Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology

[ISO-abbreviation] FASEB J.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA052443; United States / NCI NIH HHS / CA / R01 CA052443; United States / NCI NIH HHS / CA / R01 CA052443-16

[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 / 3' Untranslated Regions; 0 / Phytohemagglutinins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / zeta-Crystallins

[Other-IDs] NLM/ PMC2874474

   

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

[Title] Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin.

The B203.13 monoclonal antibody was developed by immunizing mice with the B/monocyte biphenotypic cell line B1b.

During normal hematopoiesis B203.13 is expressed on a fraction of CD34+ cells, while on mature cells it is only present on B-lymphocytes.

We tested this antibody as a marker of childhood B-acute lymphoblastic leukemia (B-ALL).

The CD10(+)/B203.13(+) phenotype was specific to B-ALL, since CD10(+)/CD20(+) cells from common acute lymphoblastic leukemia (c-ALL) did not express B203.13.

We concluded that the use of B203.13 in association with CD10 and CD20 provides meaningful information for distinguishing normal residual B-cells from leukemic B-lymphoblasts and that recurrence of a CD10(+)/B203.13(+) phenotype after transplantation may be a very early relapse indicator of early B-acute lymphoblastic leukemia.

[MeSH-major] Antigens, Neoplasm / biosynthesis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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(PMID = 18636158.001).

[ISSN] 1019-6439

[Journal-full-title] International journal of oncology

[ISO-abbreviation] Int. J. Oncol.

[Language] eng

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

[Publication-country] Greece

[Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin

   

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

[Title] V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia.

Translocations of proto-oncogenes to the B-cell or T-cell antigen receptor loci in acute T- or B-cell leukemia and lymphoma have been, in most cases, accredited to V(D)J or switch recombination depending on the location of the breakpoint at the receptor locus.

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Recombination, Genetic. Translocation, Genetic. VDJ Recombinases / metabolism

[MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cells, Cultured. DNA Breaks. DNA-Binding Proteins / genetics. Fibroblasts. Genes, T-Cell Receptor. Homeodomain Proteins / genetics. LIM Domain Proteins. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Metalloproteins / genetics. Mice. Receptors, Antigen, B-Cell / genetics. TCF Transcription Factors / genetics. Transcription Factor 7-Like 1 Protein

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(PMID = 19455608.001).

[ISSN] 1098-2264

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Receptors, Antigen, B-Cell; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Tlx1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.- / VDJ Recombinases

   

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

[Title] Numb chin syndrome as initial manifestation in a child with acute lymphoblastic leukemia.

We report on an 11-year-old male who presented with NCS as initial manifestation of acute lymphoblastic leukemia of B-cell type.

[MeSH-major] Chin / pathology. Hypesthesia / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

Genetic Alliance. consumer health - CHILD Syndrome.

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[Copyright] (c) 2008 Wiley-Liss, Inc.

(PMID = 18506757.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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

[Title] FBXW7 mutation in adult T-cell and B-cell acute lymphocytic leukemias.

Engineered FBXW7 null cells display cell cycle and chromosome stability defects.

Mutations of FBXW7 have been found in human colorectal, ovarian, endometrial tumors and T-cell acute lymphocytic leukemias.

Prompted by these findings we have examined acute myeloid leukemia, non-Hodgkin's lymphoma, T-cell acute lymphocytic leukemia, B-cell acute lymphocytic leukemia and adult T-cell leukemia DNA for mutations of the FBXW7 gene.

As expected, mutations were found in T-cell acute lymphocytic leukemias.

However mutations of FBXW7 were also found in four of 118 B-cell acute lymphocytic leukemias and one of 24 adult T-cell leukemia samples.

These observations suggest that disruption of FBXW7 has a role in several forms of lymphocytic leukemias and not exclusively T-cell acute lymphocytic leukemia.

[MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, Non-Hodgkin / genetics. Mutation / genetics. Ubiquitin-Protein Ligases / genetics

COS Scholar Universe. author profiles.

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(PMID = 18485478.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases

   

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

[Title] Expression of CD13/aminopeptidase N in precursor B-cell leukemia: role in growth regulation of B cells.

Expression of cell surface CD13 in acute B-cell leukemia (ALL-B) is often viewed, as an aberrant expression of a myeloid lineage marker.

Here, we attempted to study the stage specific expression of CD13 on ALL-B blasts and understand its role in leukemogenesis as pertaining to stage of B-cell ontogeny.

Among 68 cases of early B-cell ALL, 22 cases with distinct immunophenotype was identified as immature B-cell ALL.

This strongly indicates leukemogenesis at an early stage of B-cell development.

We also identified, the existence of a subpopulation of cells with remarkably similar phenotype in non-leukemic marrow from healthy subjects (expressing CD10, CD19, CD22, CD24, Tdt together with the co-expression of CD13).

By blocking their cell surface CD13 in leukemic blasts with monoclonal antibody we were able to inhibit their proliferation.

CD13 may thus be an important target for novel molecular therapy of early stage acute B-cell leukemia.

[MeSH-major] Antigens, CD13 / immunology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology

[MeSH-minor] Adolescent. Adult. Aged. Cell Proliferation. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Young Adult

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(PMID = 19562339.001).

[ISSN] 1432-0851

[Journal-full-title] Cancer immunology, immunotherapy : CII

[ISO-abbreviation] Cancer Immunol. Immunother.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] EC 3.4.11.2 / Antigens, CD13

   

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

[Title] Potential tumor suppressive function of miR-196b in B-cell lineage acute lymphoblastic leukemia.

Keeping in view the fact that genes coding microRNAs (miRNAs) have been found to be localized in chromosomal regions susceptible to genetic translocations, this study was addressed to identify and characterize the miRNAs that are present near/within the regions involved in genetic translocations characteristic of B-cell acute lymphoblastic leukemia (B-cell ALL).

Out of six such identified miRNAs miR-196b was not only found to be significantly down-regulated in both EB-3 cell line as well as B-cell ALL patients as compared to that found in the corresponding controls, but also had the inherent capacity to down-regulate the highly expressed c-myc gene, a consequence of genetic translocation characteristic of EB-3 cells at both transcriptional and translational level.

Also down-regulation of c-myc gene was accompanied by decreased expressions of c-myc effector genes coding for hTERT, Bcl-2, and AATF.

Based upon these results, we propose for the first time that miR-196b has the inherent capacity to down-regulate the overamplified c-myc gene recognized as a common pathognomonic feature leading to cancer in general and B-cell ALL in particular.

Hence miR-196b can be assigned with the tumor suppressor function and can be of therapeutic importance in paving the way toward the treatment of B-cell ALL.

[MeSH-major] Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. MicroRNAs / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Algorithms. Apoptosis / genetics. Apoptosis Regulatory Proteins / genetics. Case-Control Studies. Cell Line, Tumor. Cell Proliferation. Computational Biology. Down-Regulation. Humans. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-myc / genetics. Repressor Proteins / genetics. Telomerase / genetics. Transcription, Genetic. Transfection

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(PMID = 20549547.001).

[ISSN] 1573-4919

[Journal-full-title] Molecular and cellular biochemistry

[ISO-abbreviation] Mol. Cell. Biochem.

[Language] eng

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / AATF protein, human; 0 / Apoptosis Regulatory Proteins; 0 / MIRN196 microRNA, human; 0 / MYC protein, human; 0 / MicroRNAs; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / Repressor Proteins; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase

   

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

[Title] Outpatient versus inpatient autologous stem cell transplantation for malignant hematologic disorders.

: 7042 Background: High-dose chemotherapy with autologous stem cell support is utilized for the treatment of a variety of malignancies including Hodgkin/non-Hodgkins lymphoma and acute leukemias.

The aim of this study was to compare the time of engraftment and mortality rate and cost of neutropenic treatment in outpatient versus inpatient autologous stem cell transplantation (SCT).

They received conditioning regimen (CEAM for NHL and HL, busulfan and etoposide for AML) and stem cell infusion in hospital.

The day after SCT, outpatient group were discharged and followed by outpatient SCT team, and to be re-hospitalized in case of febrile neutropenia, after sepsis workup and performing chest x-ray, they were received the first dose of antibiotic in hospital and treatment continued in home.

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(PMID = 27961405.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] In vitro and in vivo anti-leukemia activity of CHR-2845, a cell-targeted HDAC inhibitor for use in monocytic leukemia.

: e14579 Background: Histone deacetylase inhibitors alter gene expression and induce apoptosis in a wide range of cancer cells including those derived from human leukemias.

METHODS: We studied the in vitro and in vivo anti-leukemia activity of CHR-2845 using cell proliferation assay, annexin V binding assay, cell cycle analysis, western blot and in vitro primary leukemia cell culture.

RESULTS: Both U937 and THP1 cells express high levels of hCE-1 whereas the myeloid cell line, HL60, does not.

In comparison to vorinostat, CHR-2845 showed increased anti-proliferative potency (IC₅₀) against monocytic cell lines (THP1, 30 nM vs 700 nM and U937, 30 nM vs 475 nM), compared to a myeloid cell line (HL60, 700nM vs 470 nM).

In a broad panel of leukemic cell lines, the potency of CHR-2845 over vorinostat correlated completely with hCE-1 expression.

In monocytic cell lines, CHR-2845 induced more apoptosis than vorinostat (THP1: 45±5% vs 11±1% and U937: 23±14% vs 6±1%), as measured by flow cytometry using Annexin V.

Biochemical assessment of histone H3 and H4 protein acetylation by Western blot also indicateed that CHR-2845 is at least 10 times more potent than vorinostat in monocytic cell lines but not in HL-60 cells.

We also studied the anti-leukemia activity of CHR-2845 in primary leukemia cells from 8 patients with acute or chronic myelomonocytic leukemia.

CONCLUSIONS: These results indicated that CHR-2845 has potential to be efficacious in the treatment of patients with monocytic leukemia.

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(PMID = 27963654.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] Three new drugs for acute lymphoblastic leukemia: nelarabine, clofarabine, and forodesine.

The search for more effective and safer anti-leukemia therapies has led to the identification of several new agents that show activity against specific types of acute lymphoblastic leukemia (ALL).

Of these, nelarabine has shown clinically meaningful benefit in patients with T-cell ALL, with overall response rates ranging from 33% to 60%, the induction of durable complete remissions, and an overall 1-year survival rate of 28% in adults.

Clofarabine has also shown promising clinical activity in pediatric patients, with an overall response rate of 30%, and some patients are able to proceed to allogeneic hematopoietic cell transplantation.

Forodesine is the most recent novel agent, with a unique mechanism that has shown single-agent activity in relapsed and refractory T- and B-cell leukemias and cutaneous lymphomas.

The rationale, pharmacology, and clinical experience to date with these agents in the treatment of patients with refractory acute leukemia are reviewed, with a highlight on ALL.

[MeSH-major] Adenine Nucleotides / pharmacology. Antineoplastic Agents / pharmacology. Arabinonucleosides / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Purine Nucleosides / pharmacology. Purine-Nucleoside Phosphorylase / drug effects. Pyrimidinones / pharmacology

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

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(PMID = 18086342.001).

[ISSN] 0093-7754

[Journal-full-title] Seminars in oncology

[ISO-abbreviation] Semin. Oncol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 0 / Purine Nucleosides; 0 / Pyrimidinones; 426X066ELK / forodesine; 60158CV180 / nelarabine; 762RDY0Y2H / clofarabine; EC 2.4.2.1 / Purine-Nucleoside Phosphorylase

[Number-of-references] 41

   

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

[Title] Development of cold agglutinin autoimmune hemolytic anemia during treatment for pediatric acute lymphoblastic leukemia.

Those most often associated with AIHA include chronic lymphocytic leukemia, B-cell lymphomas, and Burkitt-type acute lymphoblastic leukemia (ALL) and are clonal populations of mature B cells.

There have been no reports of patients with B-cell precursor ALL who developed AIHA while undergoing chemotherapy, but AIHA has been reported in a few patients with ALL after hematopoietic stem cell transplant.

The authors describe a child with B-cell precursor ALL who developed cold agglutinin AIHA during maintenance treatment while in remission after infection with influenza B.

[MeSH-major] Agglutinins. Anemia, Hemolytic / chemically induced. Anemia, Hemolytic, Autoimmune / etiology. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

Genetic Alliance. consumer health - Anemia.

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(PMID = 16012332.001).

[ISSN] 1077-4114

[Journal-full-title] Journal of pediatric hematology/oncology

[ISO-abbreviation] J. Pediatr. Hematol. Oncol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Agglutinins; 0 / Autoantibodies; 0 / Cryoglobulins; 0 / cold agglutinins

   

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

[Title] Infant acute bilineal leukemia.

Most cases of acute leukemia can be assigned to the myeloid, B or T lineage.

There are rare cases of acute leukemia, which cannot be clearly classified, because either blasts express antigens of more than one lineage (acute biphenotypic leukemias) or distinct blast populations of two lineages co-exist (acute bilineal leukemias, aBLL).

We present a 10-month-old infant with de novo aBLL, characterized by blasts of monocytic and B-cell precursor lineages.

Despite poor initial response, both to acute lymphoblastic leukemia (ALL) induction treatment and acute myeloid leukemia induction blocks, the child reached complete clinical remission with minimal residual disease negative status and was transplanted.

This case report illustrates that aBLL is a very aggressive type of acute leukemia that should be individually treated and monitored, particularly in children less than 1 year of age.

[MeSH-major] B-Lymphocytes / pathology. Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

[MeSH-minor] Cell Lineage. Hematopoietic Stem Cell Transplantation. Humans. Infant. Male. Remission Induction. Treatment Outcome

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(PMID = 19286255.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

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

[Publication-country] England

   

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

[Title] [Gene expression profile of human TGF-beta signal transduction pathway of B cell type acute lymphocytic leukemia].

This study was aimed to investigate the gene expression profile of TGF-beta signal transduction pathway in B-cell type acute lymphocytic leukemia (B-ALL).

The gene expression profiles in B-ALL primary cells and cell lines (NALM6 cells, Raji cells), B-lymphocyte of control were detected by cDNA microarray including 113 different genes in human TGF-beta/BMP signal transduction pathway, and TGF-beta(1) mRNA expression was detected by real time RT-PCR.

The B lymphocytes in peripheral blood of heacthy persons sorted by flow cytometry were used as control.

The results showed that as compared with B lymphocytes in peripheral blood of heacthy persons, the TGF-beta(1) expression in B-ALL cells, NALM6 cells and Raji cells were down-regulationed, myc and smad1 gene expressions were up-regulated, IL-6, smad 7 gene expressions were down-regulated.

It is concluded that TGF-beta signal transduction is abnormal in B-cell type acute lymphocytic leukemia.

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(PMID = 18718051.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / RNA, Messenger; 0 / Transforming Growth Factor beta

   

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

[Title] [Establishment of animal model with B lineage acute leukemia in nude mice for evaluation of new therapeutic agents].

OBJECTIVE: To establish an acute leukemia animal model for testing new therapeutic agents in vivo.

METHODS: Nude mice were intraperitoneally injected with 2 mg cyclophosphamide, 24 h later 5 x 10(6) acute B-cell leukemia Nalm-6 cells was inoculated via the tail vein, then monitored daily.

CONCLUSION: B lineage acute leukemia animal model has been successfully established in the nude mice, which is suitable for testing new therapeutic agents.

[MeSH-major] Disease Models, Animal. Precursor Cell Lymphoblastic Leukemia-Lymphoma

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(PMID = 18925721.001).

[ISSN] 1008-9292

[Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences

[ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban

[Language] chi

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

[Publication-country] China

[Chemical-registry-number] 8N3DW7272P / Cyclophosphamide

   

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

[Title] Induction of autologous CD4- and CD8-mediated T-cell responses against acute lymphocytic leukemia cell line using apoptotic tumor cell-loaded dendritic cells.

OBJECTIVE: Several studies have demonstrated that dendritic cells (DCs) pulsed with tumor lysate or apoptotic tumor cells can elicit effective T-cell responses.

We applied this approach to induce HLA class I- and class II-restricted T-cell responses directed against autologous acute lymphocytic leukemia (B-ALL) cell line NH-1.

METHODS: Autologous T cells were stimulated by apoptotic tumor cell-loaded DCs generated from a patient with ALL.

The stimulated and expanded T cells were isolated into CD8(+) T-cell line and CD4(+) T-cell line, and each of them was examined as to their functions.

RESULTS: Both CD8(+) and CD4(+) T-cell lines demonstrated cytotoxicity against NH-1 in an major histocompatibility complex-dependent manner.

Finally, we established two independent CD4(+) T-cell clones restricted to HLA-DR.

The CD4(+) T-cell line responded strongly to autologous Epstein-Barr virus-transformed lymphoblastoid cell lines (EBV-LCL) but not to autologous normal cells.

Furthermore, the T-cell clones also responded to allogeneic EBV-LCLs and B-ALL cell lines in the context of the HLA-DRB1( *)04051 molecule.

Interestingly, 293T and COS-7 cells, which had been transfected with the HLA-DRB1( *)04051, were also recognized by T-cell clones.

[MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Cell Fusion. Dendritic Cells / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

[MeSH-minor] Apoptosis / immunology. Cell Line, Tumor. Cytotoxicity Tests, Immunologic. Epitopes / immunology. Epstein-Barr Virus Nuclear Antigens / immunology. Female. HLA-DR Antigens / classification. HLA-DR Antigens / immunology. Histocompatibility Antigens Class II / immunology. Histocompatibility Antigens Class II / pharmacology. Humans. Infant. Lymphocyte Activation

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(PMID = 16459188.001).

[ISSN] 0301-472X

[Journal-full-title] Experimental hematology

[ISO-abbreviation] Exp. Hematol.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Epitopes; 0 / Epstein-Barr Virus Nuclear Antigens; 0 / HLA-DR Antigens; 0 / Histocompatibility Antigens Class II

   

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

[Title] [Biphenotypic and bilineal acute leukemias].

Human acute leukemias (AL) are classified as myeloid or lymphoid according to cytomorphology and the expression of leukocyte differentiation antigens/CD-markers.

However, in the minority of cases leukemic cells express markers of more than one lineage, which has led to the introduction of a new subgroup of acute leukemias termed mixed or biphenotypic acute leukemias (BAL).

In an effort to distinguish between BAL and those AL with aberrant expression of markers of other lineage, the European Group for the Immunological Characterization of Acute Leukemias (EGIL) has proposed a scoring system in which CD-markers are assigned a score of 0.5, 1.0 or 2.0, depending on the specificity of a particular antigen for myeloid, B- and/or T-lymphoid lineage, respectively.

In addition to BAL in which a single cell population expresses both myeloid and lymphoid differentiation markers, this new group of leukemias also comprises cases that present with two separate blast populations (acute bilineal leukemia, aBLL).

In general, BAL accounts for less than 5% of all AL cases, whereas aBLL is a rare disease constituting 1%-2% of AL cases that contains B- or T-lymphoid along with myeloid blasts.

Unfortunately, optimal therapy is not known, although regimens designed for acute lymphoblastic leukemia may result in a better response rate.

[MeSH-major] Leukemia, Biphenotypic, Acute

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(PMID = 19209464.001).

[ISSN] 1330-0164

[Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti

[ISO-abbreviation] Acta Med Croatica

[Language] hrv

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Croatia

[Number-of-references] 30

   

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

[Title] Troglitazone inhibits cell growth and induces apoptosis of B-cell acute lymphoblastic leukemia cells with t(14;18).

Peroxisome proliferator-activated receptor-gamma (PPARgamma), a member of the nuclear receptor superfamily, has been detected in several human leukemia cells.

Recent studies reported that PPARgamma ligands inhibit cell proliferation and induce apoptosis in both normal and malignant B-lineage cells.

We investigated the expression of PPARgamma and the effects of PPARgamma ligands on UTree-O2, Bay91 and 380, three B-cell acute lymphoblastic leukemia (B-ALL) cell lines with t(14;18), which show a poor prognosis, accompanying c-myc abnormality.

Western blot analysis identified expression of PPARgamma protein and real-time PCR that of PPARgamma mRNA on the three cell lines.

Troglitazone (TGZ), a synthetic PPARgamma ligand, inhibited cell growth in these cell lines in a dose-dependent manner, which was associated with G(1) cell cycle arrest and apoptosis.

We assessed the expression of c-myc, an apoptosis-regulatory gene, since c-myc abnormality was detected in most B-ALL cells with t(14;18).

TGZ was found to dose-dependently downregulate the expression of c-myc mRNA and c-myc protein in the three cell lines.

These results suggest that TGZ inhibits cell growth via induction of G(1) cell cycle arrest and apoptosis in these cell lines and that TGZ-induced apoptosis, at least in part, may be related to the downregulation of c-myc expression.

Moreover, the downregulation of c-myc expression by TGZ may depend on a PPARgamma-independent mechanism.

[MeSH-minor] Adolescent. Adult. Aged. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Female. Gene Expression Regulation, Leukemic / drug effects. Humans. Ligands. Male. Prognosis. Proto-Oncogene Proteins c-myc / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 16809887.001).

[ISSN] 0001-5792

[Journal-full-title] Acta haematologica

[ISO-abbreviation] Acta Haematol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chromans; 0 / Ligands; 0 / MYC protein, human; 0 / PPAR gamma; 0 / Proto-Oncogene Proteins c-myc; 0 / Thiazolidinediones; I66ZZ0ZN0E / troglitazone

   

[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 single population of blasts that express myeloid, T- or B-lineage antigens in various combinations and account for fewer than 4% of all acute leukemias.

An accurate diagnosis of pre-T ALL/LBL and acute biphenotypic leukemia requires a multiparametric approach, including examination of morphologic features, immunophenotype, clinical characteristics, and cytogenetic and molecular findings.

[MeSH-major] Biomarkers, Tumor / analysis. Leukemia, Lymphoid / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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(PMID = 17369128.001).

[ISSN] 0002-9173

[Journal-full-title] American journal of clinical pathology

[ISO-abbreviation] Am. J. Clin. Pathol.

[Language] eng

[Publication-type] Congresses

[Publication-country] United States

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

   

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

[Title] Acute leukemia in early childhood.

Acute leukemia in early childhood is biologically and clinically distinct.

The particular characteristics of this malignancy diagnosed during the first months of life have provided remarkable insights into the etiology of the disease.

The pro-B, CD10 negative immunophenotype is typically found in infant acute leukemia, and the most common genetic alterations are the rearrangements of the MLL gene.

The Brazilian Collaborative Study Group of Infant Acute Leukemia has found that mothers exposed to dipyrone, pesticides and hormones had an increased chance to give birth to babies with infant acute leukemia [OR = 1.48 (95%CI = 1.05-2.07), OR = 2.27 (95%CI = 1.56-3.31) and OR = 9.08 (95%CI = 2.95-27.96)], respectively.

This review aims to summarize recent clues that have facilitated the elucidation of the biology of early childhood leukemias, with emphasis on infant acute leukemia in the Brazilian population.

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(PMID = 17581672.001).

[ISSN] 0100-879X

[Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas

[ISO-abbreviation] Braz. J. Med. Biol. Res.

[Language] ENG

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

[Publication-country] Brazil

[Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

[Number-of-references] 60

   

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

[Title] T-cell acute lymphoblastic leukemia relapsing as acute myelogenous leukemia.

We present the unusual case of a 16-year-old girl with T-cell acute lymphoblastic leukemia (ALL) with an early thymocyte immunophenotype without myeloid markers, who after 13 months of complete hematological remission relapsed as acute myelogenous leukemia (AML) with minimal differentiation and died of her disease.

Whether the AML represented a relapse with lineage switch of the original immature T-cell clone or a new secondary malignancy, could not be proven due to the absence of molecular or clonal markers.

This report suggests that a subset of CD7+ T-cell leukemias without mature T-cell antigens (CD4-, CD8-) are minimally differentiated and can relapse as AML.

[MeSH-major] Antigens, Differentiation, T-Lymphocyte / analysis. Antigens, Neoplasm / analysis. Leukemia, Myeloid / pathology. Leukemia-Lymphoma, Adult T-Cell / pathology. Neoplastic Stem Cells / pathology. T-Lymphocyte Subsets / pathology

[MeSH-minor] 6-Mercaptopurine / administration & dosage. Acute Disease. Adolescent. Antigens, CD7 / analysis. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / administration & dosage. Bone Marrow / pathology. Cell Differentiation. Cell Lineage. Core Binding Factor Alpha 2 Subunit / genetics. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Diagnosis, Differential. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Etoposide / adverse effects. Fatal Outcome. Female. Gene Dosage. Histone-Lysine N-Methyltransferase. Humans. Immunophenotyping. Karyotyping. Methotrexate / administration & dosage. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / diagnosis. Proto-Oncogenes. Recurrence. Vincristine / administration & dosage

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[Copyright] (c) 2006 Wiley-Liss, Inc.

(PMID = 16206214.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD7; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Antigens, Neoplasm; 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / RUNX1 protein, human; 04079A1RDZ / Cytarabine; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin

   

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

[Title] Acute myeloid leukemia.

Acute myeloid leukemia (AML) is a heterogeneous group of leukemias that result from clonal transformation of hematopoietic precursors through the acquisition of chromosomal rearrangements and multiple gene mutations.

As a result of highly collaborative clinical research by pediatric cooperative cancer groups worldwide, disease-free survival has improved significantly during the past 3 decades.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid, Acute / therapy. Stem Cell Transplantation

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(PMID = 18242314.001).

[ISSN] 0031-3955

[Journal-full-title] Pediatric clinics of North America

[ISO-abbreviation] Pediatr. Clin. North Am.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Anthracyclines; 04079A1RDZ / Cytarabine

[Number-of-references] 229

   

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

[Title] Acute myeloid leukemia.

Acute myeloid leukemia (AML) is a heterogeneous group of leukemias that result from clonal transformation of hematopoietic precursors through the acquisition of chromosomal rearrangements and multiple gene mutations.

As a result of highly collaborative clinical research by pediatric cooperative cancer groups worldwide, disease-free survival has improved significantly during the past 3 decades.

[MeSH-major] Leukemia, Myeloid, Acute

[MeSH-minor] Antineoplastic Agents / therapeutic use. Central Nervous System Neoplasms. Child. Clone Cells / pathology. Hematopoietic Stem Cell Transplantation. Humans. Treatment Outcome

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[Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.

(PMID = 20113895.001).

[ISSN] 1558-1977

[Journal-full-title] Hematology/oncology clinics of North America

[ISO-abbreviation] Hematol. Oncol. Clin. North Am.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents

[Number-of-references] 229

   

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

[Title] [Cytomorphology of acute mixed leukemia].

[Transliterated title] Citomorfologija akutnih mjesovitih leukemija.

Biphenotypic acute leukemias (AL) with blasts expressing both myeloid and lymphoid antigens are grouped with undifferentiated AL and bilineal AL in the group of AL of ambiguous lineage.

RESULTS AND DISCUSSION: In the group of 169 adult AL patients, 116 were cytomorphologically classified as acute myeloblastic leukemias (AML), 35 as acute lymphoblastic leukemias (ALL) and 18 as acute undifferentiated leukemias (ANLM).

These observations are consistent with other studies and WHO determinations indicating that the majority of true biphenotypic leukemias are associated with immature monoblastic or myeloid cytomorphology or with lymphoid or undifferentiated characteristics, but may also express any AML cytomorphology type.

Thus, there is no direct correlation of leukemic cell cytomorphology and biphenotypic AL immunophenotype.

[MeSH-major] Leukemia, Biphenotypic, Acute / pathology

[MeSH-minor] Acute Disease. Humans. Immunophenotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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(PMID = 19205415.001).

[ISSN] 1330-0164

[Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti

[ISO-abbreviation] Acta Med Croatica

[Language] hrv

[Publication-type] English Abstract; Journal Article

[Publication-country] Croatia

   

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

[Title] The novel plant-derived agent silvestrol has B-cell selective activity in chronic lymphocytic leukemia and acute lymphoblastic leukemia in vitro and in vivo.

Therapeutic options for advanced B-cell acute lymphoblastic leukemia (ALL) and chronic lymphocytic leukemia (CLL) are limited.

Available treatments can also deplete T lymphocytes, leaving patients at risk of life-threatening infections.

In the National Cancer Institute cell line screen, the structurally unique natural product silvestrol produces an unusual pattern of cytotoxicity that suggests activity in leukemia and selectivity for B cells.

We investigated silvestrol efficacy using primary human B-leukemia cells, established B-leukemia cell lines, and animal models.

In vivo, silvestrol causes significant B-cell reduction in Emu-Tcl-1 transgenic mice and significantly extends survival of 697 xenograft severe combined immunodeficient (SCID) mice without discernible toxicity.

These data indicate silvestrol has efficacy against B cells in vitro and in vivo and identify translational inhibition as a potential therapeutic target in B-cell leukemias.

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(PMID = 19190247.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / U19 CA052956; United States / NCI NIH HHS / CA / P01CA125066; United States / NCI NIH HHS / CA / P01 CA125066; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / CA52956

[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 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Tcl1 protein, mouse; 0 / Triterpenes; 0 / silvestrol

[Other-IDs] NLM/ PMC2680369

   

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

[Title] CXC chemokine ligand 13 and CC chemokine ligand 19 cooperatively render resistance to apoptosis in B cell lineage acute and chronic lymphocytic leukemia CD23+CD5+ B cells.

We have investigated expression and functions of CXCL13/CXCR5 and CCL19/CCR7 in CD23+CD5+ and CD23+CD5- B cells from cord blood (CB) and patients with B cell lineage acute or chronic lymphocytic leukemia (B-ALL or B-CLL).

Therefore, we suggest that normal lymphocytes, especially naive B and T cells, use CXCL13/CXCR5 and CCL19/CCR7 for migration, homing, maturation, and cell homeostasis as well as secondary lymphoid tissues organogenesis.

[MeSH-major] Apoptosis / immunology. B-Lymphocyte Subsets / immunology. B-Lymphocyte Subsets / metabolism. Burkitt Lymphoma / immunology. Chemokines, CC / physiology. Chemokines, CXC / physiology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology

[MeSH-minor] Antigens, CD5 / biosynthesis. Cell Lineage / immunology. Chemokine CCL19. Chemokine CXCL13. Fetal Blood / cytology. Fetal Blood / immunology. Fetal Blood / metabolism. Humans. Lymphocyte Count. Proteins / metabolism. Proteins / physiology. Receptors, CCR7. Receptors, CXCR5. Receptors, Chemokine / biosynthesis. Receptors, IgE / biosynthesis

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(PMID = 17082584.001).

[ISSN] 0022-1767

[Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)

[ISO-abbreviation] J. Immunol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD5; 0 / CCL19 protein, human; 0 / CCR7 protein, human; 0 / CXCL13 protein, human; 0 / CXCR5 protein, human; 0 / Chemokine CCL19; 0 / Chemokine CXCL13; 0 / Chemokines, CC; 0 / Chemokines, CXC; 0 / PEG10 protein, human; 0 / Proteins; 0 / Receptors, CCR7; 0 / Receptors, CXCR5; 0 / Receptors, Chemokine; 0 / Receptors, IgE

   

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

[Title] Bioengineering a unique deimmunized bispecific targeted toxin that simultaneously recognizes human CD22 and CD19 receptors in a mouse model of B-cell metastases.

The aims were to reduce toxin immunogenicity using mutagenesis, measure the ability of mutated drug to elicit antitoxin antibody responses, and show that mutated drug was effective against systemic B-cell lymphoma in vivo.

Site-specific mutagenesis was used to mutate amino acids in seven key epitopic toxin regions that dictate B-cell generation of neutralizing antitoxin antibodies.

Finally, a powerful genetically altered luciferase xenograft model was used that could be imaged in real time to determine the effect on systemic malignant human B-cell lymphoma, Raji-luc.

Patient B-lineage acute lymphoblastic leukemia, B-cell chronic lymphocytic leukemia, and B lymphoma were high in CD22 and CD19 expression.

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[Cites] J Clin Oncol. 2001 Jan 15;19(2):376-88 [11208829.001]

(PMID = 20530709.001).

[ISSN] 1538-8514

[Journal-full-title] Molecular cancer therapeutics

[ISO-abbreviation] Mol. Cancer Ther.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA108637; United States / NCI NIH HHS / CA / R01 CA082154; United States / NCI NIH HHS / CA / CA036725-25; United States / NCI NIH HHS / CA / CA108637-05; United States / NCI NIH HHS / CA / R01 CA036725; United States / NCI NIH HHS / CA / R01-CA36725; United States / NCI NIH HHS / CA / R01-CA082154; United States / NCI NIH HHS / CA / R01 CA108637-05; United States / NCI NIH HHS / CA / R01 CA036725-25

[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 / Antibodies, Bispecific; 0 / Antigens, CD19; 0 / Bacterial Toxins; 0 / Exotoxins; 0 / Sialic Acid Binding Ig-like Lectin 2; 0 / Virulence Factors; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.31 / toxA protein, Pseudomonas aeruginosa

[Other-IDs] NLM/ NIHMS198461; NLM/ PMC2884080

   

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

[Title] Low representation of Fc receptor-like 1-5 molecules in leukemic cells from Iranian patients with acute lymphoblastic leukemia.

Recent studies have demonstrated expression of Fc receptor-like (FCRL) molecules, a newly identified family with preferential B-cell lineage expression, in some chronic B-cell leukemias with possible implication for classification and/or targeted immunotherapy.

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cell Surface / genetics. Receptors, Fc / genetics. Receptors, Immunologic / genetics

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(PMID = 18802695.001).

[ISSN] 1432-0851

[Journal-full-title] Cancer immunology, immunotherapy : CII

[ISO-abbreviation] Cancer Immunol. Immunother.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] 0 / FCRL2 protein, human; 0 / FCRL4 protein, human; 0 / FCRL5 protein, human; 0 / FCRLA protein, human; 0 / Receptors, Cell Surface; 0 / Receptors, Fc; 0 / Receptors, Immunologic

   

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

[Title] The expression of iASPP in acute leukemias.

To examine the role of iASPP in acute leukemia (AL), we analyzed iASPP mRNA expression in AL by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR).

There was no significant difference between acute lymphocytic leukemia (ALL) cells and acute myeloid leukemia (AML) cells (P = 0.593).

The expression level of iASPP gene and its overexpression in M3 and M4EO were significantly lower than in other subtypes of AML.

However, iASPP gene expression in AL cells was not associated with gender, age, initial white blood cell count or p53 type, but was associated with CD34 expression.

The results of the present study suggest that iASPP gene overexpression may play an important role in the leukemogenesis and/or disease progression of AL.

[MeSH-major] Gene Expression Regulation, Leukemic. Intracellular Signaling Peptides and Proteins / genetics. Leukemia, Myeloid, Acute / genetics. RNA, Messenger / genetics

[MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Female. Humans. Male. Mutation. Repressor Proteins. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Suppressor Protein p53 / antagonists & inhibitors. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism. Up-Regulation

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(PMID = 15607367.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / PPP1R13L protein, human; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53

   

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

[Title] Modern diagnostics in acute leukemias.

Acute leukemias are a heterogeneous group of diseases.

Improvements in patient's treatment resulting in better survival rates are closely linked to the biological understanding of the disease subtypes, which is assessed by specific diagnostic approaches.

Furthermore they are also needed for follow up studies focusing especially on minimal residual disease (MRD) to guide further treatment decisions based on the response of the disease to given treatment protocols.

Only by using a comprehensive diagnostic panel including cytomorphology, cytochemistry, multiparameter flow cytometry (MFC), cytogenetics, fluorescence in situ hybridization (FISH) and molecular genetic methods the correct diagnosis in acute leukemias can be established today.

[MeSH-major] Biomarkers, Tumor. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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(PMID = 16213152.001).

[ISSN] 1040-8428

[Journal-full-title] Critical reviews in oncology/hematology

[ISO-abbreviation] Crit. Rev. Oncol. Hematol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Ireland

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

[Number-of-references] 70

   

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

[Title] [Biological characteristics of hyperleukocytic acute leukemia].

The study was to investigate the biological characteristics of hyperleucocyte acute leukemia (HAL) and its clinical significance.

In AML, monocytic leukemia is easier to become into HAL than other leukemias.

In ALL, T-lineage antigens of HAL group are more easily expressed than those of NHAL group; the leukemia cells of HAL group are naiver than those of NHAL group, meanwhile the prognosis of HAL is poor.

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(PMID = 16800918.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD14; 0 / Antigens, CD79; 0 / Antigens, CD8; 0 / Sialic Acid Binding Ig-like Lectin 2

   

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

[Title] [Minimal residual disease in acute lymphoblastic leukemia: a new concept of complete remission].

[Transliterated title] Leucemia mínima residual: nuevo concepto de remisión completa.

INTRODUCTION: Early response to induction treatment is one of the most important prognostic factors in children with acute lymphoblastic leukemia (ALL).

More sensitive techniques are required to measure residual leukemia and establish a new definition of complete remission.

OBJECTIVE: To identify minimal residual disease (MRD) by immunological techniques and define its prognostic impact in children with ALL.

All the children achieved complete cytological remission (< 5 %) with the induction treatment and had at least one useful phenotype for follow-up: 11 % were T phenotype, one was biphenotypic and the remainder were B cell leukemias.

Continued sequential monitoring may predict recurrence before the onset of clinical or hematologic manifestations.

[MeSH-major] Neoplasm, Residual / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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(PMID = 16266612.001).

[ISSN] 1695-4033

[Journal-full-title] Anales de pediatría (Barcelona, Spain : 2003)

[ISO-abbreviation] An Pediatr (Barc)

[Language] spa

[Publication-type] English Abstract; Journal Article

[Publication-country] Spain

   

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

[Title] Advances in the molecular genetics of acute leukemia.

Acute leukemias are characterized by the unrestrained clonal proliferation of hematopoietic precursor cells coupled with aberrant or arrested differentiation.

The molecular basis of hematopoiesis and leukemogenesis is still being defined, yet it is increasingly evident that acute leukemias have recurrent molecular features that can be exploited for diagnostic, prognostic, and therapeutic purposes.

Modern molecular technologies already influence treatment strategies for these diseases, and it is likely that as such technology matures it will have an increasing impact on all aspects of acute leukemia management.

This article reviews recent developments in the molecular classification, prognostication, and treatment of the acute leukemias.

[MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia / genetics

[MeSH-minor] Cell Line, Tumor. Epigenesis, Genetic. Humans. Immunophenotyping. Karyotyping. Medical Oncology / trends. Mutation. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Pharmacogenetics / methods. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Prognosis. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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[Cites] Blood. 2003 Oct 1;102(7):2705-6 [14504076.001]

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(PMID = 16091192.001).

[ISSN] 1523-3790

[Journal-full-title] Current oncology reports

[ISO-abbreviation] Curr Oncol Rep

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / RNA, Messenger

[Number-of-references] 50

   

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

[Title] Frank hematuria as the presentation feature of acute leukemia.

Muco-cutaneous bleeding is a common presenting feature of acute leukemias.

Hematuria as an isolated or main presenting feature of acute leukemia is rare.

We describe two cases of acute leukemia, a 19 year old male with acute lymphoblastic leukemia and a 52 year old male with acute myeloid leukemia, both presenting with gross hematuria.

Our cases highlight that hematuria should be remembered as a rare presenting feature of acute leukemia.

[MeSH-major] Hematuria / etiology. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

[MeSH-minor] Blood Cell Count. Bone Marrow Examination. Fatal Outcome. Humans. Leukocyte Count. Male. Middle Aged. Thrombocytopenia / etiology. Treatment Outcome. Young Adult

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[CommentIn] Saudi J Kidney Dis Transpl. 2012 Sep;23(5):1088-9 [22982933.001]

(PMID = 20814137.001).

[ISSN] 1319-2442

[Journal-full-title] Saudi journal of kidney diseases and transplantation : an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia

[ISO-abbreviation] Saudi J Kidney Dis Transpl

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Saudi Arabia

   

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

[Title] The significance of detecting WT1 expression in childhood acute leukemias.

WT1 (Wilms' tumor gene 1) overexpression is implicated in the prognosis of acute leukemia.

The purpose of this study was to investigate WT1 expression and its clinical implication in childhood acute leukemia (AL) in Chinese population.

Bone marrow specimen from 200 children at different stages of acute leukemia and from 21 children without leukemia were studied.

The WT1 expression at diagnostic marrow specimen in both acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL) was higher than control group, whereas WT1 expression in AML was higher than in ALL, and WT1 expression level in relapse in ALL increased more significantly than in AML.

The WT1 expression level showed positive correlation with the hypodiploidy and BCR-ABL fusion gene in acute leukemia.

A rapidly decrease of WT1 expression level predicted a good response to the induction therapy and low expression of WT1 correlates with remission status.

This study suggested that WT1 expression levels in acute leukemia can potentially be a marker for evaluating therapeutic efficacy, correlating with monitoring minimal residue disease, and predicting hematological relapse in children acute leukemia.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. WT1 Proteins / genetics

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(PMID = 20863155.001).

[ISSN] 1521-0669

[Journal-full-title] Pediatric hematology and oncology

[ISO-abbreviation] Pediatr Hematol Oncol

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / WT1 Proteins; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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

[Title] [Present status in studying immunotherapy for acute leukemia and its perspective--Editorial].

One of the important approaches for further prolonging remission duration and eradicating minimal residual disease in acute leukemia is immunotherapy.

Four kinds of immunotherapy for acute leukemia are under investigation:.

(1) monoclonal antibodies, among them, Mylotarg (cytotoxic antibiotic calicheamicin linked to CD33 Mab) is given for the treatment of refractory or relapsed acute myeloid leukemia and molecular relapse in acute promyelocytic leukemia with good results, Campath-1H (antiCD52 Mab) is administered in the treatment of prolymphocytic leukemia and Rituximab (anti-CD20 Mab) in B-PLL with high complete remission rates.

Other Mabs under preclinical and clinical trials include anti-IL-2 receptor Mab for the treatment of acute T lymphocytic leukemia, anti-220 kD Mab-6G7 for acute leukemias, recombinant immune toxin BL22 (anti-CD22) for hairy cell leukemia and Mabs labeled with radio-isotopes for different types of acute leukemias;.

(2) adoptive cellular immunotherapy using cytokine-induced killer cell, alloreactive NK cells, allogeneic or autologous leukemic-specific CD8(+) cytotoxic T lymphocytes, and other immune effector cells;.

(4) leukemia vaccines of several different formulations including antigen-specific, leukemia cell-based, leukemia antigen-pulsed dendritic cell (DC) and leukemia-derived DC vaccines, the latter two formulations are more attractive.

In conclusion, up to now, the most effective example of immunotherapy in acute leukemia is provided by the administration of Mabs, and the majority of other approaches in immunotherapy for acute leukemia although promising, need further studies.

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(PMID = 15854271.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] Editorial; English Abstract

[Publication-country] China

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cancer Vaccines

   

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

[Title] [Immunologic classification used in typing of 68 cases of acute leukemias].

To evaluate the significance of immunologic classification for typing of acute leukemia (AL).

In conclusion, immunologic classification can improve the accuracy in acute leukemia diagnosis.

The diagnosis of some special AL, such as acute unidentified leukemia (AUL), AML-M(0) and so on, must rely on immunologic classification.

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(PMID = 16584588.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD14; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13

   

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

[Title] Molecular diagnostics in acute leukemias.

Acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) both represent highly heterogeneous entities on the basis of diverse cyto- and molecular genetic alterations with considerable influence on prognosis and therapeutic decisions.

Thus, molecular analysis based on various techniques, such as polymerase chain reaction (PCR) has become an essential part of the diagnostic panel for acute leukemia.

During the course of disease, the residual leukemic cell load can be monitored by highly sensitive quantitative PCR techniques ("real-time PCR").

This demonstrates that molecular diagnostics for acute leukemias are in continuous development.

This review summarizes the most important recurrent molecular markers seen in acute leukemias, their role in prognosis and therapy and provides an overview on the relevant PCR techniques.

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(PMID = 19817644.001).

[ISSN] 1437-4331

[Journal-full-title] Clinical chemistry and laboratory medicine

[ISO-abbreviation] Clin. Chem. Lab. Med.

[Language] ENG

[Publication-type] Journal Article; Review

[Publication-country] Germany

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

[Number-of-references] 78

   

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

[Title] MicroRNA expression signatures accurately discriminate acute lymphoblastic leukemia from acute myeloid leukemia.

Acute lymphoblastic leukemia (ALL) is the most common childhood cancer, whereas acute myeloid leukemia (AML) is the most common acute leukemia in adults.

Using the expression signatures of a minimum of two of these miRNAs resulted in an accuracy rate of >95% in the diagnosis of ALL and AML.

The differential expression patterns of these four miRNAs were validated further through large-scale real-time PCR on 98 acute leukemia samples covering most of the common cytogenetic subtypes, along with 10 normal control samples.

Taken together, we showed that expression signatures of as few as two miRNAs could accurately discriminate ALL from AML, and that epigenetic regulation might play an important role in the regulation of expression of miRNAs in acute leukemias.

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[Cites] N Engl J Med. 1999 Sep 30;341(14):1051-62 [10502596.001]

(PMID = 18056805.001).

[ISSN] 1091-6490

[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 / P01 CA040046; United States / NCI NIH HHS / CA / CA40046

[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 / MicroRNAs; 9007-49-2 / DNA

[Other-IDs] NLM/ PMC2148407

   

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

[Title] [Principles and potentialities of the standardization of morphocytochemical diagnosis of acute leukemias].

Under the present conditions, the competitive capacity of a health care facility is provided by the high level and timeliness of diagnosis of disease.

The diagnosis of the types of acute leukemia (AL) may be accomplished immunologically, by using a 33-marker panel and without consideration of the morphocytochemical parameters of blast cells.

Moreover, morphocytochemical data more exactly define the stages of blast cell differentiation than does the immunological phenotype.

Only M0, M6, and M7 forms of leukemia require compulsory blast cell phenotyping, particularly in the differential diagnosis of acute myeloid leukemia and acute lymphoblastic leukemia.

Search for new markers of leukemia cells, including lesions at the chromosomal or molecular levels, is under way.

Some of them are only of theoretical value while other markers have been already used by hematologists to diagnose leukemia.

Standardization in this essence is the self-assessment of a facility and reference comparison, which are based on the principles of its orientation to the patient, the adjusted system for controlling the quality of health care that is up to the world standards rather than the compliance with the state-regulated standard.

The present paper discusses the ways of establishing the uniform rates and requirements for the morphocytochemical diagnosis of acute leukemias.

[MeSH-major] Biomarkers, Tumor / analysis. Blast Crisis / diagnosis. Leukemia / diagnosis

[MeSH-minor] Acute Disease. Diagnosis, Differential. Humans. Immunohistochemistry / methods. Immunohistochemistry / standards. Immunophenotyping / methods. Immunophenotyping / standards

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(PMID = 16925061.001).

[ISSN] 0869-2084

[Journal-full-title] Klinicheskaia laboratornaia diagnostika

[ISO-abbreviation] Klin. Lab. Diagn.

[Language] rus

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Russia (Federation)

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

[Number-of-references] 8

   

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

[Title] [Methylation of Id4 gene promoter in acute leukemia].

This study was purpose to investigate the difference of Id4 gene promoter methylation between healthy individuals and acute leukemia patients.

MS-PCR methods were used to detect the status of Id4 gene methylation in healthy individuals and acute leukemia patients.

Id4 gene methylation was found in all 8 cases of relapsed acute leukemias.

It is concluded that as compared with healthy individuals, Id4 gene in acute leukemia patients was methylated in different degrees.

The change of Id4 gene methylation is thought to be associated with occurrence of acute leukemia.

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(PMID = 18088456.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

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

[Publication-country] China

[Chemical-registry-number] 0 / ID4 protein, human; 0 / Inhibitor of Differentiation Proteins

   

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

[Title] Novel therapies for relapsed acute lymphoblastic leukemia.

The outcome of salvage therapy for relapsed acute lymphoblastic leukemia (ALL) remains poor.

Novel strategies under investigation as monotherapy or in combination with chemotherapy improve the treatment of relapsed disease.

Nelarabine demonstrates activity as monotherapy in T-cell ALL and is approved by the US Food and Drug Administration.

Clofarabine, a second-generation purine analogue approved in pediatric leukemia, has shown activity in adult acute leukemias including ALL and acute myeloid leukemia.

The benefit of matched related-donor allogeneic stem cell transplantation is significant for standard-risk ALL but not for high-risk ALL.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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(PMID = 20425428.001).

[ISSN] 1558-822X

[Journal-full-title] Current hematologic malignancy reports

[ISO-abbreviation] Curr Hematol Malig Rep

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA016672

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 50

[Other-IDs] NLM/ NIHMS674650; NLM/ PMC4572835

   

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

[Title] Heat shock proteins and acute leukemias.

HSPs have also been implicated in the resistance of leukemia cells to potential therapeutic agents.

HSPs were shown highly expressed by acute myeloid leukemia (AML) cells as well as by acute lymphoblastic leukemia (ALL) cells.

[MeSH-major] Antineoplastic Agents / metabolism. Gene Expression Regulation, Leukemic / drug effects. HSP90 Heat-Shock Proteins / metabolism. Neoplasm Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Rifabutin / analogs & derivatives

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(PMID = 16019471.001).

[ISSN] 1024-5332

[Journal-full-title] Hematology (Amsterdam, Netherlands)

[ISO-abbreviation] Hematology

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Neoplasm Proteins; 1W306TDA6S / Rifabutin; 4GY0AVT3L4 / tanespimycin

[Number-of-references] 122

   

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

[Title] Mucocutaneous findings in febrile neutropenic children with acute leukemias.

Febrile neutropenia is common in children with leukemia.

The authors prospectively examined children with fever with neutropenia in acute leukemia, aged 1-15 years, who were admitted to the Department of Pediatrics, King Chulalongkorn Memorial Hospital, between September 2000 and August 2001.

The prevalence of infection was found in severe neutropenia (absolute neutrophil count, ANC less than 500 cell/cu mm), moderate neutropenia (ANC, 500-1000 cell/cu mm) and mild neutropenia (ANC, 1001-1500 cell/cu mm) was 72%, 9% and 5%, respectively.

Daily physical examination of skin and mucous membrane are suggested for proper and prompt diagnosis and treatment of febrile neutropenic children with acute leukemia to reduce mortality and morbidity in these patients.

A Guideline for the use of antimicrobial agents in neutropenic patients with acute leukemia is proposed In conclusion, infection was commonly found in severe neutropenia.

Mucocutaneous infection was the most common site of infection infebrile neutropenia in children with leukemia.

[MeSH-major] Fever. Neutropenia / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Skin Diseases / etiology

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(PMID = 16083222.001).

[ISSN] 0125-2208

[Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet

[ISO-abbreviation] J Med Assoc Thai

[Language] eng

[Publication-type] Journal Article

[Publication-country] Thailand

   

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

[Title] [Minimal residual disease in childhood acute leukemias].

Monitoring of residual leukemic cells, so called minimal residual disease (MRD) in acute leukemias is of great importance in clinical practice.

Especially evaluation of early response to treatment has a important prognostic value, and modifies the therapy schedule in a nowadays used treatment protocols.

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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(PMID = 16892899.001).

[ISSN] 0033-2240

[Journal-full-title] Przegla̧d lekarski

[ISO-abbreviation] Prz. Lek.

[Language] pol

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Poland

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

[Number-of-references] 20

   

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

[Title] Abnormalities of the P53, MDM2, BCL2 and BAX genes in acute leukemias.

Abnormalities of the P53 network have been implicated in the pathogenesis of acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML).

To gain further insight into the role of P53 network in the evolution of acute leukemias, the P53, MDM2, BCL2 and BAX mRNAexpressions in portion samples from patients with ALL and AML were analyzed using multiplex RT-PCR.

Although a low frequency of molecular disturbances of the P53 and the MDM2 genes was detected in this study, there was a high percentage of cases with increased mRNA level of P53 and MDM2.

A high frequency of BCL2 mRNA overexpression and a relatively low frequency of BAX mRNA overexpression detected in both analyzed leukemias in this study, indicate that altered transcription of these genes may be involved in leukemogenesis.

[MeSH-major] Gene Amplification. Gene Expression Profiling. Leukemia, Myeloid, Acute / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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(PMID = 16059649.001).

[ISSN] 0028-2685

[Journal-full-title] Neoplasma

[ISO-abbreviation] Neoplasma

[Language] eng

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

[Publication-country] Slovakia

[Chemical-registry-number] 0 / BAX protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2

   

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

[Title] Dose escalation of lenalidomide in relapsed or refractory acute leukemias.

We report results of a phase I dose-escalation trial of lenalidomide in relapsed or refractory acute leukemia.

PATIENTS AND METHODS: Thirty-one adults with acute myeloid leukemia (AML) and four adults with acute lymphoblastic leukemia (ALL) were enrolled.

Two of four patients who received lenalidomide as initial therapy for AML relapse after allogeneic transplantation achieved durable CR after development of cutaneous graft-versus-host disease, without donor leukocyte infusion.

[MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Thalidomide / analogs & derivatives

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[Cites] Biol Blood Marrow Transplant. 2006 Jan;12(1):61-7 [16399569.001]

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(PMID = 20956622.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / K23 CA120708; United States / NCI NIH HHS / CA / P50-CA140158; United States / NCI NIH HHS / CA / K23CA120708; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NCI NIH HHS / CA / P30 CA016058

[Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide

[Other-IDs] NLM/ PMC3020696

   

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

[Title] Acute leukemias in children with Down syndrome.

Children with Down syndrome have an increased risk for developing both acute myeloid as well as lymphoblastic leukemia.

These leukemias differ in presenting characteristics and underlying biology when compared with leukemias occurring in non-Down syndrome children.

Myeloid leukemia in children with Down syndrome is preceded by a preleukemic clone (transient leukemia or transient myeloproliferative disorder), which may disappear spontaneously, but may also need treatment in case of severe symptoms.

Twenty percent of children with transient leukemia subsequently develop myeloid leukemia.

This transition offers a unique model to study the stepwise development of leukemia and of gene dosage effects mediated by aneuploidy.

[MeSH-major] Down Syndrome / complications. Leukemia, Myeloid, Acute / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

[MeSH-minor] Child. Clone Cells / pathology. Humans. Leukemia

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[Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.

(PMID = 20113894.001).

[ISSN] 1558-1977

[Journal-full-title] Hematology/oncology clinics of North America

[ISO-abbreviation] Hematol. Oncol. Clin. North Am.

[Language] eng

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

[Publication-country] United States

[Number-of-references] 83

   

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

[Title] Acute leukemias in children with Down syndrome.

Children with Down syndrome have an increased risk for developing both acute myeloid as well as lymphoblastic leukemia.

These leukemias differ in presenting characteristics and underlying biology when compared with leukemias occurring in non-Down syndrome children.

Myeloid leukemia in children with Down syndrome is preceded by a preleukemic clone (transient leukemia or transient myeloproliferative disorder), which may disappear spontaneously, but may also need treatment in case of severe symptoms.

Twenty percent of children with transient leukemia subsequently develop myeloid leukemia.

This transition offers a unique model to study the stepwise development of leukemia, and of gene dosage effects mediated by aneuploidy.

[MeSH-major] Down Syndrome / complications. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Disease Progression. Humans. Infant. Infant, Newborn. Mutation

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(PMID = 18242315.001).

[ISSN] 0031-3955

[Journal-full-title] Pediatric clinics of North America

[ISO-abbreviation] Pediatr. Clin. North Am.

[Language] eng

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

[Publication-country] United States

[Number-of-references] 83

   

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

[Title] PHF6 mutations in T-cell acute lymphoblastic leukemia.

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with an increased incidence in males.

Mutational loss of PHF6 is importantly associated with leukemias driven by aberrant expression of the homeobox transcription factor oncogenes TLX1 and TLX3.

Overall, these results identify PHF6 as a new X-linked tumor suppressor in T-ALL and point to a strong genetic interaction between PHF6 loss and aberrant expression of TLX transcription factors in the pathogenesis of this disease.

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(PMID = 20228800.001).

[ISSN] 1546-1718

[Journal-full-title] Nature genetics

[ISO-abbreviation] Nat. Genet.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NIAID NIH HHS / AI / U54-AI057158; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / R01 CA129382-03; United States / NCI NIH HHS / CA / CA129382-03; United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01CA120196; United States / NIAID NIH HHS / AI / U54 AI057158; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NLM NIH HHS / LM / 1R01LM010140-01; United States / NCI NIH HHS / CA / U24 CA114737; United States / NLM NIH HHS / LM / R01 LM010140; United States / NCI NIH HHS / CA / R01 CA155743

[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 / Carrier Proteins; 0 / Homeodomain Proteins; 0 / PHF6 protein, human; 0 / Proto-Oncogene Proteins; 0 / TLX3 protein, human; 143275-75-6 / TLX1 protein, human

[Other-IDs] NLM/ NIHMS176587; NLM/ PMC2847364