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1. Oshiro A, Tagawa H, Ohshima K, Karube K, Uike N, Tashiro Y, Utsunomiya A, Masuda M, Takasu N, Nakamura S, Morishima Y, Seto M: Identification of subtype-specific genomic alterations in aggressive adult T-cell leukemia/lymphoma. Blood; 2006 Jun 1;107(11):4500-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of subtype-specific genomic alterations in aggressive adult T-cell leukemia/lymphoma.
  • Aggressive adult T-cell leukemia/lymphoma (ATLL) such as acute and lymphoma types are fatal diseases with poor prognosis.
  • We performed array-based comparative genomic hybridization for 17 acute and 49 lymphoma cases as well as real-time quantitative polymerase chain reaction (PCR) to identify the target genes of recurrently amplified regions.
  • Comparison of the genome profiles of acute and lymphoma types revealed that the lymphoma type had significantly more frequent gains at 1q, 2p, 4q, 7p, and 7q, and losses of 10p, 13q, 16q, and 18p, whereas the acute type showed a gain of 3/3p.
  • Of the recurrent high-level amplifications found at 1p36, 6p25, 7p22, 7q, and 14q32 in the lymphoma type, we were able to demonstrate that CARMA1 is a possible target gene of the 7p22 amplification for the lymphoma type but not for the acute type.
  • Furthermore, we found BCL11B overexpression in the acute type regardless of the 14q32 gain/amplification, but no or low expression of the gene in the lymphoma type.
  • These results suggest that acute and lymphoma types are genomically distinct subtypes, and thus may develop tumors via distinct genetic pathways.
  • [MeSH-major] Gene Amplification. Genome, Human. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis Regulatory Proteins / genetics. CARD Signaling Adaptor Proteins. Chromosomes. DNA-Binding Proteins / genetics. Female. Gene Dosage. Gene Expression Regulation, Neoplastic. Guanylate Cyclase / genetics. Humans. Lymphoma / genetics. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Polymerase Chain Reaction. Repressor Proteins / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 16484591.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BCL11B protein, human; 0 / CARD Signaling Adaptor Proteins; 0 / DNA-Binding Proteins; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins; EC 4.6.1.2 / CARD11 protein, human; EC 4.6.1.2 / Guanylate Cyclase
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2. Feldman AL, Law M, Remstein ED, Macon WR, Erickson LA, Grogg KL, Kurtin PJ, Dogan A: Recurrent translocations involving the IRF4 oncogene locus in peripheral T-cell lymphomas. Leukemia; 2009 Mar;23(3):574-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent translocations involving the IRF4 oncogene locus in peripheral T-cell lymphomas.
  • Oncogenes involved in recurrent chromosomal translocations serve as diagnostic markers and therapeutic targets in hematopoietic tumors.
  • In contrast to myeloid and B-cell neoplasms, translocations in peripheral T-cell lymphomas (PTCLs) are poorly understood.
  • Here, we identified recurrent translocations involving the multiple myeloma oncogene-1/interferon regulatory factor-4 (IRF4) locus in PTCLs.
  • IRF4 translocations exist in myeloma and some B-cell lymphomas, but have not been reported earlier in PTCLs.
  • Two cases with t(6;14)(p25;q11.2) had translocations between IRF4 and the T-cell receptor-alpha (TCRA) locus.
  • In total, 8 of the remaining 10 cases were cutaneous anaplastic large-cell lymphomas (ALCLs) without TCRA rearrangements (57% of cutaneous ALCLs tested).
  • These findings identified IRF4 translocations as a novel recurrent genetic abnormality in PTCLs.
  • Detecting these translocations may be useful in lymphoma diagnosis.

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  • (PMID = 18987657.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097274; United States / NCI NIH HHS / CA / P50 CA097274-07; United States / NCI NIH HHS / CA / P50 CA97274
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon Regulatory Factors; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / interferon regulatory factor-4
  • [Other-IDs] NLM/ NIHMS70248; NLM/ PMC2656414
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3. Ravandi F, Kantarjian H, Jones D, Dearden C, Keating M, O'Brien S: Mature T-cell leukemias. Cancer; 2005 Nov 1;104(9):1808-18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mature T-cell leukemias.
  • Mature T-cell and NK-cell leukemias are a group of relatively uncommon neoplasms derived from mature or postthymic T-cells accounting for a relatively small percentage of lymphoid malignancies.
  • The recent availability of modern immunophenotypic and molecular tools has allowed a better distinction of these disorders from their B-cell counterparts.
  • Similarly, identification of recurrent cytogenetic abnormalities, as well as plausible mechanisms through which these molecular events influence cellular signaling pathways, have created further insight into the pathogenesis of these disorders.
  • Herein, we review the clinical and pathological features of mature T-cell leukemias.
  • [MeSH-major] Leukemia, T-Cell / diagnosis
  • [MeSH-minor] Adult. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Human T-lymphotropic virus 1. Humans. Immunophenotyping. Leukemia, Lymphoid. Leukemia, Prolymphocytic / diagnosis. Leukemia, Prolymphocytic / drug therapy. Leukemia, Prolymphocytic / genetics. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / virology. Middle Aged. Tumor Virus Infections

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  • [Copyright] (c) 2005 American Cancer Society.
  • (PMID = 16136598.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 143
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4. Van Vlierberghe P, van Grotel M, Tchinda J, Lee C, Beverloo HB, van der Spek PJ, Stubbs A, Cools J, Nagata K, Fornerod M, Buijs-Gladdines J, Horstmann M, van Wering ER, Soulier J, Pieters R, Meijerink JP: The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia. Blood; 2008 May 1;111(9):4668-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The recurrent SET-NUP214 fusion as a new HOXA activation mechanism in pediatric T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is mostly characterized by specific chromosomal abnormalities, some occurring in a mutually exclusive manner that possibly delineate specific T-ALL subgroups.
  • Using a gene expression-based clustering analysis of 67 T-ALL cases with recurrent molecular genetic abnormalities and 25 samples lacking apparent aberrations, we identified 5 new patients with elevated HOXA levels.
  • Using microarray-based comparative genomic hybridization (array-CGH), a cryptic and recurrent deletion, del (9)(q34.11q34.13), was exclusively identified in 3 of these 5 patients.
  • This deletion results in a conserved SET-NUP214 fusion product, which was also identified in the T-ALL cell line LOUCY.
  • We conclude that SET-NUP214 may contribute to the pathogenesis of T-ALL by enforcing T-cell differentiation arrest.

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  • (PMID = 18299449.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA11560
  • [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 / Chromosomal Proteins, Non-Histone; 0 / Histone Chaperones; 0 / Homeodomain Proteins; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / SET protein, human; 0 / Transcription Factors; 157907-48-7 / HoxA protein
  • [Other-IDs] NLM/ PMC2343598
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5. Soulier J, Clappier E, Cayuela JM, Regnault A, García-Peydró M, Dombret H, Baruchel A, Toribio ML, Sigaux F: HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL). Blood; 2005 Jul 1;106(1):274-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HOXA genes are included in genetic and biologic networks defining human acute T-cell leukemia (T-ALL).
  • Using a combination of molecular cytogenetic and large-scale expression analysis in human T-cell acute lymphoblastic leukemias (T-ALLs), we identified and characterized a new recurrent chromosomal translocation, targeting the major homeobox gene cluster HOXA and the TCRB locus.
  • Inclusion of HOXA-translocated cases in a general molecular portrait of 92 T-ALLs based on large-scale expression analysis shows that this rearrangement defines a new homogeneous subgroup, which shares common biologic networks with the TLX1- and TLX3-related cases.
  • Because T-ALLs derive from T-cell progenitors, expression profiles of the distinct T-ALL subgroups were analyzed with respect to those of normal human thymic subpopulations.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Differentiation / genetics. Child. Child, Preschool. Female. Gene Expression Profiling. Humans. Infant. Male. Middle Aged. Multigene Family. T-Lymphocytes / cytology. T-Lymphocytes / physiology

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  • (PMID = 15774621.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 157907-48-7 / HoxA protein
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6. Russell LJ, Akasaka T, Majid A, Sugimoto KJ, Loraine Karran E, Nagel I, Harder L, Claviez A, Gesk S, Moorman AV, Ross F, Mazzullo H, Strefford JC, Siebert R, Dyer MJ, Harrison CJ: t(6;14)(p22;q32): a new recurrent IGH@ translocation involving ID4 in B-cell precursor acute lymphoblastic leukemia (BCP-ALL). Blood; 2008 Jan 01;111(1):387-91
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(6;14)(p22;q32): a new recurrent IGH@ translocation involving ID4 in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • Translocations involving the immunoglobulin heavy chain locus (IGH@) at chromosome band 14q32 are common in mature B-cell neoplasms, but are rare in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • Here, we report the translocation, t(6;14)(p22;q32), involving IGH@ as a novel recurrent translocation in 13 BCP-ALL patients.
  • Preliminary survival data suggest that this subgroup may be associated with a good response to therapy.
  • [MeSH-major] Immunoglobulin Heavy Chains / genetics. Inhibitor of Differentiation Proteins / genetics. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Base Sequence. Child. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 6. Chromosomes, Human, Pair 9. Female. Gene Deletion. Genes, p16. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Molecular Sequence Data. PAX5 Transcription Factor / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 17940204.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ MC/ U132670597
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ID4 protein, human; 0 / Immunoglobulin Heavy Chains; 0 / Inhibitor of Differentiation Proteins; 0 / PAX5 Transcription Factor; 0 / PAX5 protein, human
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7. Owatari S, Uozumi K, Tokunaga M, Tokunaga M, Haraguchi K, Suzuki S, Arima N: Adult T-cell leukemia/lymphoma in a 21-year-old man. Clin Lab Haematol; 2006 Apr;28(2):141-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukemia/lymphoma in a 21-year-old man.
  • Adult T-cell leukemia/lymphoma (ATL) is malignancy of mature T cells that caused by infection with human T-cell leukemia virus type I (HTLV-I).
  • Leukemogenesis of ATL cells considered to involve a multistep oncogenic process, resulting in a very long latency period.
  • But, we report here the case of a 21-year-old man having suffered from recurrent stomatititis who has already developed acute-type ATL.
  • ATL generally occurs after a long latency period, and the present case in a young man is thus very rare.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis
  • [MeSH-minor] Adult. Blotting, Southern. HTLV-I Antibodies / blood. Humans. Male

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  • (PMID = 16630222.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HTLV-I Antibodies
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8. Nakashima Y, Tagawa H, Suzuki R, Karnan S, Karube K, Ohshima K, Muta K, Nawata H, Morishima Y, Nakamura S, Seto M: Genome-wide array-based comparative genomic hybridization of natural killer cell lymphoma/leukemia: different genomic alteration patterns of aggressive NK-cell leukemia and extranodal Nk/T-cell lymphoma, nasal type. Genes Chromosomes Cancer; 2005 Nov;44(3):247-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genome-wide array-based comparative genomic hybridization of natural killer cell lymphoma/leukemia: different genomic alteration patterns of aggressive NK-cell leukemia and extranodal Nk/T-cell lymphoma, nasal type.
  • Natural killer (NK) cell lymphomas/leukemias are highly aggressive lymphoid malignancies, but little is known about their genomic alterations, and thus there is an urgent need for identification and analysis of NK cell lymphomas/leukemias.
  • We performed an array CGH analysis for 27 NK-cell lymphoma/leukemia cases that were classified into two disease groups based on the World Health Organization Classification (10 aggressive NK-cell leukemia cases and 17 extranodal NK/T-cell [NK/T] lymphomas, nasal type).
  • The recurrent regions characteristic of the aggressive NK-cell leukemia group compared with those of the extranodal NK/T lymphoma, nasal-type group, were gain of 1q and loss of 7p15.1-p22.3 and 17p13.1.
  • Recurrent regions characteristic of the extranodal NK/T lymphoma, nasal-type group, compared with those of the other group were gain of 2q, and loss of 6q16.1-q27, 11q22.3-q23.3, 5p14.1-p14.3, 5q34-q35.3, 1p36.23-p36.33, 2p16.1-p16.3, 4q12, and 4q31.3-q32.1.
  • Our results can be expected to provide further insights into the genetic basis of lymphomagenesis and the clinicopathologic features of NK-cell lymphomas/leukemias.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human / genetics. Genome, Human. Killer Cells, Natural / pathology. Leukemia, T-Cell / genetics. Lymphoma, T-Cell / genetics. Nose Neoplasms / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Chromosomes, Artificial, Bacterial. DNA, Neoplasm / analysis. Female. Humans. Immunoenzyme Techniques. Karyotyping. Male. Middle Aged. Nucleic Acid Hybridization

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16049916.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
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9. Metzgeroth G, Walz C, Score J, Siebert R, Schnittger S, Haferlach C, Popp H, Haferlach T, Erben P, Mix J, Müller MC, Beneke H, Müller L, Del Valle F, Aulitzky WE, Wittkowsky G, Schmitz N, Schulte C, Müller-Hermelink K, Hodges E, Whittaker SJ, Diecker F, Döhner H, Schuld P, Hehlmann R, Hochhaus A, Cross NC, Reiter A: Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma. Leukemia; 2007 Jun;21(6):1183-8
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  • [Title] Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma.
  • The FIP1L1-PDGFRA fusion gene has been described in patients with eosinophilia-associated myeloproliferative disorders (Eos-MPD).
  • Here, we report on seven FIP1L1-PDGFRA-positive patients who presented with acute myeloid leukemia (AML, n=5) or lymphoblastic T-cell non-Hodgkin-lymphoma (n=2) in conjunction with AML or Eos-MPD.
  • Patients were treated with imatinib (100 mg, n=5; 400 mg, n=2) either as monotherapy (n=2), as maintenance treatment after intensive chemotherapy (n=3) or in overt relapse 43 and 72 months, respectively, after primary diagnosis and treatment of FIP1L1-PDGFRA-positive disease (n=2).
  • We conclude that all eosinophilia-associated hematological malignancies should be screened for the presence of the FIP1L1-PDGFRA fusion gene as they are excellent candidates for treatment with tyrosine kinase inhibitors even if they present with an aggressive phenotype such as AML.
  • [MeSH-major] Eosinophilia / drug therapy. Leukemia, Myeloid / drug therapy. Oncogene Proteins, Fusion / analysis. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha. mRNA Cleavage and Polyadenylation Factors
  • [MeSH-minor] Acute Disease. Adult. Aged. Benzamides. Disease-Free Survival. Humans. Imatinib Mesylate. Male. Middle Aged. Myeloproliferative Disorders / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction / methods


10. van Vlierberghe P, Meijerink JP, Lee C, Ferrando AA, Look AT, van Wering ER, Beverloo HB, Aster JC, Pieters R: A new recurrent 9q34 duplication in pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2006 Jul;20(7):1245-53
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  • [Title] A new recurrent 9q34 duplication in pediatric T-cell acute lymphoblastic leukemia.
  • Over the last decade, genetic characterization of T-cell acute lymphoblastic leukemia (T-ALL) has led to the identification of a variety of chromosomal abnormalities.
  • In this study, we used array-comparative genome hybridization (array-CGH) and identified a novel recurrent 9q34 amplification in 33% (12/36) of pediatric T-ALL samples, which is therefore one of the most frequent cytogenetic abnormalities observed in T-ALL thus far.
  • Fluorescence in situ hybridization (FISH) analysis revealed that this 9q34 amplification was in fact a 9q34 duplication on one chromosome and could be identified in 17-39 percent of leukemic cells at diagnosis.
  • Although this leukemic subclone did not predict for poor outcome, leukemic cells carrying this duplication were still present at relapse, indicating that these cells survived chemotherapeutic treatment.
  • [MeSH-major] Chromosomes, Human, Pair 9. Gene Duplication. Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 16673019.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / NUP214-ABL1 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1
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11. Fujiwara SI, Yamashita Y, Nakamura N, Choi YL, Ueno T, Watanabe H, Kurashina K, Soda M, Enomoto M, Hatanaka H, Takada S, Abe M, Ozawa K, Mano H: High-resolution analysis of chromosome copy number alterations in angioimmunoblastic T-cell lymphoma and peripheral T-cell lymphoma, unspecified, with single nucleotide polymorphism-typing microarrays. Leukemia; 2008 Oct;22(10):1891-8
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  • [Title] High-resolution analysis of chromosome copy number alterations in angioimmunoblastic T-cell lymphoma and peripheral T-cell lymphoma, unspecified, with single nucleotide polymorphism-typing microarrays.
  • Angioimmunoblastic T-cell lymphoma (AILT) and peripheral T-cell lymphoma, unspecified (PTCL-u) are relatively frequent subtypes of T- or natural killer cell lymphoma.
  • To characterize the structural anomalies of chromosomes associated with these disorders, we here determined chromosome copy number alterations (CNAs) and loss of heterozygosity (LOH) at >55,000 single nucleotide polymorphism loci for clinical specimens of AILT (n=40) or PTCL-u (n=33).
  • Recurrent copy number gain common to both conditions was detected on chromosomes 8, 9 and 19, whereas common LOH was most frequent for a region of chromosome 2.
  • [MeSH-major] Chromosome Aberrations. Loss of Heterozygosity. Lymphoma, T-Cell / genetics. Lymphoma, T-Cell, Peripheral / genetics. Oligonucleotide Array Sequence Analysis. Polymorphism, Single Nucleotide
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. CARD Signaling Adaptor Proteins / genetics. DNA-Binding Proteins / genetics. Female. Guanylate Cyclase / genetics. Humans. Ikaros Transcription Factor / genetics. Male. Middle Aged. Neprilysin / analysis. Prognosis. Transcription Factors / genetics

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  • (PMID = 18633432.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CARD Signaling Adaptor Proteins; 0 / DNA-Binding Proteins; 0 / IKZF2 protein, human; 0 / MYCBP protein, human; 0 / Transcription Factors; 148971-36-2 / Ikaros Transcription Factor; EC 3.4.24.11 / Neprilysin; EC 4.6.1.2 / CARD11 protein, human; EC 4.6.1.2 / Guanylate Cyclase
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12. De Keersmaecker K, Marynen P, Cools J: Genetic insights in the pathogenesis of T-cell acute lymphoblastic leukemia. Haematologica; 2005 Aug;90(8):1116-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic insights in the pathogenesis of T-cell acute lymphoblastic leukemia.
  • Over the past 20 years, a large number of genes involved in the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL) has been identified by molecular characterization of recurrent chromosomal aberrations and more subtle genetic defects.
  • When reviewing the current list of oncogenes and tumor suppressor genes, it becomes clear that these can be grouped into four classes of mutations, which are involved in: (i) cell cycle deregulation;.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics

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  • (PMID = 16079112.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Number-of-references] 129
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13. Jarosova M, Urbankova H, Plachy R, Papajik T, Holzerova M, Balcarkova J, Pikalova Z, Divoky V, Indrak K: Gain of chromosome 2p in chronic lymphocytic leukemia: significant heterogeneity and a new recurrent dicentric rearrangement. Leuk Lymphoma; 2010 Feb;51(2):304-13
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  • [Title] Gain of chromosome 2p in chronic lymphocytic leukemia: significant heterogeneity and a new recurrent dicentric rearrangement.
  • Array-based comparative genomic hybridization (arrayCGH) studies in chronic lymphocytic leukemia (CLL) have revealed novel recurrent chromosomal imbalances, such as a gain of chromosome 2p.
  • We revealed significant heterogeneity of the region of gain on 2p in CLL, including a new recurrent aberration: the dicentric chromosome, dic(2;18).
  • In our cases, the region of gain involved three genes (MYCN, REL, and ALK) and was associated with an unmutated IgVH status in 14 out of 16 cases.
  • [MeSH-major] Centromere / genetics. Chromosome Aberrations. Chromosomes, Human, Pair 2 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics
  • [MeSH-minor] Adult. Aged. Comparative Genomic Hybridization. Female. Genetic Heterogeneity. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged

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  • [CommentIn] Leuk Lymphoma. 2010 Feb;51(2):186-7 [20109070.001]
  • (PMID = 20078324.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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14. Li S: Anaplastic lymphoma kinase-positive large B-cell lymphoma: a distinct clinicopathological entity. Int J Clin Exp Pathol; 2009;2(6):508-18
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  • [Title] Anaplastic lymphoma kinase-positive large B-cell lymphoma: a distinct clinicopathological entity.
  • Anaplastic lymphoma kinase-positive large B-cell lymphoma (ALK(+) LBCL) represents a distinct subtype of mature B-cell neoplasms in the most recent WHO classification of hematolymphoid neoplasms.
  • It has a characteristic immunoblastic/plasmablastic morphology, a distinct immunophenotypic profile and recurrent cytogenetic/molecular genetic abnormalities, and has been reported in both the adult and pediatric populations.
  • With the advent of new ALK inhibitors for possible targeted therapy clinical trials, it is important to recognize this new entity, particularly in the pediatric population because the prognosis is worse than the more common ALK+ anaplastic large cell lymphoma.

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  • (PMID = 19636398.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2713458
  • [Keywords] NOTNLM ; ALK / Anaplastic lymphoma kinase / CLTC/ALK / diffuse large B-cell lymphoma / t(2;17)
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15. Gorello P, La Starza R, Varasano E, Chiaretti S, Elia L, Pierini V, Barba G, Brandimarte L, Crescenzi B, Vitale A, Messina M, Grammatico S, Mancini M, Matteucci C, Bardi A, Guarini A, Martelli MF, Foà R, Mecucci C: Combined interphase fluorescence in situ hybridization elucidates the genetic heterogeneity of T-cell acute lymphoblastic leukemia in adults. Haematologica; 2010 Jan;95(1):79-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined interphase fluorescence in situ hybridization elucidates the genetic heterogeneity of T-cell acute lymphoblastic leukemia in adults.
  • BACKGROUND: Molecular lesions in T-cell acute lymphoblastic leukemias affect regulators of cell cycle, proliferation, differentiation, survival and apoptosis in multi-step pathogenic pathways.
  • DESIGN AND METHODS: We designed a combined interphase fluorescence in situ hybridization strategy to study 25 oncogenes/tumor suppressor genes in T-cell acute lymphoblastic leukemias and applied it in 23 adult patients for whom immunophenotyping, karyotyping, molecular studies, and gene expression profiling data were available.
  • The results were confirmed and integrated with those of multiplex-polymerase chain reaction analysis and gene expression profiling in another 129 adults with T-cell acute lymphoblastic leukemias.
  • It found abnormalities known to be associated with T-cell acute lymphoblastic leukemias, i.e.
  • CDKN2A-B/9p21 and GRIK2/6q16 deletions, TCR and TLX3 rearrangements, SIL-TAL1, CALM-AF10, MLL-translocations, del(17)(q12)/NF1 and other cryptic genomic imbalances, i.e.
  • 9q34, 11p, 12p, and 17q11 duplication, del(5)(q35), del(7)(q34), del(9)(q34), del(12)(p13), and del(14)(q11).
  • In two cases with cryptic del(9)(q34), fluorescence in situ hybridization and reverse transcriptase polymerase chain reaction detected the TAF_INUP214 fusion and gene expression profiling identified a signature characterized by HOXA and NUP214 upregulation and TAF_I, FNBP1, C9orf78, and USP20 down-regulation.
  • Multiplex-polymerase chain reaction analysis and gene expression profiling of 129 further cases found five additional cases of TAF_I-NUP214-positive T-cell acute lymphoblastic leukemia.
  • CONCLUSIONS: Our combined interphase fluorescence in situ hybridization strategy greatly improved the detection of genetic abnormalities in adult T-cell acute lymphoblastic leukemias.
  • The estimated incidence of TAF_I-NUP214, a new recurrent fusion in adult T-cell acute lymphoblastic leukemias, was 4.6% (7/152).
  • [MeSH-major] Comparative Genomic Hybridization. Genetic Heterogeneity. In Situ Hybridization, Fluorescence. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Adolescent. Adult. Age Factors. Female. Gene Expression Profiling / methods. Humans. Male. Middle Aged. Mutation / genetics. Young Adult

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  • (PMID = 20065082.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2805748
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16. Yin CC, Abruzzo LV, Qiu X, Apostolidou E, Cortes JE, Medeiros LJ, Lu G: del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia. Cancer Genet Cytogenet; 2009 Jul;192(1):18-23
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  • [Title] del(15q) is a recurrent minor-route cytogenetic abnormality in the clonal evolution of chronic myelogenous leukemia.
  • The del(15q) chromosomal abnormality is known to occur in acute leukemias, but has rarely been described in chronic myelogenous leukemia (CML).
  • Described here are five cases of CML associated with del(15q): four men and one woman.
  • Bone marrow aspirate smears showed increased blasts in all cases at the time of del(15q) detection, in accelerated phase in two cases and myeloid blast phase in three.
  • Conventional cytogenetic analysis showed t(9;22) and del(15q), as well as other inconsistent clonal abnormalities.
  • All patients received imatinib mesylate; four received additional chemotherapy, and two had allogeneic stem cell transplantation (ASCT).
  • Of the three patients who did not receive ASCT, one died, one was in persistent blast phase, and one was in clinical remission with molecular evidence of residual disease at 16, 6, and 34 months, respectively, after identification of the del(15q).
  • Of the two patients who had ASCT, one died and one was in clinical remission with molecular evidence of disease at 15 and 64 months, respectively, after identification of the del(15q).
  • These findings indicate that del(15q) is a recurrent cytogenetic abnormality that may be seen at initial presentation of advanced disease or may emerge during disease progression.
  • Del(15q) appears to be associated with a poor prognosis in CML.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 15. Clone Cells / pathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • [MeSH-minor] Adult. Bone Marrow Cells / pathology. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Chromosome Aberrations. Female. Follow-Up Studies. Gene Frequency. Humans. Karyotyping. Male. Middle Aged

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  • (PMID = 19480932.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS627187; NLM/ PMC4167428
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17. Elstrom RL, Martin P, Ostrow K, Barrientos J, Chadburn A, Furman R, Ruan J, Shore T, Schuster M, Cerchietti L, Melnick A, Coleman M, Leonard JP: Response to second-line therapy defines the potential for cure in patients with recurrent diffuse large B-cell lymphoma: implications for the development of novel therapeutic strategies. Clin Lymphoma Myeloma Leuk; 2010 Jun;10(3):192-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Response to second-line therapy defines the potential for cure in patients with recurrent diffuse large B-cell lymphoma: implications for the development of novel therapeutic strategies.
  • BACKGROUND: Patients with diffuse large B-cell lymphoma (DLBCL) who are not cured by initial therapy sometimes experience disease-free survival after autologous stem cell transplantation.
  • PATIENTS AND METHODS: We identified patients with relapsed or refractory DLBCL at Weill Cornell Medical Center for whom data on responses to second-line chemotherapy were available.
  • RESULTS: A total of 74 patients with relapsed or refractory DLBCL who underwent second-line chemotherapy between 1996 and 2007 were identified.
  • CONCLUSION: Our data demonstrate that patients with recurrent DLBCL not responding to second-line chemotherapy demonstrate dismal outcomes.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / surgery. Neoplasm Recurrence, Local / surgery. Salvage Therapy / methods
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Female. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Prognosis. Stem Cell Transplantation. Treatment Outcome. Young Adult

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  • (PMID = 20511164.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Lowe T, Luu T, Shen J, Bhatia S, Shibata S, Stein A, Somlo G: Male breast cancer 15 years after allogeneic hematopoietic cell transplantation including total body irradiation for recurrent acute lymphoblastic leukemia. Onkologie; 2008 May;31(5):266-9
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  • [Title] Male breast cancer 15 years after allogeneic hematopoietic cell transplantation including total body irradiation for recurrent acute lymphoblastic leukemia.
  • CASE REPORTS: We report here the case of a 34-year-old man who developed stage IIB node-positive breast cancer almost 15 years following total body irradiation and allogeneic hematopoietic cell transplantation for acute lymphoblastic leukemia.
  • [MeSH-major] Breast Neoplasms, Male / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Neoplasms, Radiation-Induced / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Whole-Body Irradiation / adverse effects
  • [MeSH-minor] Adult. Humans. Longitudinal Studies. Male. Neoplasm Recurrence, Local


19. Speleman F, Cauwelier B, Dastugue N, Cools J, Verhasselt B, Poppe B, Van Roy N, Vandesompele J, Graux C, Uyttebroeck A, Boogaerts M, De Moerloose B, Benoit Y, Selleslag D, Billiet J, Robert A, Huguet F, Vandenberghe P, De Paepe A, Marynen P, Hagemeijer A: A new recurrent inversion, inv(7)(p15q34), leads to transcriptional activation of HOXA10 and HOXA11 in a subset of T-cell acute lymphoblastic leukemias. Leukemia; 2005 Mar;19(3):358-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new recurrent inversion, inv(7)(p15q34), leads to transcriptional activation of HOXA10 and HOXA11 in a subset of T-cell acute lymphoblastic leukemias.
  • Chromosomal translocations with breakpoints in T-cell receptor (TCR) genes are recurrent in T-cell malignancies.
  • These translocations involve the TCRalphadelta gene (14q11), the TCRbeta gene (7q34) and to a lesser extent the TCRgamma gene at chromosomal band 7p14 and juxtapose T-cell oncogenes next to TCR regulatory sequences leading to deregulated expression of those oncogenes.
  • Here, we describe a new recurrent chromosomal inversion of chromosome 7, inv(7)(p15q34), in a subset of patients with T-cell acute lymphoblastic leukemia characterized by CD2 negative and CD4 positive, CD8 negative blasts.
  • This is the first report of a recurrent chromosome rearrangement targeting the HOXA gene cluster in T-cell malignancies resulting in deregulated HOXA gene expression (particularly HOXA10 and HOXA11) and is in keeping with a previous report suggesting HOXA deregulation in MLL-rearranged T- and B cell lymphoblastic leukemia as the key factor in leukaemic transformation.
  • [MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 7 / genetics. DNA-Binding Proteins / genetics. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Transcriptional Activation / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Cytogenetic Analysis. Female. Gene Expression Regulation, Neoplastic. Gene Rearrangement, T-Lymphocyte / genetics. Humans. Immunophenotyping. Male. Middle Aged. Translocation, Genetic / genetics

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  • (PMID = 15674412.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / HOXA11 protein, human; 0 / Homeodomain Proteins; 140441-81-2 / HOXA10 protein, human
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20. Jung SI, Cho HS, Lee CH, Jung BC: A case of adult B lymphoblastic leukemia with ider(9)(q10)t(9;22)(q34;q11.2) and der(19)t(1;19)(q23;p13.3). Korean J Lab Med; 2010 Dec;30(6):585-90

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of adult B lymphoblastic leukemia with ider(9)(q10)t(9;22)(q34;q11.2) and der(19)t(1;19)(q23;p13.3).
  • In B lymphoblastic leukemia/lymphoma (B-ALL/LBL), t(9;22)(q34;q11.2) and t(1;19)(q23;p13.3) are recurrent cytogenetic abnormalities.
  • Here, we report a case of adult B-ALL with ider(9)(q10)t(9;22)(q34;q11.2) and der(19)t(1;19)(q23;p13.3).
  • This abnormality is specific to precursor B-lymphoid neoplasms, such as B-ALL or B-lymphoid blast phase of CML, and is associated with disease progression or short survival.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Translocation, Genetic

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  • (PMID = 21157143.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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21. Sinclair P, Harrison CJ, Jarosová M, Foroni L: Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36). Haematologica; 2005 May;90(5):602-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36).
  • BACKGROUND AND OBJECTIVES: Many clinically important oncogenes and tumor suppressor genes have been identified through analysis of recurrent chromosomal rearrangements in acute leukemia.
  • In this study we investigated the significance of novel translocations and inversions of 6q in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).
  • RESULTS: Six of seven breakpoints in ALL and two in a single case of AML were localized to within a 10.5 Mb hotspot at 6q22-q23 with five analyzed to the level of a single probe.
  • INTERPRETATION AND CONCLUSIONS: We identified a new primary recurrent translocation t(6;7) (q22;q23 through q26) in pediatric T-ALL.
  • Other translocations interrupting the 6q22-q23 breakpoint cluster region did not appear to be recurrent and may contribute to leukemogenesis through a novel mechanism.
  • [MeSH-major] Chromosome Breakage. Chromosome Inversion / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Genes, myb. Leukemia, Myeloid / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Acute Disease. Adaptor Proteins, Signal Transducing / genetics. Adolescent. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Banding. Clone Cells / pathology. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 15921375.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AHI1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Oncogene Proteins, Fusion
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22. Le QH, Thomas X, Ecochard R, Iwaz J, Lhéritier V, Michallet M, Fiere D: Proportion of long-term event-free survivors and lifetime of adult patients not cured after a standard acute lymphoblastic leukemia therapeutic program: adult acute lymphoblastic leukemia-94 trial. Cancer; 2007 May 15;109(10):2058-67
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  • [Title] Proportion of long-term event-free survivors and lifetime of adult patients not cured after a standard acute lymphoblastic leukemia therapeutic program: adult acute lymphoblastic leukemia-94 trial.
  • BACKGROUND: In adult acute lymphoblastic leukemia, treatment results generally are expressed in terms of overall survival or disease-free survival at 3 years.
  • In this investigation, the authors attempted to express the results in terms of the proportion of long-term disease-free survivors and in terms of lifetime in patients who developed recurrent disease or died.
  • METHODS: Univariate and multivariate analyses were used to assess the influence of different covariates on the 2 result criteria in 922 participants in the Adult Acute Lymphoblastic Leukemia-94 multicenter trial.
  • The proportion decreased with increasing age, white blood cell count, and lactate dehydrogenase level.
  • It was longer in men than in women and was shorter with increasing age, performance status, hemoglobin level, and white blood cell count.
  • CONCLUSIONS: The results of this study highlighted and specified the importance of some classic prognostic factors in patients with acute lymphoblastic leukemia.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Female. Follow-Up Studies. Genes, abl / genetics. Humans. Karyotyping. L-Lactate Dehydrogenase / blood. Leukocyte Count. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Odds Ratio. Oncogene Proteins, Fusion / genetics. Prognosis. Risk Factors. Survival Rate. Treatment Failure

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  • [Copyright] (c) 2007 American Cancer Society
  • (PMID = 17407135.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL-AF4 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 1.1.1.27 / L-Lactate Dehydrogenase
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23. Tanvetyanon T, Stiff PJ: Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations. Leuk Lymphoma; 2005 Jan;46(1):151-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations.
  • However, to date, recurrent acute pancreatitis has never been described in association with MDS.
  • Finally, his MDS transformed into acute myeloid leukemia (AML); severe acute pancreatitis closely accompanied.
  • A subsequent pancreatitis attack with pseudocyst formation occurred, but again was controlled with corticosteroids, although this was followed closely by another relapse of AML.
  • All etiologies for recurrent acute pancreatitis were ruled out.
  • [MeSH-minor] Abdomen / pathology. Adult. Cell Transformation, Neoplastic. Humans. Male. Recurrence. Time Factors


24. Pan J, Xue Y, Wu Y, Wang Y, Shen J: Dicentric (7;9)(p11;p11) is a rare but recurrent abnormality in acute lymphoblastic leukemia: a study of 7 cases. Cancer Genet Cytogenet; 2006 Sep;169(2):159-63
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  • [Title] Dicentric (7;9)(p11;p11) is a rare but recurrent abnormality in acute lymphoblastic leukemia: a study of 7 cases.
  • A clinical and experimental study of acute lymphoblastic leukemia (ALL) with a dic(7;9)(p11;p11) included 7 patients (5 males and 2 females) with a median age of 32 years.
  • We consider the dic(7;9) a rare but recurrent abnormality, which may represent a distinct cytogenetic subgroup in B-ALL.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 9. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Centromere. Child. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged

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  • (PMID = 16938575.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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25. Hori T, Suzuki N, Mizue N, Hatakeyama N, Takamuro M, Tsutsumi H: Relapse of T-cell all after stem cell transplant presenting as hypertrophic cardiomyopathy: the value of non-invasive diagnostic imaging in detecting cardiac leukemia. Pediatr Blood Cancer; 2006 Jan;46(1):108-11
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  • [Title] Relapse of T-cell all after stem cell transplant presenting as hypertrophic cardiomyopathy: the value of non-invasive diagnostic imaging in detecting cardiac leukemia.
  • We describe a 14-year-old female with acute lymphoblastic leukemia (ALL) with a mediastinal mass at diagnosis who developed hypertrophic cardiomyopathy (HC) after stem cell transplantation (SCT).
  • During refractory relapse after SCT using bone marrow from her HLA-matched sibling, she underwent whole thorax irradiation because of pleural effusion and a recurrent mediastinal mass.
  • However, isolated cardiac relapse was finally diagnosed by several non-invasive imaging techniques.
  • [MeSH-major] Cardiomyopathy, Hypertrophic / etiology. Diagnostic Imaging. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration. Myocardium / pathology
  • [MeSH-minor] Adolescent. Female. Humans. Magnetic Resonance Imaging. Recurrence. Stem Cell Transplantation. Tomography, X-Ray Computed

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  • (PMID = 16078227.001).
  • [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
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26. Clappier E, Cuccuini W, Kalota A, Crinquette A, Cayuela JM, Dik WA, Langerak AW, Montpellier B, Nadel B, Walrafen P, Delattre O, Aurias A, Leblanc T, Dombret H, Gewirtz AM, Baruchel A, Sigaux F, Soulier J: The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children. Blood; 2007 Aug 15;110(4):1251-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children.
  • The C-Myb transcription factor is essential for hematopoiesis, including in the T-cell lineage.
  • The C-Myb locus is a common site of retroviral insertional mutagenesis, however no recurrent genomic involvement has been reported in human malignancies.
  • Here, we identified 2 types of genomic alterations involving the C-MYB locus at 6q23 in human T-cell acute leukemia (T-ALL).
  • Strikingly, profiling of the T-ALLs by clinical, genomic, and large-scale gene expression analyses shows that the TCRB-MYB translocation defines a new T-ALL subtype associated with a very young age for T-cell leukemia (median, 2.2 years) and with a proliferation/mitosis expression signature.
  • By contrast, the MYB(dup) alteration was associated with the previously defined T-ALL subtypes.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Proto-Oncogene Proteins c-myb / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Base Sequence. Child. Child, Preschool. Female. Gene Dosage. Gene Expression Profiling. Genome, Human. Humans. Infant. Male. Middle Aged. Molecular Sequence Data. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Sequence Homology, Nucleic Acid

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  • (PMID = 17452517.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA101859
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb
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27. Balgobind BV, Van Vlierberghe P, van den Ouweland AM, Beverloo HB, Terlouw-Kromosoeto JN, van Wering ER, Reinhardt D, Horstmann M, Kaspers GJ, Pieters R, Zwaan CM, Van den Heuvel-Eibrink MM, Meijerink JP: Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis. Blood; 2008 Apr 15;111(8):4322-8
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  • [Title] Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis.
  • Patients with NF1 have a higher risk to develop juvenile myelomonocytic leukemia (JMML) with a possible progression toward acute myeloid leukemia (AML).
  • In an oligo array comparative genomic hybridization-based screening of 103 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL) and 71 patients with MLL-rearranged AML, a recurrent cryptic deletion, del(17)(q11.2), was identified in 3 patients with T-ALL and 2 patients with MLL-rearranged AML.
  • Mutation analysis in 4 of these del(17)(q11.2)-positive patients revealed that mutations in the remaining NF1 allele were present in 3 patients, confirming its role as a tumor-suppressor gene in cancer.
  • NF1 inactivation may provide an additional proliferative signal toward the development of leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation / genetics. Neurofibromatoses / genetics. Neurofibromin 1 / genetics

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  • (PMID = 18172006.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neurofibromin 1; 0 / RNA, Messenger
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28. Hamaki T, Kami M, Kanda Y, Yuji K, Inamoto Y, Kishi Y, Nakai K, Nakayama I, Murashige N, Abe Y, Ueda Y, Hino M, Inoue T, Ago H, Hidaka M, Hayashi T, Yamane T, Uoshima N, Miyakoshi S, Taniguchi S: Reduced-intensity stem-cell transplantation for adult acute lymphoblastic leukemia: a retrospective study of 33 patients. Bone Marrow Transplant; 2005 Mar;35(6):549-56
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduced-intensity stem-cell transplantation for adult acute lymphoblastic leukemia: a retrospective study of 33 patients.
  • Efficacy of reduced-intensity stem-cell transplantation (RIST) for acute lymphoblastic leukemia (ALL) was investigated in 33 patients (median age, 55 years).
  • Disease status at RIST was first remission (n=13), second remission (n=6), and induction failure or relapse (n=14).
  • Six patients received donor lymphocyte infusion (DLI), for prophylaxis (n=1) or treatment of recurrent ALL (n=5).
  • The 1-year relapse-free and overall survival rates were 29.8 and 39.6%, respectively.
  • Of the 14 patients transplanted in relapse, five remained relapse free for longer than 6 months.
  • These findings suggest the presence of a graft-versus-leukemia effect for ALL.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Graft Survival. Graft vs Host Disease. Humans. Male. Middle Aged. Retrospective Studies. Risk Factors. Survival Analysis. Transplantation Conditioning / methods. Treatment Outcome

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  • (PMID = 15756282.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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29. Robak T, Smolewski P, Cebula B, Szmigielska-Kaplon A, Chojnowski K, Blonski JZ: Rituximab combined with cladribine or with cladribine and cyclophosphamide in heavily pretreated patients with indolent lymphoproliferative disorders and mantle cell lymphoma. Cancer; 2006 Oct 1;107(7):1542-50
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  • [Title] Rituximab combined with cladribine or with cladribine and cyclophosphamide in heavily pretreated patients with indolent lymphoproliferative disorders and mantle cell lymphoma.
  • Fifty-four adult patients with recurrent or refractory, low-grade non-Hodgkin lymphoma (LG-NHL) and B-cell chronic lymphocytic leukemia (B-CLL) were treated according to the RC/RCC regimens.
  • RESULTS: Thirty-three patients with B-CLL, 12 patients with LG-NHL and 9 patients with mantle cell lymphoma (MCL) entered the study.
  • Thirty-three patients (61%) had recurrent disease after prior therapy, and 21 patients (39%) had refractory disease.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols. Cladribine / therapeutic use. Cyclophosphamide / therapeutic use. Lymphoma, Mantle-Cell / drug therapy. Lymphoproliferative Disorders / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Murine-Derived. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. Rituximab. Treatment Outcome

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 16948126.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 47M74X9YT5 / Cladribine; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide
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30. Huang Y, de Reyniès A, de Leval L, Ghazi B, Martin-Garcia N, Travert M, Bosq J, Brière J, Petit B, Thomas E, Coppo P, Marafioti T, Emile JF, Delfau-Larue MH, Schmitt C, Gaulard P: Gene expression profiling identifies emerging oncogenic pathways operating in extranodal NK/T-cell lymphoma, nasal type. Blood; 2010 Feb 11;115(6):1226-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene expression profiling identifies emerging oncogenic pathways operating in extranodal NK/T-cell lymphoma, nasal type.
  • Biopsies and cell lines of natural killer/T-cell lymphoma, nasal type (NKTCL) were subject to combined gene expression profiling and array-based comparative genomic hybridization analyses.
  • Compared with peripheral T-cell lymphoma, not otherwise specified, NKTCL had greater transcript levels for NK-cell and cytotoxic molecules, especially granzyme H.
  • Notably, platelet-derived growth factor receptor alpha and its phosphorylated form were confirmed at the protein level, and in vitro the MEC04 NKTCL cell line was sensitive to imatinib.
  • Deregulation of the AKT, Janus kinase-signal transducers and activators of transcription, and nuclear factor-kappaB pathways was corroborated by nuclear expression of phosphorylated AKT, signal transducers and activators of transcription 3, and RelA in NKTCL, and several deregulated genes in these pathways mapped to regions of recurrent copy number aberrations (AKT3 [1q44], IL6R [1q21.3], CCL2 [17q12], TNFRSF21 [6p12.3]).
  • [MeSH-major] Epstein-Barr Virus Infections / genetics. Gene Expression Profiling. Killer Cells, Natural / pathology. Lymphoma, Extranodal NK-T-Cell / genetics. Nasopharyngeal Neoplasms / genetics. Oncogenes / physiology
  • [MeSH-minor] Adult. Aged. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Blotting, Western. Cell Proliferation. Cells, Cultured. Comparative Genomic Hybridization. Female. Herpesvirus 4, Human / physiology. Humans. Immunoenzyme Techniques. Male. Middle Aged. Nasal Mucosa / metabolism. Nasal Mucosa / pathology. Oligonucleotide Array Sequence Analysis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, Platelet-Derived Growth Factor / genetics. Receptors, Platelet-Derived Growth Factor / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Ubiquitin-Protein Ligases / genetics. Ubiquitin-Protein Ligases / metabolism


31. Gong H, Liu WL, Zhou JF, Xu HZ: [Expression of mitosis checkpoint gene CHFR in acute leukemia]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1085-8
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  • [Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].
  • OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.
  • METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
  • The cell cycle was examined by flow cytometric analysis.
  • (1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
  • CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.
  • Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 16029562.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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32. van Grotel M, Meijerink JP, Beverloo HB, Langerak AW, Buys-Gladdines JG, Schneider P, Poulsen TS, den Boer ML, Horstmann M, Kamps WA, Veerman AJ, van Wering ER, van Noesel MM, Pieters R: The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols. Haematologica; 2006 Sep;91(9):1212-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The outcome of molecular-cytogenetic subgroups in pediatric T-cell acute lymphoblastic leukemia: a retrospective study of patients treated according to DCOG or COALL protocols.
  • BACKGROUND AND OBJECTIVES: Subgroups of T-cell acute lymphoblastic leukemia (T-ALL), defined according to recurrent cytogenetic aberrations, may have different prognoses.
  • RESULTS: In our cohort study, CALM-AF10 was associated with an immature immunophenotype and poor outcome (p=0.005).
  • HOX11L2 was associated with both immunophenotypically immature cases as well as cases committed to the gammadelta-lineage.
  • HOX11L2 was significantly associated with poor outcome (p=0.01), independently of the expression of CD1 or the presence of NOTCH1 mutations.
  • TAL1 abnormalities were associated with alphabeta-lineage commitment, and tended to be associated with a good outcome.
  • In relation to the expression of early T-cell transcription factors, high TAL1 levels were found in immunophenotypically-advanced cases, whereas high LYL1 levels were found in immature subgroups.
  • In our cohort, this cytogenetic aberration was associated with a poor outcome.
  • Our data on CALM-AF10 rearranged T-ALL, albeit based on only three patients, suggest that this type of leukemia is associated with a poor outcome.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Cytogenetic Analysis. Leukemia-Lymphoma, Adult T-Cell / diagnosis

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  • [CommentIn] Haematologica. 2006 Sep;91(9):1156A [16956809.001]
  • (PMID = 16956820.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / AF10-CALM fusion protein, human; 0 / Oncogene Proteins, Fusion
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33. Sandler ES, Homans A, Mandell L, Amylon M, Wall DA, Devidas M, Buchanan GR, Lipton JM, Billett AL: Hematopoietic stem cell transplantation after first marrow relapse of non-T, non-B acute lymphoblastic leukemia: a pediatric oncology group pilot feasibility study. J Pediatr Hematol Oncol; 2006 Apr;28(4):210-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematopoietic stem cell transplantation after first marrow relapse of non-T, non-B acute lymphoblastic leukemia: a pediatric oncology group pilot feasibility study.
  • BACKGROUND: Relapsed acute lymphoblastic leukemia (ALL) in children is associated with a poor outcome, especially for those patients whose relapse occurs during the first 36 months after diagnosis.
  • This study was designed to evaluate the feasibility of enrolling children with recurrent ALL in a standardized treatment protocol that included receipt of a hematopoietic stem cell transplant (HSCT).
  • PROCEDURE: Eligible patients with a bone marrow relapse of non-T, non-B ALL underwent a common induction and consolidation followed by receipt of either an allogeneic HSCT from a human leukocyte antigen (HLA)-identical sibling or an autologous HSCT purged with B-4 blocked ricin.
  • Fourteen patients did not receive a transplant during the study, because of toxicity (4), relapse (1), inadequate purging (1), and parental or physician preference for an alternative donor transplant (8).
  • CONCLUSION: We conclude that well designed and controlled prospective studies are necessary to define the role of HSCTs in children with recurrent ALL.
  • Autologous HSC transplantation may have a role in the treatment of relapsed ALL, but further studies are needed.
  • [MeSH-major] Bone Marrow / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols. Child. Child, Preschool. Female. Humans. Male. Pilot Projects. Recurrence. Treatment Outcome


34. Paulsson K, Cazier JB, Macdougall F, Stevens J, Stasevich I, Vrcelj N, Chaplin T, Lillington DM, Lister TA, Young BD: Microdeletions are a general feature of adult and adolescent acute lymphoblastic leukemia: Unexpected similarities with pediatric disease. Proc Natl Acad Sci U S A; 2008 May 06;105(18):6708-13
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  • [Title] Microdeletions are a general feature of adult and adolescent acute lymphoblastic leukemia: Unexpected similarities with pediatric disease.
  • We present here a genome-wide map of abnormalities found in diagnostic samples from 45 adults and adolescents with acute lymphoblastic leukemia (ALL).
  • Importantly, the pattern of deletions resembled that recently reported in pediatric ALL, suggesting that adult, adolescent, and childhood cases may be more similar on the genetic level than previously thought.
  • Furthermore, several genes not previously implicated in the pathogenesis of ALL were identified as possible recurrent targets of deletion.
  • Our findings provide insights into the leukemogenic process and may be clinically important in adult and adolescent ALL.
  • [MeSH-major] Gene Deletion. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. B-Lymphocytes / pathology. Cell Cycle / genetics. Child. Chromosome Aberrations. Genes, Neoplasm. Genome, Human / genetics. Humans. Lymphopoiesis / genetics. Middle Aged. Polymorphism, Single Nucleotide / genetics

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  • (PMID = 18458336.001).
  • [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
  • [Databank-accession-numbers] GEO/ GSE9611
  • [Grant] United Kingdom / Cancer Research UK / / CRUK/ A6438; United Kingdom / Cancer Research UK / / CRUK/ A6789
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2373322
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35. An Q, Wright SL, Moorman AV, Parker H, Griffiths M, Ross FM, Davies T, Harrison CJ, Strefford JC: Heterogeneous breakpoints in patients with acute lymphoblastic leukemia and the dic(9;20)(p11-13;q11) show recurrent involvement of genes at 20q11.21. Haematologica; 2009 Aug;94(8):1164-9
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  • [Title] Heterogeneous breakpoints in patients with acute lymphoblastic leukemia and the dic(9;20)(p11-13;q11) show recurrent involvement of genes at 20q11.21.
  • The dic(9;20)(p11-13;q11) is a recurrent chromosomal abnormality in patients with acute lymphoblastic leukemia.
  • From an initial cohort of 58 with acute lymphoblastic leukemia patients with this translocation, breakpoint mapping with fluorescence in situ hybridization on 26 of them revealed breakpoint heterogeneity of both chromosomes.
  • This study provides insight into the breakpoint complexity underlying dicentric chromosomal formation in acute lymphoblastic leukemia and highlights putative target gene loci.
  • [MeSH-major] Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. B-Cell-Specific Activator Protein / genetics. Base Sequence. Centromere / genetics. Child. Child, Preschool. Chromosome Breakage. Chromosome Mapping. Cohort Studies. Female. Genetic Heterogeneity. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Molecular Sequence Data. Nuclear Proteins / genetics. Recurrence. Repressor Proteins / genetics. Sequence Homology, Nucleic Acid. Transcription Factors / genetics. Young Adult

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  • (PMID = 19586940.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / ASXL1 protein, human; 0 / B-Cell-Specific Activator Protein; 0 / FRG1 protein, human; 0 / Nuclear Proteins; 0 / PAX5 protein, human; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / ZCCHC7 protein, human
  • [Other-IDs] NLM/ PMC2719040
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36. Burmeister T, Macleod RA, Reinhardt R, Mansmann V, Loddenkemper C, Marinets O, Drexler HG, Thiel E, Blau IW: A novel sporadic Burkitt lymphoma cell line (BLUE-1) with a unique t(6;20)(q15;q11.2) rearrangement. Leuk Res; 2006 Nov;30(11):1417-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel sporadic Burkitt lymphoma cell line (BLUE-1) with a unique t(6;20)(q15;q11.2) rearrangement.
  • We report the establishment and characterization, including HLA-typing, immunophenotypic and molecular cytogenetic analysis, of a novel EBV-negative cell line (BLUE-1) derived from adult relapsed sporadic Burkitt lymphoma.
  • BLUE-1 carries the pathognomonic t(8;14)(q24;q32) effecting MYC/IgHJ fusion and a novel t(6;20)(q15;q11.2) originally present in the patient, analysis of which may facilitate identification of gene target(s) of recurrent 6q rearrangements in B-cell neoplasia.
  • Our findings are discussed in light of the current understanding of endemic and sporadic Burkitt lymphoma.
  • BLUE-1 grows well in culture and should be a useful lymphoma research tool.
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Line, Tumor. Chromosomes, Human, Pair 20 / genetics. Chromosomes, Human, Pair 6 / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Cytogenetic Analysis / methods. HLA Antigens / genetics. Histocompatibility Testing. Humans. Immunohistochemistry. Immunophenotyping. Male. Oligonucleotide Array Sequence Analysis / methods

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  • (PMID = 16697040.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA Antigens
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37. Pan Q, Zhu YJ, Gu BW, Cai X, Bai XT, Yun HY, Zhu J, Chen B, Weng L, Chen Z, Xue YQ, Chen SJ: A new fusion gene NUP98-IQCG identified in an acute T-lymphoid/myeloid leukemia with a t(3;11)(q29q13;p15)del(3)(q29) translocation. Oncogene; 2008 May 29;27(24):3414-23
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  • [Title] A new fusion gene NUP98-IQCG identified in an acute T-lymphoid/myeloid leukemia with a t(3;11)(q29q13;p15)del(3)(q29) translocation.
  • NUP98 has been involved in multiple recurrent chromosome rearrangements in leukemia.
  • We identified a novel fusion between NUP98 and IQ motif containing G (IQCG) gene from a de novo acute T-lymphoid/myeloid leukemia harboring t(3;11)(q29q13;p15)del(3)(q29).
  • Expression of NUP98-IQCG inhibited 32Dcl3 cell apoptosis induced by Ara-C, and partially blocked granulocyte differentiation induced by G-CSF.
  • Taken together, our data indicate that newly identified NUP98-IQCG fusion protein may play an essential role in leukemogenesis, but by itself may not be sufficient to induce leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 3 / genetics. Leukemia, Myeloid, Acute / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Pore Complex Proteins / genetics. Recombinant Fusion Proteins / genetics. ras GTPase-Activating Proteins / genetics
  • [MeSH-minor] Adult. Amino Acid Sequence. Animals. Apoptosis. Base Sequence. Blotting, Western. COS Cells. Cell Differentiation. Cell Proliferation. Cell Survival. Cercopithecus aethiops. Fluorescent Antibody Technique. Humans. In Situ Hybridization, Fluorescence. Molecular Sequence Data. Phylogeny. Translocation, Genetic / genetics

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  • (PMID = 18084320.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IQ motif containing GTPase activating protein 1; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Recombinant Fusion Proteins; 0 / ras GTPase-Activating Proteins
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38. Moorman AV, Harrison CJ, Buck GA, Richards SM, Secker-Walker LM, Martineau M, Vance GH, Cherry AM, Higgins RR, Fielding AK, Foroni L, Paietta E, Tallman MS, Litzow MR, Wiernik PH, Rowe JM, Goldstone AH, Dewald GW, Adult Leukaemia Working Party, Medical Research Council/National Cancer Research Institute: Karyotype is an independent prognostic factor in adult acute lymphoblastic leukemia (ALL): analysis of cytogenetic data from patients treated on the Medical Research Council (MRC) UKALLXII/Eastern Cooperative Oncology Group (ECOG) 2993 trial. Blood; 2007 Apr 15;109(8):3189-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Karyotype is an independent prognostic factor in adult acute lymphoblastic leukemia (ALL): analysis of cytogenetic data from patients treated on the Medical Research Council (MRC) UKALLXII/Eastern Cooperative Oncology Group (ECOG) 2993 trial.
  • However, its usefulness in adult acute lymphoblastic leukemia (ALL) is generally limited to the presence of the Philadelphia (Ph) chromosome because of the low incidence of other recurrent abnormalities.
  • We present centrally reviewed cytogenetic data from 1522 adult patients enrolled on the Medical Research Council (MRC) UKALLXII/Eastern Cooperative Oncology Group (ECOG) 2993 trial.
  • Patients with a Ph chromosome, t(4;11)(q21;q23), t(8;14)(q24.1;q32), complex karyotype (5 or more chromosomal abnormalities), or low hypodiploidy/near triploidy (Ho-Tr) all had inferior rates of event-free and overall survival when compared with other patients.
  • In contrast, patients with high hyperdiploidy or a del(9p) had a significantly improved outcome.
  • Multivariate analysis demonstrated that the prognostic relevance of t(8;14), complex karyotype, and Ho-Tr was independent of sex, age, white cell count, and T-cell status among Ph-negative patients.
  • The observation that Ho-Tr and, for the first time, karyotype complexity confer an increased risk of treatment failure demonstrates that cytogenetic subgroups other than the Ph chromosome can and should be used to risk stratify adults with ALL in future trials.
  • [MeSH-major] Chromosome Deletion. Philadelphia Chromosome. Ploidies. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Disease-Free Survival. Humans. Karyotyping. Leukocyte Count. Multivariate Analysis. Risk Factors. Survival Rate. Treatment Failure

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  • (PMID = 17170120.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ MC/ U137686856
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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39. Fortune AF, Kelly K, Sargent J, O'Brien D, Quinn F, Chadwick N, Flynn C, Conneally E, Browne P, Crotty GM, Thornton P, Vandenberghe E: Large granular lymphocyte leukemia: natural history and response to treatment. Leuk Lymphoma; 2010 May;51(5):839-45
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  • [Title] Large granular lymphocyte leukemia: natural history and response to treatment.
  • Large granular lymphocyte leukemia (T-LGL) is an indolent T lymphoproliferative disorder that was difficult to diagnose with certainty until clonality testing of the T cell receptor gene became routinely available.
  • We studied the natural history and response to treatment in 25 consecutive patients with T-LGL diagnosed between 2004 and 2008 in which the diagnosis was confirmed by molecular analysis, to define an effective treatment algorithm.
  • The median age at diagnosis was 61 years (range 27-78), with a male to female ratio of 1:1.8 and presenting features of fatigue (n = 13), recurrent infections (n = 9), and/or abnormal blood counts (n = 5).
  • The overall survival (OS) and progression-free survival (PFS) 37 months from diagnosis were 80% and 52%, respectively.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclosporine / therapeutic use. Immunosuppressive Agents / therapeutic use. Leukemia, Large Granular Lymphocytic / drug therapy
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / administration & dosage. Drug Therapy, Combination. Female. Humans. Male. Methotrexate / administration & dosage. Middle Aged. Pentostatin / administration & dosage. Survival Rate. Treatment Outcome

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  • (PMID = 20367569.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Immunosuppressive Agents; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab; 83HN0GTJ6D / Cyclosporine; YL5FZ2Y5U1 / Methotrexate
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40. Samassekou O, Ntwari A, Hébert J, Yan J: Individual telomere lengths in chronic myeloid leukemia. Neoplasia; 2009 Nov;11(11):1146-54
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  • [Title] Individual telomere lengths in chronic myeloid leukemia.
  • Chronic myeloid leukemia (CML) is a neoplasia characterized by proliferation of a myeloid cell lineage and chromosome translocation t(9;22) (q34;q11.2).
  • We observed recurrent telomere length changes as well as telomere length maintenance and elongation in some individual telomeres.
  • We suggest that individual telomere length maintenance is chromosome arm-specific associated with leukemia cells.
  • [MeSH-major] Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Telomere / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Young Adult

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  • (PMID = 19881950.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC2767216
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41. Van Vlierberghe P, Homminga I, Zuurbier L, Gladdines-Buijs J, van Wering ER, Horstmann M, Beverloo HB, Pieters R, Meijerink JP: Cooperative genetic defects in TLX3 rearranged pediatric T-ALL. Leukemia; 2008 Apr;22(4):762-70
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  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.
  • Array-CGH analysis revealed five recurrent genomic deletions in TLX3 rearranged T-ALL, including del(1)(p36.31), del(5)(q35), del(13)(q14.3), del(16)(q22.1) and del(19)(p13.2).
  • From these, the cryptic deletion, del(5)(q35), was exclusively identified in about 25% of TLX3 rearranged T-ALL cases.
  • [MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion
  • [MeSH-minor] Cell Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics

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  • (PMID = 18185524.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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42. Yamamoto K, Nagata K, Morita Y, Inagaki K, Hamaguchi H: Isodicentric Philadelphia chromosome in acute lymphoblastic leukemia with der(7;12)(q10;q10). Leuk Res; 2007 May;31(5):713-8
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  • [Title] Isodicentric Philadelphia chromosome in acute lymphoblastic leukemia with der(7;12)(q10;q10).
  • We describe here the first case of acute lymphoblastic leukemia (ALL) with an isodicentric Philadelphia [idic(Ph)] chromosome.
  • The idic(Ph) chromosome was spindle-shaped and supposed to be formed by two Ph chromosomes joined at their q terminals, whereas idic(Ph) chromosomes in chronic myelogenous leukemia (CML) have been shown to be fused at the satellite regions of p arms.
  • Furthermore, considering other three reported cases, der(7;12)(q10;q10) may be one of the recurrent translocations in ALL.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 7. Philadelphia Chromosome. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male

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  • (PMID = 16979235.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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43. Clappier E, Cuccuini W, Cayuela JM, Vecchione D, Baruchel A, Dombret H, Sigaux F, Soulier J: Cyclin D2 dysregulation by chromosomal translocations to TCR loci in T-cell acute lymphoblastic leukemias. Leukemia; 2006 Jan;20(1):82-6
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  • [Title] Cyclin D2 dysregulation by chromosomal translocations to TCR loci in T-cell acute lymphoblastic leukemias.
  • While the cyclin D1 and D3 genes (CCND1 and CCND3) are recurrently involved in genomic rearrangements, especially in B-cell lymphoid neoplasias, no clear involvement of the cyclin D2 gene (CCND2) has been reported to date.
  • Here, we identified chromosomal translocations targeting the CCND2 locus at 12p13, and the T-cell receptor beta (TCRB) or the TCRA/D loci in T-cell acute lymphoblastic leukemias (T-ALLs).
  • In order to evaluate dysregulation in T-ALL with respect to normal T-cell differentiation, we analyzed CCND2 expression in normal purified human thymic subpopulations.
  • CCND2 levels were downregulated through progression from the early stages of human T-cell differentiation, further suggesting that the massive and sustained expression in the CCND2-rearranged T-ALL cases was oncogenic.
  • This report is the first clear evidence of a direct involvement of cyclin D2 in human cancer due to recurrent somatic genetic alterations.
  • [MeSH-major] Chromosomes, Human, Pair 12 / genetics. Cyclins / biosynthesis. Cyclins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Antigen, T-Cell / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Cell Separation. Child. Cyclin D2. Cytogenetic Analysis. DNA Mutational Analysis. Gene Rearrangement. Humans

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  • (PMID = 16270038.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Receptors, Antigen, T-Cell
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44. Yanada M, Kiyoi H, Murata M, Suzuki M, Iwai M, Yokozawa T, Baba H, Emi N, Naoe T: Micafungin, a novel antifungal agent, as empirical therapy in acute leukemia patients with febrile neutropenia. Intern Med; 2006;45(5):259-64
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  • [Title] Micafungin, a novel antifungal agent, as empirical therapy in acute leukemia patients with febrile neutropenia.
  • RESULTS: A total of 31 patients with acute leukemia who developed febrile neutropenia were enrolled in the study.
  • Among them, 18 patients fulfilling the protocol-defined criteria, including 10 with persistent fever and 8 with recurrent fever, received MCFG empirically.
  • Underlying diseases consisted of acute myeloid leukemia (n=15) and acute lymphoblastic leukemia (n=3).
  • [MeSH-minor] Adolescent. Adult. Algorithms. Echinocandins. Female. Fever / etiology. Humans. Leukemia, Myeloid / complications. Lipopeptides. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Prospective Studies

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  • (PMID = 16595990.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 0 / Lipopeptides; 0 / Lipoproteins; 0 / Peptides, Cyclic; R10H71BSWG / micafungin
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45. Dickson BC, Chung CT, Patterson BJ, Riddell RH, Kamel-Reid S, Messner HA, Lipton JH: Precursor lymphoblastic lymphoma reoccurring as a donor-derived neoplasm: a case report and review of the literature. Arch Pathol Lab Med; 2008 Aug;132(8):1342-5
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  • [Title] Precursor lymphoblastic lymphoma reoccurring as a donor-derived neoplasm: a case report and review of the literature.
  • Precursor lymphoblastic lymphoma is an uncommon neoplasm.
  • We report the case of a man who presented with precursor T lymphoblastic lymphoma and ultimately received an allogeneic bone marrow transplant from his human leukocyte antigen-identical sister.
  • Four years later he developed recurrent disease.
  • By means of DNA probing for the amelogenin locus and fluorescence in situ hybridization, the neoplastic cells of the recurrent lesion were found to be of donor origin.
  • We offer the report of a patient with an unusual lymphoblastic lymphoma who, after successful bone marrow transplantation, developed the same disease of donor cell origin; further, we offer a literature review on donor cell lymphoma.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Kidney Neoplasms / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Testicular Neoplasms / surgery
  • [MeSH-minor] Adult. Amelogenin / genetics. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Mapping. Fatal Outcome. Humans. In Situ Hybridization, Fluorescence. Male. Siblings. Tissue Donors


46. Strefford JC, Worley H, Barber K, Wright S, Stewart AR, Robinson HM, Bettney G, van Delft FW, Atherton MG, Davies T, Griffiths M, Hing S, Ross FM, Talley P, Saha V, Moorman AV, Harrison CJ: Genome complexity in acute lymphoblastic leukemia is revealed by array-based comparative genomic hybridization. Oncogene; 2007 Jun 21;26(29):4306-18
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  • [Title] Genome complexity in acute lymphoblastic leukemia is revealed by array-based comparative genomic hybridization.
  • Chromosomal abnormalities are important for the classification and risk stratification of patients with acute lymphoblastic leukemia (ALL).
  • However, approximately 30% of childhood and 50% of adult patients lack abnormalities with clinical relevance.
  • Deletions of 6q (del(6q)) were heterogeneous in size, in agreement with previous data, demonstrating the sensitivity of aCGH to measure CNA.
  • Six patients showed del(12p), with a common region encompassing the ETV6 gene.
  • Chromosome 21 CNA shared a common region of gain, with associated subtelomeric deletions.
  • Other recurrent findings included dim(13q), dim(16q) and enh(17q).
  • [MeSH-major] Burkitt Lymphoma / genetics. Gene Expression Profiling. Genome, Human. Leukemia-Lymphoma, Adult T-Cell / genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Female. Gene Dosage. Humans. Infant. Male. Middle Aged. Tumor Cells, Cultured

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  • (PMID = 17237825.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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47. Robak T, Lech-Maranda E, Janus A, Blonski J, Wierzbowska A, Gora-Tybor J: Cladribine combined with cyclophosphamide and mitoxantrone is an active salvage therapy in advanced non-Hodgkin's lymphoma. Leuk Lymphoma; 2007 Jun;48(6):1092-101
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  • [Title] Cladribine combined with cyclophosphamide and mitoxantrone is an active salvage therapy in advanced non-Hodgkin's lymphoma.
  • The aim of this study was to determine the feasibility, efficacy and toxicity of the combined therapy consisting of cladribine (2-CdA), mitoxantrone and cyclophosphamide (CMC regimen) in patients with refractory or relapsed non-Hodgkin's lymphoma (NHL).
  • Thirty six patients, 14 with mantle cell lymphoma (MCL), 10 with diffuse large B-cell lymphoma (DLBCL), 5 with follicular lymphoma (FL), 3 with small lymphocytic lymphoma (SLL), and 4 with T-cell lymphoma were enrolled to the study.
  • The CMC protocol consisted of 2-CdA at a dose of 0.12 mg/kg in a 2-hour infusion on days 1 through 3, mitoxantrone 10 mg/m(2) i.v. on day 1 and cyclophosphamide 650 mg/m(2) i.v. on day 1.
  • When different disease status before CMC treatment was considered, a trend toward longer survival of recurrent patients was observed (log rank test, P = 0.08).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cladribine / adverse effects. Cladribine / therapeutic use. Cyclophosphamide / adverse effects. Cyclophosphamide / therapeutic use. Feasibility Studies. Female. Humans. Male. Middle Aged. Mitoxantrone / adverse effects. Mitoxantrone / therapeutic use. Salvage Therapy / adverse effects. Survival Analysis. Treatment Outcome

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  • (PMID = 17577772.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 47M74X9YT5 / Cladribine; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; CMC protocol 2
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48. Tosello V, Mansour MR, Barnes K, Paganin M, Sulis ML, Jenkinson S, Allen CG, Gale RE, Linch DC, Palomero T, Real P, Murty V, Yao X, Richards SM, Goldstone A, Rowe J, Basso G, Wiernik PH, Paietta E, Pieters R, Horstmann M, Meijerink JP, Ferrando AA: WT1 mutations in T-ALL. Blood; 2009 Jul 30;114(5):1038-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.
  • We used single nucleotide polymorphism array analysis to analyze paired diagnostic and relapsed T-ALL samples to identify recurrent genetic alterations in T-ALL.
  • This analysis showed that diagnosis and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at diagnosis, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at diagnosis.
  • In addition, we identified deletions and associated mutations in the WT1 tumor suppressor gene in 2 of 9 samples.
  • Subsequent analysis showed WT1 mutations in 28 of 211 (13.2%) of pediatric and 10 of 85 (11.7%) of adult T-ALL cases.
  • Survival analysis demonstrated that WT1 mutations do not confer adverse prognosis in pediatric and adult T-ALL.
  • Overall, these results identify the presence of WT1 mutations as a recurrent genetic alteration in T-ALL.
  • [MeSH-major] Genes, Wilms Tumor. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Child. Chromosome Aberrations. Clone Cells / chemistry. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Genes, Homeobox. Humans. Kaplan-Meier Estimate. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Oncogenes. Polymorphism, Single Nucleotide. Prognosis. Recurrence. WT1 Proteins / chemistry. WT1 Proteins / genetics. Zinc Fingers / genetics

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  • (PMID = 19494353.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE15931
  • [Grant] United States / NCI NIH HHS / CA / CA114737; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United Kingdom / Medical Research Council / / MRC/ MC/ U137686856; United States / NCI NIH HHS / CA / CA02111; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United Kingdom / Medical Research Council / / MRC/ G0500389; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA120196-03
  • [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 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC2721784
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49. Hijiya N, Ness KK, Ribeiro RC, Hudson MM: Acute leukemia as a secondary malignancy in children and adolescents: current findings and issues. Cancer; 2009 Jan 1;115(1):23-35
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute leukemia as a secondary malignancy in children and adolescents: current findings and issues.
  • Secondary acute leukemia is a devastating complication in children and adolescents who have been treated for cancer.
  • Secondary acute lymphoblastic leukemia (s-ALL) was rarely reported previously but can be distinguished today from recurrent primary ALL by comparison of immunoglobulin and T-cell receptor rearrangement.
  • Secondary acute myeloid leukemia (s-AML) is much more common, and some cases actually may be second primary cancers.
  • The magnitude of the risk associated with these factors depends on several variables, including the administration schedule, concomitant medications, and host factors.
  • The prevalence of alkylator-associated s-AML has diminished among pediatric oncology patients with the reduction of cumulative alkylator dose and limited use of the more leukemogenic alkylators.
  • The best-documented topoisomerase II inhibitor-associated s-AML is s-AML associated with epipodophyllotoxins.
  • Studies in survivors of adult cancers suggest that, contrary to previous beliefs, the outcome of s-AML is not necessarily worse than that of de novo AML when adjusted for cytogenetic features.

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  • [Copyright] Copyright (c) 2008 American Cancer Society.
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  • (PMID = 19072983.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / P30 CA021765-31
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] L36H50F353 / Podophyllotoxin
  • [Number-of-references] 99
  • [Other-IDs] NLM/ NIHMS135594; NLM/ PMC2767267
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50. Boerma EG, Siebert R, Kluin PM, Baudis M: Translocations involving 8q24 in Burkitt lymphoma and other malignant lymphomas: a historical review of cytogenetics in the light of todays knowledge. Leukemia; 2009 Feb;23(2):225-34
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  • [Title] Translocations involving 8q24 in Burkitt lymphoma and other malignant lymphomas: a historical review of cytogenetics in the light of todays knowledge.
  • Burkitt lymphoma (BL) has a characteristic clinical presentation, morphology, immunophenotype and primary chromosomal aberration, that is, the translocation t(8;14)(q24;q32) or its variants.
  • However, diagnostic dilemmas may arise in daily practice due to overlap of BL with subsets of other aggressive, mature B-cell lymphomas such as diffuse large B-cell lymphomas (DLBCL).
  • In the remaining cases, additional recurrent but partially exclusive abnormalities included gains at chromosomes 1q, 7 and 12, and losses of 6q, 13q32-34 and 17p.
  • Within the core subset, no differences were found between pediatric and adult patients.
  • We suggest that, concordant with the WHO classification to be published in 2008, the diagnosis of BL should be restricted to cases with expression of CD10 and BCL6, absence or very weak expression of BCL2 protein, a homogeneously very high proliferation index and a proven IG-MYC translocation without evidence of a chromosomal translocation typical for other lymphoma entities.
  • In addition, a high number of nonspecific cytogenetic abnormalities should suggest need for a critical review of the diagnosis of BL.
  • [MeSH-major] Burkitt Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosomes, Human, Pair 8. Cytogenetics / history. Gene Expression Profiling. History, 20th Century. History, 21st Century. Humans. Lymphoma / classification. Lymphoma / diagnosis. Lymphoma / genetics

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  • (PMID = 18923440.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Historical Article; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 59
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51. Han Y, Xue Y, Zhang J, Wu Y, Pan J, Wang Y, Shen J, Dai H, Bai S: Translocation (14;14)(q11;q32) with simultaneous involvement of the IGH and CEBPE genes in B-lineage acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2008 Dec;187(2):125-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation (14;14)(q11;q32) with simultaneous involvement of the IGH and CEBPE genes in B-lineage acute lymphoblastic leukemia.
  • Translocation (14;14)(q11;q32) is one of the recurrent chromosome aberrations in ataxia-teleangiectasia (AT) and T-cell malignancies.
  • However, t(14;14)(q11;q32) is an exceedingly rare phenomenon in B-lineage acute lymphoblastic leukemia (B-ALL).
  • Here, we report another B-ALL case with t(14;14)(q11;q32) in a 39-year-old female.
  • Fluorescence in situ hybridization (FISH) demonstrated trisomy 4 and the simultaneous involvement of the IGH gene at 14q32 and the CEBPE gene at 14q11, which differs from the genes involved in T-cell leukemias.
  • Later, she received allogeneic peripheral blood stem cell transplantation.
  • We suggest that t(14;14)(q11;q32) involving the IGH and CEBPE genes in B-ALL is rare, but it is a recurrent abnormality that could identify a new subgroup of B-ALL.
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Chromosomes, Human, Pair 14 / genetics. Immunoglobulin Heavy Chains / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / genetics. Daunorubicin / therapeutic use. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Prednisone / therapeutic use. Trisomy. Vincristine / therapeutic use

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  • (PMID = 19027493.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CCAAT-Enhancer-Binding Proteins; 0 / Immunoglobulin Heavy Chains; 142805-41-2 / CEBPE protein, human; 5J49Q6B70F / Vincristine; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; VDP protocol
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52. Karst C, Gross M, Haase D, Wedding U, Höffken K, Liehr T, Mkrtchyan H: Novel cryptic chromosomal rearrangements detected in acute lymphoblastic leukemia detected by application of new multicolor fluorescent in situ hybridization approaches. Int J Oncol; 2006 Apr;28(4):891-7
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel cryptic chromosomal rearrangements detected in acute lymphoblastic leukemia detected by application of new multicolor fluorescent in situ hybridization approaches.
  • However, it is often difficult to obtain good karyotypes, especially of cells from cases with acute lymphoblastic leukemia (ALL) because of poor morphology and spreading.
  • Thus, we detected the following recurrent cryptic chromosomal aberrations: del(12)(pter) [8 cases], del(9)(qter) [3 cases], and del(11)(pter) [2 cases].
  • In summary, mMCB and subCTM were proven to be powerful methods in the screening for new cryptic chromosomal aberrations, which considerably increased the accuracy of cytogenetic diagnosis.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Spectral Karyotyping / methods. Translocation, Genetic / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Child, Preschool. Chromosome Banding / methods. Female. Humans. Male. Middle Aged. Telomere / genetics

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  • (PMID = 16525638.001).
  • [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
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53. Pan JL, Xue YQ, Jiang HY, Zhu YJ, Ma L, Li TY, Wang Y, Wu YF: [Clinical and experimental study of 7 cases of acute lymphoblastic leukemia with dic(7;9) (pll;pll)]. Zhonghua Xue Ye Xue Za Zhi; 2005 Aug;26(8):485-8
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical and experimental study of 7 cases of acute lymphoblastic leukemia with dic(7;9) (pll;pll)].
  • OBJECTIVE: To investigate the laboratory and clinical features of 7 cases of acute lymphoblastic leukemia (ALL) with dic(7;9) (pll;pll).
  • CONCLUSION: dic(7;9) was a rare, but recurrent chromosome abnormality in ALL and had some clinical and laboratory features.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Chromosomes, Human, Pair 7 / genetics. Chromosomes, Human, Pair 9 / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Translocation, Genetic

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  • (PMID = 16383241.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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54. Persson M, Andrén Y, Mark J, Horlings HM, Persson F, Stenman G: Recurrent fusion of MYB and NFIB transcription factor genes in carcinomas of the breast and head and neck. Proc Natl Acad Sci U S A; 2009 Nov 3;106(44):18740-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent fusion of MYB and NFIB transcription factor genes in carcinomas of the breast and head and neck.
  • We suggest that deletion of these target sites may disrupt repression of MYB leading to overexpression of MYB-NFIB transcripts and protein and to activation of critical MYB targets, including genes associated with apoptosis, cell cycle control, cell growth/angiogenesis, and cell adhesion.
  • [MeSH-minor] Adult. Aged. Base Sequence. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 8 / genetics. Female. Gene Expression Regulation, Neoplastic. Humans. Leukemia-Lymphoma, Adult T-Cell / genetics. Male. MicroRNAs / genetics. Middle Aged. Molecular Sequence Data. RNA, Messenger / genetics. RNA, Messenger / metabolism. Translocation, Genetic

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  • (PMID = 19841262.001).
  • [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
  • [Databank-accession-numbers] GENBANK/ FJ969915/ FJ969916/ FJ969917
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MYB-NFIB fusion protein, human; 0 / MicroRNAs; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger
  • [Other-IDs] NLM/ PMC2773970
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55. Huh JY, Chung S, Oh D, Kang MS, Eom HS, Cho EH, Han MH, Kong SY: Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature. Korean J Lab Med; 2010 Apr;30(2):117-21
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  • [Title] Clathrin assembly lymphoid myeloid leukemia-AF10-positive acute leukemias: a report of 2 cases with a review of the literature.
  • The translocation t(10;11)(p13;q14q21) has been found to be recurrent in acute lymphoblastic and myeloid leukemias, and results in the fusion of the clathrin assembly lymphoid myeloid leukemia (CALM) gene with the AF10 gene; these genes are present on chromosomes 11 and 10, respectively.
  • Because the CALM-AF10 rearrangement is a rare chromosomal abnormality, it is not included in routine molecular tests for acute leukemia.
  • The first patient (case 1) was diagnosed with T-cell ALL, and the second patient (case 2) was diagnosed with AML.
  • Both patient samples showed expression of the homeobox A gene cluster and the histone methyltransferase hDOT1L, which suggests that they mediate leukemic transformation in CALM-AF10-positive and mixed-lineage leukemia-AF10-positive leukemias.
  • The first patient (case 1) relapsed after double-unit cord blood transplantation; there was no evidence of relapse in the second patient (case 2) after allogenic peripheral blood stem cell transplantation.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Monomeric Clathrin Assembly Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adolescent. Adult. Bone Marrow / pathology. Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 11. Cord Blood Stem Cell Transplantation. Female. Histone-Lysine N-Methyltransferase / genetics. Histone-Lysine N-Methyltransferase / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Male. Recurrence. Translocation, Genetic

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  • (PMID = 20445327.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLLT10 protein, human; 0 / Monomeric Clathrin Assembly Proteins; 0 / Oncogene Proteins, Fusion; 0 / PICALM protein, human; 0 / Transcription Factors; EC 2.1.1.- / histone methyltransferase; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 14
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56. Buhmann R, Simoes B, Stanglmaier M, Yang T, Faltin M, Bund D, Lindhofer H, Kolb HJ: Immunotherapy of recurrent B-cell malignancies after allo-SCT with Bi20 (FBTA05), a trifunctional anti-CD3 x anti-CD20 antibody and donor lymphocyte infusion. Bone Marrow Transplant; 2009 Mar;43(5):383-97
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  • [Title] Immunotherapy of recurrent B-cell malignancies after allo-SCT with Bi20 (FBTA05), a trifunctional anti-CD3 x anti-CD20 antibody and donor lymphocyte infusion.
  • Donor lymphocyte infusions (DLIs) after allo-SCT displayed limited use in CLL and highly malignant non-Hodgkin's lymphoma (NHL).
  • Here we studied whether Bi20 (FBTA05), a novel trifunctional bispecific antibody targeting CD20 on lymphoma cells and CD3 on T cells, could induce GVL responses in combination with DLI or mobilized PBSCT after allogeneic transplantation in these diseases.
  • [MeSH-major] Adoptive Transfer. Antibodies, Bispecific / therapeutic use. Hematopoietic Stem Cell Transplantation. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Lymphoma, Large B-Cell, Diffuse / therapy
  • [MeSH-minor] Adult. Female. Graft vs Host Disease / etiology. Humans. Male. Middle Aged. Pilot Projects. Recurrence. Tissue Donors. Transplantation, Homologous

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  • (PMID = 18850012.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Bispecific; 0 / Bi20 antibody
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57. Bashey A, Medina B, Corringham S, Pasek M, Carrier E, Vrooman L, Lowy I, Solomon SR, Morris LE, Holland HK, Mason JR, Alyea EP, Soiffer RJ, Ball ED: CTLA4 blockade with ipilimumab to treat relapse of malignancy after allogeneic hematopoietic cell transplantation. Blood; 2009 Feb 12;113(7):1581-8
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  • [Title] CTLA4 blockade with ipilimumab to treat relapse of malignancy after allogeneic hematopoietic cell transplantation.
  • Relapse of malignancy after allogeneic hematopoietic cell transplantation (allo-HCT) remains a therapeutic challenge.
  • Twenty-nine patients with malignancies that were recurrent or progressive after allo-HCT, received ipilimumab as a single infusion at dose cohorts between 0.1 and 3.0 mg/kg.
  • Organ-specific immune adverse events (IAE) were seen in 4 patients (grade 3 arthritis, grade 2 hyperthyroidism, recurrent grade 4 pneumonitis).
  • Three patients with lymphoid malignancy developed objective disease responses following ipilimumab: complete remission (CR) in 2 patients with Hodgkin disease and partial remission (PR) in a patient with refractory mantle cell lymphoma.

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  • (PMID = 18974373.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00060372
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 9389-01A1
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / ipilimumab
  • [Other-IDs] NLM/ PMC2644086
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58. Bittencourt AL, de Oliveira Mde F: Cutaneous manifestations associated with HTLV-1 infection. Int J Dermatol; 2010 Oct;49(10):1099-110
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cutaneous manifestations associated with HTLV-1 infection.
  • Skin lesions are frequent in human T-cell lymphotropic virus type 1 (HTLV-1) infection and may constitute an alert for the diagnosis of this condition.
  • The most severe skin diseases related to this virus are adult T-cell leukemia/lymphoma (ATLL), an aggressive form of leukemia/lymphoma that fails to respond to chemotherapy, and infective dermatitis associated with HTLV-1 (IDH), a severe and recurrent form of eczema occurring in childhood.
  • IDH may progress to HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and to ATLL.
  • Adult onset IDH and reactional and inflammatory dermatoses found in carriers and also in patients with HAM/TSP will be considered.
  • Other dermatological diseases that occur more frequently in HTLV-1-infected individuals such as xerosis, acquired ichthyosis, seborrheic dermatitis and infectious and parasitic dermatoses will also be discussed.
  • [MeSH-major] Lymphoma, T-Cell / pathology. Lymphoma, T-Cell / virology
  • [MeSH-minor] Antiviral Agents / therapeutic use. Carrier State. Diagnosis, Differential. Drug Resistance, Neoplasm. HTLV-I Infections. Human T-lymphotropic virus 1. Humans. Ichthyosis / diagnosis. Ichthyosis / virology. Immunohistochemistry. Interferon-alpha / therapeutic use. Scabies / diagnosis. Skin / pathology. Skin Diseases, Viral / diagnosis. Treponemal Infections / diagnosis. Zidovudine / therapeutic use

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  • [Copyright] © 2010 The International Society of Dermatology.
  • (PMID = 20883400.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 4B9XT59T7S / Zidovudine
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59. Bielen D, Mortelé K, Peters H, Lombard D, Ros R: Small bowel obstruction secondary to disseminated candidiasis in an immunocompromised patient: radiologic-pathologic correlation. JBR-BTR; 2005 Jan-Feb;88(1):20-2
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  • AIDS, leukemia), is increasingly encountered in daily medical practice.
  • We report on a case of a 33-year-old immunocompromised woman with a history of recurrent T-cell lymphoblastic lymphoma, which presented with abdominal pain.
  • [MeSH-major] Candidiasis / diagnosis. Immunocompromised Host. Intestinal Obstruction / microbiology. Jejunal Diseases / microbiology. Opportunistic Infections / diagnosis
  • [MeSH-minor] Adult. Enteritis / microbiology. Fatal Outcome. Female. Humans. Lymphoma, T-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 15792164.001).
  • [ISSN] 0302-7430
  • [Journal-full-title] JBR-BTR : organe de la Société royale belge de radiologie (SRBR) = orgaan van de Koninklijke Belgische Vereniging voor Radiologie (KBVR)
  • [ISO-abbreviation] JBR-BTR
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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60. Manoukian G, Hagemeister F: Denileukin diftitox: a novel immunotoxin. Expert Opin Biol Ther; 2009 Nov;9(11):1445-51
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  • RESULTS: In 1999, the FDA approved the use of denileukin diftitox for patients with persistent or relapsed CD25-positive cutaneous T-cell lymphoma (CTCL), but Ontak has been reported to be an effective therapy for other neoplastic and non-neoplastic conditions.
  • Oncological uses include therapy for CD25-negative T-cell lymphoma, recurrent and refractory chronic lymphocytic leukemia (CLL), non-Hodgkin's B-cell lymphoma (NHL), and human T-cell lymphotropic virus- 1 (HTLV-1)-associated adult T-cell leukemia/lymphoma (ATL).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Diphtheria Toxin / therapeutic use. Interleukin-2 / therapeutic use. Lymphoma, T-Cell / drug therapy

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  • (PMID = 19817678.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 25E79B5CTM / denileukin diftitox
  • [Number-of-references] 37
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61. Maser RS, Choudhury B, Campbell PJ, Feng B, Wong KK, Protopopov A, O'Neil J, Gutierrez A, Ivanova E, Perna I, Lin E, Mani V, Jiang S, McNamara K, Zaghlul S, Edkins S, Stevens C, Brennan C, Martin ES, Wiedemeyer R, Kabbarah O, Nogueira C, Histen G, Aster J, Mansour M, Duke V, Foroni L, Fielding AK, Goldstone AH, Rowe JM, Wang YA, Look AT, Stratton MR, Chin L, Futreal PA, DePinho RA: Chromosomally unstable mouse tumours have genomic alterations similar to diverse human cancers. Nature; 2007 Jun 21;447(7147):966-71
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  • Here we engineered lymphoma-prone mice with chromosomal instability to assess the usefulness of mouse models in cancer gene discovery and the extent of cross-species overlap in cancer-associated copy number aberrations.
  • Along with targeted re-sequencing, our comparative oncogenomic studies identified FBXW7 and PTEN to be commonly deleted both in murine lymphomas and in human T-cell acute lymphoblastic leukaemia/lymphoma (T-ALL).
  • The murine cancers acquire widespread recurrent amplifications and deletions targeting loci syntenic to those not only in human T-ALL but also in diverse human haematopoietic, mesenchymal and epithelial tumours.
  • [MeSH-major] Chromosomal Instability / genetics. Chromosome Aberrations. Conserved Sequence / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell / genetics

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  • (PMID = 17515920.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE7615
  • [Grant] United Kingdom / Medical Research Council / / MRC/ G0500389; United Kingdom / Wellcome Trust / / WT077012; United Kingdom / Wellcome Trust / / WT088340; United Kingdom / Wellcome Trust / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2714968; NLM/ UKMS27310
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62. Rutar T, Cockerham KP: Periorbital zygomycosis (mucormycosis) treated with posaconazole. Am J Ophthalmol; 2006 Jul;142(1):187-188
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  • RESULTS: A 22-year-old male undergoing induction chemotherapy for acute lymphoblastic leukemia presented with periorbital cellulitis attributable to Rhizopus.
  • Despite recurrent profound neutropenia, the periorbital infection resolved, he tolerated reconstructive procedures, and he did not develop orbital invasion.
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Humans. Male. Microbial Sensitivity Tests. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Tomography, X-Ray Computed

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  • (PMID = 16815283.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Antineoplastic Agents; 0 / Triazoles; 6TK1G07BHZ / posaconazole
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63. Murakami Y, Saigo K, Takashima H, Minami M, Okanoue T, Bréchot C, Paterlini-Bréchot P: Large scaled analysis of hepatitis B virus (HBV) DNA integration in HBV related hepatocellular carcinomas. Gut; 2005 Aug;54(8):1162-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • HBV integration recurrently targeted the human telomerase reverse transcriptase gene (three cases) and genes belonging to distinct pathways: calcium signalling related genes, 60s ribosomal protein encoding genes, and platelet derived growth factor and mixed lineage leukaemia encoding genes.
  • CONCLUSIONS: In 61/68 (89.7%) cases, HBV DNA was integrated into cellular genes potentially providing cell growth advantage.
  • Identification of recurrent viral integration sites into genes of the same family allows recognition of common cell signalling pathways activated in hepatocarcinogenesis.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Calcium Signaling / genetics. DNA Transposable Elements / genetics. DNA-Binding Proteins. Female. Genes, Tumor Suppressor. Humans. Leukemia / genetics. Male. Middle Aged. Neoplasm Proteins / genetics. Platelet-Derived Growth Factor / genetics. Polymerase Chain Reaction / methods. Ribosomal Proteins / genetics. Telomerase / genetics. Viral Proteins / genetics

  • Genetic Alliance. consumer health - Hepatitis.
  • MedlinePlus Health Information. consumer health - Hepatitis B.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
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  • (PMID = 16009689.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Transposable Elements; 0 / DNA, Viral; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / Platelet-Derived Growth Factor; 0 / Ribosomal Proteins; 0 / Viral Proteins; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC1774867
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64. Gué M, Sun JS, Boudier T: Simultaneous localization of MLL, AF4 and ENL genes in interphase nuclei by 3D-FISH: MLL translocation revisited. BMC Cancer; 2006;6:20
MedlinePlus Health Information. consumer health - Genes and Gene Therapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MLL translocation in acute leukaemia) and two models have been proposed to explain the origins of recurrent reciprocal translocation.
  • METHODS: Using triple labeling 3D FISH experiments, we have determined the relative positions of MLL, AF4 and ENL genes, in two lymphoblastic and two myeloid human cell lines.
  • RESULTS: In all cell lines, the ENL gene is significantly closer to the MLL gene than the AF4 gene (with P value < 0.0001).
  • [MeSH-major] Cell Nucleus / chemistry. DNA-Binding Proteins / genetics. Genes. Imaging, Three-Dimensional. In Situ Hybridization, Fluorescence / methods. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adolescent. Adult. Cell Line, Transformed / chemistry. Cell Line, Transformed / ultrastructure. Cell Line, Tumor / chemistry. Cell Line, Tumor / ultrastructure. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 19 / genetics. Chromosomes, Human, Pair 19 / ultrastructure. Chromosomes, Human, Pair 4 / genetics. Chromosomes, Human, Pair 4 / ultrastructure. HL-60 Cells / chemistry. HL-60 Cells / ultrastructure. Herpesvirus 4, Human. Histone-Lysine N-Methyltransferase. Humans. Interphase. Leukemia, Monocytic, Acute / genetics. Leukemia, Monocytic, Acute / pathology. Male. Models, Genetic. Multiple Myeloma / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic

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  • (PMID = 16433901.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 150826-18-9 / AFF1 protein, human; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Other-IDs] NLM/ PMC1388228
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65. Chapiro E, Russell LJ, Struski S, Cavé H, Radford-Weiss I, Valle VD, Lachenaud J, Brousset P, Bernard OA, Harrison CJ, Nguyen-Khac F: A new recurrent translocation t(11;14)(q24;q32) involving IGH@ and miR-125b-1 in B-cell progenitor acute lymphoblastic leukemia. Leukemia; 2010 Jul;24(7):1362-4
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new recurrent translocation t(11;14)(q24;q32) involving IGH@ and miR-125b-1 in B-cell progenitor acute lymphoblastic leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 14 / genetics. Immunoglobulin Heavy Chains / genetics. MicroRNAs / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Base Sequence. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Molecular Sequence Data. Sequence Homology, Nucleic Acid

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  • (PMID = 20485370.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / MIRN125 microRNA, human; 0 / MicroRNAs
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