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1. Wolach B, Ash S, Gavrieli R, Stark B, Yaniv I, Roos D: Acute lymphoblastic leukemia in a patient with chronic granulomatous disease and a novel mutation in CYBB: first report. Am J Hematol; 2005 Sep;80(1):50-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute lymphoblastic leukemia in a patient with chronic granulomatous disease and a novel mutation in CYBB: first report.
  • We report for the first time a child with chronic granulomatous disease (CGD) who developed acute lymphoblastic leukemia (ALL).
  • During the course of ALL and later, he suffered from recurrent severe pyogenic infections, but careful detection of the etiological agent and promptly instituted specific treatment resulted in his complete recovery.
  • [MeSH-major] Granulomatous Disease, Chronic / genetics. Membrane Glycoproteins / genetics. Mutation. NADPH Oxidase / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16138344.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CYBB protein, human; 0 / Membrane Glycoproteins; EC 1.6.3.1 / NADPH Oxidase
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2. Tavil B, Secmeer G, Balc YI, Tezer H, Aksoy C, Alan S, Gumruk F, Yetgin S: Chronic recurrent multifocal osteomyelitis as the first presentation of acute lymphoblastic leukemia in a 2-year-old boy. J Pediatr Hematol Oncol; 2010 May;32(4):e151-2
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  • [Title] Chronic recurrent multifocal osteomyelitis as the first presentation of acute lymphoblastic leukemia in a 2-year-old boy.
  • SUMMARY: We present herein a 2-year-old boy who suffered from chronic recurrent multifocal osteomyelitis for 6 months and was later diagnosed as acute lymphoblastic leukemia.
  • In view of the rarity of bilateral symmetric and multifocal lesions in osteomyelitis in children, we suggest that leukemia should be investigated with bone marrow aspiration in such patients, even if complete blood count parameters are normal, and there is no hepatosplenomegaly.
  • [MeSH-major] Osteomyelitis / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


3. Ballen KK, Haley NR, Kurtzberg J, Lane TA, Lindgren BR, Miller JP, Newman B, McCullough J: Outcomes of 122 diverse adult and pediatric cord blood transplant recipients from a large cord blood bank. Transfusion; 2006 Dec;46(12):2063-70
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  • RESULTS: Most patients had acute myelogeneous leukemia (21%), genetic disorders (22%), or acute lymphoblastic leukemia (18%).
  • Thirty percent of patients experienced Grades III to IV acute graft-versus-host disease (GVHD).
  • Survival at 1 year after transplant was 35 percent, with recurrent disease the major cause of death.


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4. 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
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  • [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

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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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5. 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.
  • (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

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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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6. 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

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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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7. Horton TM, Thompson PA, Berg SL, Adamson PC, Ingle AM, Dolan ME, Delaney SM, Hedge M, Weiss HL, Wu MF, Blaney SM, Children's Oncology Group Study: Phase I pharmacokinetic and pharmacodynamic study of temozolomide in pediatric patients with refractory or recurrent leukemia: a Children's Oncology Group Study. J Clin Oncol; 2007 Nov 1;25(31):4922-8
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  • [Title] Phase I pharmacokinetic and pharmacodynamic study of temozolomide in pediatric patients with refractory or recurrent leukemia: a Children's Oncology Group Study.
  • PURPOSE: To determine the tolerability, pharmacokinetics, and mechanisms of temozolomide resistance in children with relapsed or refractory leukemia.
  • Pretreatment leukemia cell O6-methylguanine-DNA methyltransferase (MGMT) activity, tumor and plasma MGMT promoter methylation, and microsatellite instability (MSI) were examined in 14 of 16 study patients and in tissue bank samples from children with acute leukemia not treated with temozolomide (MGMT, n = 67; MSI, n = 65).
  • RESULTS: Sixteen patients (nine female, seven male; acute lymphoblastic leukemia [ALL], n = 8; acute myeloid leukemia [AML], n = 8), median age 11 years (range, 1 to 19 years), received either 200 mg/m2/d (nine enrolled, three assessable for toxicity) or 260 mg/m2/d (seven enrolled, three assessable for toxicity) of temozolomide.
  • MGMT activity in leukemia cells was quite variable and was highest in patients with relapsed ALL.
  • CONCLUSION: Temozolomide was well tolerated at doses as high as 260 mg/m2/d for 5 days in children with relapsed or refractory leukemia.
  • Increased MGMT activity may account for the temozolomide resistance in children with relapsed leukemia.
  • Leukemia cell MGMT activity was higher in pediatric ALL than AML (P < .0001).
  • [MeSH-major] Antineoplastic Agents, Alkylating / pharmacokinetics. Dacarbazine / analogs & derivatives. Drug Resistance, Neoplasm / genetics. Leukemia / drug therapy. Neoplasm Recurrence, Local / drug therapy

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  • (PMID = 17971589.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K12CA90433; United States / NCI NIH HHS / CA / P30 CA14599; United States / NCI NIH HHS / CA / U01CA63187; United States / NCI NIH HHS / CA / UO1-CA97452
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes
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8. 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).
  • [MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion

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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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9. Teitell MA, Pandolfi PP: Molecular genetics of acute lymphoblastic leukemia. Annu Rev Pathol; 2009;4:175-98
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  • [Title] Molecular genetics of acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is mainly a disease of childhood that arises from recurrent genetic insults that block precursor B and T cell differentiation and drive aberrant cell proliferation and survival.
  • Recurrent defects including chromosomal translocations, aneuploidies, and gene-specific alterations generate molecular subgroups of B- and T-ALL with differing clinical courses and distinct responses to therapy.
  • Recent discoveries arising from genome-wide surveys and adoptive transfer of leukemia-initiating cells have uncovered multiple gene copy number aberrations and have yielded new insight into at least one type of ALL-originating cell.
  • Here, we review the spectrum of genetic aberrations that promote acute B and T cell leukemias and the mechanisms of cell transformation and malignant progression that are reinforced by mouse models of human ALL.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Gene Expression Regulation, Leukemic. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18783329.001).
  • [ISSN] 1553-4014
  • [Journal-full-title] Annual review of pathology
  • [ISO-abbreviation] Annu Rev Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 153
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10. Reid AG, Seppa L, von der Weid N, Niggli FK, Betts DR: A t(12;17)(p13;q12) identifies a distinct TEL rearrangement-negative subtype of precursor-B acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2006 Feb;165(1):64-9
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  • [Title] A t(12;17)(p13;q12) identifies a distinct TEL rearrangement-negative subtype of precursor-B acute lymphoblastic leukemia.
  • Structural rearrangements involving the short arm of chromosome 12 are common in acute lymphoblastic leukemia (ALL) and often involve the TEL locus at 12p13.
  • The balanced t(12;17)(p13;q12) is a rare but recurrent aberration in ALL.

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  • (PMID = 16490598.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / TEL-AML1 fusion protein
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11. Seegmiller AC, Kroft SH, Karandikar NJ, McKenna RW: Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia. Am J Clin Pathol; 2009 Dec;132(6):940-9
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  • [Title] Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia.
  • Morphologic distinction of leukemic lymphoblasts in B acute lymphoblastic leukemia (B-ALL) from their nonneoplastic counterparts in bone marrow (hematogones) can be difficult.
  • Specific aberrancies correlate with recurrent cytogenetic abnormalities in B-ALL.
  • [MeSH-major] Bone Marrow Cells / pathology. Immunophenotyping / methods. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Precursor Cells, B-Lymphoid / pathology

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  • (PMID = 19926587.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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12. Nowak NJ, Sait SN, Zeidan A, Deeb G, Gaile D, Liu S, Ford L, Wallace PK, Wang ES, Wetzler M: Recurrent deletion of 9q34 in adult normal karyotype precursor B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2010 May;199(1):15-20
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  • [Title] Recurrent deletion of 9q34 in adult normal karyotype precursor B-cell acute lymphoblastic leukemia.
  • The prognosis of adult normal karyotype (NK) precursor B-cell acute lymphoblastic leukemia (B-ALL) has not improved over the last decade, mainly because separation into distinct molecular subsets has been lacking and no targeted treatments are available.

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20417863.001).
  • [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 CA016056; None / None / / P30 CA016056-33; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / P30 CA016056-33
  • [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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Homeodomain Proteins; 157907-48-7 / HoxA protein
  • [Other-IDs] NLM/ NIHMS173834; NLM/ PMC2862995
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13. Lundin C, Heidenblad M, Strombeck B, Borg A, Hovland R, Heim S, Johansson B: Tiling resolution array CGH of dic(7;9)(p11 approximately 13;p11 approximately 13) in B-cell precursor acute lymphoblastic leukemia reveals clustered breakpoints at 7p11.2 approximately 12.1 and 9p13.1. Cytogenet Genome Res; 2007;118(1):13-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tiling resolution array CGH of dic(7;9)(p11 approximately 13;p11 approximately 13) in B-cell precursor acute lymphoblastic leukemia reveals clustered breakpoints at 7p11.2 approximately 12.1 and 9p13.1.
  • The dic(7;9)(p11 approximately 13;p11 approximately 13) is a recurrent chromosomal abnormality in acute lymphoblastic leukemia (ALL), mainly of B-lineage.

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  • [Copyright] Copyright (c) 2007 S. Karger AG, Basel.
  • (PMID = 17901695.001).
  • [ISSN] 1424-859X
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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14. Brugnoletti F, Morris EB, Laningham FH, Patay Z, Pauley JL, Pui CH, Jeha S, Inaba H: Recurrent intrathecal methotrexate induced neurotoxicity in an adolescent with acute lymphoblastic leukemia: Serial clinical and radiologic findings. Pediatr Blood Cancer; 2009 Feb;52(2):293-5
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  • [Title] Recurrent intrathecal methotrexate induced neurotoxicity in an adolescent with acute lymphoblastic leukemia: Serial clinical and radiologic findings.
  • Systemic and intrathecal methotrexate (MTX) are integral components of acute lymphoblastic leukemia (ALL) therapy, but can be associated with neurotoxicity.
  • We describe here the case of an adolescent male with T-cell ALL who developed recurrent episodes of subacute neurotoxicity characterized by slurred speech, emotional lability, and hemiparesis after intrathecal MTX administration.
  • Serial magnetic resonance imaging with diffusion-weighted imaging showed recurrent areas of restricted diffusion within cerebral hemispheric white matter, which correlated chronologically with the administration of intrathecal therapy and severity of clinical symptoms.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
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  • (PMID = 18831032.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-29; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / P30 CA021765-29
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ NIHMS75296; NLM/ PMC2605174
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15. 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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  • [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.
  • 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


16. Jeannet R, Mastio J, Macias-Garcia A, Oravecz A, Ashworth T, Geimer Le Lay AS, Jost B, Le Gras S, Ghysdael J, Gridley T, Honjo T, Radtke F, Aster JC, Chan S, Kastner P: Oncogenic activation of the Notch1 gene by deletion of its promoter in Ikaros-deficient T-ALL. Blood; 2010 Dec 16;116(25):5443-54
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  • The Notch pathway is frequently activated in T-cell acute lymphoblastic leukemias (T-ALLs).
  • Of the Notch receptors, Notch1 is a recurrent target of gain-of-function mutations and Notch3 is expressed in all T-ALLs, but it is currently unclear how these receptors contribute to T-cell transformation in vivo.
  • [MeSH-major] Ikaros Transcription Factor / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Receptor, Notch1 / genetics. Transcriptional Activation / physiology


17. Roche-Lestienne C, Deluche L, Corm S, Tigaud I, Joha S, Philippe N, Geffroy S, Laï JL, Nicolini FE, Preudhomme C, Fi-LMC group: RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance. Blood; 2008 Apr 1;111(7):3735-41
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  • Acquired molecular abnormalities (mutations or chromosomal translocations) of the RUNX1 transcription factor gene are frequent in acute myeloblastic leukemias (AMLs) and in therapy-related myelodysplastic syndromes, but rarely in acute lymphoblastic leukemias (ALLs) and chronic myelogenous leukemias (CMLs).
  • Among 18 BCR-ABL+ leukemias presenting acquired trisomy of chromosome 21, we report a high frequency (33%) of recurrent point mutations (4 in myeloid blast crisis [BC] CML and one in chronic phase CML) within the DNA-binding region of RUNX1.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Blast Crisis / genetics. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Drug Resistance, Neoplasm / genetics. Fusion Proteins, bcr-abl / genetics. Leukemia / genetics. Piperazines / administration & dosage. Pyrimidines / administration & dosage. Transcription Factors / genetics. Trisomy / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Benzamides. Chromosomes, Human. Chronic Disease. Disease-Free Survival. Female. Humans. Imatinib Mesylate. Male. Middle Aged. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Myelodysplastic Syndromes / metabolism. Myelodysplastic Syndromes / mortality. Phenotype. Point Mutation. Retrospective Studies. Survival Rate. Translocation, Genetic / drug effects. Translocation, Genetic / genetics

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  • (PMID = 18202228.001).
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / PRDM16 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / RUNX1 protein, human; 0 / Transcription Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [General-notes] NLM/ Investigator list not found.
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18. Noble SL, Sherer E, Hannemann RE, Ramkrishna D, Vik T, Rundell AE: Using adaptive model predictive control to customize maintenance therapy chemotherapeutic dosing for childhood acute lymphoblastic leukemia. J Theor Biol; 2010 Jun 7;264(3):990-1002
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  • [Title] Using adaptive model predictive control to customize maintenance therapy chemotherapeutic dosing for childhood acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is a common childhood cancer in which nearly one-quarter of patients experience a disease relapse.
  • During the course of treatment, the patient-specific parameters are adaptively identified using recurrent complete blood count measurements, which sufficiently constrain the patient parameter uncertainty to support customized adjustments of the drug dose.
  • [MeSH-major] 6-Mercaptopurine / therapeutic use. Dose-Response Relationship, Drug. Models, Biological. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20138060.001).
  • [ISSN] 1095-8541
  • [Journal-full-title] Journal of theoretical biology
  • [ISO-abbreviation] J. Theor. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, American Recovery and Reinvestment Act; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; E7WED276I5 / 6-Mercaptopurine
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19. Sino US Leukemia Cooperative Group of Shanghai: [Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification]. Zhonghua Xue Ye Xue Za Zhi; 2007 Jul;28(7):444-8
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  • [Title] [Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification].
  • OBJECTIVE: To evaluate WHO classification of acute leukemia (AL) in Shanghai and compare the difference between WHO and FAB classification.
  • METHODS: Successive and unselected leukemia patients were referred to Sino-US Leukemia Cooperative Group of Shanghai from 2003 to 2006.
  • RESULTS: Of the 572 AL patients, 436 (76.2%) were diagnosed as acute myeloid leukemia (AML), 119 (20.8%) acute lymphoblastic leukemia (ALL).
  • AML with recurrent cytogenetic abnormalities accounted for 35.3%, and with multilineage dysplasia for 13.1%, therapy-related AML accounted for 0.9%, and AML not otherwise categorized for 50.7%.
  • Comparing to the AL data of Shanghai Leukemia Group between 1984 and 1994, the percentage of AML-M4 was increased, but that of AML-M1 and M5 were decreased.
  • [MeSH-major] Leukemia / classification
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. China. Female. Humans. Karyotyping. Male. Middle Aged

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  • (PMID = 18072625.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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20. Moon HW, Chang YH, Kim TY, Oh BR, Min HC, Kim BK, Ahn HS, Cho HI, Lee DS: Incidence of submicroscopic deletions vary according to disease entities and chromosomal translocations in hematologic malignancies: investigation by fluorescence in situ hybridization. Cancer Genet Cytogenet; 2007 Jun;175(2):166-8
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  • Submicroscopic deletions of genes in recurrent chromosomal rearrangements occur frequently in hematologic malignancies, but their incidences have not been reported clearly.
  • A fluorescence in situ hybridization (FISH) study was conducted in 336 patients with acute lymphoblastic leukemia, 223 patients with acute myeloid leukemia, and 79 patients with chronic myelogenous leukemia.

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  • (PMID = 17556074.001).
  • [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
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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21. Stanulla M, Schrappe M: Treatment of childhood acute lymphoblastic leukemia. Semin Hematol; 2009 Jan;46(1):52-63
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  • [Title] Treatment of childhood acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is the most common malignancy of childhood.
  • While the goal of effective therapy for the majority of children with ALL has been achieved, significant numbers of patients still die due to recurrent disease or the toxicity of treatment.
  • Thus, future research must extend our molecular understanding of leukemia and host factors in order to even more specifically identify the mechanisms underlying the differences in treatment response and outcome, and to finally address the therapeutic needs of the individual child.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


22. Sørensen GV, Helgestad J, Rosthøj S: [Herpes zoster-associated morbidity in children undergoing chemotherapy for acute lymphoblastic leukaemia]. Ugeskr Laeger; 2009 Nov 9;171(46):3350-4
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  • [Title] [Herpes zoster-associated morbidity in children undergoing chemotherapy for acute lymphoblastic leukaemia].
  • We aimed to assess morbidity from herpes zoster in children with acute lymphoblastic leukemia (ALL).
  • Three children on prolonged intensive chemotherapy had recurrent zoster episodes.
  • CONCLUSION: Chemotherapy causes zoster eruptions in approximately one quarter of children with ALL, and with intensive protocols recurrent zoster can cause significant morbidity.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Herpes Zoster / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19925740.001).
  • [ISSN] 1603-6824
  • [Journal-full-title] Ugeskrift for laeger
  • [ISO-abbreviation] Ugeskr. Laeg.
  • [Language] dan
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antiviral Agents; X4HES1O11F / Acyclovir
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23. Pihan G: Detection of gene fusions in acute leukemia using bead microarrays. Curr Protoc Cytom; 2006 Feb;Chapter 13:Unit13.7
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  • [Title] Detection of gene fusions in acute leukemia using bead microarrays.
  • This unit describes a method for the rapid and simultaneous detection of hybrid mRNAs (hRNA; also known as gene fusions, RNA fusions, or chimeric RNA), resulting from recurrent chromosome translocations or inversions in acute leukemia.
  • The assay is designed to detect the most common risk-stratifying translocation in pediatric acute lymphoblastic leukemia, satisfying the demand for inclusion of genetic data in the diagnosis of acute leukemia as predicated by the current WHO classification of hematopoietic and lymphoid neoplasms.

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  • (PMID = 18770837.001).
  • [ISSN] 1934-9300
  • [Journal-full-title] Current protocols in cytometry
  • [ISO-abbreviation] Curr Protoc Cytom
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / RNA, Messenger; 0 / RNA, Neoplasm
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24. 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.
  • 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.
  • [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

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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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25. 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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  • [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.
  • 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

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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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26. Alexander BM, Wechsler D, Braun TM, Levine J, Herman J, Yanik G, Hutchinson R, Pierce LJ: Utility of cranial boost in addition to total body irradiation in the treatment of high risk acute lymphoblastic leukemia. Int J Radiat Oncol Biol Phys; 2005 Nov 15;63(4):1191-6
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  • [Title] Utility of cranial boost in addition to total body irradiation in the treatment of high risk acute lymphoblastic leukemia.
  • PURPOSE: Total body irradiation (TBI) as part of a conditioning regimen before hematopoietic stem cell transplant (HSCT) is an important component in the management of acute lymphoblastic leukemia (ALL) that has relapsed or has other certain high-risk features.
  • RESULTS: At the time of analysis, 30 (45%) patients were alive with no evidence of disease, 8 (12%) were alive with recurrence of leukemia, 7 (10.5%) had recurrent ALL but with successful salvage, 7 (11%) died subsequent to recurrence, 14 (21%) died from complications related to HCST, and 1 patient was lost to follow-up (1.5%).
  • [MeSH-major] Brain Neoplasms / prevention & control. Cranial Irradiation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control. Whole-Body Irradiation


27. Abbas S, Lugthart S, Kavelaars FG, Schelen A, Koenders JE, Zeilemaker A, van Putten WJ, Rijneveld AW, Löwenberg B, Valk PJ: Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value. Blood; 2010 Sep 23;116(12):2122-6
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  • [Title] Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value.
  • Somatic mutations in isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) were recently demonstrated in acute myeloid leukemia (AML), but their prevalence and prognostic impact remain to be explored in large extensively characterized AML series, and also in various other hematologic malignancies.
  • Moreover, we identified IDH mutations in 2 JAK2 V617F myeloproliferative neoplasias (n = 96), a single case of acute lymphoblastic leukemia (n = 96), and none in chronic myeloid leukemias (n = 81).
  • [MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

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  • (PMID = 20538800.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / Janus Kinase 2
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28. 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.
  • 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


29. 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.
  • 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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30. Qureshi A, Mitchell C, Richards S, Vora A, Goulden N: Asparaginase-related venous thrombosis in UKALL 2003- re-exposure to asparaginase is feasible and safe. Br J Haematol; 2010 May;149(3):410-3
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  • We report the incidence and outcome of venous thrombosis (VT) in the UK acute lymphoblastic leukaemia (ALL) 2003 trial.
  • There were no episodes of bleeding or recurrent thrombosis.
  • [MeSH-minor] Adolescent. Anticoagulants / therapeutic use. Child. Child, Preschool. Feasibility Studies. Female. Heparin, Low-Molecular-Weight / therapeutic use. Humans. Infant. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Prospective Studies

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  • (PMID = 20201945.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0300130; United Kingdom / Medical Research Council / / MC/ U137686856
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticoagulants; 0 / Antineoplastic Agents; 0 / Heparin, Low-Molecular-Weight; EC 3.5.1.1 / Asparaginase
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31. Prabhu S, Gottlieb DJ, Varikatt W, St Heaps L, Diaz S, Smith A: Adult B-cell acute lymphoblastic leukemia with two unrelated abnormal cytogenetic clones. Cancer Genet Cytogenet; 2010 Aug;201(1):24-7
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  • [Title] Adult B-cell acute lymphoblastic leukemia with two unrelated abnormal cytogenetic clones.
  • On the basis of the morphology, flow cytometry, and lack of myeloid-associated markers, a diagnosis of precursor B-cell acute lymphoblastic leukemia (B-ALL) was made.
  • The dic(7;9) is a rare but recurrent abnormality in B-ALL, while trisomy 8 as a sole abnormality is most commonly associated with myeloid malignancies.
  • [MeSH-major] Leukemia, B-Cell / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20633764.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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32. Pérez-Vera P, Salas C, Montero-Ruiz O, Frías S, Dehesa G, Jarquín B, Rivera-Luna R: Analysis of gene rearrangements using a fluorescence in situ hybridization method in Mexican patients with acute lymphoblastic leukemia: experience at a single institution. Cancer Genet Cytogenet; 2008 Jul 15;184(2):94-8
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  • [Title] Analysis of gene rearrangements using a fluorescence in situ hybridization method in Mexican patients with acute lymphoblastic leukemia: experience at a single institution.
  • We evaluated the prevalence of BCR/ABL, MLL, and ETV6/RUNX1 rearrangements as well as CDKN2A (alias p16) deletion in a group of Mexican children with acute lymphoblastic leukemia (ALL) to determine whether the changes coexist, and to compare the incidences found with other reports in the literature.
  • The coexistence of two recurrent abnormalities with specific prognostic significance in the same patient was not found.
  • [MeSH-major] Chromosome Aberrations. In Situ Hybridization, Fluorescence / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Child. Child, Preschool. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 19. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Core Binding Factor Alpha 2 Subunit / genetics. Female. Gene Frequency. Genes, abl. Genes, p16. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Male. Mexico. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 18617057.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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33. Sato TS, Ferguson PJ, Khanna G: Primary multifocal osseous lymphoma in a child. Pediatr Radiol; 2008 Dec;38(12):1338-41
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  • The differential diagnoses for such a presentation include histiocytosis X, chronic recurrent multifocal osteomyelitis, acute lymphoblastic leukemia, metastatic disease, and primary bone lymphoma.

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  • [ISSN] 0301-0449
  • [Journal-full-title] Pediatric radiology
  • [ISO-abbreviation] Pediatr Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
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34. 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

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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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35. da Silva Silveira V, Canalle R, Scrideli CA, Queiroz RG, Bettiol H, Valera ET, Tone LG: Polymorphisms of xenobiotic metabolizing enzymes and DNA repair genes and outcome in childhood acute lymphoblastic leukemia. Leuk Res; 2009 Jul;33(7):898-901
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  • [Title] Polymorphisms of xenobiotic metabolizing enzymes and DNA repair genes and outcome in childhood acute lymphoblastic leukemia.
  • The interindividual variation in the activity of xenobiotic metabolizing enzymes and DNA repair genes could modify an individual's risk of recurrent malignancy and response to therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. DNA Repair Enzymes / genetics. Polymorphism, Genetic / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [CommentIn] Leuk Res. 2009 Jul;33(7):889-90 [19243820.001]
  • (PMID = 19162321.001).
  • [ISSN] 1873-5835
  • [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 / DNA-Binding Proteins; 0 / Interleukin-3; 0 / Recombinant Fusion Proteins; 0 / Recombinant Proteins; 0 / X-ray repair cross complementing protein 1; 0 / myelopoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 1.14.14.1 / Cytochrome P-450 CYP2D6; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.1.1.45 / Thymidylate Synthase; EC 3.3.2.- / Epoxide Hydrolases; EC 3.3.2.9 / EPHX1 protein, human; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human; EC 6.5.1.- / DNA Repair Enzymes
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36. 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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  • [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.
  • 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

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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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37. Rabin KR, Man TK, Yu A, Folsom MR, Zhao YJ, Rao PH, Plon SE, Naeem RC: Clinical utility of array comparative genomic hybridization for detection of chromosomal abnormalities in pediatric acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Aug;51(2):171-7
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  • [Title] Clinical utility of array comparative genomic hybridization for detection of chromosomal abnormalities in pediatric acute lymphoblastic leukemia.
  • BACKGROUND: Accurate detection of recurrent chromosomal abnormalities is critical to assign patients to risk-based therapeutic regimens for pediatric acute lymphoblastic leukemia (ALL).

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  • (PMID = 18253961.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K12 CA090433; United States / NCI NIH HHS / CA / CA90433-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS570929; NLM/ PMC4063297
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38. Griffin TC, Weitzman S, Weinstein H, Chang M, Cairo M, Hutchison R, Shiramizu B, Wiley J, Woods D, Barnich M, Gross TG, Children's Oncology Group: A study of rituximab and ifosfamide, carboplatin, and etoposide chemotherapy in children with recurrent/refractory B-cell (CD20+) non-Hodgkin lymphoma and mature B-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group. Pediatr Blood Cancer; 2009 Feb;52(2):177-81
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  • [Title] A study of rituximab and ifosfamide, carboplatin, and etoposide chemotherapy in children with recurrent/refractory B-cell (CD20+) non-Hodgkin lymphoma and mature B-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group.
  • BACKGROUND: To estimate the response rate and therapy related toxicities of the anti-CD20 monoclonal antibody rituximab when combined with chemotherapy including ifosfamide, carboplatin, and etoposide (ICE) in patients with relapsed and refractory B-cell non-Hodgkin lymphoma and mature B-cell acute lymphoblastic leukemia (B-ALL).


39. Parker H, An Q, Barber K, Case M, Davies T, Konn Z, Stewart A, Wright S, Griffiths M, Ross FM, Moorman AV, Hall AG, Irving JA, Harrison CJ, Strefford JC: The complex genomic profile of ETV6-RUNX1 positive acute lymphoblastic leukemia highlights a recurrent deletion of TBL1XR1. Genes Chromosomes Cancer; 2008 Dec;47(12):1118-25
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  • [Title] The complex genomic profile of ETV6-RUNX1 positive acute lymphoblastic leukemia highlights a recurrent deletion of TBL1XR1.
  • The ETV6-RUNX1 fusion is the molecular consequence of the t(12;21)(p13;q22) seen in approximately 25% of children with acute lymphoblastic leukemia (ALL).
  • Studies have shown that the fusion alone is insufficient for the initiation of leukemia; additional genetic changes are required.
  • This study identifies deletions of TBL1XR1 as a recurrent abnormality in ETV6-RUNX1 positive ALL.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cytoplasmic and Nuclear / genetics. Repressor Proteins / genetics. Sequence Deletion

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  • (PMID = 18767146.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Repressor Proteins; 0 / TBL1XR1 protein, human; 0 / TEL-AML1 fusion protein
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40. 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
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  • 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.
  • [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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41. Shimoyama M, Yamamoto K, Nishikawa S, Minagawa K, Katayama Y, Matsui T: Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia. Cancer Genet Cytogenet; 2009 Oct;194(1):38-43
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  • [Title] Duplication of isodicentric chromosome 21, idic(21)(p11.2), leading to pentasomy 21q in acute myeloid leukemia with multilineage dysplasia.
  • Isodicentric chromosome 21, idic(21)(p11.2), is a rare but recurrent cytogenetic aberration in acute lymphoblastic leukemia.
  • We describe here a novel case of acute myeloid leukemia (AML) with double idic(21)(p11.2).
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 21 / genetics. Gene Duplication. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Adult. Antigens, CD / blood. Antigens, CD13 / blood. Antigens, CD34 / blood. Antigens, CD7 / blood. Antigens, Differentiation, Myelomonocytic / blood. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. HLA-DR Antigens / blood. Humans. In Situ Hybridization, Fluorescence. Male. Sialic Acid Binding Ig-like Lectin 3. Spectral Karyotyping

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  • (PMID = 19737652.001).
  • [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 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, CD7; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / HLA-DR Antigens; 0 / RUNX1 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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42. Jarosova M, Takacova S, Holzerova M, Priwitzerova M, Divoka M, Lakoma I, Mihal V, Indrak K, Divoky V: Cryptic MLL-AF10 fusion caused by insertion of duplicated 5' part of MLL into 10p12 in acute leukemia: a case report. Cancer Genet Cytogenet; 2005 Oct 15;162(2):179-82
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  • [Title] Cryptic MLL-AF10 fusion caused by insertion of duplicated 5' part of MLL into 10p12 in acute leukemia: a case report.
  • Chromosomal translocations involving the mixed lineage leukemia gene (MLL) located at 11q23 belong to common chromosomal abnormalities in both acute lymphoblastic (ALL) and acute myeloid leukemias (AML).
  • One of the recurrent translocations in AML-M5 involves chromosomal locus 10p12 and results in the MLL-AF10 fusion gene.
  • [MeSH-major] Chromosomes, Human, Pair 10. Leukemia, Monocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics

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  • (PMID = 16213369.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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43. 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
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  • [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.
  • [MeSH-major] Immunoglobulin Heavy Chains / genetics. Inhibitor of Differentiation Proteins / genetics. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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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 / / 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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44. Gandemer V, Rio AG, de Tayrac M, Sibut V, Mottier S, Ly Sunnaram B, Henry C, Monnier A, Berthou C, Le Gall E, Le Treut A, Schmitt C, Le Gall JY, Mosser J, Galibert MD: Five distinct biological processes and 14 differentially expressed genes characterize TEL/AML1-positive leukemia. BMC Genomics; 2007;8:385
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  • [Title] Five distinct biological processes and 14 differentially expressed genes characterize TEL/AML1-positive leukemia.
  • BACKGROUND: The t(12;21)(p13;q22) translocation is found in 20 to 25% of cases of childhood B-lineage acute lymphoblastic leukemia (B-ALL).
  • RESULTS: We compared the leukemia cell gene expression profiles of 16 TEL/AML1-positive ALL patients to those of 44 TEL/AML1-negative patients, whose blast cells did not contain any additional recurrent translocation.
  • CONCLUSION: Gene expression analyses of leukemia cells from 60 children with TEL/AML1-positive and -negative B-lineage ALL led to the identification of five biological processes, associated with 14 validated genes characterizing and highlighting the biology of the TEL/AML1-positive ALL sub-group.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Profiling / methods. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17956600.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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  • [Other-IDs] NLM/ PMC2211320
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45. Zweier-Renn LA, Hawley TS, Burkett S, Ramezani A, Riz I, Adler RL, Hickstein DD, Hawley RG: Hematopoietic immortalizing function of the NKL-subclass homeobox gene TLX1. Genes Chromosomes Cancer; 2010 Feb;49(2):119-31
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  • Translocations resulting in ectopic expression of the TLX1 homeobox gene (previously known as HOX11) are recurrent events in human T-cell acute lymphoblastic leukemia (T-ALL).

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  • (PMID = 19862821.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01HL65519; United States / NHLBI NIH HHS / HL / R01 HL065519-08; United States / NHLBI NIH HHS / HL / R01 HL066305-05; United States / NHLBI NIH HHS / HL / HL065519-08; United States / NHLBI NIH HHS / HL / R01 HL065519; United States / Intramural NIH HHS / / ; United States / NHLBI NIH HHS / HL / R01 HL066305; United States / NHLBI NIH HHS / HL / HL066305-05; United States / NHLBI NIH HHS / HL / R01HL66305
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 143275-75-6 / TLX1 protein, human
  • [Other-IDs] NLM/ NIHMS155591; NLM/ PMC2795049
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46. Kuiper RP, Waanders E, van der Velden VH, van Reijmersdal SV, Venkatachalam R, Scheijen B, Sonneveld E, van Dongen JJ, Veerman AJ, van Leeuwen FN, van Kessel AG, Hoogerbrugge PM: IKZF1 deletions predict relapse in uniformly treated pediatric precursor B-ALL. Leukemia; 2010 Jul;24(7):1258-64
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  • Relapse is the most common cause of treatment failure in pediatric acute lymphoblastic leukemia (ALL) and is often difficult to predict.
  • To explore the prognostic impact of recurrent DNA copy number abnormalities on relapse, we performed high-resolution genomic profiling of 34 paired diagnosis and relapse ALL samples.
  • Recurrent lesions detected at diagnosis, including PAX5, CDKN2A and EBF1, were frequently absent at relapse, indicating that they represent secondary events that may be absent in the relapse-prone therapy-resistant progenitor cell.
  • [MeSH-major] Gene Deletion. Ikaros Transcription Factor / genetics. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics


47. Benesch M, Sovinz P, Krammer B, Lackner H, Mann G, Schwinger W, Gadner H, Urban C: Feasibility and toxicity of intrathecal liposomal cytarabine in 5 children and young adults with refractory neoplastic meningitis. J Pediatr Hematol Oncol; 2007 Apr;29(4):222-6
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  • We studied feasibility and toxicity of IT administered liposomal cytarabine on a compassionate basis in 5 patients (male, n=4; female, n=1; age at diagnosis 5 to 18 y) with recurrent acute lymphoblastic leukemia (n=3), primary refractory acute myeloid leukemia (n=1), or relapsed medulloblastoma (n=1).

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  • (PMID = 17414563.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Liposomes; 04079A1RDZ / Cytarabine
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48. Davidsson J, Paulsson K, Lindgren D, Lilljebjörn H, Chaplin T, Forestier E, Andersen MK, Nordgren A, Rosenquist R, Fioretos T, Young BD, Johansson B: Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations. Leukemia; 2010 May;24(5):924-31
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  • [Title] Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations.
  • Although childhood high hyperdiploid acute lymphoblastic leukemia is associated with a favorable outcome, 20% of patients still relapse.
  • No single aberration was linked to relapse, but four deletions, involving IKZF1, PAX5, CDKN2A/B or AK3, were recurrent.
  • [MeSH-major] Chromosome Deletion. Diploidy. Genes, ras / genetics. Mutation / genetics. Neoplasm Recurrence, Local / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor Protein-Tyrosine Kinases / genetics


49. Chan GS, Chim S, Fan YS, Chan KW: Focal segmental glomerulosclerosis after membranous glomerulonephritis in remission: temporal diversity of glomerulopathy after bone marrow transplantation. Hum Pathol; 2006 Dec;37(12):1607-10
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  • We describe a 13-year-old boy who had matched unrelated donor allogeneic BMT for relapsed acute lymphoblastic leukemia, complicated by chronic graft-versus-host disease.
  • Recurrent significant proteinuria after BMT is not necessarily due to previous renal lesion, and a repeat renal biopsy is indicated.


50. Gaikwad A, Rye CL, Devidas M, Heerema NA, Carroll AJ, Izraeli S, Plon SE, Basso G, Pession A, Rabin KR: Prevalence and clinical correlates of JAK2 mutations in Down syndrome acute lymphoblastic leukaemia. Br J Haematol; 2009 Mar;144(6):930-2
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  • [Title] Prevalence and clinical correlates of JAK2 mutations in Down syndrome acute lymphoblastic leukaemia.
  • Recurrent, prognostically significant chromosomal abnormalities occur in approximately 75% of paediatric acute lymphoblastic leukaemia (ALL), but only infrequently in children with Down syndrome (DS) and ALL.

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  • [Cites] Blood. 2007 Mar 1;109(5):2202-4 [17068151.001]
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  • (PMID = 19120350.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K12 CA090433; United States / NCI NIH HHS / CA / K12 CA090433-06; United States / NCI NIH HHS / CA / CA90433-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / Janus Kinase 2
  • [Other-IDs] NLM/ NIHMS127709; NLM/ PMC2724897
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51. Carlsson G, Aprikyan AA, Ericson KG, Stein S, Makaryan V, Dale DC, Nordenskjöld M, Fadeel B, Palmblad J, Hentera JI: Neutrophil elastase and granulocyte colony-stimulating factor receptor mutation analyses and leukemia evolution in severe congenital neutropenia patients belonging to the original Kostmann family in northern Sweden. Haematologica; 2006 May;91(5):589-95
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  • [Title] Neutrophil elastase and granulocyte colony-stimulating factor receptor mutation analyses and leukemia evolution in severe congenital neutropenia patients belonging to the original Kostmann family in northern Sweden.
  • BACKGROUND AND OBJECTIVES: Severe congenital neutropenia (SCN) or Kostmann syndrome was originally reported to be an autosomal recessive disease of neutrophil production causing recurrent, life-threatening infections.
  • As a young adult this patient sequentially acquired two mutations in the gene for the G-CSF receptor (G-CSFR) and therefore recently received a hematopoietic stem cell transplant, due to the risk of evolution to leukemia.
  • Moreover, another patient developed acute leukemia and was treated with transplantation.
  • INTERPRETATION AND CONCLUSIONS: Our data are the first to document leukemia evolution and G-CSFR gene mutations in the original Kostmann kindred.
  • [MeSH-major] Leukocyte Elastase / genetics. Neoplasm Proteins / genetics. Neutropenia / congenital. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Preleukemia / genetics. Receptors, Granulocyte Colony-Stimulating Factor / genetics

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  • (PMID = 16670064.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / GFI1 protein, human; 0 / Neoplasm Proteins; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 0 / Transcription Factors; 0 / Wiskott-Aldrich Syndrome Protein; EC 3.4.21.37 / Leukocyte Elastase
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52. 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.
  • 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.
  • [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


53. Bungaro S, Dell'Orto MC, Zangrando A, Basso D, Gorletta T, Lo Nigro L, Leszl A, Young BD, Basso G, Bicciato S, Biondi A, te Kronnie G, Cazzaniga G: Integration of genomic and gene expression data of childhood ALL without known aberrations identifies subgroups with specific genetic hallmarks. Genes Chromosomes Cancer; 2009 Jan;48(1):22-38
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  • Pediatric acute lymphoblastic leukemia (ALL) comprises genetically distinct subtypes.
  • To identify variation in expression of genes directly or indirectly affected by recurrent genomic alterations, we integrated genomic and gene expression data generated by microarray analyses of the same samples.
  • [MeSH-major] Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18803328.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Calcium-Binding Proteins; 0 / ETS translocation variant 6 protein; 0 / Genetic Markers; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / PAX5 protein, human; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / Smad1 Protein; 134324-36-0 / Serrate proteins
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54. Struski S, Hélias C, Gervais C, Leymarie V, Audhuy B, Moskovtchenko P, Lutz P, Gaub MP, Lessard M: Confirmation of a novel recurrent association: BCR-ABL t(9;22) and t(19;21). Cancer Genet Cytogenet; 2007 Dec;179(2):127-31
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  • [Title] Confirmation of a novel recurrent association: BCR-ABL t(9;22) and t(19;21).
  • Association of a t(9;22)(q34;q11), BCR/ABL-positive, with a dic(19;21)(p13;p13) has been described in acute lymphoblastic leukemia in relapse, raising the question of whether this association is recurrent.
  • Described here are two cases, one of myeloproliferative disease and one of acute lymphoblastic leukemia, both presenting a masked t(9;22) and t(19;21).

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  • (PMID = 18036399.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
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55. Hah JO: Anaplastic oligodendroglioma after childhood acute lymphoblastic leukemia: chemotherapy and autologous peripheral blood stem cell transplantation. J Pediatr Hematol Oncol; 2008 Oct;30(10):764-7
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  • [Title] Anaplastic oligodendroglioma after childhood acute lymphoblastic leukemia: chemotherapy and autologous peripheral blood stem cell transplantation.
  • Secondary brain tumors after cranial irradiation occur in survivors of childhood acute lymphoblastic leukemia (ALL).
  • High-dose chemotherapy with stem cell rescue seems to be potentially effective for multiple recurrent anaplastic oligodendroglioma occurring after childhood ALL.
  • [MeSH-major] Neoplasms, Second Primary / therapy. Oligodendroglioma / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


56. Chang HH, Lu MY, Jou ST, Lin KH, Tien HF, Lin DT: Cytogenetics in childhood acute lymphoblastic leukemia in Taiwan: a single-institutional experience. Pediatr Hematol Oncol; 2006 Sep;23(6):495-506
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  • [Title] Cytogenetics in childhood acute lymphoblastic leukemia in Taiwan: a single-institutional experience.
  • Of the patients with abnormal karyotypes, recurrent structural abnormalities were determined in 31 (50%) cases, with the most frequent t(9;22).
  • [MeSH-major] Chromosome Aberrations / statistics & numerical data. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


57. 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


58. Seif AE, Barrett DM, Milone M, Brown VI, Grupp SA, Reid GS: Long-term protection from syngeneic acute lymphoblastic leukemia by CpG ODN-mediated stimulation of innate and adaptive immune responses. Blood; 2009 Sep 17;114(12):2459-66
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  • [Title] Long-term protection from syngeneic acute lymphoblastic leukemia by CpG ODN-mediated stimulation of innate and adaptive immune responses.
  • Acute lymphoblastic leukemia (ALL) is the most common childhood cancer and remains a major cause of mortality in children with recurrent disease and in adults.
  • Despite observed graft-versus-leukemia effects after stem cell transplantation, successful immune therapies for ALL have proven elusive.
  • CpG ODN induced early killing of leukemia by innate immune effectors both in vitro and in vivo.
  • Mice were treated with CpG ODN starting 7 days after injection with leukemia to mimic a minimal residual disease state and achieved T cell-dependent remissions of more than 6 months.
  • In addition, mice in remission after CpG ODN treatment were protected from leukemia rechallenge, and adoptive transfer of T cells from mice in remission conferred protection against leukemia growth.

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  • (PMID = 19636062.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K12 CA076931; United States / NCI NIH HHS / CA / 2K12CA076931-11; United States / NCI NIH HHS / CA / T32 CA009615; United States / NCI NIH HHS / CA / R03-CA123554; United States / NCI NIH HHS / CA / R03 CA123554
  • [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 / CPG-oligonucleotide; 0 / Oligodeoxyribonucleotides
  • [Other-IDs] NLM/ PMC2746473
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59. Limongi ZM, Curatolo A, Pelliccia F, Rocchi A: Biallelic deletion and loss of expression analysis of genes at FRA2G common fragile site in tumor-derived cell lines. Cancer Genet Cytogenet; 2005 Sep;161(2):181-6
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  • Much evidence suggests that CFSs are causally related to cancer as breakpoints in recurrent chromosome mutations and as sites of viral integration.
  • Moreover, we observed loss of expression (LOE) of the DHRS9 gene (alias RDHL), one of the deleted genes in the DAUDI cell line, in MOLT-14 and Raji cell lines derived from Burkitt lymphoma and from T-cell acute lymphoblastic leukemia, respectively.

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  • (PMID = 16102592.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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60. Iwanami H, Odaka M, Hirata K: [A case of acute lymphocytic leukemia relapsed as meningoradiculoneuropathy after bone marrow transplantation]. Rinsho Shinkeigaku; 2006 Feb;46(2):157-9
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  • [Title] [A case of acute lymphocytic leukemia relapsed as meningoradiculoneuropathy after bone marrow transplantation].
  • We report a 21-year-old woman who had acute lymphocytic leukemia with a relapse in the peripheral nervous system after bone marrow transplantation.
  • Based on the diagnosis of recurrent acute lymphocytic leukemia with tumor infiltration to the meninges (meningeal leukemia), she received chemotherapy, after which her neurological symptoms and signs gradually improved.
  • We would like to emphasize that neurological examination is important to detect CNS relapse in a patient with leukemia, even in hematological complete remission.
  • [MeSH-major] Bone Marrow Transplantation. Meningeal Neoplasms / etiology. Peripheral Nervous System Neoplasms / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 16619843.001).
  • [ISSN] 0009-918X
  • [Journal-full-title] Rinshō shinkeigaku = Clinical neurology
  • [ISO-abbreviation] Rinsho Shinkeigaku
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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61. Keckler SJ, Spilde TL, St Peter SD, Tsao K, Ostlie DJ: Treatment of bronchopleural fistula with small intestinal mucosa and fibrin glue sealant. Ann Thorac Surg; 2007 Oct;84(4):1383-6
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  • We present a case of bronchopleural fistula occurring after pulmonary lobectomy for aspergilloma in a patient with recurrent acute lymphoblastic leukemia.
  • [MeSH-minor] Aspergillosis / complications. Aspergillosis / diagnosis. Aspergillosis / surgery. Bronchoscopy / methods. Child. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Intestine, Small. Lung Diseases, Fungal / complications. Lung Diseases, Fungal / diagnosis. Lung Diseases, Fungal / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Risk Assessment. Treatment Outcome

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  • (PMID = 17889008.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Fibrin Tissue Adhesive
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62. Jeong EG, Kim MS, Nam HK, Min CK, Lee S, Chung YJ, Yoo NJ, Lee SH: Somatic mutations of JAK1 and JAK3 in acute leukemias and solid cancers. Clin Cancer Res; 2008 Jun 15;14(12):3716-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Somatic mutations of JAK1 and JAK3 in acute leukemias and solid cancers.
  • EXPERIMENTAL DESIGN: We analyzed 494 tissues from 186 acute adulthood leukemias, 30 multiple myelomas, and 278 common solid cancers, including 90 breast, 47 gastric, 47 colon, 47 lung, and 47 hepatocellular carcinomas by single-strand conformation polymorphism analysis.
  • RESULTS: Overall, we found six JAK1 mutations (four in acute leukemias, one in a lung carcinoma, and one in a breast carcinoma) and three JAK3 mutations (two in breast carcinomas and one in a gastric carcinoma).
  • These recurrent mutations in identical and homologous sites suggest a possibility that alterations of these amino acids might be important for tumor pathogenesis.
  • With respect to the cancer types, T-acute lymphoblastic leukemia (T-ALL) showed the highest incidence of the mutations (3 of 11; 27.3%).
  • [MeSH-major] Breast Neoplasms / genetics. Carcinoma / genetics. Janus Kinase 1 / genetics. Janus Kinase 3 / genetics. Leukemia / genetics. Mutation
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Base Sequence. Colorectal Neoplasms / genetics. DNA Mutational Analysis. Humans. Liver Neoplasms / genetics. Middle Aged. Stomach Neoplasms / genetics

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  • (PMID = 18559588.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / JAK3 protein, human; EC 2.7.010.2 / JAK1 protein, human; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3
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63. Tomizawa D, Koh K, Hirayama M, Miyamura T, Hatanaka M, Saikawa Y, Ishii E: Outcome of recurrent or refractory acute lymphoblastic leukemia in infants with MLL gene rearrangements: A report from the Japan Infant Leukemia Study Group. Pediatr Blood Cancer; 2009 Jul;52(7):808-13
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  • [Title] Outcome of recurrent or refractory acute lymphoblastic leukemia in infants with MLL gene rearrangements: A report from the Japan Infant Leukemia Study Group.
  • BACKGROUND: Despite the poor outcome of recurrent or refractory acute lymphoblastic leukemia (ALL) in infants with MLL gene rearrangement, few studies have focused on this specific group.
  • We conducted a retrospective analysis of infants with recurrent or refractory ALL from two previous consecutive Japanese studies to clarify the characteristics and prognostic factors among these patients PROCEDURE: All recurrent or refractory ALL infants with MLL gene rearrangement (MLL-R) who were registered in two consecutive Japanese nation-wide multicentric trials (MLL96 and MLL98; between 1995 and 2001) were eligible for the study.
  • CONCLUSIONS: The prognosis of infants with recurrent or refractory MLL-R ALL is extremely poor despite alternative treatments including HSCT; therefore, it is necessary to develop novel treatment strategies.
  • [MeSH-major] Drug Resistance, Neoplasm. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasm Recurrence, Local / genetics. Neoplasm Recurrence, Local / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19229974.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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64. Kawamata N, Ogawa S, Zimmermann M, Kato M, Sanada M, Hemminki K, Yamatomo G, Nannya Y, Koehler R, Flohr T, Miller CW, Harbott J, Ludwig WD, Stanulla M, Schrappe M, Bartram CR, Koeffler HP: Molecular allelokaryotyping of pediatric acute lymphoblastic leukemias by high-resolution single nucleotide polymorphism oligonucleotide genomic microarray. Blood; 2008 Jan 15;111(2):776-84
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  • [Title] Molecular allelokaryotyping of pediatric acute lymphoblastic leukemias by high-resolution single nucleotide polymorphism oligonucleotide genomic microarray.
  • Pediatric acute lymphoblastic leukemia (ALL) is a malignant disease resulting from accumulation of genetic alterations.
  • Three common genetic alterations were found: deletion of ETV6, deletion of p16INK4A, and hyperdiploidy, as well as a number of novel recurrent genetic alterations.
  • [MeSH-major] Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Gene Deletion. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 17890455.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
  • [Other-IDs] NLM/ PMC2200831
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65. Hamamoto K, Oriuchi N, Kanazawa T, Higuchi T, Endo K: Mesial temporal sclerosis associated with methotrexate-induced leukoencephalopathy. Pediatr Neurol; 2009 Apr;40(4):306-9
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  • Mesial temporal sclerosis is a common form of symptomatic, localization-related epilepsy in children and adolescents, but its occurrence with acute lymphoblastic leukemia is rare.
  • We present clinical records and neuroimaging results of a 13-year-old patient with acute lymphoblastic leukemia who developed recurrent partial seizures after an episode of leukoencephalopathy thought to be caused by methotrexate.
  • Mesial temporal sclerosis was not previously reported in acute lymphoblastic leukemia patients with methotrexate-induced leukoencephalopathy.
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child, Preschool. Female. Fluorodeoxyglucose F18. Humans. Magnetic Resonance Imaging. Positron-Emission Tomography. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sclerosis

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  • (PMID = 19302946.001).
  • [ISSN] 0887-8994
  • [Journal-full-title] Pediatric neurology
  • [ISO-abbreviation] Pediatr. Neurol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0Z5B2CJX4D / Fluorodeoxyglucose F18; YL5FZ2Y5U1 / Methotrexate
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66. Harrison CJ: Cytogenetics of paediatric and adolescent acute lymphoblastic leukaemia. Br J Haematol; 2009 Jan;144(2):147-56
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  • [Title] Cytogenetics of paediatric and adolescent acute lymphoblastic leukaemia.
  • Cytogenetics has determined the incidence and prognostic significance of chromosomal abnormalities in acute lymphoblastic leukaemia (ALL).
  • (ii) intrachromosomal amplification of chromosome 21 is a new recurrent abnormality in precursor-B ALL (BCP-ALL);.
  • [MeSH-major] Chromosome Aberrations. Cytogenetic Analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19006567.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 74
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67. Küker W, Bader P, Herrlinger U, Heckl S, Nägele T: Transient encephalopathy after intrathekal methotrexate chemotherapy: diffusion-weighted MRI. J Neurooncol; 2005 May;73(1):47-9
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  • However, acute neurotoxicity with confusion, disorientation, seizures and focal deficits has also been reported.
  • Because acute neurological symptoms in patients under chemotherapy for neoplastic disorders may have many reasons, MR-imaging is usually necessary to identify the underlying pathology.
  • We report on clinical and imaging findings of reversibly restricted diffusion in a patient with transient encephalopathy after intrathecal administration of MTX for recurrent acute lymphatic leukaemia.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Brain Diseases / chemically induced. Methotrexate / adverse effects. Neurotoxicity Syndromes / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • [ISSN] 0167-594X
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  • [Language] eng
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68. Thomas DA, Sarris AH, Cortes J, Faderl S, O'Brien S, Giles FJ, Garcia-Manero G, Rodriguez MA, Cabanillas F, Kantarjian H: Phase II study of sphingosomal vincristine in patients with recurrent or refractory adult acute lymphocytic leukemia. Cancer; 2006 Jan 1;106(1):120-7
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  • [Title] Phase II study of sphingosomal vincristine in patients with recurrent or refractory adult acute lymphocytic leukemia.
  • BACKGROUND: Outcomes with salvage therapy for patients with recurrent or refractory acute lymphocytic leukemia (ALL) are poor, with complete response (CR) rates reported to be 20-30% and a median survival ranging from 2-6 months.
  • METHODS: A Phase II clinical trial of single-agent SV given at a dose of 2.0 mg/m2 every 2 weeks was conducted in patients with recurrent or refractory ALL.
  • Five patients (36%) had transient reductions in bone marrow leukemia infiltrate with subsequent regrowth of the leukemia between SV infusions.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Salvage Therapy. Vincristine / therapeutic use

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  • [Copyright] Copyright 2005 American Cancer Society.
  • [ErratumIn] Cancer. 2006 Apr 1;106(7):1641
  • (PMID = 16331634.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Liposomes; 0 / Sphingomyelins; 5J49Q6B70F / Vincristine
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69. 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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  • 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.
  • 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

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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 Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; 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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70. Yamamoto-Ogasawara A, Asakawa M, Yoshino K, Nagamoto T, Inoue M, Hirakata A: Anterior complications in case of recurrent acute lymphoblastic leukaemia diagnosed by biopsy of aqueous humour. Clin Exp Ophthalmol; 2009 Sep;37(7):739-41
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  • [Title] Anterior complications in case of recurrent acute lymphoblastic leukaemia diagnosed by biopsy of aqueous humour.
  • [MeSH-major] Anterior Chamber / pathology. Aqueous Humor / cytology. Leukemic Infiltration. Neoplasm Recurrence, Local / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19788673.001).
  • [ISSN] 1442-9071
  • [Journal-full-title] Clinical & experimental ophthalmology
  • [ISO-abbreviation] Clin. Experiment. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Glucocorticoids; EC 3.4.24.11 / Neprilysin
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71. Linsenmeier C, Thoennessen D, Negretti L, Bourquin JP, Streller T, Lütolf UM, Oertel S: Total body irradiation (TBI) in pediatric patients. A single-center experience after 30 years of low-dose rate irradiation. Strahlenther Onkol; 2010 Nov;186(11):614-20
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  • A total of 18 patients suffered from acute lymphoblastic leukemia (ALL), 5 from acute and 2 from chronic myelogenous leukemia, 1 from non-Hodgkin lymphoma, and 2 from anaplastic anemia.
  • The cohort consisted of 15 patients referred after first remission and 13 patients with relapsed leukemia.
  • Eight patients died of recurrent disease, 1 of graft vs. host reaction, 2 of sepsis, and 2 patients died of a secondary malignancy.
  • Overall survival was significantly inferior in patients treated after relapse compared to those treated for newly diagnosed leukemia (24% versus 74%; p=0.004).
  • [MeSH-major] Anemia, Aplastic / radiotherapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / radiotherapy. Leukemia, Myeloid, Acute / radiotherapy. Lymphoma, Non-Hodgkin / radiotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Whole-Body Irradiation

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  • (PMID = 21069270.001).
  • [ISSN] 1439-099X
  • [Journal-full-title] Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al]
  • [ISO-abbreviation] Strahlenther Onkol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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72. 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
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  • [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].
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Spectral Karyotyping / methods. Translocation, Genetic / 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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73. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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).
  • 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

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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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74. Ege MJ, Meyer LH, Debatin KM, Stahnke K: Coincidence of recurrent hemiparesis and detection of ALL in a 4-year-old girl: one or two diseases? Klin Padiatr; 2009 Nov-Dec;221(6):386-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coincidence of recurrent hemiparesis and detection of ALL in a 4-year-old girl: one or two diseases?
  • In childhood leukemia, stroke like symptoms at presentation are rare and normally caused by cerebral bleedings.
  • Here we report a patient who presented with classical stroke symptoms and hemiparesis prior to the diagnosis of acute lymphoblastic leukemia without proven CNS infiltration by leukemic cells.
  • In general, acute leukemia or cerebral lymphoma do not lead to extensive defects of brain tissue.
  • This unusual case suggests that acute lymphoblastic leukemia may present with stroke like CNS symptoms including hemiparesis.
  • [MeSH-major] Paresis / complications. Paresis / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Stroke / complications. Stroke / diagnosis

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  • [Copyright] Georg Thieme Verlag KG Stuttgart.New York.
  • (PMID = 19890794.001).
  • [ISSN] 1439-3824
  • [Journal-full-title] Klinische Pädiatrie
  • [ISO-abbreviation] Klin Padiatr
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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75. Harrison CJ, Moorman AV, Barber KE, Broadfield ZJ, Cheung KL, Harris RL, Jalali GR, Robinson HM, Strefford JC, Stewart A, Wright S, Griffiths M, Ross FM, Harewood L, Martineau M: Interphase molecular cytogenetic screening for chromosomal abnormalities of prognostic significance in childhood acute lymphoblastic leukaemia: a UK Cancer Cytogenetics Group Study. Br J Haematol; 2005 May;129(4):520-30
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  • [Title] Interphase molecular cytogenetic screening for chromosomal abnormalities of prognostic significance in childhood acute lymphoblastic leukaemia: a UK Cancer Cytogenetics Group Study.
  • Summary Interphase fluorescence in situ hybridization (iFISH) was used independently to reveal chromosomal abnormalities of prognostic importance in a large, consecutive series of children (n = 2367) with acute lymphoblastic leukaemia (ALL).
  • We were thus able to define amplification of AML1 as a new recurrent abnormality in ALL, associated with a poor prognosis.
  • Amplification involving the ABL gene, a rare recurrent abnormality confined to T ALL patients, was identified for the first time.
  • [MeSH-major] Chromosome Aberrations. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Core Binding Factor Alpha 2 Subunit. Cytogenetic Analysis. DNA-Binding Proteins / genetics. Fusion Proteins, bcr-abl / genetics. Gene Amplification. Gene Rearrangement. Genes, abl. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Infant. Interphase. Myeloid-Lymphoid Leukemia Protein. Oncogene Proteins, Fusion / genetics. Prognosis. Proto-Oncogenes / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / genetics

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  • (PMID = 15877734.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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76. Reismüller B, Attarbaschi A, Peters C, Dworzak MN, Pötschger U, Urban C, Fink FM, Meister B, Schmitt K, Dieckmann K, Henze G, Haas OA, Gadner H, Mann G, Austrian Berlin-Frankfurt-Münster (BFM) Study Group: Long-term outcome of initially homogenously treated and relapsed childhood acute lymphoblastic leukaemia in Austria--a population-based report of the Austrian Berlin-Frankfurt-Münster (BFM) Study Group. Br J Haematol; 2009 Feb;144(4):559-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcome of initially homogenously treated and relapsed childhood acute lymphoblastic leukaemia in Austria--a population-based report of the Austrian Berlin-Frankfurt-Münster (BFM) Study Group.
  • Relapsed acute lymphoblastic leukaemia (ALL) is the most common cause for a fatal outcome in paediatric oncology.
  • Although initial ALL cure rates have improved up to 80%, the prognosis of recurrent ALL remains dismal with event-free-survival (EFS) rates about 35%.
  • Of these, 203 (23%) suffered from recurrent disease.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19077160.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Investigator] Ausserer B; Busch U; Müller G; Kurz R; Urban Ch; Berger H; Fink FM; Meister B; Kaulfersch W; Messner H; Mutz I; Stöllinger O; Tulzer W; Schmidt K; Ebetsberger T; Grienberger H; Jones N; Jones R; Rücker J; Haas H; Ploier R; Gadner H; Grümayer-Panzer ER; Krepler P; Mann G; Pichler E; Jürgenssen O; Slavc I; Höcker P; Knapp W; Pickl WF; Haas OA; Lion T; Kärcher KH; Hawlicek R; Pötter R; Dieckmann K
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77. Lundin C, Davidsson J, Hjorth L, Behrendtz M, Johansson B: Tiling resolution array-based comparative genomic hybridisation analyses of acute lymphoblastic leukaemias in children with Down syndrome reveal recurrent gain of 8q and deletions of 7p and 9p. Br J Haematol; 2009 Jun;146(1):113-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tiling resolution array-based comparative genomic hybridisation analyses of acute lymphoblastic leukaemias in children with Down syndrome reveal recurrent gain of 8q and deletions of 7p and 9p.
  • [MeSH-major] Down Syndrome / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [CommentOn] Blood. 2009 Jan 15;113(3):646-8 [18927438.001]
  • [CommentOn] Br J Haematol. 2008 Sep;142(6):934-45 [18557744.001]
  • (PMID = 19344409.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comment; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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78. Haltrich I, Csóka M, Kovács G, Fekete G: [Cytogenetic and FISH findings are complementary in childhood ALL]. Magy Onkol; 2008 Sep;52(3):283-91
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  • Primary genetic abnormalities of leukemia cells have important prognostic significance in childhood acute leukemia.
  • In the last two years 30 newly diagnosed or recurrent childhood ALL bone marrow samples were analyzed for chromosomal abnormalities with conventional G-banding and interphase-fluorescence in situ hybridization (I-FISH) using probes to detect BCR/ABL fusions, cryptic TEL/AML1 and MLL rearrangements and p16(9p21) tumor suppressor gene deletions.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 21. Gene Rearrangement. In Situ Hybridization, Fluorescence. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Chromosome Banding. Core Binding Factor Alpha 2 Subunit / genetics. Female. Fusion Proteins, bcr-abl / genetics. Gene Deletion. Histone-Lysine N-Methyltransferase. Humans. Interphase. Karyotyping / methods. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Predictive Value of Tests. Prognosis. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Risk Factors. Sensitivity and Specificity

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  • (PMID = 18845499.001).
  • [ISSN] 0025-0244
  • [Journal-full-title] Magyar onkologia
  • [ISO-abbreviation] Magy Onkol
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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79. Lilljebjörn H, Soneson C, Andersson A, Heldrup J, Behrendtz M, Kawamata N, Ogawa S, Koeffler HP, Mitelman F, Johansson B, Fontes M, Fioretos T: The correlation pattern of acquired copy number changes in 164 ETV6/RUNX1-positive childhood acute lymphoblastic leukemias. Hum Mol Genet; 2010 Aug 15;19(16):3150-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The correlation pattern of acquired copy number changes in 164 ETV6/RUNX1-positive childhood acute lymphoblastic leukemias.
  • The ETV6/RUNX1 fusion gene, present in 25% of B-lineage childhood acute lymphoblastic leukemia (ALL), is thought to represent an initiating event, which requires additional genetic changes for leukemia development.
  • In total, 45 recurrent CNAs were identified with an average number of 3.5 recurrent changes per case (range 0-13).
  • Twenty-six percent of cases displayed a set of recurrent CNAs identical to that of other cases in the data set.
  • The majority (74%), however, displayed a unique pattern of recurrent CNAs, indicating a large heterogeneity within this ALL subtype.

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  • (PMID = 20513752.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA026038-31; United States / NCI NIH HHS / CA / R01 CA026038-32; United States / NCI NIH HHS / CA / CA026038-30A2; United States / NCI NIH HHS / CA / R01 CA026038; United States / NCI NIH HHS / CA / R01 CA026038-30A2
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
  • [Other-IDs] NLM/ PMC3146010
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80. Gottfredsson M, Steingrímsdóttir H: Disseminated invasive aspergillosis in a patient with acute leukaemia. Acta Biomed; 2006;77 Suppl 2:10-3
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  • [Title] Disseminated invasive aspergillosis in a patient with acute leukaemia.
  • A 46-year-old previously healthy woman was diagnosed with acute lymphoblastic leukaemia.
  • Following this infection the patient developed recurrent fever and new pulmonary infiltrates were noted.
  • Bronchoscopy was performed and treatment was administered with liposomal amphotericin B (L-AmB, AmBisome) for two days, but was complicated by acute renal failure.
  • [MeSH-major] Amphotericin B / therapeutic use. Antifungal Agents / therapeutic use. Aspergillosis / complications. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Acute Kidney Injury / chemically induced. Anti-Bacterial Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bacteremia / complications. Bacteremia / drug therapy. Chlamydophila Infections / complications. Chlamydophila Infections / drug therapy. Chlamydophila pneumoniae. Doxorubicin / administration & dosage. Drug Resistance, Multiple, Fungal. Drug Therapy, Combination. Echinocandins. Fatal Outcome. Female. Humans. Immunocompromised Host. Liposomes. Lung Diseases, Fungal / complications. Lung Diseases, Fungal / drug therapy. Medical Futility. Methotrexate / administration & dosage. Middle Aged. Neuroaspergillosis / drug therapy. Neuroaspergillosis / etiology. Peptides, Cyclic / administration & dosage. Peptides, Cyclic / therapeutic use. Pneumonia, Bacterial / complications. Pyrimidines / therapeutic use. Streptococcal Infections / complications. Streptococcal Infections / drug therapy. Triazoles / therapeutic use. Vincristine / administration & dosage. Voriconazole

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  • Hazardous Substances Data Bank. AMPHOTERICIN B .
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  • [ErratumIn] Acta Biomed. 2006;77 Suppl 4:following 33
  • (PMID = 16918060.001).
  • [ISSN] 0392-4203
  • [Journal-full-title] Acta bio-medica : Atenei Parmensis
  • [ISO-abbreviation] Acta Biomed
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antifungal Agents; 0 / Echinocandins; 0 / Liposomes; 0 / Peptides, Cyclic; 0 / Pyrimidines; 0 / Triazoles; 0 / liposomal amphotericin B; 5J49Q6B70F / Vincristine; 7XU7A7DROE / Amphotericin B; 80168379AG / Doxorubicin; F0XDI6ZL63 / caspofungin; JFU09I87TR / Voriconazole; YL5FZ2Y5U1 / Methotrexate
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81. Gmidène A, Elghezal H, Sennana H, Ben Youssef Y, Meddeb B, Elloumi M, Khlif A, Saad A: ETV6-RUNX1 Rearrangement in Tunisian Pediatric B-Lineage Acute Lymphoblastic Leukemia. Adv Hematol; 2009;2009:924301
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  • [Title] ETV6-RUNX1 Rearrangement in Tunisian Pediatric B-Lineage Acute Lymphoblastic Leukemia.
  • In this study, Forty-one out of fifty-seven Tunisian children with B-lineage acute lymphoblastic leukemia (B-ALL), and without cytogenetically detectable recurrent abnormalities at the time of the diagnosis, were evaluated by fluorescence in situ hybridization (FISH) for the t(12;21).

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  • (PMID = 20049174.001).
  • [ISSN] 1687-9112
  • [Journal-full-title] Advances in hematology
  • [ISO-abbreviation] Adv Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
  • [Other-IDs] NLM/ PMC2799269
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82. Emerenciano M, Bungaro S, Cazzaniga G, Dorea MD, Coser VM, Magalhães IQ, Biondi A, Pombo-de-Oliveira MS: ETV6-RUNX1 fusion gene and additional genetic changes in infant leukemia: a genome-wide analysis. Cancer Genet Cytogenet; 2009 Sep;193(2):86-92
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  • [Title] ETV6-RUNX1 fusion gene and additional genetic changes in infant leukemia: a genome-wide analysis.
  • Acute lymphoblastic leukemia (ALL) in infants is characterized by a high frequency of MLL gene rearrangements.
  • In a series of Brazilian infant leukemia cases, however, four younger cases harbored ETV6-RUNX1, at ages 2, 3, 5, and 7 months.
  • This finding could represent a unique model for delineating the additional genomic hits required to accelerate the emergence of a frank leukemia in these t(12;21)-positive cases.
  • Recurrent deletions, including 9p21.3 (CDKN2A, CKDN2B, and MTAP), 11p13 (CD44), 12p13.2 (ETV6), and patient-specific abnormalities were identified.
  • Although infant cases with t(12;21) did not display specific genetic abnormalities explaining the short latency to overt leukemia, the frequency of copy number abnormalities increased proportionally with age.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Fusion. Genome-Wide Association Study. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19665068.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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83. Stanulla M, Cario G, Meissner B, Schrauder A, Möricke A, Riehm H, Schrappe M: Integrating molecular information into treatment of childhood acute lymphoblastic leukemia--a perspective from the BFM Study Group. Blood Cells Mol Dis; 2007 Sep-Oct;39(2):160-3
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  • [Title] Integrating molecular information into treatment of childhood acute lymphoblastic leukemia--a perspective from the BFM Study Group.
  • Acute lymphoblastic leukemia (ALL) is the most common malignancy of childhood and is treated with chemotherapy alone or, in particular subgroups, with additional radiation therapy and/or stem cell transplantation.
  • However, although overall long-term cure rates for childhood ALL treated on risk-adapted protocols have dramatically improved over the last decades and, to date, are higher than 75%, a significant number of patients still die due to recurrent disease or the toxicity of treatment applied.
  • One goal in future BFM trials will be to take advantage of a better molecular understanding of leukemia and host characteristics to dissect the mechanisms underlying the differences in treatment response.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 17532236.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 18
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84. Harned TM, Gaynon P: Relapsed acute lymphoblastic leukemia: current status and future opportunities. Curr Oncol Rep; 2008 Nov;10(6):453-8
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  • [Title] Relapsed acute lymphoblastic leukemia: current status and future opportunities.
  • Significant improvements in primary therapy for childhood acute lymphoblastic leukemia (ALL) have led to dramatic increases in cure rates over the past few decades.
  • The high likelihood of achieving a third remission may discourage participation in single-agent trials of new drugs, despite the critical need for novel agents with activity against resistant disease that may improve outcomes for recurrent ALL.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 18928659.001).
  • [ISSN] 1534-6269
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 44
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85. 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.
  • [MeSH-major] Cardiomyopathy, Hypertrophic / etiology. Diagnostic Imaging. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration. Myocardium / pathology


86. Martineau M, Jalali GR, Barber KE, Broadfield ZJ, Cheung KL, Lilleyman J, Moorman AV, Richards S, Robinson HM, Ross F, Harrison CJ: ETV6/RUNX1 fusion at diagnosis and relapse: some prognostic indications. Genes Chromosomes Cancer; 2005 May;43(1):54-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This study was undertaken in order to compare the interphase and metaphase cytogenetics of 28 patients with ETV6/RUNX1 positive acute lymphoblastic leukemia, at diagnosis and relapse.
  • Other recurrent cytogenetic features included a second copy of the fusion signal in six cases, partial duplication of the long arm of the X chromosome in two cases, and trisomy 10 in three cases.
  • [MeSH-major] Artificial Gene Fusion. DNA-Binding Proteins / genetics. Nuclear Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins / genetics. Repressor Proteins / genetics. Transcription Factors / genetics

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15704129.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / ETS translocation variant 6 protein; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins; 0 / Transcription Factors
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87. 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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  • [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.
  • [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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88. Kim MJ, Yoon HS, Lim G, Kim SY, Lee HJ, Suh JT, Lee J, Lee WI, Park TS: ABL1 gene deletion without BCR/ABL1 rearrangement in a young adolescent with precursor B-cell acute lymphoblastic leukemia: clinical study and literature review. Cancer Genet Cytogenet; 2010 Jan 15;196(2):184-8
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  • [Title] ABL1 gene deletion without BCR/ABL1 rearrangement in a young adolescent with precursor B-cell acute lymphoblastic leukemia: clinical study and literature review.
  • Here we describe a fifth case of ABL1 deletion without BCR/ABL1 rearrangement in an adolescent patient with precursor B-cell lymphoblastic leukemia (B-ALL) and review the relevant literature.
  • It is not clear how ABL1 deletion affects leukemogenesis; however, it is plausible that ABL1 deletion without BCR/ABL1 rearrangement is a rare but recurrent genetic abnormality in precursor B-ALL patients.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Gene Deletion. Gene Rearrangement. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20082857.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 24
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89. Kearney L, Horsley SW: Molecular cytogenetics in haematological malignancy: current technology and future prospects. Chromosoma; 2005 Sep;114(4):286-94
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  • Cytogenetics has played a pivotal role in haematological malignancy, both as an aid to diagnosis and in identifying recurrent chromosomal rearrangements, an essential prerequisite to identifying genes involved in leukaemia and lymphoma pathogenesis.
  • In the acute leukaemias, the finding of characteristic gene expression signatures corresponding to biological subgroups has heralded gene expression profiling as a possible future alternative to current cytogenetic and morphological methods for diagnosis.
  • [MeSH-minor] Child. Humans. In Situ Hybridization, Fluorescence. Nucleic Acid Hybridization. Polyploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16003502.001).
  • [ISSN] 0009-5915
  • [Journal-full-title] Chromosoma
  • [ISO-abbreviation] Chromosoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Austria
  • [Number-of-references] 66
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90. Jones D, Thomas D, Yin CC, O'Brien S, Cortes JE, Jabbour E, Breeden M, Giles FJ, Zhao W, Kantarjian HM: Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL kinase inhibitors. Cancer; 2008 Sep 1;113(5):985-94
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  • [Title] Kinase domain point mutations in Philadelphia chromosome-positive acute lymphoblastic leukemia emerge after therapy with BCR-ABL kinase inhibitors.
  • BACKGROUND: BCR-ABL kinase domain (KD) mutations are detected in approximately 45% of patients with imatinib-resistant chronic myeloid leukemia.
  • Patterns of KD mutations in Philadelphia chromosome (Ph)-positive acute lympho- blastic leukemia (ALL) are less well studied.
  • METHODS: The authors assessed KD mutations in patients with recurrent Ph-positive ALL after treatments that included 1 or more kinase inhibitors (n = 24 patients) or no prior kinase inhibitor (KI) therapy (n = 12 patients).
  • RESULTS: ABL KD mutations were detected by direct sequencing in 15 of 17 patients (88%) who had recurrent Ph-positive ALL and received prior imatinib (n = 16) or dasatinib (n = 1) treatment and in 6 of 7 patients (86%) who had resistant/recurrent tumors treated with >or=2 KIs compared with 0 of 12 patients with recurrent Ph-positive ALL who never received KIs.
  • Using a more sensitive pyrosequencing method, mutations were not detected at codons 315 and 253 in the diagnostic samples from those 12 patients or in 30 patients with Ph-positive ALL who never developed recurrent disease.

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  • [Copyright] (c) 2008 American Cancer Society.
  • (PMID = 18615627.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / P50 CA100632-010007; United States / NCI NIH HHS / CA / P50 CA100707; United States / NCI NIH HHS / CA / 1P50CA100707-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS58345; NLM/ PMC4204653
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91. Carpenter PA, Snyder DS, Flowers ME, Sanders JE, Gooley TA, Martin PJ, Appelbaum FR, Radich JP: Prophylactic administration of imatinib after hematopoietic cell transplantation for high-risk Philadelphia chromosome-positive leukemia. Blood; 2007 Apr 1;109(7):2791-3
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  • [Title] Prophylactic administration of imatinib after hematopoietic cell transplantation for high-risk Philadelphia chromosome-positive leukemia.
  • Relapse occurs frequently after allogeneic hematopoietic cell transplantation (HCT) for treatment of high-risk Philadelphia chromosome-positive (Ph+) leukemia.
  • Administration of imatinib early after HCT might provide an effective approach for preventing recurrent Ph+ leukemia, but the feasibility of this approach has not been systematically tested.
  • Twenty-two patients, 15 with Ph+ acute lymphoblastic leukemia and 7 with high-risk chronic myelogenous leukemia, were enrolled in a prospective study and given imatinib from the time of engraftment until 365 days after HCT.

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  • (PMID = 17119111.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA018029; United States / NCI NIH HHS / CA / CA18029
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Other-IDs] NLM/ PMC1852215
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92. Lu G, Gurevich I, Vo BT, Chen SS: t(10; 12) (q24; p13) as the sole abnormality in a case with refractory acute myeloid leukemia: The first case report and literature review. Beijing Da Xue Xue Bao; 2009 Aug 18;41(4):480-3
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  • [Title] t(10; 12) (q24; p13) as the sole abnormality in a case with refractory acute myeloid leukemia: The first case report and literature review.
  • ETV6 rearrangements are more often observed in acute lymphoblastic leukemia than in acute myeloid leukemia (AML), where ETV6 gene deletions are more common than rearrangements.
  • Here, we report an AML case with the recurrent t(10;. 12) (q24;.
  • [MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 12 / genetics. Gene Rearrangement / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic

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  • (PMID = 19727243.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
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93. von Bergh AR, van Drunen E, van Wering ER, van Zutven LJ, Hainmann I, Lönnerholm G, Meijerink JP, Pieters R, Beverloo HB: High incidence of t(7;12)(q36;p13) in infant AML but not in infant ALL, with a dismal outcome and ectopic expression of HLXB9. Genes Chromosomes Cancer; 2006 Aug;45(8):731-9
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  • The t(7;12)(q36;p13) is a recurrent translocation involving the ETV6/TEL gene (12p13) and a heterogeneous breakpoint at 7q36.
  • To study the incidence of t(7;12) in infant and childhood acute leukemia, we screened 320 cases <36 months using FISH.
  • The t(7;12) is associated with a poor outcome and an ectopic expression of HLXB9 is commonly involved in this genetic subtype of leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 7. Homeodomain Proteins / genetics. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Transcription Factors / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Child, Preschool. Chromosome Breakage. Cohort Studies. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Infant, Newborn. Male. Models, Genetic. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 16646086.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / Homeodomain Proteins; 0 / MNX1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins; 0 / Transcription Factors
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94. Tsuzuki S, Karnan S, Horibe K, Matsumoto K, Kato K, Inukai T, Goi K, Sugita K, Nakazawa S, Kasugai Y, Ueda R, Seto M: Genetic abnormalities involved in t(12;21) TEL-AML1 acute lymphoblastic leukemia: analysis by means of array-based comparative genomic hybridization. Cancer Sci; 2007 May;98(5):698-706
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  • [Title] Genetic abnormalities involved in t(12;21) TEL-AML1 acute lymphoblastic leukemia: analysis by means of array-based comparative genomic hybridization.
  • The TEL (ETV6)-AML1 (RUNX1) chimeric gene fusion is the most common genetic abnormality in childhood acute lymphoblastic leukemias.
  • Evidence suggests that this chimeric gene fusion constitutes an initiating mutation that is necessary but insufficient for the development of leukemia.
  • In a search for additional genetic events that could be linked to the development of leukemia, we applied a genome-wide array-comparative genomic hybridization technique to 24 TEL-AML1 leukemia samples and two cell lines.
  • Recurrent regions of chromosomal imbalance (>10% of cases) and representative involved genes were gain of chromosomes 10 (17%) and 21q (25%; RUNX1) and loss of 12p13.2 (87%; TEL), 9p21.3 (29%; p16INK4a/ARF), 9p13.2 (25%; PAX5), 12q21.3 (25%; BTG1), 3p21 (21%; LIMD1), 6q21 (17%; AIM1 and BLIMP1), 4q31.23 (17%; NR3C2), 11q22-q23 (13%;.
  • Together, these findings suggest that some of the genes identified as lost by array-comparative genomic hybridization may partly account for the development of leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 17374122.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 146835-72-5 / BTG1 protein, human
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95. Chelghoum Y, Vey N, Raffoux E, Huguet F, Pigneux A, Witz B, Pautas C, de Botton S, Guyotat D, Lioure B, Fegueux N, Garban F, Saad H, Thomas X: Acute leukemia during pregnancy: a report on 37 patients and a review of the literature. Cancer; 2005 Jul 1;104(1):110-7
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  • [Title] Acute leukemia during pregnancy: a report on 37 patients and a review of the literature.
  • BACKGROUND: Acute leukemia (AL) requiring cytotoxic treatment occurring during pregnancy poses a very difficult therapeutic dilemma.
  • RESULTS: Thirty-one patients had acute myeloid leukemia (AML), and 6 patients had acute lymphoblastic leukemia (ALL).
  • Ten patients developed recurrent disease.
  • Overall, 12 of 37 pregnant women died from leukemia.
  • [MeSH-major] Leukemia / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pregnancy Complications, Neoplastic
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Leukemia, Myeloid / drug therapy. Pregnancy. Pregnancy Outcome. Pregnancy Trimesters. Remission Induction

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  • (PMID = 15912518.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 13
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96. Einsiedel HG, von Stackelberg A, Hartmann R, Fengler R, Schrappe M, Janka-Schaub G, Mann G, Hählen K, Göbel U, Klingebiel T, Ludwig WD, Henze G: Long-term outcome in children with relapsed ALL by risk-stratified salvage therapy: results of trial acute lymphoblastic leukemia-relapse study of the Berlin-Frankfurt-Münster Group 87. J Clin Oncol; 2005 Nov 1;23(31):7942-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcome in children with relapsed ALL by risk-stratified salvage therapy: results of trial acute lymphoblastic leukemia-relapse study of the Berlin-Frankfurt-Münster Group 87.
  • PURPOSE: Approximately 20% of children with acute lymphoblastic leukemia (ALL) suffer a relapse, and their prognosis is unfavorable.
  • Between 1987 and 1990, the multicenter trial Acute Lymphoblastic Leukemia-Relapse Study of the Berlin-Frankfurt-Münster Group (ALL-REZ BFM) 87 was conducted to establish a uniform treatment for these children in Germany and Austria.
  • CONCLUSION: With the ALL-REZ BFM 87 protocol, more than one-third of patients may be regarded as cured from recurrent ALL with second complete remissions lasting more than 10 years.
  • [MeSH-major] Neoplasm Recurrence, Local / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Salvage Therapy

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  • [ErratumIn] J Clin Oncol. 2008 May 1;26(13):2238
  • (PMID = 16258094.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] FTK8U1GZNX / Thioguanine; YL5FZ2Y5U1 / Methotrexate
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97. Wang HY, Tirado CA: t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected]. Hum Pathol; 2010 Feb;41(2):286-92
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  • [Title] t(8;21)(q22;q22) Translocation involving AML1 and ETO in B lymphoblastic leukemia [corrected].
  • t(8;21)(q22;q22) giving rise to RUNX1/RUNX1T1 fusion transcript is a recurrent non-random chromosomal translocation, accounting for approximately 5% of cases of acute myeloid leukemia and 10% of acute myeloid leukemia with maturation.
  • Studies have demonstrated so far that t(8;21)(q22;q22) occurs only in acute myeloid leukemia, and B lymphoblastic leukemia with t(8;21)(q22;q22) has not been reported in the literature.
  • In the present study, we report a 44-year-old woman with a diagnosis of a B lymphoblastic leukemia based on morphology and immunophenotype.
  • [MeSH-major] Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • [ErratumIn] Hum Pathol. 2010 Apr;41(4):620
  • (PMID = 19896694.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Proto-Oncogene Proteins; 0 / RUNX1 protein, human; 0 / RUNX1T1 protein, human; 0 / Transcription Factors
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98. Strehl S, Nebral K, König M, Harbott J, Strobl H, Ratei R, Struski S, Bielorai B, Lessard M, Zimmermann M, Haas OA, Izraeli S: ETV6-NCOA2: a novel fusion gene in acute leukemia associated with coexpression of T-lymphoid and myeloid markers and frequent NOTCH1 mutations. Clin Cancer Res; 2008 Feb 15;14(4):977-83
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  • [Title] ETV6-NCOA2: a novel fusion gene in acute leukemia associated with coexpression of T-lymphoid and myeloid markers and frequent NOTCH1 mutations.
  • Cytogenetic analysis of six cases of childhood acute lymphoblastic leukemia revealed a novel recurrent t(8;12)(q13;p13), suggesting involvement of ETV6.
  • RESULTS: We have identified a novel recurrent t(8;12)(q13;p13), which results in a fusion between the transcriptional repressor ETV6 (TEL) and the transcriptional coactivator NCOA2 (TIF2) in six cases of childhood leukemia expressing both T-lymphoid and myeloid antigens.
  • In addition, ETV6-NCOA2 leukemia shows a high frequency of heterozygous activating NOTCH1 mutations, which disrupt the heterodimerization or the PEST domains.
  • CONCLUSIONS: The ETV6-NCOA2 fusion may define a novel subgroup of acute leukemia with T-lymphoid and myeloid features, which is associated with a high prevalence of NOTCH1 mutations.
  • [MeSH-major] Nuclear Receptor Coactivator 2 / genetics. Oncogene Fusion / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 18281529.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ETS translocation variant 6 protein; 0 / NCOA2 protein, human; 0 / NOTCH1 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / Receptor, Notch1; 0 / Repressor Proteins
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99. Edkins S, O'Meara S, Parker A, Stevens C, Reis M, Jones S, Greenman C, Davies H, Dalgliesh G, Forbes S, Hunter C, Smith R, Stephens P, Goldstraw P, Nicholson A, Chan TL, Velculescu VE, Yuen ST, Leung SY, Stratton MR, Futreal PA: Recurrent KRAS codon 146 mutations in human colorectal cancer. Cancer Biol Ther; 2006 Aug;5(8):928-32
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  • [Title] Recurrent KRAS codon 146 mutations in human colorectal cancer.
  • We report here the identification of recurrent somatic missense mutations at alanine 146, a highly conserved residue in the guanine nucleotide binding domain.
  • We did, however, identify a KRAS A146 mutation in the ML-2 acute myeloid leukemia cell line and an NRAS A146 mutation in the NALM-6 B-cell acute lymphoblastic leukemia line, suggesting that the contribution of codon 146 mutations is not entirely restricted to colorectal cancers or to KRAS.
  • [MeSH-minor] Adenocarcinoma / genetics. Amino Acid Sequence. Carcinoma, Large Cell / genetics. DNA Mutational Analysis. DNA, Neoplasm / genetics. Hong Kong. Humans. Leukemia, Myeloid, Acute / genetics. Molecular Sequence Data. Neoplasm Staging. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Homology, Amino Acid. United States

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  • (PMID = 16969076.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA121113; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / R01 CA121113; United States / NCI NIH HHS / CA / CA062924; United Kingdom / Wellcome Trust / / 077012
  • [Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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  • [Other-IDs] NLM/ PMC2714972; NLM/ UKMS27311
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100. De Keersmaecker K, Real PJ, Gatta GD, Palomero T, Sulis ML, Tosello V, Van Vlierberghe P, Barnes K, Castillo M, Sole X, Hadler M, Lenz J, Aplan PD, Kelliher M, Kee BL, Pandolfi PP, Kappes D, Gounari F, Petrie H, Van der Meulen J, Speleman F, Paietta E, Racevskis J, Wiernik PH, Rowe JM, Soulier J, Avran D, Cavé H, Dastugue N, Raimondi S, Meijerink JP, Cordon-Cardo C, Califano A, Ferrando AA: The TLX1 oncogene drives aneuploidy in T cell transformation. Nat Med; 2010 Nov;16(11):1321-7
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  • The TLX1 oncogene (encoding the transcription factor T cell leukemia homeobox protein-1) has a major role in the pathogenesis of T cell acute lymphoblastic leukemia (T-ALL).
  • Here we show that transgenic expression of human TLX1 in mice induces T-ALL with frequent deletions and mutations in Bcl11b (encoding B cell leukemia/lymphoma-11B) and identify the presence of recurrent mutations and deletions in BCL11B in 16% of human T-ALLs.

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  • (PMID = 20972433.001).
  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA129382-04; United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / R01 CA120196-04; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA129382-04; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / CA120196-04; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737
  • [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 / BCL11B protein, human; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins; 143275-75-6 / TLX1 protein, human
  • [Other-IDs] NLM/ NIHMS238550; NLM/ PMC2974790
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