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1. Signer RA, Montecino-Rodriguez E, Witte ON, Dorshkind K: Immature B-cell progenitors survive oncogenic stress and efficiently initiate Ph+ B-acute lymphoblastic leukemia. Blood; 2010 Oct 7;116(14):2522-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immature B-cell progenitors survive oncogenic stress and efficiently initiate Ph+ B-acute lymphoblastic leukemia.
  • Philadelphia chromosome-positive (Ph(+)) B-acute lymphoblastic leukemia (B-ALL) can initiate in committed B-cell progenitors.
  • However, the stages of B-cell differentiation in which disease can initiate and the efficiency with which this occurs are unclear.
  • We now demonstrate that B-cell progenitors, up to and including the pro-B cell, efficiently initiate Ph(+) B-ALL.
  • However, cells at the pre-B-cell stage of development did not initiate disease.
  • We show that this difference in leukemia initiating potential is due to the level at which the Arf tumor suppressor gene is induced in specific stages of B lymphopoiesis.
  • Whereas immature B-cell progenitors survive the relatively low levels of Arf that are induced after oncogene expression, pre-B cells express the tumor suppressor gene at high levels and undergo massive apoptosis.
  • These data demonstrate that the molecular events that control Ph(+) B-ALL initiation and tumor suppression in the B-cell lineage are developmentally regulated.

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  • [Cites] Blood. 2000 Feb 1;95(3):1007-13 [10648416.001]
  • [Cites] Blood. 2009 Nov 12;114(20):4451-9 [19759355.001]
  • [Cites] Leukemia. 2000 Jun;14(6):1122-6 [10865978.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] Rev Clin Exp Hematol. 2002 Jun;6(2):142-60; discussion 200-2 [12196213.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):10002-7 [12890867.001]
  • [Cites] Annu Rev Immunol. 2004;22:247-306 [15032571.001]
  • [Cites] N Engl J Med. 2004 Aug 12;351(7):657-67 [15306667.001]
  • [Cites] Nature. 1973 Jun 1;243(5405):290-3 [4126434.001]
  • [Cites] J Immunol. 1981 Nov;127(5):2027-34 [6975306.001]
  • [Cites] J Immunol. 1983 Dec;131(6):2635-40 [6417229.001]
  • [Cites] J Immunol. 1986 Jun 15;136(12):4438-43 [3519770.001]
  • [Cites] J Immunol. 1987 Feb 15;138(4):1082-7 [3492541.001]
  • [Cites] Science. 1988 Jul 1;241(4861):58-62 [2898810.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Sep;87(17):6649-53 [2204061.001]
  • [Cites] J Exp Med. 1991 May 1;173(5):1213-25 [1827140.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Oct 1;88(19):8661-5 [1924327.001]
  • [Cites] Cell. 1992 Mar 6;68(5):869-77 [1547488.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3755-9 [8475126.001]
  • [Cites] EMBO J. 1994 Feb 1;13(3):683-91 [8313913.001]
  • [Cites] Leukemia. 1996 May;10(5):795-802 [8656674.001]
  • [Cites] Cell. 1997 Nov 28;91(5):661-72 [9393859.001]
  • [Cites] J Exp Med. 1999 May 3;189(9):1399-412 [10224280.001]
  • [Cites] Exp Gerontol. 2004 Nov-Dec;39(11-12):1751-9 [15582292.001]
  • [Cites] Nat Med. 2005 Jun;11(6):630-7 [15908956.001]
  • [Cites] Genes Dev. 2005 Jun 15;19(12):1438-43 [15964995.001]
  • [Cites] Cell. 2005 Jul 1;121(7):1109-21 [15989959.001]
  • [Cites] Mutat Res. 2005 Aug 25;576(1-2):22-38 [15878778.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6306-15 [16155013.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6688-93 [16618932.001]
  • [Cites] Immunity. 2007 Jun;26(6):703-14 [17582343.001]
  • [Cites] Blood. 2007 Sep 15;110(6):1831-9 [17554060.001]
  • [Cites] Adv Immunol. 2007;95:1-50 [17869609.001]
  • [Cites] Genes Dev. 2007 Sep 15;21(18):2283-7 [17761812.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]
  • [Cites] Genes Dev. 2008 Jun 1;22(11):1411-5 [18519632.001]
  • [Cites] Cancer Cell. 2008 Jul 8;14(1):47-58 [18598943.001]
  • [Cites] Cell. 2008 Oct 17;135(2):227-39 [18957199.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4184-92 [18755985.001]
  • [Cites] Nature. 2008 Dec 4;456(7222):593-8 [19052619.001]
  • [Cites] Genes Dev. 2008 Nov 15;22(22):3115-20 [19056891.001]
  • [Cites] Annu Rev Pathol. 2009;4:175-98 [18783329.001]
  • [Cites] Bioessays. 2009 Jun;31(6):600-9 [19444834.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2008;73:461-7 [19028987.001]
  • [Cites] J Exp Med. 2009 Aug 3;206(8):1739-53 [19620627.001]
  • [Cites] J Clin Oncol. 2009 Nov 1;27(31):5175-81 [19805687.001]
  • [Cites] N Engl J Med. 2000 Apr 6;342(14):998-1006 [10749961.001]
  • (PMID = 20562326.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-16042; United States / NIA NIH HHS / AG / R01 AG021450; United States / NIAID NIH HHS / AI / AI-28697; United States / NCI NIH HHS / CA / P30 CA016042; United States / NIAID NIH HHS / AI / R01 AI021256; United States / NIAID NIH HHS / AI / P30 AI028697; United States / Howard Hughes Medical Institute / / ; United States / NIA NIH HHS / AG / AG021450; United States / NIAID NIH HHS / AI / AI21256; United States / NIAID NIH HHS / AI / R37 AI021256
  • [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 / Cdkn2a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p16
  • [Other-IDs] NLM/ PMC2953887
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2. Airoldi I, Cocco C, Di Carlo E, Disarò S, Ognio E, Basso G, Pistoia V: Methylation of the IL-12Rbeta2 gene as novel tumor escape mechanism for pediatric B-acute lymphoblastic leukemia cells. Cancer Res; 2006 Apr 15;66(8):3978-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Methylation of the IL-12Rbeta2 gene as novel tumor escape mechanism for pediatric B-acute lymphoblastic leukemia cells.
  • The aim of this study was to investigate (i) whether the IL-12Rbeta2 gene is silenced in B-cell acute lymphoblastic leukemia (B-ALL) cells, and (ii) what the functional implications of such silencing for tumor growth are.
  • Here, we show that although mature B cells expressed both chains of the IL-12R, normal pro-B and pre-B cells failed to express the IL-12Rbeta2 chain.
  • Similarly, primary tumor cells from pediatric pro-B, early pre-B, and pre-B ALL (30 cases) did not express the IL-12Rbeta2 chain.
  • Such methylation was not detected in normal early B cells that when differentiated into mature B cells expressed the IL-12Rbeta2 gene.
  • Detection of IL-12Rbeta2 mRNA and protein in the tumorigenic 697 pre-B-ALL cell line allowed to perform functional experiments in severe combined immunodeficient/nonobese diabetic mice receiving 697 cells with or without human recombinant IL-12 (hrIL-12).
  • [MeSH-major] Burkitt Lymphoma / genetics. DNA Methylation. Receptors, Interleukin / genetics

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  • (PMID = 16618714.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / IL12RB2 protein, human; 0 / Il12rb2 protein, mouse; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-12
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3. Chung HY, Kim KH, Jun KR, Jang S, Park CJ, Chi HS, Im HJ, Seo JJ, Seo EJ: [Prognostic significance of TEL/AML1 rearrangement and its additional genetic changes in Korean childhood precursor B-acute lymphoblastic leukemia]. Korean J Lab Med; 2010 Feb;30(1):1-8
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  • [Title] [Prognostic significance of TEL/AML1 rearrangement and its additional genetic changes in Korean childhood precursor B-acute lymphoblastic leukemia].
  • BACKGROUND: TEL (ETV6)/AML1 (RUNX1) rearrangement is observed in approximately 20-25% of childhood precursor B-ALL and is associated with a favorable outcome.
  • We evaluated the prevalence and prognostic significance of TEL/AML1 rearrangement and additional genetic changes in the TEL and AML1 genes in Korean childhood precursor B-ALL.
  • METHODS: We performed FISH using LSITEL/AML1 ES probe (Vysis, USA) in 123 children diagnosed as having precursor B-ALL and assessed clinical relevance of the TEL/AML1 rearrangement and additional genetic abnormalities.
  • RESULTS: The frequency of TEL/AML1 was 17.1% (21/123) in patients with precursor B-ALL.
  • [MeSH-major] Asian Continental Ancestry Group / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Translocation, Genetic

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  • (PMID = 20197715.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins
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4. Stanciu-Herrera C, Morgan C, Herrera L: Anti-CD19 and anti-CD22 monoclonal antibodies increase the effectiveness of chemotherapy in Pre-B acute lymphoblastic leukemia cell lines. Leuk Res; 2008 Apr;32(4):625-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-CD19 and anti-CD22 monoclonal antibodies increase the effectiveness of chemotherapy in Pre-B acute lymphoblastic leukemia cell lines.
  • The monoclonal antibodies (MAbs) HD37 and RFB4 bind to receptors on precursor B acute lymphoblastic leukemia (ALL) cells.
  • HD37 and not RFB4 increased the in vitro cytotoxicity of daunorubicin (DNR) and vincristine (VCR) in three Pre-B ALL cell lines.

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  • [Cites] Arch Pathol Lab Med. 2003 Jan;127(1):42-8 [12521365.001]
  • [Cites] Am J Clin Pathol. 2002 Mar;117(3):380-9 [11888077.001]
  • [Cites] J Clin Oncol. 2003 Jul 15;21(14):2787-99 [12860957.001]
  • [Cites] Anticancer Drugs. 2003 Oct;14(9):669-82 [14551500.001]
  • [Cites] Cytometry B Clin Cytom. 2003 Nov;56(1):30-42 [14582135.001]
  • [Cites] Clin Cancer Res. 2004 Feb 15;10(4):1274-81 [14977825.001]
  • [Cites] Exp Cell Res. 2004 Aug 15;298(2):560-73 [15265702.001]
  • [Cites] J Immunol. 1987 May 1;138(9):2793-9 [2437199.001]
  • [Cites] Leuk Res. 1988;12(2):135-41 [3282129.001]
  • [Cites] Blood. 1988 Jul;72(1):299-307 [3291983.001]
  • [Cites] Cancer Res. 1989 Sep 1;49(17):4906-12 [2667754.001]
  • [Cites] J Immunol. 1991 Dec 1;147(11):3663-71 [1719083.001]
  • [Cites] Crit Rev Oncol Hematol. 1991 Dec;11(4):267-97 [1777090.001]
  • [Cites] Blood. 1992 Nov 1;80(9):2315-20 [1384801.001]
  • [Cites] Blood. 1993 Nov 1;82(9):2624-33 [8219217.001]
  • [Cites] Blood. 1994 Mar 1;83(5):1329-36 [7509655.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):4048-52 [7513431.001]
  • [Cites] Curr Opin Oncol. 1994 Jan;6(1):14-22 [8204688.001]
  • [Cites] J Immunol. 1995 Apr 1;154(7):3096-104 [7534787.001]
  • [Cites] Blood. 1995 Jun 15;85(12):3457-65 [7780133.001]
  • [Cites] Leuk Lymphoma. 1995 Aug;18(5-6):385-97 [8528044.001]
  • [Cites] Curr Biol. 1997 Feb 1;7(2):133-43 [9016707.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7509-14 [9207122.001]
  • [Cites] Leuk Res. 1998 Jul;22(7):567-79 [9680106.001]
  • [Cites] J Immunol. 1998 Sep 15;161(6):3176-85 [9743386.001]
  • [Cites] Exp Hematol. 2005 Feb;33(2):199-211 [15676214.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):694-704 [15681517.001]
  • [Cites] J Clin Oncol. 2005 Jun 1;23(16):3676-85 [15738535.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 18;102(42):15178-83 [16217038.001]
  • [Cites] Leukemia. 2003 Feb;17(2):334-8 [12592332.001]
  • [Cites] Clin Cancer Res. 1999 Dec;5(12):3920-7 [10632321.001]
  • [Cites] Clin Cancer Res. 2000 Apr;6(4):1302-13 [10778955.001]
  • [Cites] Immunity. 2000 Jul;13(1):47-57 [10933394.001]
  • [Cites] Br J Haematol. 2001 Sep;114(4):800-9 [11564066.001]
  • [Cites] J Biol Chem. 2001 Nov 23;276(47):44315-22 [11551923.001]
  • [CommentIn] Leuk Res. 2008 Jun;32(6):847-9 [18191203.001]
  • (PMID = 17706771.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101897-04; United States / NCI NIH HHS / CA / K01 CA101897-04
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / Antineoplastic Agents, Phytogenic; 0 / Sialic Acid Binding Ig-like Lectin 2; 5J49Q6B70F / Vincristine; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS42262; NLM/ PMC2276361
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5. Attarbaschi A, Mann G, König M, Steiner M, Strehl S, Schreiberhuber A, Schneider B, Meyer C, Marschalek R, Borkhardt A, Pickl WF, Lion T, Gadner H, Haas OA, Dworzak MN: Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity. Clin Cancer Res; 2006 May 15;12(10):2988-94
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mixed lineage leukemia-rearranged childhood pro-B and CD10-negative pre-B acute lymphoblastic leukemia constitute a distinct clinical entity.
  • PURPOSE: Mixed lineage leukemia (MLL) abnormalities occur in approximately 50% of childhood pro-B acute lymphoblastic leukemia (ALL).
  • However, the incidence and type of MLL rearrangements have not been determined in common ALL (cALL) and CD10+ or CD10- pre-B ALL.
  • EXPERIMENTAL DESIGN: To address this question, we analyzed 29 patients with pro-B ALL, 11 patients with CD10- pre-B ALL, 23 pre-B, and 26 cALL patients with CD10 on 20% to 80%, as well as 136 pre-B and 143 cALL patients with CD10 > or = 80% of blasts.
  • RESULTS: We found that 15 of 29 pro-B ALL, 7 of 11 CD10- pre-B ALL, and 1 of 2 French-American-British classification L1 mature B-cell leukemia cases had a MLL rearrangement.
  • However, no 11q23/MLL translocation was identified among the CD10+ pre-B and cALL patients.
  • MLL-rearranged pro-B and CD10- pre-B ALL cases had similar clinical and immunophenotypic (coexpression of CDw65 and CD15) features at initial diagnosis.
  • CONCLUSIONS: The striking similarities between the two CD10- ALL subsets imply that CD10- pre-B ALL variants may represent pro-B ALL cases that maintained the propensity to rearrange and express their immunoglobulin heavy chain rather than actual pre-B ALL forms transformed at this later stage of B-cell differentiation.
  • [MeSH-major] Chromosome Aberrations. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16707593.001).
  • [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 / Immunoglobulin Heavy Chains; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 3.4.24.11 / Neprilysin
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6. Cocco C, Canale S, Frasson C, Di Carlo E, Ognio E, Ribatti D, Prigione I, Basso G, Airoldi I: Interleukin-23 acts as antitumor agent on childhood B-acute lymphoblastic leukemia cells. Blood; 2010 Nov 11;116(19):3887-98
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-23 acts as antitumor agent on childhood B-acute lymphoblastic leukemia cells.
  • The aim of this study was to investigate the potential direct antitumor activity of IL-23 in pediatric B-acute lymphoblastic leukemia (B-ALL) cells and to unravel the molecular mechanisms involved.
  • Here, we show, for the first time, that IL-23R is up-regulated in primary B-ALL cells, compared with normal early B lymphocytes, and that IL-23 dampens directly tumor growth in vitro and in vivo through the inhibition of tumor cell proliferation and induction of apoptosis.
  • [MeSH-major] Interleukin-23 Subunit p19 / immunology. Interleukin-23 Subunit p19 / pharmacology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Child. Child, Preschool. Female. Gene Expression / drug effects. Genes, bcl-2 / drug effects. Humans. In Vitro Techniques. Infant. Male. Mice. Mice, Inbred NOD. Mice, SCID. MicroRNAs / antagonists & inhibitors. MicroRNAs / genetics. Recombinant Proteins / genetics. Recombinant Proteins / immunology. Recombinant Proteins / pharmacology. Signal Transduction / immunology

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  • (PMID = 20671120.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IL23A protein, human; 0 / Interleukin-23 Subunit p19; 0 / MIRN15 microRNA, human; 0 / MicroRNAs; 0 / Recombinant Proteins
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7. Abdelhaleem M, Yi Q, Beimnet K, Hitzler J: A novel TEL-AML1 fusion transcript involving the pro-apoptotic gene BCL-G in pediatric precursor B acute lymphoblastic leukemia. Leukemia; 2006 Jul;20(7):1294
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel TEL-AML1 fusion transcript involving the pro-apoptotic gene BCL-G in pediatric precursor B acute lymphoblastic leukemia.
  • [MeSH-major] Apoptosis / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics

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  • (PMID = 16673018.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL2L14 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / TEL-AML1 fusion protein
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8. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • Thus, the presence of aberrant antigen expression detectable by flow cytometry may be critical for diagnosis of B-ALL and detection of minimal residual disease.
  • Of 200 cases, 9.0% aberrantly expressed T cell-associated antigens.
  • 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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9. Lin RF, Li JY, Lu H, Wu YJ, Qiu HR, Xiao B, Zhang JF, Yang H: [Bone marrow necrosis as an initial manifestation of Philadelphia chromosome and myeloid antigens positive B acute lymphoblastic leukemia--a case report]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Aug;14(4):832-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Bone marrow necrosis as an initial manifestation of Philadelphia chromosome and myeloid antigens positive B acute lymphoblastic leukemia--a case report].
  • Many diseases cause bone marrow necrosis (BMN), especially lymphocytic leukemia.
  • To explore the complexity of the pathogenesis and pathology of BMN and understand the multiplicity of clinical features, a case of Philadelphia chromosome positive (Ph+) B acute lymphoblastic leukemia (ALL) expressing myeloid antigens was reported.
  • The results indicated that the clinical features of this case were complicated and multiplex, the diagnosis was confirmed by using bone marrow smear and biopsy, immunophenotype analysis, conventional cytogenetics and fluorescence in situ hybridization (FISH), the prognosis of patients improved by active treatment for primary disease.
  • In conclusion, the Ph+ B ALL expressing myeloid antigen with BMN is very rare, its diagnosis should be confirmed by using multiple methods, and the active treatments should be performed.

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  • (PMID = 16928333.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm
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10. Herrera L, Stanciu-Herrera C, Morgan C, Ghetie V, Vitetta ES: Anti-CD19 immunotoxin enhances the activity of chemotherapy in severe combined immunodeficient mice with human pre-B acute lymphoblastic leukemia. Leuk Lymphoma; 2006 Nov;47(11):2380-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-CD19 immunotoxin enhances the activity of chemotherapy in severe combined immunodeficient mice with human pre-B acute lymphoblastic leukemia.
  • The anti-CD19 immunotoxin (IT) (HD37-dgRTA) is effective in killing B-lineage leukemia cells and in curing severe combined immunodeficient mice with acute lymphoblastic leukemia.
  • [MeSH-major] Antibodies / immunology. Antigens, CD19 / immunology. Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / immunology. Immunotoxins / immunology
  • [MeSH-minor] Animals. Cell Line, Tumor. DNA / biosynthesis. Humans. Male. Mice. Mice, SCID. Survival Rate

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  • (PMID = 17107913.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD19; 0 / Immunotoxins; 9007-49-2 / DNA
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11. Nishida H, Yamazaki H, Yamada T, Iwata S, Dang NH, Inukai T, Sugita K, Ikeda Y, Morimoto C: CD9 correlates with cancer stem cell potentials in human B-acute lymphoblastic leukemia cells. Biochem Biophys Res Commun; 2009 Apr 24;382(1):57-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD9 correlates with cancer stem cell potentials in human B-acute lymphoblastic leukemia cells.
  • Cancer stem cell (CSC) theory suggests that only a small subpopulation of cells having stem cell-like potentials can initiate tumor development.
  • While recent data on acute lymphoblastic leukemia (ALL) are conflicting, some studies have demonstrated the existence of such cells following CD34-targeted isolation of primary samples.
  • Although CD34 is a useful marker for the isolation of CSCs in leukemias, the identification of other specific markers besides CD34 has been relatively unsuccessful.
  • To identify new markers, we first performed extensive analysis of surface markers on several B-ALL cell lines.
  • Our data demonstrated that every B-ALL cell line tested did not express CD34 but certain lines contained cell populations with marked heterogeneity in marker expression.
  • Moreover, the CD9(+) cell population possessed stem cell characteristics within the clone, as demonstrated by in vitro and transplantation experiments.
  • [MeSH-major] Antigens, CD / biosynthesis. Antigens, Neoplasm / biosynthesis. Biomarkers, Tumor / biosynthesis. Membrane Glycoproteins / biosynthesis. Neoplastic Stem Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Animals. Antigens, CD9. Cell Line, Tumor. Humans. Mice. Transplantation, Heterologous

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  • (PMID = 19254692.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD9; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CD9 protein, human; 0 / Cd9 protein, mouse; 0 / Membrane Glycoproteins
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12. Berretta R, Barone A, Rolla M, Bertolini P, Nardelli GB: Isolated ovarian relapse of pre-B acute lymphoblastic leukemia: a case report. J Pediatr Adolesc Gynecol; 2009 Aug;22(4):e65-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolated ovarian relapse of pre-B acute lymphoblastic leukemia: a case report.
  • BACKGROUND: Acute lymphoblastic leukemia is a malignant disease of the bone marrow in which early lymphoid precursors proliferate and replace normal marrow hematopoietic cells, resulting in a marked decrease in the production of normal blood cells.
  • CASE REPORT: We report a case of isolated ovarian relapse 7 years after the primary diagnosis in a patient, who was seemingly in clinical remission following unilateral ovariectomy and second-line chemotherapy.
  • CONCLUSION: In contrast to testicular relapse, ovarian relapses in acute lymphoblastic leukemia are rarely reported.
  • [MeSH-major] Ovarian Neoplasms / secondary. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19493520.001).
  • [ISSN] 1873-4332
  • [Journal-full-title] Journal of pediatric and adolescent gynecology
  • [ISO-abbreviation] J Pediatr Adolesc Gynecol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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13. Babusíková O, Zelezníková T, Mlcáková A, Kusenda J, Stevulová L: The knowledge on the 3rd type hematogones could contribute to more precise detection of small numbers of precursor B-acute lymphoblastic leukemia. Neoplasma; 2005;52(6):502-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The knowledge on the 3rd type hematogones could contribute to more precise detection of small numbers of precursor B-acute lymphoblastic leukemia.
  • Bone marrow hematogones (benign B-lymphocyte precursors) may cause diagnostic problems due to their morphologic and immunophenotypic similarities with neoplastic lymphoblasts.
  • Bone marrow hematogones were separately assessed as hematogones 1 population of early stage and hematogones 2 of mid-stage precursor B-cells, respectively.
  • In some (about 30%) of hematogones a third type hematogones could be assessed in bone marrow samples.
  • This small B-cell subpopulation was defined by CD10-positivity, coexpressing more mature markers CD19,CD20,CD22 and CD45bright.
  • These cells obviously blended with those of mature B-lymphocytes (CD10-negative) on CD45/SSC, and could be better recognized on CD10-gating.
  • Quantitative immunophenotyping of this study completed the percent antigen expression data in two main hematogone subtypes and lymphocytes in 16 bone marrow specimens and precursor B-ALL lymphoblasts in some samples.
  • Increased information on benign B-lymphocyte precursors, especially that of existence of the 3rd type hematogones could provide a basis for better discrimination of B-leukemia cells even in a very small amounts.
  • [MeSH-major] Antigens, CD / analysis. B-Lymphocytes / immunology. Bone Marrow / immunology. Bone Marrow Cells / cytology. Burkitt Lymphoma / diagnosis. Immunophenotyping

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  • (PMID = 16284697.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD
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14. Bloomfield CD: Importance of genetic heterogeneity in curing adult acute leukemia (AL). J Clin Oncol; 2009 May 20;27(15_suppl):s1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Importance of genetic heterogeneity in curing adult acute leukemia (AL).
  • Publication of the French-American-British classification 34 years ago resulted in acceptance that morphology and cytochemistry separated AL into two different diseases, acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL), that required separate treatment.
  • The most striking example of increased curability of AL is acute promyelocytic leukemia, in which targeted therapy combined with chemotherapy has increased survival from a 2-week median to an 80% cure rate.
  • Among adult de novo AML 40%-45% are cytogenetically normal (CN); the striking molecular heterogeneity of CN-AML is now being recognized and promises to allow individualized approaches that improve substantially upon the current cure rate of 40%.
  • New approaches to studying the leukemia genome and epigenome should improve our understanding of AL heterogeneity, identify new therapeutic targets, and allow the cure of most patients.

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  • (PMID = 27962366.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Smith MA, Morton CL, Carol H, Gorlick RG, Kang MH, Keir ST, Kolb EA, Lock RB, Maris JM, Houghton PJ: Pediatric Preclinical Testing Program (PPTP) testing of the CENP-E inhibitor GSK923295A. J Clin Oncol; 2009 May 20;27(15_suppl):10015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: The PPTP includes a molecularly characterized in vitro panel of cell lines (n = 27) and in vivo panel of xenografts (n = 60) representing most of the common types of childhood solid tumors and childhood acute lymphoblastic leukemia (ALL).
  • RESULTS: GSK923295A demonstrated potent in vitro activity against the PPTP cell line panel with a median IC50 of 27 nM (range 12 nM to > 10 μM).

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  • (PMID = 27962529.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Yeh C, Ma W, Kantarjian H, Zhang ZJ, Cortes J, Albitar M: BCR-ABL truncation due to premature translation termination as a mechanism of resistance to kinase inhibitors. J Clin Oncol; 2009 May 20;27(15_suppl):7028

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7028 Background: The major mechanism underlying imatinib resistance in patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with point mutations in the BCR-ABL tyrosine kinase.
  • We describe three novel ABL premature termination mutations leading to BCR-ABL truncation in leukemia patients with multidrug (imatinib/nilotinib/dasatinib) resistance.
  • Total nucleic acids were purified and subjected to two rounds of PCR analysis, with the first PCR designed to eliminate amplification of the wild-type, non-translocated ABL gene.
  • HL60 cells (a Ph-negative myeloid leukemia cell line) and peripheral blood of healthy subjects were used as negative controls; a human CML cell line (K562) was used as a positive control.
  • RESULTS: We identified an exon 7 deletion in three CML patients, a 4-nt insertion (908insCAGG) near the exon 5/6 junction in one CML case, and an exon 6 point mutation (997C>T) in one patient with acute lymphoblastic leukemia (ALL).

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  • (PMID = 27961401.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Fauzdar A, Mahajan A, Jain D, Mishra M, Raina V: Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report. J Clin Oncol; 2009 May 20;27(15_suppl):e21000

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report.
  • : e21000 Background: Chromosome abnormalities of leukemia cells have important prognostic significance in childhood acute lymphoblastic leukemia (ALL).
  • B-cell precursor acute lymphoblastic leukemia (BCP-ALL) ETV6/RUNX1 (alias TEL/AML1) is most frequent i.e.
  • We report two new cases with Pre B- cell ALL without ETV6/RUNX1 rearrangement, showing amplification of AML1 gene detected by FISH analysis.
  • RESULTS: In first case a 3-year girl with four copies of AML (RUNX1) gene were observed in 95% of the cell with normal two copies of TEL (ETV6) gene in both interphase and metaphase FISH.

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  • (PMID = 27960689.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Zuo Z, Jones DM, Thomas DA, O'Brien S, Ravandi F, Kantarjian HM, Medeiros LJ, Luthra R, Chen SS: A nine-gene predictor of therapy response in adult Philadelphia-chromosome positive acute lymphoblastic leukemia (Ph+ ALL). J Clin Oncol; 2009 May 20;27(15_suppl):7014

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A nine-gene predictor of therapy response in adult Philadelphia-chromosome positive acute lymphoblastic leukemia (Ph+ ALL).
  • There was no statistical difference in age, initial peripheral blood white cell and BM blast counts, and initial normalized BCR/ABL1 levels between groups.

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  • (PMID = 27961387.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Mukhopadhyay A, Gupta P, Mukhopadhyay S, Dey S, Basak J, Pandey R: Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country. J Clin Oncol; 2009 May 20;27(15_suppl):10046

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country.
  • : 10046 Background: Acute Lymphatic Leukemia is a curable disease in the range of 80 - 90% in developed countries by aggressive protocol like BFM, St. Judes' but result is much less in adolescence age group (60-70%).
  • CONCLUSIONS: The data of acute lymphatic leukemia in adolescent is not satisfactory as compared to other pediatric patients.

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  • (PMID = 27962472.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Iacobucci I, Storlazzi C, Lonetti A, Ferrari A, Messina M, Cilloni D, Papayannidis C, Baccarani M, Foà R, Martinelli G: IKZF1 (IKAROS) deletions as a prognostic marker in BCR-ABL1 positive acute lymphoblastic leukemia patients: A GIMEMA ALL WP Report. J Clin Oncol; 2009 May 20;27(15_suppl):11005

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IKZF1 (IKAROS) deletions as a prognostic marker in BCR-ABL1 positive acute lymphoblastic leukemia patients: A GIMEMA ALL WP Report.
  • : 11005 Expression of BCR-ABL1 in hematopoietic stem cells can alone induce a chronic myeloid leukemia (CML) but cooperating oncogenic lesions are required for the generation of a blastic leukemia.
  • To identify oncogenic sub-microscopic lesions that cooperate with BCR-ABL1 to induce ALL, by high resolution single nucleotide polymorphism (SNP) arrays (250K NspI and SNP 6.0, Affymetrix) we studied 106 patients (pts) with de novo adult BCR-ABL1-positive ALL.
  • A variable number of nucleotides (patient-specific) were inserted at the conjunction and maintained with fidelity at the time of relapse.
  • Gene expression profiling analysis of pts with IKZF1 deletion vs wild-type pts identified a unique signature characterized by a down-regulation of genes involved in pre-B-cell differentiation (e.g.
  • VPREB1, VPREB3, IGLL3, BLK), demonstrating that genomic IKZF1 alterations have a strong impact on trascriptoma and contribute to an impaired B-cell differentiation.
  • Univariate analysis showed that the IKZF1 deletion is a negative prognostic marker influencing the cumulative incidence of relapse (10.1 months for pts with deletion vs 56.1 months for wild-type pts, p=0.0103) and disease-free survival (DFS) (10.1 months vs 32.1 months, respectively, p=0.0229).

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  • (PMID = 27964054.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Ikawa Y, Sugimoto N, Koizumi S, Yachie A, Saikawa Y: Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene. J Clin Oncol; 2009 May 20;27(15_suppl):10045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene.
  • While CD10 negativity reflects an earlier stage of B-cell development, complete IgH gene rearrangements (VDJ<sub>H</sub>) show more mature IgH status.
  • METHODS: CD10-negative infant ALL with MLL/AF4, CD10-positive infant ALL with germ-line MLL, CD10-positive pre-B ALL cell line, infant AML (M5) with MLL/AF9 and pediatric AML (M2) with AML1/ETO were analyzed for VDJ<sub>H</sub> status and methylation of CD10 gene promoters.
  • Bisulfite sequencing of CD 10 type 1 and 2 promoters identified more than 84% of methylated CpG dinucleotides in all three CD10-negative infant ALL cases with MLL/AF4.

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  • (PMID = 27962471.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Bose P, Thompson CL, Gandhi DG, Ghabach BS, Ozer H: Response of AIDS-related plasmablastic lymphoma (PBL) to bortezomib. J Clin Oncol; 2009 May 20;27(15_suppl):e19562

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • They are terminally differentiated B-cell neoplasms, and typically lack common B-cell markers but uniformly express plasma cell markers.
  • Flow cytometry was negative for CD45 and all common epithelial, T-cell and B-cell markers, but was positive for CD138 and p63(VS38c).
  • The diagnosis was stage IVBE PBL.
  • The WHO classifies PBL as a variant of diffuse large B-cell lymphoma.
  • However, studies of their immunophenotype and molecular histogenesis suggest that PBL are more closely related to plasma cell neoplasms.
  • Bortezomib is a proteasome inhibitor widely used in multiple myeloma and mantle cell lymphoma.
  • We chose bortezomib based on our patient's poor performance status and immune function, the desire to avoid combination chemotherapy, and translocations involving the immunoglobulin heavy chain gene locus (8;14) similar to those seen in multiple myeloma(4;14, 14;16) and mantle cell lymphoma(11;14).
  • A shift in the paradigm of treatment of PBL towards agents effective in plasma cell malignancies may be necessary.

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  • (PMID = 27961065.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Te Loo DM, van Schie RM, Hoogerbrugge PM: Effect of azole antifungal therapy on vincristine toxicity in childhood acute lymphoblastic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):10049

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of azole antifungal therapy on vincristine toxicity in childhood acute lymphoblastic leukemia.
  • : 10049 Background: Vincristine is one of the corner stitches in the treatment of children with acute lymphoblastic leukemia (ALL).
  • Constipation and other peripheral and central neurotoxicities are the most common side effects.
  • METHODS: In total, twenty pediatric patients with de novo ALL were included in this study.

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  • (PMID = 27962456.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Khattab TM, Jastaniah WA, Felimban SK, Elemam N, Abdullah K, Ahmed B: How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia. J Clin Oncol; 2009 May 20;27(15_suppl):10048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.
  • : 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.
  • Our published data showed that T-ALL phenotype patients fared poorly with 5 year survival of 27% versus 83% for precursor B-ALL (Recent Advances Research Update: 2006, 7; 1, P 51-56).
  • OBJECTIVES: We reviewed all patients diagnosed with T-ALL to assess risk classification according to NCI criteria, type of therapy received, overall survival and causes of mortality.
  • METHODS: Retrospective review of all patients files diagnosed with T-ALL from 1989 until now with data collection including; sex, age, white cell count (WBCs), CNS disease, type of protocol used, length of survival, overall survival, cause of death (toxic, disease).
  • Median WBCs 50,000/Cmm (range: 1.500-619,000/Cmm) and positive CNS at diagnosis 10/52 (20%).
  • Further risk and response stratification in addition to intensification of therapy for T-cell ALL in our center may prove to be beneficial.

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  • (PMID = 27962474.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Morris B, Khan R, Ledet D, Howell C, Pui C, Hudson M, Ness K: Neurological morbidity in survivors of childhood acute lymphoblastic leukemia (ALL). J Clin Oncol; 2009 May 20;27(15_suppl):9529

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neurological morbidity in survivors of childhood acute lymphoblastic leukemia (ALL).
  • METHODS: After obtaining IRB approval, all long-term ALL survivors (≥ 5 years since diagnosis) aged 6-28 years who remained active patients at our institution were identified.
  • Complaints of fatigue, dizziness, and chronic back pain were also relatively common.
  • Although headache was a common complaint, its prevalence may not differ significantly from a normal age-matched population.

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  • (PMID = 27964517.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Tai E, Richardson L, Townsend J, Steele B: Differences in length of stay among hospitalized children with acute lymphoblastic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):10044

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differences in length of stay among hospitalized children with acute lymphoblastic leukemia.
  • : 10044 Background: Acute lymphoblastic leukemia (ALL) is the most common malignancy among children in the United States.
  • CONCLUSIONS: Race/ethnicity, age, sex, household income, insurance status, admission source, hospital type and region, transfusion, bone marrow transplant, and neutropenia were significantly associated with longer LOS.

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  • (PMID = 27962470.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Lonetti A, Iacobucci I, Ferrari A, Messina M, Cilloni D, Soverini S, Papayannidis C, Baccarani M, Foà R, Martinelli G: Expression of different isoforms of the B-cell mutator activation-induced cytidine deaminase (AID) in BCR-ABL1-positive acute lymphoblastic leukemia (ALL) patients. J Clin Oncol; 2009 May 20;27(15_suppl):7049

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of different isoforms of the B-cell mutator activation-induced cytidine deaminase (AID) in BCR-ABL1-positive acute lymphoblastic leukemia (ALL) patients.
  • : 7049 Since the activation-induced cytidine deaminase (AID) enzyme can target non-immunoglobulin (Ig) genes and may even act as a genome-wide mutator, we investigated AID expression in BCR-ABL1-positive ALL and in chronic myeloid leukemia (CML) at the time of progression to blast crisis.
  • On the 61 de novo adult BCR-ABL1-positive ALL patients (pts), AID mRNA and protein were detected in 36 (59%); their expression correlated with BCR-ABL1 transcript levels and disappeared after treatment with tyrosine kinase inhibitors at the time of remission.
  • Different isoforms of AID were identified: 13/61 (21%) pts expressed the full-length isoform; 19/61 (31%) co-expressed the wild-type and different AID splice variants with deaminase activity (AIDΔE4a, with a 30 bp deletion of exon 4; AIDΔE4, with the exon 4 deletion; AIDins3, with the retention of intron 3-4); 4/61 (7%) expressed the AIDΔE3-E4 isoform without deaminase activity (deletion of exons 2 and 3).
  • Patients who expressed wild-type AID had a higher number of alterations compared to AID-negative (median copy number alteration of 14 versus 4. respectively, p < 0.03).
  • Our findings show that BCR-ABL1-positive ALL cells aberrantly express different isoforms of AID that can act as mutator outside the Ig gene loci in promoting genetic instability in leukemia cells.

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  • (PMID = 27961429.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Lipshultz SE, Scully RE, Lipsitz SR, Sallan SE, Silverman LB, Miller TL, Orav EJ, Colan SD: Gender differences in long-term dexrazoxane cardioprotection in doxorubicin-treated children with acute lymphoblastic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):10005

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gender differences in long-term dexrazoxane cardioprotection in doxorubicin-treated children with acute lymphoblastic leukemia.
  • Adding dexrazoxane (DZR) to DOX treatment resulted in reduced myocardial injury in children with acute lymphoblastic leukemia (ALL) during Dana-Farber Cancer Institute Protocol 95-01.

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  • (PMID = 27962530.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Bernard N, Devevey L, Jacquemont C, Chrétien P, Helissey P, Guillosson JJ, Arock M, Nafziger J: A new model of pre-B acute lymphoblastic leukemia chemically induced in rats. Exp Hematol; 2005 Oct;33(10):1130-9
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  • [Title] A new model of pre-B acute lymphoblastic leukemia chemically induced in rats.
  • OBJECTIVE: Although B acute lymphoblastic leukemia (B-ALL) is the most common leukemia among children, no chemically inducible model of this leukemia has yet been described in vivo.
  • METHODS: Leukemia was chemically induced in male WKAH/Hkm rats by a nitrosourea derivative, N-butylnitrosourea (BNU), an alkylating agent, administered orally 5 days a week for 24 weeks.
  • Development of leukemia was monitored by clinical observation, follow-up of blood parameters, and appearance of blast cells in peripheral blood samples.
  • The phenotype of the leukemia was determined by cytological examination, cytochemical reactions, and by immunophenotyping of bone marrow cells using various markers.
  • The feasibility of leukemia transplantation was investigated.
  • RESULTS: We observed the appearance of acute leukemia in 60% of the rats treated with BNU.
  • Of these, 65% developed pre-B-ALL, which was serially transplantable to healthy WKAH/Hkm male rats.
  • Clonality determined by immunoglobulin gene rearrangement sequencing disclosed that the pre-B-ALL were mostly oligoclonal.
  • CONCLUSION: This new in vivo model of inducible pre-B-ALL might be useful for investigating the effects of co-initiating or promoting agents suspected to be involved in leukemia development, and for disclosing new molecular events leading to leukemogenic processes.
  • [MeSH-major] Carcinogens / toxicity. Leukemia, Experimental / pathology. Nitrosourea Compounds / toxicity. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 16219535.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitrosourea Compounds; 869-01-2 / N-nitrosobutylurea
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30. Russell T, Oliver JM, Wilson BS, Tarleton CA, Winter SS, Meng X: Differential expression of Ikaros isoforms in monozygotic twins with MLL-rearranged precursor-B acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2008 Dec;30(12):941-4
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  • [Title] Differential expression of Ikaros isoforms in monozygotic twins with MLL-rearranged precursor-B acute lymphoblastic leukemia.
  • Infant leukemia associated with rearrangement of the MLL gene typically presents with high-risk clinical features.
  • Relapse is common despite aggressive therapy and perturbations in signaling pathways may contribute to disease resistance.
  • We evaluated twin 4-month-old monozygotic baby boys who presented with MLL-rearranged precursor-B acute lymphoblastic leukemia.
  • However, the dominant-negative Ik8 isoform was detected in only 1 boy, suggesting a common genetic ontogeny that was modulated by leukemic evolution.
  • [MeSH-major] Diseases in Twins / genetics. Gene Rearrangement. Ikaros Transcription Factor / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Twins, Monozygotic
  • [MeSH-minor] Acid Anhydride Hydrolases / genetics. Acute Disease. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Female. Histone-Lysine N-Methyltransferase. Humans. Infant. Neoplasm Proteins / genetics. Oncogene Proteins, Fusion / genetics. Protein Isoforms / genetics. Translocation, Genetic. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 19131787.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IKZF1 protein, human; 0 / MLL protein, human; 0 / MLL-AF4 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Protein Isoforms; 0 / fragile histidine triad protein; 148971-36-2 / Ikaros Transcription Factor; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.6.- / Acid Anhydride Hydrolases
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31. Han X, Garcia-Manero G, McDonnell TJ, Lozano G, Medeiros LJ, Xiao L, Rosner G, Nguyen M, Fernandez M, Valentin-Vega YA, Barboza J, Jones DM, Rassidakis GZ, Kantarjian HM, Bueso-Ramos CE: HDM4 (HDMX) is widely expressed in adult pre-B acute lymphoblastic leukemia and is a potential therapeutic target. Mod Pathol; 2007 Jan;20(1):54-62
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  • [Title] HDM4 (HDMX) is widely expressed in adult pre-B acute lymphoblastic leukemia and is a potential therapeutic target.
  • HDM4 has not been assessed in precursor B (pre-B) lymphoblastic leukemia (ALL).
  • We examined bone marrow samples obtained at time of diagnosis from 55 adults with pre-B ALL.
  • p53 (P<0.05) and p21 (P<0.001) were expressed significantly more often in Ph+ pre-B ALL.
  • HDM4 expression in most cases of adult pre-B ALL suggests that HDM4 is a potential therapeutic target.
  • [MeSH-major] Biomarkers, Tumor / analysis. Bone Marrow / pathology. Nuclear Proteins / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Proto-Oncogene Proteins / analysis
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p21 / analysis. Disease-Free Survival. Female. Follow-Up Studies. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Mutation. Philadelphia Chromosome. Prognosis. Proportional Hazards Models. Proto-Oncogene Proteins c-mdm2 / analysis. RNA, Messenger / analysis. Time Factors. Treatment Outcome. Tumor Suppressor Protein p53 / analysis. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17143258.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / MDM4 protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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32. Niizuma H, Fujii K, Sato A, Fujiwara I, Takeyama J, Imaizumi M: PTHrP-independent hypercalcemia with increased proinflammatory cytokines and bone resorption in two children with CD19-negative precursor B acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Dec;49(7):990-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PTHrP-independent hypercalcemia with increased proinflammatory cytokines and bone resorption in two children with CD19-negative precursor B acute lymphoblastic leukemia.
  • Hypercalcemia in childhood acute lymphoblastic leukemia (ALL) is rare and occasionally associated with parathyroid hormone-related protein (PTHrP).
  • We report two children with precursor B ALL who had marked hypercalcemia (15.8 and 16.6 mg/dl, respectively) and disseminated osteolysis.
  • These findings suggest that increased osteoclastic bone resorption via stimulation with TNF-alpha and IL-6 may be mechanism causing PTHrP-independent hypercalcemia in some patients with precursor B ALL lacking CD19 expression.
  • [MeSH-major] Bone Resorption / complications. Cytokines / blood. Diphosphonates / administration & dosage. Hypercalcemia / complications. Parathyroid Hormone-Related Protein / blood. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • [Copyright] 2007 Wiley-Liss, Inc
  • (PMID = 16496289.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Bone Density Conservation Agents; 0 / Cytokines; 0 / Diphosphonates; 0 / Parathyroid Hormone-Related Protein; 90032-33-0 / deoxypyridinoline
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33. Nygren MK, Døsen-Dahl G, Stubberud H, Wälchli S, Munthe E, Rian E: beta-catenin is involved in N-cadherin-dependent adhesion, but not in canonical Wnt signaling in E2A-PBX1-positive B acute lymphoblastic leukemia cells. Exp Hematol; 2009 Feb;37(2):225-33
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] beta-catenin is involved in N-cadherin-dependent adhesion, but not in canonical Wnt signaling in E2A-PBX1-positive B acute lymphoblastic leukemia cells.
  • OBJECTIVE: The t(1;19)(q23;13) translocation, resulting in the production of the E2A-PBX1 chimeric protein, is a common nonrandom translocation in pediatric B-lineage acute lymphoblastic leukemia (B-ALL).
  • Localization of beta-catenin in the cell membrane and its involvement in leukemia-stroma interaction were studied by confocal microscopy.
  • RESULTS: In contrast to previous reports, we detected no effects on cell viability or proliferation upon modulation of the Wnt16 levels.
  • Instead, beta-catenin was located in the cell membrane along with N-cadherin.
  • E2A-PBX1-positive leukemia cells adhered strongly to bone marrow stroma cells, and we showed that adherence junctions stained strongly for both proteins.
  • Moreover, knockdown of beta-catenin reduced the adhesion of E2A-PBX1-positive leukemia cells to N-cadherin, suggesting that beta-catenin and N-cadherin play a central role in homotypic cell-to-cell adhesion and in leukemia-stroma adhesion.
  • Instead, beta-catenin is involved in N-cadherin-dependent adherence junctions, suggesting for the first time that leukemia-stroma interactions may be mediated via an N-cadherin-dependent mechanism.
  • [MeSH-major] Cadherins / metabolism. Homeodomain Proteins / metabolism. Leukemia, B-Cell / metabolism. Oncogene Proteins, Fusion / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Signal Transduction. Wnt Proteins / metabolism. beta Catenin / metabolism
  • [MeSH-minor] Adherens Junctions / genetics. Adherens Junctions / metabolism. Cell Adhesion / genetics. Cell Line, Tumor. Child. Child, Preschool. Chromosomes, Human / genetics. Chromosomes, Human / metabolism. Humans. Translocation, Genetic / genetics

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  • [ErratumIn] Exp Hematol. 2009 Mar;37(3):421
  • (PMID = 19101069.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cadherins; 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / WNT16 protein, human; 0 / Wnt Proteins; 0 / beta Catenin; 146150-85-8 / E2A-Pbx1 fusion protein
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34. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • We identified a t(12;17) in 2 of 398 childhood ALL patients karyotyped at presentation in our institute.
  • Both cases had a precursor-B immunophenotype and were CD10 negative and CD33 positive.
  • Comparison of these and previously published cases demonstrates that the translocation predominately occurs in children and young adults with precursor B-ALL and is typically characterized by low CD10 expression and high CD33 expression.
  • [MeSH-major] Burkitt Lymphoma / genetics. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 17. Core Binding Factor Alpha 2 Subunit / genetics. Gene Rearrangement. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Translocation, Genetic

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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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35. El Demellawy D, Sur M, Ross C, DeNardi F, Alowami S: Composite multifocal basal cell carcinoma and precursor B acute lymphoblastic leukemia: case report. Diagn Pathol; 2007;2:32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Composite multifocal basal cell carcinoma and precursor B acute lymphoblastic leukemia: case report.
  • Moreover, simultaneous occurrence of synchronous tumors involving the same tissue or organ at multiple sites is even less common.
  • We report a case of acute lymphoblastic leukemia (ALL) and basal cell carcinoma (BCC) occurring simultaneously in multiple skin sites.

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  • [Cites] Med Pediatr Oncol. 1991;19(6):508-10 [1961139.001]
  • [Cites] Arch Dermatol. 1990 Jan;126(1):102, 104-5 [2404459.001]
  • [Cites] Arch Dermatol. 1973 Oct;108(4):523-7 [4126803.001]
  • [Cites] Cancer. 1970 Jan;25(1):61-71 [4312028.001]
  • [Cites] Int J Hematol. 1993 Dec;59(1):67-71 [8161737.001]
  • [Cites] Pediatr Dermatol. 1996 Jan-Feb;13(1):54-7 [8919528.001]
  • (PMID = 17718899.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2000862
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36. Chapiro E, Russell L, Radford-Weiss I, Bastard C, Lessard M, Struski S, Cave H, Fert-Ferrer S, Barin C, Maarek O, Della-Valle V, Strefford JC, Berger R, Harrison CJ, Bernard OA, Nguyen-Khac F: Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia. Blood; 2006 Nov 15;108(10):3560-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia.
  • The CEBPA protein is known to regulate the balance between cell proliferation and differentiation during early hematopoietic development and myeloid differentiation.
  • In human myeloid leukemia, CEBPA is frequently inactivated by mutation and indirect and posttranslational mechanisms, in keeping with tumor suppressor properties.
  • We report that CEBPA is activated by juxtaposition to the immunoglobulin gene enhancer upon its rearrangement with the immunoglobulin heavy-chain locus in precursor B-cell acute lymphoblastic leukemia harboring t(14;19)(q32;q13).
  • [MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 16873674.001).
  • [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 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Immunoglobulin Heavy Chains; 0 / RNA, Neoplasm
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37. Brummel B, Bernbeck B, Schneider DT: Complicated but successful treatment of a patient with ataxia telangiectasia and pre-B-acute lymphoblastic leukemia. Klin Padiatr; 2010 Nov;222(6):391-4
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  • [Title] Complicated but successful treatment of a patient with ataxia telangiectasia and pre-B-acute lymphoblastic leukemia.
  • Pediatric patients may develop lymphomas and acute lymphoblastic leukaemia (ALL), especially of the T-lineage.
  • CASE REPORT: Here, we first report on a patient with AT and pre B-cell ALL.
  • CONCLUSION: A general recommendation for dose modification in these patients group cannot be made due to the low number of patients suffering from AT and leukaemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Ataxia Telangiectasia / diagnosis. Ataxia Telangiectasia / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


38. Lee K, Bang J, Kim K: Proteome analysis of malignant pleural effusion. J Clin Oncol; 2009 May 20;27(15_suppl):e22194

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Twenty microliters of pleural effusions(PEs) from 3 patients with non-small cell lung cancer(NSCLC) and 3 patients with tuberculous pleurisy(TBC) were used for proteome analysis.
  • Among the identified proteins, we found the biomarker candidates that significantly have different expression levels in malignant effusion; apolipoprotein B precursor, vitronectin, complement factor B, histidine-rich glycoprotein precursor, coagulation factor II precursor variant.
  • CONCLUSIONS: We found that several pleural effusion proteins may serve as potential biomarker candidates for differential diagnosis between maligant and tuberculous pleural effusion.

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  • (PMID = 27963631.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Meyer LH, Zangrando A, Eckhoff SM, Queudeville M, Vendramini E, Basso G, Te Kronnie G, Debatin K: Association of time to leukemia (TTL) in NOD/SCID mice with expression of apoptosis regulators in pediatric ALL. J Clin Oncol; 2009 May 20;27(15_suppl):10042

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Association of time to leukemia (TTL) in NOD/SCID mice with expression of apoptosis regulators in pediatric ALL.
  • : 10042 Background: Acute lymphoblastic leukemia (ALL) is the most frequent malignant disease in childhood.
  • In a recent study we transplanted pediatric leukemia samples from newly diagnosed BCP-ALL patients into NOD/SCID mice.
  • Time to leukemia (TTL) was analyzed for each patient sample as time from transplant to overt leukemia in the recipients.
  • Patients whose leukemia cells engrafted rapidly showed a clearly inferior relapse free survival in contrast to patient samples with prolonged in vivo growth.
  • METHODS: Gene expression profiles of ALL samples (N = 14) with short versus long TTL in the xenograft model were analyzed using a human whole genome array (Affymetrix U133 Plus 2.0) correlating gene expression values (relative expression) to the time from transplant to manifestation of leukemia in the NOD/SCID mice (TTL, in weeks) by quantitative traits analysis (QTA).
  • Patient samples exhibiting a short time to overt leukemia in the xenotransplant model associated with poor relapse free survival showed down-regulated XAF1 and impaired caspase-3 activation leading to decreased apoptosis of the leukemia cells.
  • CONCLUSIONS: Taken together, we used a novel approach directly correlating gene expression values to time from transplant to overt leukemia (TTL) identifying the apoptosis regulator XAF1 to be associated with poor outcome of patients.

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  • (PMID = 27962468.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Epenetos AA, Kousparou C, Stylianou S: Inhibition of Notch and tumor regression. J Clin Oncol; 2009 May 20;27(15_suppl):e14623

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14623 Background: Notch signaling is an evolutionary-conserved pathway in vertebrates and invertebrates which is involved many developmental processes, including cell fate decisions, apoptosis, proliferation, and stem-cell self renewal.
  • Increasing evidence suggests that the Notch signaling pathway is frequently up regulated in many forms of cancer including acute T-cell lymphoblastic leukemia, cervical, prostate, lung, breast and others.
  • RESULTS: Our data show that ANTP/DN MAML fusion protein, TR4 contains signals for proper cell targeting, internalization and nuclear transport.

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  • (PMID = 27964214.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. Faderl S, Thomas DA, Gandhi V, Huang X, Borthakur G, O'Brien S, Ravandi F, Plunkett W, Bretz JL, Kantarjian HM: Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL). J Clin Oncol; 2009 May 20;27(15_suppl):7020

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL).
  • The continual reassessment method (CRM) was used to determine the maximum tolerated dose (MTD) from 4 pre-defined dose levels.
  • Twenty-one pts had pre-B ALL, 5 pts pre-T/T ALL, 1 pt mature B ALL, and 3 pts biphenotypic acute leukemias.
  • All pts had pre-B ALL.

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  • (PMID = 27961382.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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42. Callera F, Lopes CO, Rosa ES, Mulin CC: Adult transitional pre-B acute lymphoblastic leukemia associated with ring chromosome 16. Cancer Genet Cytogenet; 2008 Jun;183(2):131-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult transitional pre-B acute lymphoblastic leukemia associated with ring chromosome 16.
  • [MeSH-major] Burkitt Lymphoma / genetics. Chromosomes, Human, Pair 16. Ring Chromosomes

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  • (PMID = 18503834.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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43. Hafeez M, Shaharyar A, Zia N, Rasheed H: A phase II feasibility study of cytarabine and idarubicin combination in relapsed or refractory adult acute lymphoblastic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e18002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II feasibility study of cytarabine and idarubicin combination in relapsed or refractory adult acute lymphoblastic leukemia.

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  • (PMID = 27964000.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Bernard N, Alberdi AJ, Tanguy ML, Brugere H, Helissey P, Hubert C, Gendrey N, Guillosson JJ, Nafziger J: Assessing the potential leukemogenic effects of 50 Hz magnetic fields and their harmonics using an animal leukemia model. J Radiat Res; 2008 Nov;49(6):565-77

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessing the potential leukemogenic effects of 50 Hz magnetic fields and their harmonics using an animal leukemia model.
  • To answer the still unresolved question of the possible leukemogenic effects of extremely low frequency magnetic fields (ELF-MFs) and of their harmonics on the incidence of B acute lymphoblastic leukemia in children, we used an animal model to explore the possible co-initiating or co-promoting effects of ELF-MFs on the development of leukemia.
  • We used a rat model in which B acute lymphoblastic leukemia is chemically induced by a nitrosurea derivative.
  • We compared body weight and survival time, percentage of bone marrow blast cells, cumulative incidence of leukemia and type of leukemia in the unexposed groups and in the groups exposed to 50 Hz MFs, with and without harmonics.
  • Significant changes in the leukemia type obtained after gamma-irradiation of the leukemia model, showed its sensitivity to a physical agent.
  • Our results do not support the hypothesis that ELF-MFs, with or without harmonics, affect the development of B acute lymphoblastic leukemia in children.
  • [MeSH-major] Leukemia, Radiation-Induced / etiology. Leukemia, Radiation-Induced / physiopathology. Risk Assessment / methods. Whole-Body Irradiation / methods

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  • (PMID = 18838845.001).
  • [ISSN] 0449-3060
  • [Journal-full-title] Journal of radiation research
  • [ISO-abbreviation] J. Radiat. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
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45. Gobbi G, Mirandola P, Malinverno C, Sponzilli I, Carubbi C, Ricci F, Binazzi R, Basso G, Giuliani-Piccari G, Ramazzotti G, Pasquantonio G, Cocco L, Vitale M: Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin. Int J Oncol; 2008 Aug;33(2):371-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin.
  • The B203.13 monoclonal antibody was developed by immunizing mice with the B/monocyte biphenotypic cell line B1b.
  • During normal hematopoiesis B203.13 is expressed on a fraction of CD34+ cells, while on mature cells it is only present on B-lymphocytes.
  • We tested this antibody as a marker of childhood B-acute lymphoblastic leukemia (B-ALL).
  • The CD10(+)/B203.13(+) phenotype was specific to B-ALL, since CD10(+)/CD20(+) cells from common acute lymphoblastic leukemia (c-ALL) did not express B203.13.
  • We concluded that the use of B203.13 in association with CD10 and CD20 provides meaningful information for distinguishing normal residual B-cells from leukemic B-lymphoblasts and that recurrence of a CD10(+)/B203.13(+) phenotype after transplantation may be a very early relapse indicator of early B-acute lymphoblastic leukemia.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18636158.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
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46. Safa M, Kazemi A, Zand H, Azarkeivan A, Zaker F, Hayat P: Inhibitory role of cAMP on doxorubicin-induced apoptosis in pre-B ALL cells through dephosphorylation of p53 serine residues. Apoptosis; 2010 Feb;15(2):196-203
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory role of cAMP on doxorubicin-induced apoptosis in pre-B ALL cells through dephosphorylation of p53 serine residues.
  • Exposure of cells to chemotherapeutic drug doxorubicin, a DNA-damaging agent, induces an increase in the levels and activity of the wild-type p53 protein.
  • Here we show that elevation of cAMP in pre-B acute lymphoblastic leukemia NALM-6 cells significantly attenuated phosphorylation state of p53 at Ser6, Ser9, Ser15, Ser20, Ser37, Ser46 and Ser392 upon exposure to doxorubicin.
  • [MeSH-major] Apoptosis / drug effects. Cyclic AMP / pharmacology. Doxorubicin / pharmacology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Serine / metabolism
  • [MeSH-minor] Ataxia Telangiectasia Mutated Proteins. Caspase 3 / metabolism. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Checkpoint Kinase 2. DNA Damage. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Leukemic / drug effects. Humans. Intracellular Space / drug effects. Intracellular Space / metabolism. Okadaic Acid / pharmacology. Phosphoprotein Phosphatases / metabolism. Phosphorylation / drug effects. Phosphoserine / metabolism. Protein Phosphatase 1 / metabolism. Protein Phosphatase 2 / metabolism. Protein-Serine-Threonine Kinases / metabolism. Tumor Suppressor Protein p53 / metabolism. Tumor Suppressor Proteins / metabolism. bcl-2-Associated X Protein / metabolism

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  • (PMID = 19882354.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / bcl-2-Associated X Protein; 17885-08-4 / Phosphoserine; 1W21G5Q4N2 / Okadaic Acid; 452VLY9402 / Serine; 80168379AG / Doxorubicin; E0399OZS9N / Cyclic AMP; EC 2.7.1.11 / Checkpoint Kinase 2; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / CHEK2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 1; EC 3.1.3.16 / Protein Phosphatase 2; EC 3.1.3.16 / protein phosphatase 2C; EC 3.4.22.- / Caspase 3
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47. Cui L, Li Z, Wu M, Li W, Gao C, Deng G: Combined analysis of minimal residual disease at two time points and its value for risk stratification in childhood B-lineage acute lymphoblastic leukemia. Leuk Res; 2010 Oct;34(10):1314-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined analysis of minimal residual disease at two time points and its value for risk stratification in childhood B-lineage acute lymphoblastic leukemia.
  • The study was aimed to explore the value of minimal residual disease (MRD) for risk stratification in childhood precursor-B-acute lymphoblastic leukemia.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 20034668.001).
  • [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 / Immunoglobulin Heavy Chains
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48. Papadhimitriou SI, Polychronopoulou S, Tsakiridou AA, Androutsos G, Paterakis GS, Athanassiadou F: p16 inactivation associated with aggressive clinical course and fatal outcome in TEL/AML1-positive acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2005 Dec;27(12):675-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] p16 inactivation associated with aggressive clinical course and fatal outcome in TEL/AML1-positive acute lymphoblastic leukemia.
  • The authors describe a 7-year-old boy with TEL/AML1-positive pre-B acute lymphoblastic leukemia, with hemizygous 9p21 deletion at presentation and no p16(INK4A) protein expression.
  • Despite an initial response to a standard chemotherapy regimen, the patient suffered two hematologic relapses and died 34 months after diagnosis.
  • The authors discuss the possibility that complete p16(INK4A) gene inactivation may adversely modify the prognostic significance of TEL/AML1 fusion in childhood acute lymphoblastic leukemia, and present evidence from clinical and in vitro observations in favor of this assumption.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Deletion. Genes, p16. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16344676.001).
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; AIEOP acute lymphoblastic leukemia protocol
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49. Specchia G, Albano F, Anelli L, Zagaria A, Liso A, Pannunzio A, Archidiacono N, Liso V, Rocchi M: Molecular cytogenetic study of instability at 1q21 approximately q32 in adult acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2005 Jan 1;156(1):54-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular cytogenetic study of instability at 1q21 approximately q32 in adult acute lymphoblastic leukemia.
  • In the present paper, we report a molecular cytogenetic study of 1q abnormalities associated with t(8;14)(q24;q32) in an adult common B acute lymphoblastic leukemia case with FAB-L2 morphology.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 1. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 15588856.001).
  • [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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50. Naithani R, Rai S, Choudhry VP: Septic arthritis of hip in a neutropenic child caused by Salmonella typhi. J Pediatr Hematol Oncol; 2008 Feb;30(2):182-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A 5-year-old male child was undergoing chemotherapy for pre-B acute lymphoblastic leukemia.
  • [MeSH-major] Arthritis, Infectious / etiology. Hip Joint. Neutropenia / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Typhoid Fever / complications

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  • (PMID = 18376276.001).
  • [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; Review
  • [Publication-country] United States
  • [Number-of-references] 32
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51. Talby L, Chambost H, Roubaud MC, N'Guyen C, Milili M, Loriod B, Fossat C, Picard C, Gabert J, Chiappetta P, Michel G, Schiff C: The chemosensitivity to therapy of childhood early B acute lymphoblastic leukemia could be determined by the combined expression of CD34, SPI-B and BCR genes. Leuk Res; 2006 Jun;30(6):665-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The chemosensitivity to therapy of childhood early B acute lymphoblastic leukemia could be determined by the combined expression of CD34, SPI-B and BCR genes.
  • We have identified genes differentially expressed in childhood early B acute lymphoblastic leukemia at diagnosis, according to chemosensitivity.
  • [MeSH-major] Antigens, CD34 / biosynthesis. Burkitt Lymphoma / metabolism. DNA-Binding Proteins / biosynthesis. Drug Resistance, Neoplasm. Gene Expression Regulation, Leukemic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-bcr / biosynthesis. Transcription Factors / biosynthesis

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  • (PMID = 16297978.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antigens, CD34; 0 / DNA-Binding Proteins; 0 / Transcription Factors; 148350-00-9 / SPIB protein, human; 5J49Q6B70F / Vincristine; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr; EC 3.5.1.1 / Asparaginase; V27W9254FZ / Cortisone; FRALLE 93 protocol
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52. van der Velden VH, de Bie M, van Wering ER, van Dongen JJ: Immunoglobulin light chain gene rearrangements in precursor-B-acute lymphoblastic leukemia: characteristics and applicability for the detection of minimal residual disease. Haematologica; 2006 May;91(5):679-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoglobulin light chain gene rearrangements in precursor-B-acute lymphoblastic leukemia: characteristics and applicability for the detection of minimal residual disease.
  • We analyzed the frequency and characteristics of Vk-Jk and Vlambda-Jlambda rearrangements inpatients with precursor-B-acute lymphoblastic leukemia (ALL) and evaluated the applicability of these rearrangements as targets for minimal residual disease (MRD) detection.
  • Vk-Jk rearrangements were particularly frequent in common-ALL, children between 5-10 years, and TEL-AML1-positive patients.
  • Vk-Jk and Vlambda-Jlambda rearrangements showed a good stability between diagnosis and relapse and reached good sensitivities in real-time quantitative polymerase chain reaction analysis.
  • Our data show that Vk-Jk and Vlambda-Jlambda rearrangements can be successfully applied for MRD detection in a subset of patients with precursor-B-ALL.
  • [MeSH-major] DNA, Neoplasm / genetics. Gene Rearrangement, B-Lymphocyte, Light Chain. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16627258.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Neoplasm; 0 / Immunoglobulin Variable Region
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53. Abrams MT, Robertson NM, Litwack G, Wickstrom E: Evaluation of glucocorticoid sensitivity in 697 pre-B acute lymphoblastic leukemia cells after overexpression or silencing of MAP kinase phosphatase-1. J Cancer Res Clin Oncol; 2005 Jun;131(6):347-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of glucocorticoid sensitivity in 697 pre-B acute lymphoblastic leukemia cells after overexpression or silencing of MAP kinase phosphatase-1.
  • PURPOSE: To determine the effect of modulating MAP kinase phosphatase-1 (MKP-1) expression levels on cell death induced by glucocorticoid (GC) or hydroxyurea (HU) treatment in the human pre-B acute lymphoblastic leukemia cell line 697.
  • METHODS: Stable MKP-1 overexpressing transformants of the 697 pre-B acute lymphoblastic leukemia cell line were created and tested for sensitivity to the GC triamcinolone acetonide (TA) and HU, and compared to a control 697 cell line containing normal MKP-1 expression levels.
  • Small interfering RNAs (siRNAs) were designed to inhibit MKP-1 expression and evaluated for their effect on GC-mediated cell death.
  • [MeSH-major] Cell Cycle Proteins / metabolism. Gene Silencing. Glucocorticoids / pharmacology. Immediate-Early Proteins / metabolism. Phosphoprotein Phosphatases / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Tyrosine Phosphatases / metabolism. Triamcinolone Acetonide / pharmacology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Base Sequence. Caspase 3. Caspases / metabolism. Cell Line, Tumor. Drug Resistance, Neoplasm. Dual Specificity Phosphatase 1. Humans. Hydroxyurea / pharmacology. Immunoblotting. Molecular Sequence Data. Protein Phosphatase 1. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Transfection

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  • (PMID = 15856297.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cell Cycle Proteins; 0 / Glucocorticoids; 0 / Immediate-Early Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 1; EC 3.1.3.48 / DUSP1 protein, human; EC 3.1.3.48 / Dual Specificity Phosphatase 1; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; F446C597KA / Triamcinolone Acetonide; X6Q56QN5QC / Hydroxyurea
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54. Sandler ES, Homans A, Mandell L, Amylon M, Wall DA, Devidas M, Buchanan GR, Lipton JM, Billett AL: Hematopoietic stem cell transplantation after first marrow relapse of non-T, non-B acute lymphoblastic leukemia: a pediatric oncology group pilot feasibility study. J Pediatr Hematol Oncol; 2006 Apr;28(4):210-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hematopoietic stem cell transplantation after first marrow relapse of non-T, non-B acute lymphoblastic leukemia: a pediatric oncology group pilot feasibility study.
  • BACKGROUND: Relapsed acute lymphoblastic leukemia (ALL) in children is associated with a poor outcome, especially for those patients whose relapse occurs during the first 36 months after diagnosis.
  • This study was designed to evaluate the feasibility of enrolling children with recurrent ALL in a standardized treatment protocol that included receipt of a hematopoietic stem cell transplant (HSCT).
  • PROCEDURE: Eligible patients with a bone marrow relapse of non-T, non-B ALL underwent a common induction and consolidation followed by receipt of either an allogeneic HSCT from a human leukocyte antigen (HLA)-identical sibling or an autologous HSCT purged with B-4 blocked ricin.
  • A common conditioning regimen was used for all patients.
  • [MeSH-major] Bone Marrow / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation


55. Tirado CA, Chen W, Huang LJ, Laborde C, Hiemenz MC, Valdez F, Ho K, Winick N, Lou Z, Koduru P: Novel JAK2 rearrangement resulting from a t(9;22)(p24;q11.2) in B-acute lymphoblastic leukemia. Leuk Res; 2010 Dec;34(12):1674-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel JAK2 rearrangement resulting from a t(9;22)(p24;q11.2) in B-acute lymphoblastic leukemia.
  • We report a novel JAK2 rearrangement resulting from a t(9;22)(p24;q11.2) in a 14-year-old male with a diagnosis of B lymphoblastic leukemia.
  • This case brings the total number of JAK2 rearranged lymphoblastic leukemia cases in the literature to seven.
  • [MeSH-major] Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 9 / genetics. Janus Kinase 2 / genetics. Leukemia, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20594592.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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56. Mihalcik SA, Tschumper RC, Jelinek DF: Transcriptional and post-transcriptional mechanisms of BAFF-receptor dysregulation in human B lineage malignancies. Cell Cycle; 2010 Dec 15;9(24):4884-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this study, we used primary cells and cell lines to interrogate the mechanisms underlying aberrant BAFF-R expression in precursor B acute lymphoblastic leukemia (precursor B-ALL) and mature B chronic lymphocytic leukemia (CLL).
  • Here we demonstrate the aberrant expression of BAFF-R in precursor B-ALL cell lines and reveal that these cells acquire BAFF-R expression through premature transcriptional activation of the BAFF-R promoter in coordination with regulatory transcription factor c-Rel.
  • Investigations using primary CLL cells provide a crucial counterpoint through their paucity of BAFF-R relative to their benign mature B cell counterparts, which we establish as functionally significant in its depletion of the CLL cells' BAFF-binding capacity.

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  • [Cites] J Immunol. 2001 Jan 1;166(1):6-10 [11123269.001]
  • [Cites] Arthritis Rheum. 2001 Jun;44(6):1313-9 [11407690.001]
  • [Cites] Exp Hematol. 2002 Feb;30(2):135-41 [11823048.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2973-9 [12351410.001]
  • [Cites] Ann Rheum Dis. 2003 Feb;62(2):168-71 [12525388.001]
  • [Cites] Arthritis Rheum. 2003 Apr;48(4):982-92 [12687540.001]
  • [Cites] Blood. 2004 Jan 15;103(2):679-88 [14504101.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1840-7 [10477712.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1848-54 [10477713.001]
  • [Cites] J Clin Oncol. 2006 Feb 20;24(6):983-7 [16432079.001]
  • [Cites] Immunology. 2006 Jul;118(3):281-92 [16827889.001]
  • [Cites] Arthritis Res Ther. 2006;8(1):R6 [16356193.001]
  • [Cites] Blood. 2007 Jan 15;109(2):703-10 [16973958.001]
  • [Cites] Haematologica. 2007 Sep;92(9):1284-5 [17768131.001]
  • [Cites] Blood. 2007 Dec 1;110(12):3959-67 [17687108.001]
  • [Cites] Arthritis Rheum. 2008 Aug;58(8):2453-9 [18668552.001]
  • [Cites] Leuk Res. 2009 Jan;33(1):162-5 [18556064.001]
  • [Cites] Nat Immunol. 2009 Jul;10(7):778-85 [19483719.001]
  • [Cites] Leuk Res. 2009 Oct;33(10):1319-27 [19395025.001]
  • [Cites] Arthritis Rheum. 2009 Jul;60(7):2083-93 [19565488.001]
  • [Cites] Cancer Res. 2010 Jun 1;70(11):4346-56 [20460528.001]
  • [Cites] J Immunol. 2010 Jul 15;185(2):1045-54 [20554963.001]
  • [CommentIn] Cell Cycle. 2011 Jan 15;10(2):189-90 [21239884.001]
  • (PMID = 21099364.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA062242; United States / NCI NIH HHS / CA / R01 CA105258; United States / NCI NIH HHS / CA / CA062242; United States / NCI NIH HHS / CA / CA105258
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell Activating Factor; 0 / B-Cell Activation Factor Receptor
  • [Other-IDs] NLM/ PMC3047811
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57. Jastaniah WA, Alessandri AJ, Reid GS, Schultz KR: HLA-DM expression is elevated in ETV6-AML1 translocation-positive pediatric acute lymphoblastic leukemia. Leuk Res; 2006 Apr;30(4):487-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HLA-DM expression is elevated in ETV6-AML1 translocation-positive pediatric acute lymphoblastic leukemia.
  • ETV6-AML1-positive precursor-B acute lymphoblastic leukemia (pre-B ALL) is associated with good outcome and late relapse.
  • The HLA-DR(high)/CLIP(low)/HLA-DM(high) phenotype strongly suggests that ETV6-AML1 leukemia will induce favorable immune responses and may in part explain the characteristic late relapses associated with ETV6-AML1 pre-B ALL.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. HLA-D Antigens / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics. Translocation, Genetic

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  • (PMID = 16191436.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / HLA-D Antigens; 0 / HLA-DM antigens; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins
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58. Escher R, Wilson P, Carmichael C, Suppiah R, Liu M, Kavallaris M, Cannon P, Michaud J, Scott HS: A pedigree with autosomal dominant thrombocytopenia, red cell macrocytosis, and an occurrence of t(12:21) positive pre-B acute lymphoblastic leukemia. Blood Cells Mol Dis; 2007 Jul-Aug;39(1):107-14
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A pedigree with autosomal dominant thrombocytopenia, red cell macrocytosis, and an occurrence of t(12:21) positive pre-B acute lymphoblastic leukemia.
  • Here we describe a new autosomal dominant inherited phenotype of thrombocytopenia and red cell macrocytosis in a four-generation pedigree.
  • Interestingly, in the youngest generation, a 2-year-old boy presenting with these familial features has developed acute lymphoblastic leukemia characterized by a t(12;21) translocation.
  • Tri-lineage involvement of platelets, red cells and white cells may suggest a genetic defect in an early multiliear progenitor or a stem cell.
  • Functional assays in EBV-transformed cell lines revealed a defect in cell proliferation and tubulin dynamics.
  • [MeSH-major] Anemia, Macrocytic / genetics. Burkitt Lymphoma / genetics. Chromosome Disorders / genetics. Genetic Predisposition to Disease. Pedigree. Thrombocytopenia / genetics

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  • (PMID = 17434765.001).
  • [ISSN] 1079-9796
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Clinical Trial; 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 / RUNX1 protein, human; 0 / Transcription Factors; 0 / ZFPM1 protein, human
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59. Healy J, Bélanger H, Beaulieu P, Larivière M, Labuda D, Sinnett D: Promoter SNPs in G1/S checkpoint regulators and their impact on the susceptibility to childhood leukemia. Blood; 2007 Jan 15;109(2):683-92
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter SNPs in G1/S checkpoint regulators and their impact on the susceptibility to childhood leukemia.
  • Mutations leading to the alteration of cell-cycle checkpoint functions are a common feature of most cancers.
  • Because of the highly regulated nature of the cell cycle, it seems likely that variation in gene dosage of key components due to functional regulatory polymorphisms could play an important role in cancer development.
  • Here we provide evidence of the involvement of promoter single-nucleotide polymorphisms (pSNPs) in the cyclin-dependent-kinase inhibitor genes CDKN2A, CDKN2B, CDKN1A, and CDKN1B in the etiology of childhood pre-B acute lymphoblastic leukemia (ALL).
  • A case-control study, conducted in 240 patients with pre-B ALL and 277 healthy controls, combined with a family-based analysis using 135 parental trios, all of French-Canadian origin, were used to evaluate single-site genotypic as well as multilocus haplotypic associations for a total of 10 pSNPs.
  • These findings suggest that variable expression levels of cell-cycle inhibitor genes CDKN2A, CDKN2B, and CDKN1B due to regulatory polymorphisms could indeed influence the risk of childhood pre-B ALL and contribute to carcinogenesis.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor Proteins / genetics. Genetic Predisposition to Disease. Polymorphism, Single Nucleotide. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics

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  • (PMID = 17008550.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor Proteins
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60. Gleissner B, Goekbuget N, Rieder H, Arnold R, Schwartz S, Diedrich H, Schoch C, Heinze B, Fonatsch C, Bartram CR, Hoelzer D, Thiel E, GMALL Study Group: CD10- pre-B acute lymphoblastic leukemia (ALL) is a distinct high-risk subgroup of adult ALL associated with a high frequency of MLL aberrations: results of the German Multicenter Trials for Adult ALL (GMALL). Blood; 2005 Dec 15;106(13):4054-6
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD10- pre-B acute lymphoblastic leukemia (ALL) is a distinct high-risk subgroup of adult ALL associated with a high frequency of MLL aberrations: results of the German Multicenter Trials for Adult ALL (GMALL).
  • Immunophenotyping disclosed CD10 negativity in 70 of 2408 cases of B-lineage acute lymphoblastic leukemia (ALL), although other criteria followed classification of pre-B ALL (eg, cytoplasmic immunoglobulin positivity).
  • Although 83% of the patients achieved complete remission, the remission duration remained remarkably low: 141 days for MLL rearrangement-positive and 245 days for MLL rearrangement-negative CD10(-) pre-B ALL.
  • Thus, the overall survival probability 3 years after diagnosis was 0.34 +/- 0.20 SE in MLL-rearrangement-negative versus 0.12 +/- 0.06 SE in MLL rearrangement-positive CD10- pre-B ALL.
  • Our data identify CD10- cytoplasmic immunoglobulin-positive pre-B ALL as a rare (2.2%) but distinct immuno-subtype of adult ALL that is characterized by a high MLL rearrangement rate and a worse outcome.
  • [MeSH-major] Chromosome Aberrations. Neprilysin / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 16123216.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.24.11 / Neprilysin
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61. Morisot S, Wayne AS, Bohana-Kashtan O, Kaplan IM, Gocke CD, Hildreth R, Stetler-Stevenson M, Walker RL, Davis S, Meltzer PS, Wheelan SJ, Brown P, Jones RJ, Shultz LD, Civin CI: High frequencies of leukemia stem cells in poor-outcome childhood precursor-B acute lymphoblastic leukemias. Leukemia; 2010 Nov;24(11):1859-66
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High frequencies of leukemia stem cells in poor-outcome childhood precursor-B acute lymphoblastic leukemias.
  • In order to develop a xenograft model to determine the efficacy of new therapies against primary human precursor-B acute lymphoblastic leukemia (ALL) stem cells (LSCs), we used the highly immunodeficient non-obese diabetic (NOD).Cg-Prkdc(scid)IL2rg(tmlWjl)/SzJ (NOD-severe combined immune deficient (scid) IL2rg(-/-)) mouse strain.
  • Intravenous transplantation of 2 of 2 ALL cell lines and 9 of 14 primary ALL cases generated leukemia-like proliferations in recipient mice by 1-7 months after transplant.
  • Leukemias were retransplantable, and the immunophenotypes, gene rearrangements and expression profiles were identical or similar to those of the original primary samples.
  • NOD-scid mice transplanted with the same primary samples developed similar leukemias with only a slightly longer latency than did NOD-scid-IL2Rg(-/-) mice.
  • In this highly sensitive NOD-scid-IL2Rg(-/-)-based assay, 1-100 unsorted primary human ALL cells from five of five tested patients, four of whom eventually experienced leukemia relapse, generated leukemias in recipient mice.


62. Gruber TA, Chang MS, Sposto R, Müschen M: Activation-induced cytidine deaminase accelerates clonal evolution in BCR-ABL1-driven B-cell lineage acute lymphoblastic leukemia. Cancer Res; 2010 Oct 1;70(19):7411-20
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activation-induced cytidine deaminase accelerates clonal evolution in BCR-ABL1-driven B-cell lineage acute lymphoblastic leukemia.
  • Occasionally, AID can target non-Ig genes and thereby promote GC B-cell lymphomagenesis.
  • We recently showed that the oncogenic BCR-ABL1 kinase induces aberrant expression of AID in pre-B acute lymphoblastic leukemia (ALL) and lymphoid chronic myelogenous leukemia blast crisis.
  • Mice transplanted with BCR-ABL1-transduced AID(-/-) bone marrow had prolonged survival compared with mice transplanted with leukemia cells generated from AID(+/+) bone marrow.
  • Consistent with a causative role of AID in genetic instability, AID(-/-) leukemia had a lower frequency of amplifications and deletions and a lower frequency of mutations in non-Ig genes, including Pax5 and Rhoh compared with AID(+/+) leukemias.

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  • [Copyright] © 2010 AACR.
  • [Cites] J Clin Oncol. 2009 Nov 1;27(31):5175-81 [19805687.001]
  • [Cites] Cancer Cell. 2009 Sep 8;16(3):232-45 [19732723.001]
  • [Cites] Nature. 2010 Feb 25;463(7284):1042-7 [20027182.001]
  • [Cites] Nature. 2010 Feb 25;463(7284):1101-5 [20098412.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):12963-8 [12297621.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):145-60 [12620409.001]
  • [Cites] J Exp Med. 2003 May 19;197(10):1291-6 [12756266.001]
  • [Cites] Nature. 2003 May 22;423(6938):452-6 [12761551.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Nat Genet. 2004 May;36(5):453-61 [15098032.001]
  • [Cites] Blood. 1992 Feb 15;79(4):1029-36 [1737087.001]
  • [Cites] Genes Dev. 1993 Dec;7(12B):2520-32 [8276236.001]
  • [Cites] Nucleic Acids Res. 1995 Feb 25;23(4):628-33 [7899083.001]
  • [Cites] Nat Med. 1995 Oct;1(10):1052-6 [7489362.001]
  • [Cites] Immunol Rev. 1998 Apr;162:107-16 [9602357.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3780-92 [9808572.001]
  • [Cites] J Biol Chem. 1999 Jun 25;274(26):18470-6 [10373455.001]
  • [Cites] Nature. 2004 Dec 2;432(7017):635-9 [15577913.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1467-75 [15494435.001]
  • [Cites] Nature. 2006 Mar 2;440(7080):105-9 [16400328.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2752-7 [16477013.001]
  • [Cites] N Engl J Med. 2006 Jun 15;354(24):2531-41 [16775234.001]
  • [Cites] Nat Med. 2006 Oct;12(10):1175-80 [16998483.001]
  • [Cites] Clin Cancer Res. 2006 Dec 15;12(24):7374-9 [17189410.001]
  • [Cites] J Exp Med. 2007 May 14;204(5):1157-66 [17485517.001]
  • [Cites] Adv Immunol. 2007;94:75-107 [17560272.001]
  • [Cites] Blood. 2000 Feb 15;95(4):1144-50 [10666183.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):9168-73 [10908648.001]
  • [Cites] Mol Cell. 2000 Aug;6(2):409-19 [10983987.001]
  • [Cites] Cell. 2000 Sep 1;102(5):553-63 [11007474.001]
  • [Cites] Cell. 2000 Sep 1;102(5):565-75 [11007475.001]
  • [Cites] Mol Cell Biol. 2000 Dec;20(23):9018-27 [11074000.001]
  • [Cites] Nature. 2000 Nov 9;408(6809):216-21 [11089977.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 22;98(11):6192-7 [11353846.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):341-6 [11460166.001]
  • [Cites] J Exp Med. 2002 May 6;195(9):F37-41 [11994429.001]
  • [Cites] Cancer Cell. 2007 Nov;12(5):467-78 [17996650.001]
  • [Cites] Nat Genet. 2008 Jan;40(1):108-12 [18066064.001]
  • [Cites] Nature. 2008 Feb 14;451(7180):841-5 [18273020.001]
  • [Cites] Methods Enzymol. 2008;439:365-93 [18374178.001]
  • [Cites] Nature. 2008 May 1;453(7191):110-4 [18408710.001]
  • [Cites] Cancer Chemother Pharmacol. 2008 Jul;62(2):363-8 [17899082.001]
  • [Cites] J Natl Cancer Inst. 2008 Jul 2;100(13):926-39 [18577747.001]
  • [Cites] Cell. 2008 Jul 11;134(1):62-73 [18614011.001]
  • [Cites] Gene Ther. 2008 Nov;15(21):1411-23 [18496571.001]
  • [Cites] Cell. 2008 Dec 12;135(6):1028-38 [19070574.001]
  • [Cites] Cell. 2008 Dec 12;135(6):1130-42 [19070581.001]
  • [Cites] Nat Rev Cancer. 2009 Feb;9(2):95-107 [19165225.001]
  • [Cites] Leukemia. 2010 Jan;24(1):66-73 [19759560.001]
  • (PMID = 20876806.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32CA09659; United States / NCI NIH HHS / CA / T32 CA009659; United States / NCI NIH HHS / CA / R21 CA152497; United States / NCI NIH HHS / CA / R21CA152497; United States / NCI NIH HHS / CA / R01CA137060; United States / NCI NIH HHS / CA / R01 CA139032; United States / NCI NIH HHS / CA / R01CA139032; United States / NCI NIH HHS / CA / R01 CA137060
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / src-Family Kinases; EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / Cytidine Deaminase
  • [Other-IDs] NLM/ NIHMS228027; NLM/ PMC2948648
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63. Fu JF, Hsu HC, Shih LY: MLL is fused to EB1 (MAPRE1), which encodes a microtubule-associated protein, in a patient with acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2005 Jun;43(2):206-10
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MLL is fused to EB1 (MAPRE1), which encodes a microtubule-associated protein, in a patient with acute lymphoblastic leukemia.
  • We have shown that the EB1 (MAPRE1) gene, at 20q11.2, is fused to MLL in an adult patient with pro-B acute lymphoblastic leukemia.
  • Southern blot analysis indicated that a rearrangement of the MLL gene was involved in the chromosomal abnormality. cDNA panhandle polymerase chain reaction (PCR) identified the fusion transcript, in which MLL exon 6 was fused in-frame with EB1 exon 5.
  • EB1 is a microtubule-associated protein that interacts with the colorectal adenomatous polyposis coli tumor-suppressor protein and plays important roles in regulating microtubule dynamics, cell polarity, and chromosome stability.
  • [MeSH-major] DNA-Binding Proteins / genetics. Microtubule-Associated Proteins / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. DNA Primers. Histone-Lysine N-Methyltransferase. Humans. Molecular Sequence Data. Myeloid-Lymphoid Leukemia Protein

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 15751040.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY752858/ AY752859/ AY752860/ AY752861
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / MAPRE1 protein, human; 0 / MLL protein, human; 0 / Microtubule-Associated Proteins; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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64. Seifert G, Reindl T, Lobitz S, Seeger K, Henze G: Fatal course after administration of rituximab in a boy with relapsed all: a case report and review of literature. Haematologica; 2006 Jun;91(6 Suppl):ECR23
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We are reporting on a 14-year-old boy with a very early relapse of pre-B acute lymphoblastic leukemia (ALL) and anaplastic astrocytoma WHO degrees III; the astrocytoma was subtotally resected and subsequently treated with irradiation and chemotherapy.
  • After a small fraction of the standard dose (375 mg/m(2)) had been administered, the infusion had to be interrupted because of an acute attack of pain in the lumbar region.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antineoplastic Agents / adverse effects. Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Burkitt Lymphoma / drug therapy

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  • (PMID = 16785126.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 27
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65. Wimmer-Kleikamp SH, Nievergall E, Gegenbauer K, Adikari S, Mansour M, Yeadon T, Boyd AW, Patani NR, Lackmann M: Elevated protein tyrosine phosphatase activity provokes Eph/ephrin-facilitated adhesion of pre-B leukemia cells. Blood; 2008 Aug 1;112(3):721-32
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevated protein tyrosine phosphatase activity provokes Eph/ephrin-facilitated adhesion of pre-B leukemia cells.
  • Signaling by Eph receptors and cell-surface ephrin ligands modulates adhesive cell properties and thereby coordinates cell movement and positioning in normal and oncogenic development.
  • While cell contact-dependent Eph activation frequently leads to cell-cell repulsion, also the diametrically opposite response, cell-cell adhesion, is a probable outcome.
  • We have examined cell-biologic mechanisms underlying this switch by analyzing ephrin-A5-induced cell-morphologic changes of EphA3-positive LK63 pre-B acute lymphoblastic leukemia cells.
  • Their exposure to ephrin-A5 surfaces leads to a rapid conversion from a suspended/nonpolarized to an adherent/polarized cell type, a transition that relies on EphA3 functions operating in the absence of Eph-kinase signaling.
  • Cell morphology change and adhesion of LK63 cells are effectively attenuated by endogenous protein tyrosine phosphatase (PTP) activity, whereby PTP inhibition and productive EphA3-phosphotyrosine signaling reverse the phenotype to nonadherent cells with a condensed cytoskeleton.
  • [MeSH-major] Cell Adhesion. Ephrins / physiology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Protein Tyrosine Phosphatases / metabolism. Receptors, Eph Family / physiology
  • [MeSH-minor] Cell Line. Cell Line, Tumor. Cell Polarity. Cell Shape. Ephrin-A5 / physiology. Humans. Phosphorylation. Receptor, EphA3 / physiology. Signal Transduction

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  • [CommentIn] Blood. 2008 Aug 1;112(3):455-6 [18650455.001]
  • (PMID = 18385452.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ephrin-A5; 0 / Ephrins; EC 2.7.10.1 / Receptor, EphA3; EC 2.7.10.1 / Receptors, Eph Family; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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66. Papayannidis C, Derenzini E, Iacobucci I, Curti A, Paolini S, Cilloni D, Baccarani M, Martinelli G: Successful combination treatment of clofarabine, cytarabine, and gemtuzumab-ozogamicin in adult refractory B-acute lymphoblastic leukemia. Am J Hematol; 2009 Dec;84(12):849-50
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful combination treatment of clofarabine, cytarabine, and gemtuzumab-ozogamicin in adult refractory B-acute lymphoblastic leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Salvage Therapy

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  • (PMID = 19844989.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Arabinonucleosides; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 762RDY0Y2H / clofarabine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
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67. Kraal K, Schalij-Delfos N, van Buchem M, Egeler M, Ball L: Optic nerve relapse in a child with common acute lymphoblastic leukemia, treated with systemic anti-CD-20 (rituximab). Haematologica; 2005 Nov;90 Suppl:ECR24
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  • [Title] Optic nerve relapse in a child with common acute lymphoblastic leukemia, treated with systemic anti-CD-20 (rituximab).
  • We describe a two- year old boy who was diagnosed with pre-B acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD20 / immunology. Antineoplastic Agents / therapeutic use. Leukemic Infiltration / drug therapy. Optic Nerve / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16266915.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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68. Morrissette JJ, Halligan GE, Punnett HH, McKenzie AS, Guerrero F, de Chadarévian JP: Down syndrome with low hypodiploidy in precursor B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2006 Aug;169(1):58-61
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  • [Title] Down syndrome with low hypodiploidy in precursor B-cell acute lymphoblastic leukemia.
  • We describe the rare finding of a 33-month-old child neonatally diagnosed with Down syndrome, who presented with pre-B acute lymphoblastic leukemia (ALL) with a pretreatment bone marrow karyotype in which a low hypodiploid cell line (38 chromosomes) was identified in 17/19 cells studied.
  • The abnormal cell line retained the extra constitutional chromosome 21.
  • Hypodiploidy (loss of one or more chromosomes) is seen in approximately 5% of all childhood pre-B ALL cases and in approximately 2.2% cases of individuals with a constitutional trisomy 21.
  • [MeSH-major] Burkitt Lymphoma / genetics. Diploidy. Down Syndrome / genetics

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  • (PMID = 16875938.001).
  • [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
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69. Pradeep R, Madhumathi DS, Lakshmidevi V, Premalata CS, Appaji L, Patil SA, Swapnil B: Bilateral nephromegaly simulating wilms tumor: a rare initial manifestation of acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2008 Jun;30(6):471-3
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  • [Title] Bilateral nephromegaly simulating wilms tumor: a rare initial manifestation of acute lymphoblastic leukemia.
  • A 7-year-old boy was referred with a provisional diagnosis of bilateral Wilms tumor.
  • Immunohistochemistry on paraffin sections showed a pre-B phenotype of acute lymphoblastic leukemia.
  • Finally, a diagnosis of pre-B acute lymphoblastic leukemia infiltrating both the kidneys was made.
  • [MeSH-major] Kidney Diseases / etiology. Kidney Neoplasms / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Wilms Tumor / pathology
  • [MeSH-minor] Biopsy, Fine-Needle. Child. Diagnosis, Differential. Humans. Immunohistochemistry. Male. Tomography, X-Ray Computed


70. Colović N, Terzić T, Andelić B, Sretenović M, Mihaljević B, Lipkovski JM, Colović M: Nephrotic syndrome and acute renal failure in non-Hodgkin lymphoplasmacytic lymphoma. Med Oncol; 2008;25(4):458-61
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  • [Title] Nephrotic syndrome and acute renal failure in non-Hodgkin lymphoplasmacytic lymphoma.
  • Two patients with lymphoplasmacytic lymphoma, and monoclonal proteins of IgM in one, and IgG and lambda light chains in the second patient, nephrotic syndrome and acute renal failure are reported.
  • A 58-year-old man previously treated for pre-B acute lymphoblastic leukemia, developed 3 years later nephrotic syndrome as a complication of lymphoplasmacytic lymphoma and high-paraprotein IgM kappa type.
  • The second patient is a 42-year-old female diagnosed with lymphoplasmacytic lymphoma and paraprotein IgG lambda type.
  • The course of the disease was fulminant with developing nephrotic syndrome and fatal acute renal failure.
  • [MeSH-major] Acute Kidney Injury / complications. Lymphoma, Non-Hodgkin / complications. Nephrotic Syndrome / complications. Waldenstrom Macroglobulinemia / complications

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  • (PMID = 18214715.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Immunoglobulin M
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71. Moleti ML, Testi AM, Giona F, Malandruccolo L, Pescarmona E, Martino P, Paoloni F, Barberi W, Palumbo G, Mandelli F, Foa R: CODOX-M/IVAC (NCI 89-C-41) in children and adolescents with Burkitt's leukemia/lymphoma and large B-cell lymphomas: a 15-year monocentric experience. Leuk Lymphoma; 2007 Mar;48(3):551-9
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  • [Title] CODOX-M/IVAC (NCI 89-C-41) in children and adolescents with Burkitt's leukemia/lymphoma and large B-cell lymphomas: a 15-year monocentric experience.
  • During the last 15 years, we have used the National Cancer Institute (NCI) 89-C-41 protocol in patients aged younger than 21 years with Burkitt's leukemia/lymphoma (BLL) and diffuse large B-cell lymphoma (DLBCL).
  • Two responders relapsed after 2 months and one presented early B acute lymphoblastic leukemia 33 months from the end of therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma / drug therapy. Leukemia / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy

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  • (PMID = 17454598.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; UM20QQM95Y / Ifosfamide; YL5FZ2Y5U1 / Methotrexate; ANAVACYM protocol; IVAC protocol
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72. Healy J, Bourgey M, Richer C, Sinnett D, Roy-Gagnon MH: Detection of fetomaternal genotype associations in early-onset disorders: evaluation of different methods and their application to childhood leukemia. J Biomed Biotechnol; 2010;2010:369534
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  • [Title] Detection of fetomaternal genotype associations in early-onset disorders: evaluation of different methods and their application to childhood leukemia.
  • Using this approach, we examined fetomaternal associations between 29 SNPs in 12 cell-cycle genes and childhood pre-B acute lymphoblastic leukemia (ALL).

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  • [Cites] Lancet. 1999 Oct 30;354(9189):1499-503 [10551495.001]
  • [Cites] Am J Hum Genet. 1993 Nov;53(5):1114-26 [8213835.001]
  • [Cites] Leuk Res. 1997 Sep;21(9):817-23 [9393596.001]
  • [Cites] Am J Hum Genet. 1998 Apr;62(4):969-78 [9529360.001]
  • [Cites] Am J Hum Genet. 1998 Jul;63(1):259-66 [9634505.001]
  • [Cites] Am J Epidemiol. 1998 Nov 1;148(9):893-901 [9801020.001]
  • [Cites] Proc Biol Sci. 1998 Dec 7;265(1412):2273-8 [9881472.001]
  • [Cites] Science. 1999 Jan 15;283(5400):387-90 [9888853.001]
  • [Cites] Blood. 1999 Mar 1;93(5):1496-501 [10029576.001]
  • [Cites] Dev Cell. 2005 Feb;8(2):153-66 [15691758.001]
  • [Cites] Environ Health Perspect. 2005 Jun;113(6):787-92 [15929905.001]
  • [Cites] Am J Epidemiol. 2005 Oct 1;162(7):676-85 [16093287.001]
  • [Cites] Am J Hum Genet. 2005 Oct;77(4):627-36 [16175508.001]
  • [Cites] Nat Rev Cancer. 2006 Mar;6(3):193-203 [16467884.001]
  • [Cites] Genomics. 2006 Jun;87(6):704-10 [16500075.001]
  • [Cites] Am J Epidemiol. 2006 Jun 15;163(12):1091-100 [16597704.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2336-41 [17164354.001]
  • [Cites] Am J Epidemiol. 2007 Jan 1;165(1):27-35 [17035343.001]
  • [Cites] Blood. 2007 Jan 15;109(2):683-92 [17008550.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • [Cites] Am Nat. 2008 May;171(5):580-96 [18419568.001]
  • [Cites] Eur J Hum Genet. 2008 Jul;16(7):783-5 [18398431.001]
  • [Cites] Am J Epidemiol. 2008 Sep 1;168(5):541-7 [18650222.001]
  • [Cites] Genet Epidemiol. 2009 Feb;33(2):136-44 [18759250.001]
  • [Cites] PLoS One. 2011;6(5):e19368 [21573116.001]
  • [Cites] Lancet. 1999 Nov 20;354(9192):1819 [10577664.001]
  • [Cites] Am J Hum Genet. 2000 Jan;66(1):335-8 [10631165.001]
  • [Cites] Eur J Cancer. 1999 Dec;35(14):1941-53 [10711237.001]
  • [Cites] Leukemia. 2000 Mar;14(3):513-7 [10720153.001]
  • [Cites] Am J Hum Genet. 2002 Jan;70(1):124-41 [11719900.001]
  • [Cites] Cancer. 2002 Oct 15;95(8):1786-94 [12365028.001]
  • [Cites] Am J Hum Genet. 2002 Dec;71(6):1312-9 [12439825.001]
  • [Cites] Genet Epidemiol. 2003 Jan;24(1):1-13 [12508251.001]
  • [Cites] Am J Hum Genet. 2003 Feb;72(2):438-47 [12533786.001]
  • [Cites] Genes Chromosomes Cancer. 2003 May;37(1):36-43 [12661004.001]
  • [Cites] Nucleic Acids Res. 2003 Jul 1;31(13):3576-9 [12824369.001]
  • [Cites] Genet Epidemiol. 2004 Apr;26(3):167-85 [15022205.001]
  • [Cites] EMBO J. 1983;2(5):679-84 [6641714.001]
  • [Cites] Lancet. 1997 Feb 1;349(9048):344-9 [9024390.001]
  • (PMID = 20617153.001).
  • [ISSN] 1110-7251
  • [Journal-full-title] Journal of biomedicine & biotechnology
  • [ISO-abbreviation] J. Biomed. Biotechnol.
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2896672
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73. Zunino SJ, Ducore JM, Storms DH: Parthenolide induces significant apoptosis and production of reactive oxygen species in high-risk pre-B leukemia cells. Cancer Lett; 2007 Aug 28;254(1):119-27
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  • [Title] Parthenolide induces significant apoptosis and production of reactive oxygen species in high-risk pre-B leukemia cells.
  • We investigated whether parthenolide, the principal bioactive component of the herb feverfew (Tanacetum parthenium) induced apoptosis in pre-B acute lymphoblastic leukemia (ALL) lines, including cells carrying the t(4;11)(q21;q23) chromosomal translocation.
  • Parthenolide induced rapid apoptotic cell death distinguished by loss of nuclear DNA, externalization of cell membrane phosphatidylserine, and depolarization of mitochondrial membranes at concentrations ranging from 5 to 100 microM.
  • Using reactive oxygen species (ROS)-specific dyes, an increase in nitric oxide and superoxide anion was detected in the cells by 4 h after exposure to parthenolide.
  • These data suggest parthenolide may have potential as a potent and novel therapeutic agent against pre-B ALLs.
  • [MeSH-minor] Dose-Response Relationship, Drug. Flow Cytometry. Humans. Membrane Potential, Mitochondrial / drug effects. Nitric Oxide / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Risk Factors. Tumor Cells, Cultured

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  • (PMID = 17470383.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Reactive Oxygen Species; 0 / Sesquiterpenes; 2RDB26I5ZB / parthenolide; 31C4KY9ESH / Nitric Oxide
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74. Zunino SJ, Storms DH: Carnosol delays chemotherapy-induced DNA fragmentation and morphological changes associated with apoptosis in leukemic cells. Nutr Cancer; 2009;61(1):94-102
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  • Carnosol, from the herb rosemary, has been shown to induce apoptotic cell death in high-risk pre-B acute lymphoblastic leukemia (ALL).
  • In the present study, carnosol was tested for its ability to sensitize leukemia cells to chemotherapeutic agents.
  • Carnosol reduced the percentage of cell death in the pre-B ALL lines SEM, RS4;11, and REH when combined with cytarabine, methotrexate, or vincristine compared to the chemotherapeutic agents alone.
  • These data show that carnosol blocks the terminal apoptotic events induced by chemotherapeutic drugs and suggest that increased dietary intake of carnosol may potentially decrease the effectiveness of some standard chemotherapy treatments used for leukemia.
  • [MeSH-major] Antineoplastic Agents / pharmacology. DNA Fragmentation / drug effects. Diterpenes, Abietane / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Caspase 3 / drug effects. Caspase 3 / metabolism. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Synergism. Humans. Mitochondrial Membranes / drug effects

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  • (PMID = 19116879.001).
  • [ISSN] 1532-7914
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diterpenes, Abietane; 5957-80-2 / carnosol; EC 3.4.22.- / Caspase 3
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75. Al-Anazi KA, Eltayeb KI, Bakr M, Al-Mohareb FI: Methotrexate-induced acute leukemia: report of three cases and review of the literature. Clin Med Case Rep; 2009;2:43-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Methotrexate-induced acute leukemia: report of three cases and review of the literature.
  • For many years, methotrexate has been used in the treatment of certain chronic medical disorders e.g. rheumatoid arthritis and psoriasis as well as a number of malignant disorders e.g. acute lymphoblastic leukemia, certain types of lymphoma and breast carcinoma.
  • In patients treated with methotrexate, the development of leukemia has been attributed to either the primary disorder e.g. rheumatoid arthritis or to other drugs used concomitantly e.g. cyclophosphamide.
  • Two of these patients developed acute myeloid leukemia on myelodysplastic syndrome background, while the third patient developed pre-B acute lymphoblastic leukemia that expressed few myeloid markers and had a positive philadelphia chromosome.
  • To our knowledge, these are the first reported cases of methotrexate-induced acute leukemia.

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  • (PMID = 24179373.001).
  • [ISSN] 1178-6450
  • [Journal-full-title] Clinical medicine. Case reports
  • [ISO-abbreviation] Clin Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3785348
  • [Keywords] NOTNLM ; acute lymphoblastic leukemia / acute myeloid leukemia / methotrexate / myelodysplastic syndrome / rheumatoid arthritis
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76. Salzer WL, Devidas M, Shuster JJ, Wang C, Chauvenet A, Asselin BL, Camitta BM, Kurtzberg J, Children's Oncology Group: Intensified PEG-L-asparaginase and antimetabolite-based therapy for treatment of higher risk precursor-B acute lymphoblastic leukemia: a report from the Children's Oncology Group. J Pediatr Hematol Oncol; 2007 Jun;29(6):369-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intensified PEG-L-asparaginase and antimetabolite-based therapy for treatment of higher risk precursor-B acute lymphoblastic leukemia: a report from the Children's Oncology Group.
  • The Pediatric Oncology Group 9203 pilot protocol was designed to determine the feasibility of delivering 29 biweekly doses of polyethylene glycol (PEG)-L-asparaginase, on a backbone of intensive multiagent antimetabolite-based consolidation and maintenance in higher risk B-precursor acute lymphoblastic leukemia.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asparaginase / therapeutic use. Polyethylene Glycols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 17551397.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 30969; United States / NCI NIH HHS / CA / CA 98543; United States / NCI NIH HHS / CA / U10 CA 29139
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / pegaspargase; 30IQX730WE / Polyethylene Glycols; EC 3.5.1.1 / Asparaginase
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77. Healy J, Roy-Gagnon MH, Sinnett D: No evidence for association between TGFB1 promoter SNPs and the risk of childhood pre-B acute lymphoblastic leukemia among French Canadians. Haematologica; 2009 Jul;94(7):1034-5
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  • [Title] No evidence for association between TGFB1 promoter SNPs and the risk of childhood pre-B acute lymphoblastic leukemia among French Canadians.
  • [MeSH-major] Polymorphism, Single Nucleotide. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic. Transforming Growth Factor beta1 / genetics

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  • [Cites] Anal Biochem. 1999 Nov 1;275(1):84-92 [10542112.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2610-5 [12750287.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 May;13(5):759-64 [15159307.001]
  • [Cites] Genet Epidemiol. 2004 Jul;27(1):21-32 [15185400.001]
  • [Cites] Am J Hum Genet. 2004 Oct;75(4):561-70 [15290652.001]
  • [Cites] Cancer Res. 2008 Feb 15;68(4):1236-44 [18281501.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):2078-93 [15774796.001]
  • [Cites] Lung Cancer. 2006 Apr;52(1):1-7 [16499994.001]
  • [Cites] Genomics. 2006 Jun;87(6):704-10 [16500075.001]
  • [Cites] Blood. 2007 Jan 15;109(2):683-92 [17008550.001]
  • [Cites] Am J Hum Genet. 1998 Jul;63(1):259-66 [9634505.001]
  • (PMID = 19491338.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Transforming Growth Factor beta1
  • [Other-IDs] NLM/ PMC2704319
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78. Mosad E, Hamed HB, Bakry RM, Ezz-Eldin AM, Khalifa NM: Persistence of TEL-AML1 fusion gene as minimal residual disease has no additive prognostic value in CD 10 positive B-acute lymphoblastic leukemia: a FISH study. J Hematol Oncol; 2008;1:17
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Persistence of TEL-AML1 fusion gene as minimal residual disease has no additive prognostic value in CD 10 positive B-acute lymphoblastic leukemia: a FISH study.
  • There was a significant correlation between TEL-AML1 fusion gene both at diagnosis (r = 0.5, P = 0.003) and as a MRD (r = 0.4, P = 0.01) with favorable course.
  • Kaplan-Meier curve for the presence of TEL-AML1 fusion at the diagnosis was associated with a better probability of overall survival (OS); mean survival time was 47 +/- 1 month, in contrast to 28 +/- 5 month in its absence (P = 0.006).
  • So, persistence of TEL-AML1 fusion as a MRD had no additive prognostic value over its measurement at diagnosis in terms of predicting the probability of OS.
  • CONCLUSION: For most patients, the presence of TEL-AML1 fusion gene at diagnosis suggests a favorable prognosis.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Child. Child, Preschool. Female. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm, Residual / diagnosis. Neoplasm, Residual / genetics. Prognosis

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  • [Cites] Pediatr Int. 2003 Jun;45(3):275-80 [12828580.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1253-8 [11830473.001]
  • [Cites] Med Pediatr Oncol. 1990;18(4):273-9 [2355886.001]
  • [Cites] N Engl J Med. 1990 Aug 16;323(7):448-55 [2095753.001]
  • [Cites] Blood. 1991 Aug 1;78(3):739-47 [1859886.001]
  • [Cites] Leukemia. 1992 Apr;6(4):282-8 [1316978.001]
  • [Cites] Br J Haematol. 1993 Mar;83(3):412-8 [8485046.001]
  • [Cites] Lancet. 1994 Jan 22;343(8891):196-200 [7904666.001]
  • [Cites] Leukemia. 1994 Mar;8(3):395-401 [8127144.001]
  • [Cites] Leukemia. 1995 Dec;9(12):1985-9 [8609706.001]
  • [Cites] Blood. 1996 Apr 1;87(7):2891-9 [8639909.001]
  • [Cites] Cancer Genet Cytogenet. 1996 Jun;88(2):151-4 [8640725.001]
  • [Cites] Blood. 1996 Jul 1;88(1):302-8 [8704188.001]
  • [Cites] Blood. 1996 Dec 1;88(11):4252-8 [8943861.001]
  • [Cites] Med Pediatr Oncol. 1997 Jan;28(1):48-53 [8950336.001]
  • [Cites] J Clin Oncol. 1997 Mar;15(3):1150-7 [9060558.001]
  • [Cites] Br J Haematol. 1997 May;97(2):460-2 [9163615.001]
  • [Cites] Br J Haematol. 1997 Jun;97(3):607-11 [9207408.001]
  • [Cites] Br J Haematol. 1997 Oct;99(1):240-1 [9359534.001]
  • [Cites] Blood. 1997 Dec 15;90(12):4933-7 [9389711.001]
  • [Cites] Blood. 1998 Mar 1;91(5):1716-22 [9473238.001]
  • [Cites] Jpn J Cancer Res. 1998 Jul;89(7):783-8 [9738986.001]
  • [Cites] Blood. 1998 Dec 15;92(12):4792-7 [9845546.001]
  • [Cites] Leukemia. 1999 Jan;13(1):19-21 [10049054.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1116-23 [16195338.001]
  • [Cites] Rev Immunogenet. 1999;1(2):265-78 [11253952.001]
  • [Cites] Mol Cell Probes. 2001 Apr;15(2):99-103 [11292328.001]
  • [Cites] Blood. 2001 Aug 1;98(3):558-64 [11468150.001]
  • [Cites] J Clin Oncol. 1989 Dec;7(12):1807-15 [2685179.001]
  • (PMID = 18928518.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [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/ PMC2577682
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79. Cairo MS, Gerrard M, Sposto R, Auperin A, Pinkerton CR, Michon J, Weston C, Perkins SL, Raphael M, McCarthy K, Patte C, FAB LMB96 International Study Committee: Results of a randomized international study of high-risk central nervous system B non-Hodgkin lymphoma and B acute lymphoblastic leukemia in children and adolescents. Blood; 2007 Apr 1;109(7):2736-43
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  • [Title] Results of a randomized international study of high-risk central nervous system B non-Hodgkin lymphoma and B acute lymphoblastic leukemia in children and adolescents.
  • The prognosis for higher risk childhood B-cell non-Hodgkin lymphoma has improved over the past 20 years but the optimal intensity of treatment has yet to be determined.
  • Children 21 years old or younger with newly diagnosed B-cell non-Hodgkin lymphoma/B-cell acute lymphoblastic leukemia (B-NHL/B-ALL) with higher risk factors (bone marrow [BM] with or without CNS involvement) were randomized to standard intensity French-American-British/Lymphoma Malignancy B (FAB/LMB) therapy or reduced intensity (reduced cytarabine plus etoposide and deletion of 3 maintenance courses M2, M3, M4).
  • Patients with either combined BM/CNS disease at diagnosis or poor response to cyclophosphamide, Oncovin [vincristine], prednisone (COP) reduction therapy had a significantly inferior EFS and S (P < .001).
  • [MeSH-major] Burkitt Lymphoma / drug therapy. Central Nervous System Neoplasms / drug therapy. Lymphoma, B-Cell / drug therapy


80. Řezáčová M, Vávrová J, Vokurková D: Ionizing Radiation Sensitizes Leukemic MOLT-4 Cells to TRAIL-induced Apoptosis. Acta Medica (Hradec Kralove); 2008;51(2):101-105

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  • However, leukemia cells studied to date have shown variable susceptibility to TRAIL.
  • Our study demonstrates that cells of acute T-lymphoblastic leukemia MOLT-4 are resistant to TRAIL and that ionizing radiation in the therapeutically achievable dose of 1 Gy sensitizes TRAIL-resistant cells MOLT-4 to the TRAIL-induced apoptosis by increase in death receptors for TRAIL DR5.
  • When TRAIL is applied after the irradiation in the time of increased DR5 positivity more efficient cell killing is achieved.

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  • (PMID = 28550838.001).
  • [ISSN] 1211-4286
  • [Journal-full-title] Acta medica (Hradec Kralove)
  • [ISO-abbreviation] Acta Medica (Hradec Kralove)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Czech Republic
  • [Keywords] NOTNLM ; Apoptosis / DR5 / Ionizing radiation / Leukemia / TRAIL
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81. Brown VI, Hulitt J, Fish J, Sheen C, Bruno M, Xu Q, Carroll M, Fang J, Teachey D, Grupp SA: Thymic stromal-derived lymphopoietin induces proliferation of pre-B leukemia and antagonizes mTOR inhibitors, suggesting a role for interleukin-7Ralpha signaling. Cancer Res; 2007 Oct 15;67(20):9963-70
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  • [Title] Thymic stromal-derived lymphopoietin induces proliferation of pre-B leukemia and antagonizes mTOR inhibitors, suggesting a role for interleukin-7Ralpha signaling.
  • Understanding the pathogenesis of leukemia in the context of lymphopoiesis may reveal novel therapeutic targets.
  • Previously, we have shown that mTOR inhibitors (MTI) show activity in vitro and in preclinical models of both human and murine precursor B acute lymphoblastic leukemia (pre-B ALL), inhibiting cell proliferation and inducing apoptosis.
  • These MTI-mediated effects can be reversed by interleukin-7 (IL-7), an important regulator of early B-cell development.
  • TSLP is closely related to IL-7 and active in lymphopoiesis, but an effect of TSLP on leukemia cells has not been described.
  • We examined the effect of TSLP on pre-B ALL cells and their response to MTIs.
  • Here, we show that TSLP stimulates proliferation of pre-B ALL cell lines.
  • TSLP also partially reverses the effects of MTI on proliferation, apoptosis, and ribosomal protein S6 and 4E-BP1 phosphorylation in cell lines, with similar biological effects seen in some primary human lymphoblast samples.
  • These data show that TSLP can promote survival of pre-B ALL cells and antagonize the effects of MTIs.
  • These findings suggest that IL-7Ralpha chain is responsible for transducing the survival signal that overcomes MTI-mediated growth inhibition in pre-B ALL.

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  • (PMID = 17942929.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 5K08-CA104882; United States / NCI NIH HHS / CA / K08 CA104882-04; United States / NCI NIH HHS / CA / K08 CA104882; United States / NCI NIH HHS / CA / CA104882-04; United States / NCI NIH HHS / CA / R01-CA102646
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Carrier Proteins; 0 / Cytokines; 0 / Eif4ebp1 protein, mouse; 0 / Interleukin-7; 0 / Interleukin-7 Receptor alpha Subunit; 0 / Phosphoproteins; 0 / Protein Kinase Inhibitors; 0 / Recombinant Proteins; 0 / Ribosomal Protein S6; 0 / STAT5 Transcription Factor; 0 / thymic stromal lymphopoietin; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.10.2 / Janus Kinase 1; EC 2.7.10.2 / Janus Kinase 3; W36ZG6FT64 / Sirolimus
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82. Reid GS, She K, Terrett L, Food MR, Trudeau JD, Schultz KR: CpG stimulation of precursor B-lineage acute lymphoblastic leukemia induces a distinct change in costimulatory molecule expression and shifts allogeneic T cells toward a Th1 response. Blood; 2005 May 1;105(9):3641-7
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  • [Title] CpG stimulation of precursor B-lineage acute lymphoblastic leukemia induces a distinct change in costimulatory molecule expression and shifts allogeneic T cells toward a Th1 response.
  • Pediatric precursor B acute lymphoblastic leukemia (B-ALL) cells express low levels of costimulatory molecules and are generally poor stimulators of T-cell responses.
  • In this study, we evaluated the impact of CpG stimulation on precursor B-ALL cell lines and pediatric patient-derived samples.
  • In contrast to both nonleukemic B-cell precursors and mature B cells, the response of precursor B-ALL cells was characterized by increased CD40 expression but only small changes in CD86 levels and no induction of CD80 expression.
  • These results demonstrate the functional relevance of CpG stimulation of precursor B-ALL cells and provide a rational basis for study of these agents for use in treatment of this disease.
  • [MeSH-major] Dinucleoside Phosphates / pharmacology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Th1 Cells / immunology
  • [MeSH-minor] Animals. B-Lymphocytes / drug effects. B-Lymphocytes / immunology. B-Lymphocytes / pathology. Cell Line, Tumor. DNA-Binding Proteins / physiology. Humans. Interleukins / biosynthesis. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Oligodeoxyribonucleotides / pharmacology. Receptors, Cell Surface / physiology. T-Lymphocyte Subsets / immunology. Toll-Like Receptor 9. Transplantation, Heterologous

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  • (PMID = 15650062.001).
  • [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 / DNA-Binding Proteins; 0 / Dinucleoside Phosphates; 0 / Interleukins; 0 / Oligodeoxyribonucleotides; 0 / Receptors, Cell Surface; 0 / TLR9 protein, human; 0 / Tlr9 protein, mouse; 0 / Toll-Like Receptor 9; 2382-65-2 / cytidylyl-3'-5'-guanosine
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83. Nasr MR, Rosenthal N, Syrbu S: Expression profiling of transcription factors in B- or T-acute lymphoblastic leukemia/lymphoma and burkitt lymphoma: usefulness of PAX5 immunostaining as pan-Pre-B-cell marker. Am J Clin Pathol; 2010 Jan;133(1):41-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression profiling of transcription factors in B- or T-acute lymphoblastic leukemia/lymphoma and burkitt lymphoma: usefulness of PAX5 immunostaining as pan-Pre-B-cell marker.
  • The optimal use of transcription factors to determine B-lineage specificity in B-acute lymphoblastic leukemia/lymphoma (B-ALL) has not been fully investigated.
  • We undertook an extensive immunohistochemical study of a panel of B-cell transcription factors in B- and T-ALL and Burkitt lymphoma to evaluate those with the best specificity and sensitivity.
  • Tissue microarrays were constructed from 34 B-ALL, 19 T-ALL, and 30 Burkitt lymphoma samples.
  • Burkitt lymphoma cases were positive for PAX5 (30/30 [100%]), BOB.1 (27/30 [90%]), PU.1 (23/30 [77%]), CD79a (29/30 [97%]), CD22 (14/30 [47%]), CD20 (30/30 [100%]), OCT-2 (23/30 [77%]), and MUM1 (5/30 [17%]).
  • T-ALLs were only positive for PU.1 (15/19 [79%]) and BOB.1 (12/19 [63%]).
  • [MeSH-major] B-Cell-Specific Activator Protein / metabolism. Biomarkers, Tumor / metabolism. Burkitt Lymphoma / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cells, B-Lymphoid / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Bone Marrow Cells. Cell Lineage. Flow Cytometry. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Immunophenotyping. Oligonucleotide Array Sequence Analysis. Predictive Value of Tests. Tissue Array Analysis

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  • (PMID = 20023257.001).
  • [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 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human
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84. van Zelm MC, van der Burg M, de Ridder D, Barendregt BH, de Haas EF, Reinders MJ, Lankester AC, Révész T, Staal FJ, van Dongen JJ: Ig gene rearrangement steps are initiated in early human precursor B cell subsets and correlate with specific transcription factor expression. J Immunol; 2005 Nov 1;175(9):5912-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ig gene rearrangement steps are initiated in early human precursor B cell subsets and correlate with specific transcription factor expression.
  • The role of specific transcription factors in the initiation and regulation of Ig gene rearrangements has been studied extensively in mouse models, but data on normal human precursor B cell differentiation are limited.
  • We purified five human precursor B cell subsets, and assessed and quantified their IGH, IGK, and IGL gene rearrangement patterns and gene expression profiles.
  • Pro-B cells already massively initiate D(H)-J(H) rearrangements, which are completed with V(H)-DJ(H) rearrangements in pre-B-I cells.
  • Large cycling pre-B-II cells are selected for in-frame IGH gene rearrangements.
  • The first IGK/IGL gene rearrangements were initiated in pre-B-I cells, but their frequency increased enormously in small pre-B-II cells, and in-frame selection was found in immature B cells.
  • Transcripts of the RAG1 and RAG2 genes and earlier defined transcription factors, such as E2A, early B cell factor, E2-2, PAX5, and IRF4, were specifically up-regulated at stages undergoing Ig gene rearrangements.
  • Based on the combined Ig gene rearrangement status and gene expression profiles of consecutive precursor B cell subsets, we identified 16 candidate genes involved in initiation and/or regulation of Ig gene rearrangements.
  • These analyses provide new insights into early human precursor B cell differentiation steps and represent an excellent template for studies on oncogenic transformation in precursor B acute lymphoblastic leukemia and B cell differentiation blocks in primary Ab deficiencies.
  • [MeSH-minor] Adolescent. Cell Separation. Child. Child, Preschool. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Gene Rearrangement, B-Lymphocyte, Light Chain. Humans

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  • [ErratumIn] J Immunol. 2006 Jun 15;176(12):7787
  • (PMID = 16237084.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Transcription Factors
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85. Wandroo F, Bell A, Darbyshire P, Pratt G, Stankovic T, Gordon J, Lawson S, Moss P: ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia. Int J Lab Hematol; 2008 Apr;30(2):149-57
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  • [Title] ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia.
  • ZAP-70 is, however, expressed in adult B cell chronic lymphocytic leukemia where it correlates with a poor prognosis.
  • We wished to determine if ZAP-70 is also expressed in pediatric B cell malignancy.
  • A quantitative PCR assay for ZAP-70 expression was established and ZAP-70 expression in a range of human B cell lines was compared with expression in the Jurkat T cell line.
  • ZAP-70 expression was then determined in bone marrow lymphoblasts obtained from 12 patients with pre-B cell acute lymphoblastic leukemia (ALL).
  • ZAP-70 expression was not detected in mature B cell lines but was detected in pre-B cell lines at a level comparable to that seen in T cells.
  • ZAP-70 expression was strongly expressed in nine of the 12 cases of primary pre-B cell lymphoblastic leukemia.
  • The T cell-associated protein kinase ZAP-70 is highly expressed in pre-B lineage cells and most cases of pre-B acute lymphoblastic leukemia.
  • ZAP-70 expression may hold prognostic value for pre-B ALL and raises the prospect of a novel therapeutic target.
  • [MeSH-major] B-Lymphocytes / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cells, B-Lymphoid / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism
  • [MeSH-minor] Adolescent. Blotting, Western. Bone Marrow Cells / metabolism. Cell Line, Transformed. Cell Line, Tumor. Child. Child, Preschool. Female. Flow Cytometry. Gene Expression. Humans. Jurkat Cells. Male. Polymerase Chain Reaction

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  • (PMID = 18333847.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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86. Menendez P, Catalina P, Rodríguez R, Melen GJ, Bueno C, Arriero M, García-Sánchez F, Lassaletta A, García-Sanz R, García-Castro J: Bone marrow mesenchymal stem cells from infants with MLL-AF4+ acute leukemia harbor and express the MLL-AF4 fusion gene. J Exp Med; 2009 Dec 21;206(13):3131-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone marrow mesenchymal stem cells from infants with MLL-AF4+ acute leukemia harbor and express the MLL-AF4 fusion gene.
  • MLL-AF4 fusion is a hallmark genetic abnormality in infant B-acute lymphoblastic leukemia (B-ALL) known to arise in utero.
  • BM mesenchymal stem cells (BM-MSC) from 38 children diagnosed with cytogenetically different acute leukemias were screened for leukemic fusion genes.
  • Fusion genes were absent in BM-MSCs of childhood leukemias carrying TEL-AML1, BCR-ABL, AML1-ETO, MLL-AF9, MLL-AF10, MLL-ENL or hyperdiploidy.
  • The absence of monoclonal rearrangements in MLL-AF4(+) BM-MSCs precludes the possibility of cellular plasticity or de-differentiation of B-ALL blasts and suggests that MLL-AF4 might arise in a population of prehematopoietic precursors.
  • [MeSH-major] Mesenchymal Stromal Cells / metabolism. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • [Cites] Dev Dyn. 2007 Dec;236(12):3297-308 [18000980.001]
  • [Cites] Carcinogenesis. 2009 Sep;30(9):1628-37 [19587093.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] Cell Stem Cell. 2007 Dec 13;1(6):597-8 [18371398.001]
  • [Cites] Genes Dev. 2008 Sep 1;22(17):2308-41 [18765787.001]
  • [Cites] Dev Cell. 2008 Dec;15(6):801-12 [19081070.001]
  • [Cites] J Cell Mol Med. 2008 Dec;12(6B):2552-65 [19210755.001]
  • [Cites] Exp Cell Res. 1999 Dec 15;253(2):519-22 [10585275.001]
  • [Cites] Cell. 2000 Jan 7;100(1):157-68 [10647940.001]
  • [Cites] Lancet. 2000 May 13;355(9216):1688-91 [10905245.001]
  • [Cites] Leukemia. 2000 Aug;14(8):1493-9 [10942248.001]
  • [Cites] Stem Cells. 2001;19(5):408-18 [11553849.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Bone Marrow Transplant. 2001 Oct;28(7):665-72 [11704789.001]
  • [Cites] Development. 2002 Jun;129(11):2773-83 [12015303.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):639-49 [12951583.001]
  • [Cites] Curr Opin Genet Dev. 2003 Oct;13(5):537-42 [14550421.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2474-86 [14562124.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2318-57 [14562125.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2257-317 [14671650.001]
  • [Cites] N Engl J Med. 2004 Jul 15;351(3):250-9 [15254283.001]
  • [Cites] Immunity. 2004 Jul;21(1):31-41 [15345218.001]
  • [Cites] Blood. 1983 Jul;62(1):1-13 [6407542.001]
  • [Cites] Nature. 1993 May 27;363(6427):358-60 [8497319.001]
  • [Cites] Blood. 1995 May 1;85(9):2422-35 [7537114.001]
  • [Cites] Mol Ther. 2004 Dec;10(6):1109-20 [15564142.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2733-40 [15591120.001]
  • [Cites] Haematologica. 2005 Jul;90(7):906-13 [15996928.001]
  • [Cites] Development. 2005 Oct;132(19):4363-74 [16141227.001]
  • [Cites] Leukemia. 2005 Nov;19(11):2016-8 [16151462.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3559-66 [16046533.001]
  • [Cites] Cytotherapy. 2006;8(4):315-7 [16923606.001]
  • [Cites] Stem Cell Rev. 2005;1(3):277-84 [17142866.001]
  • [Cites] Exp Hematol. 2007 Feb;35(2):221-9 [17258071.001]
  • [Cites] Leukemia. 2007 May;21(5):1079-88 [17344918.001]
  • [Cites] Cell. 2007 Jun 15;129(6):1097-110 [17574023.001]
  • [Cites] Stem Cell Rev. 2007 Jan;3(1):7-17 [17873377.001]
  • [Cites] J Biol Chem. 2007 Oct 26;282(43):31703-12 [17711862.001]
  • [Cites] Methods Mol Biol. 2009;538:7-27 [19277581.001]
  • [Cites] Neoplasia. 2009 Apr;11(4):397-407 [19308294.001]
  • [Cites] Leukemia. 2009 Apr;23(4):664-72 [19151777.001]
  • [Cites] Leuk Res. 2009 Jul;33(7):980-90 [18930318.001]
  • [Cites] Cell Res. 2009 Jun;19(6):698-709 [19308090.001]
  • [Cites] Cell. 2008 Feb 22;132(4):612-30 [18295579.001]
  • (PMID = 19995953.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [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-AF4 fusion protein, human; 0 / MLL-AF9 fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
  • [Other-IDs] NLM/ PMC2806455
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87. Bumbea H, Serghei L, Vlădăreanu AM, Stefan LM, Casleanu D, Voican I, Begu M: Cryptic genomic abnormalities associated with coexpression of KOR-SA3544 and NG.2 in proB acute lymphoblastic leukemia. Rom J Intern Med; 2007;45(4):387-91
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  • [Title] Cryptic genomic abnormalities associated with coexpression of KOR-SA3544 and NG.2 in proB acute lymphoblastic leukemia.
  • Balanced translocations and chromosomal rearrangements are rare events involved in acute lymphoblastic leukemogenesis, yet little is known about the actual gene anomalies responsible for it.
  • Initially we have investigated by imunophenotyping 28 patients with acute lymphoblastic leukemia, admitted in the Department of Hematology during the last year.
  • Of those 15 patients, 7 had pro-B acute lymphoblastic leukemia immunophenotype: CD19+CD10+CD34+.
  • [MeSH-major] Antigens / metabolism. Chromosome Aberrations. Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proteoglycans / metabolism. Receptors, Opioid, kappa / metabolism

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  • (PMID = 18767415.001).
  • [ISSN] 1220-4749
  • [Journal-full-title] Romanian journal of internal medicine = Revue roumaine de médecine interne
  • [ISO-abbreviation] Rom J Intern Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Antigens; 0 / OPRK1 protein, human; 0 / Proteoglycans; 0 / Receptors, Opioid, kappa; 0 / chondroitin sulfate proteoglycan 4
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88. Mantadakis E, Anagnostatou N, Smyrnaki P, Spanaki AM, Papavasiliou ES, Briassoulis G, Kalmanti M: Life-threatening hypercalcemia complicated by pancreatitis in a child with acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2005 May;27(5):288-92
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  • [Title] Life-threatening hypercalcemia complicated by pancreatitis in a child with acute lymphoblastic leukemia.
  • The authors describe a 9-year-old girl with precursor-B acute lymphoblastic leukemia (ALL) who presented with dehydration and severe hypercalcemia.
  • The hypercalcemia resolved with specific antileukemic therapy along with supportive care and administration of calcitonin.
  • Hypercalcemia is an uncommon metabolic abnormality in children with ALL, but it can be life-threatening.
  • [MeSH-major] Burkitt Lymphoma / complications. Hypercalcemia / complications
  • [MeSH-minor] Acute Disease. Calcium / administration & dosage. Calcium / therapeutic use. Child. Dehydration / complications. Dexamethasone / therapeutic use. Dietary Supplements. Female. Humans. Methotrexate / therapeutic use. Pancreatitis / complications. Treatment Outcome. Vitamin D / administration & dosage. Vitamin D / therapeutic use

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  • (PMID = 15891568.001).
  • [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] 1406-16-2 / Vitamin D; 7S5I7G3JQL / Dexamethasone; SY7Q814VUP / Calcium; YL5FZ2Y5U1 / Methotrexate
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89. Horie O, Saigo K, Murayama T, Ryo R: Differential expression of proteinase inhibitor-9 and granzyme B mRNAs in activated immunocompetent cells. Tohoku J Exp Med; 2005 Feb;205(2):103-13
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  • While the strongest expression of PI-9 mRNA was observed in a NK cell line YT-N10, it was also expressed in a B-acute lymphoblastic leukemia cell line U-Tree02, an Epstein-Barr Virus (EBV)-transformed B cell clone, a CD8+ T lymphocyte clone and a megakaryocytic cell line CMK, but not in a T cell line Jurkat.
  • PMA increased PI-9 mRNA expression in the EBV-transformed B cell clone and CMK cells, but IL-6 showed no effect.
  • We therefore examined the expression of PI-9 and GrB mRNAs in eight patients after allogeneic hematopoietic stem cell transplantation with GVHD (n = 4) or without chronic GVHD (n = 4).
  • [MeSH-minor] Cells, Cultured. Gene Expression Regulation / drug effects. Granzymes. Hematopoietic Stem Cell Transplantation. Humans. Interleukins / pharmacology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Tetradecanoylphorbol Acetate / pharmacology. Transplantation, Homologous

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  • (PMID = 15673968.001).
  • [ISSN] 0040-8727
  • [Journal-full-title] The Tohoku journal of experimental medicine
  • [ISO-abbreviation] Tohoku J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Interleukins; 0 / RNA, Messenger; 0 / Serpins; EC 3.4.21.- / GZMB protein, human; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Serine Endopeptidases; NI40JAQ945 / Tetradecanoylphorbol Acetate
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90. Hansson F, Toporski J, Månsson R, Johansson B, Norén-Nyström U, Jacobsen SE, Wiebe T, Larsson M, Sigvardsson M, Castor A: Exit of pediatric pre-B acute lymphoblastic leukaemia cells from the bone marrow to the peripheral blood is not associated with cell maturation or alterations in gene expression. Mol Cancer; 2008;7:67

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exit of pediatric pre-B acute lymphoblastic leukaemia cells from the bone marrow to the peripheral blood is not associated with cell maturation or alterations in gene expression.
  • BACKGROUND: Childhood pre-B acute lymphoblastic leukemia (ALL) is a bone marrow (BM) derived disease, which often disseminates out of the BM cavity, where malignant cells to a variable degree can be found circulating in the peripheral blood (PB).
  • Normal pre-B cells are absolutely dependent on BM stroma for survival and differentiation.
  • It is not known whether transformed pre-B ALL cells retain any of this dependence, which possibly could impact on drug sensitivity or MRD measurements.
  • RESULTS: Pre-B ALL cells, highly purified by a novel method using surface expression of CD19 and immunoglobulin light chains, from BM and PB show a very high degree of similarity in gene expression patterns, with differential expression of vascular endothelial growth factor (VEGF) as a notable exception.
  • In addition, the cell sorting procedure revealed that in 2 out of five investigated patients, a significant fraction of the malignant cells had matured beyond the pre-B cell stage.
  • This might indicate an independence of BM stroma on the part of transformed pre-B cells, which contrasts with that of their normal counterparts.
  • [MeSH-major] Blood Cells / metabolism. Bone Marrow Cells / metabolism. Gene Expression. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Cell Differentiation. Cell Lineage. Cell Movement. Child. Gene Expression Profiling. Humans. Immunoglobulins / metabolism. In Situ Hybridization, Fluorescence. Stromal Cells / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • [Cites] Leukemia. 2000 Dec;14(12):2205-22 [11187912.001]
  • [Cites] Genes Dev. 2000 Aug 15;14(16):1983-91 [10950862.001]
  • [Cites] J Clin Invest. 2000 Aug;106(4):511-21 [10953026.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):19069-74 [16354839.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2223-33 [11187913.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2247-56 [11187916.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2267-75 [11187918.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):31-6 [11134512.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Nature. 2002 Jun 27;417(6892):954-8 [12087404.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2951-9 [12730115.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] J Exp Med. 1996 Dec 1;184(6):2217-29 [8976177.001]
  • [Cites] Blood. 1998 Dec 1;92(11):4150-66 [9834220.001]
  • [Cites] Cell. 2005 Apr 22;121(2):295-306 [15851035.001]
  • [Cites] Nat Med. 2005 Jun;11(6):630-7 [15908956.001]
  • (PMID = 18694513.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501838
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulins; 0 / Vascular Endothelial Growth Factor A
  • [Other-IDs] NLM/ PMC2525657
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91. Dunphy CH: Gene expression profiling data in lymphoma and leukemia: review of the literature and extrapolation of pertinent clinical applications. Arch Pathol Lab Med; 2006 Apr;130(4):483-520
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  • [Title] Gene expression profiling data in lymphoma and leukemia: review of the literature and extrapolation of pertinent clinical applications.
  • OBJECTIVES: To review the literature regarding GE data that may provide important information regarding pathogenesis and that may be extrapolated for use in diagnosing and prognosticating lymphomas and leukemias; to present GE findings in Hodgkin and non-Hodgkin lymphomas, acute leukemias, and chronic myeloid leukemia in detail; and to summarize the practical clinical applications in tables that are referenced throughout the text.
  • CONCLUSIONS: Gene expression profiling of lymphomas and leukemias aids in the diagnosis and prognostication of these diseases.
  • Flow cytometric and immunohistochemical applications of the information gained from GE profiling assist in the management of chronic lymphocytic leukemia, other low-grade B-cell non-Hodgkin lymphomas and leukemias, diffuse large B-cell lymphoma, nodular lymphocyte-predominant Hodgkin lymphoma, and classic Hodgkin lymphoma.
  • For practical clinical use, GE profiling of precursor B acute lymphoblastic leukemia, precursor T acute lymphoblastic leukemia, and acute myeloid leukemia has supported most of the information that has been obtained by cytogenetic and molecular studies (except for the identification of FLT3 mutations for molecular analysis), but extrapolation of the analyses leaves much to be gained based on the GE profiling data.
  • [MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Leukemia / diagnosis. Leukemia / genetics. Lymphoma / diagnosis. Lymphoma / genetics

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  • (PMID = 16594743.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  • [Number-of-references] 173
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92. Liu Y, Li ZG, Zhao W, Li B, Gong WY, Wu MY: [Immunophenotypic characteristics of children with acute lymphoblastic leukemia carrying TEL-AML1 fusion gene]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Aug;14(4):714-6
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  • [Title] [Immunophenotypic characteristics of children with acute lymphoblastic leukemia carrying TEL-AML1 fusion gene].
  • To investigate the immunological and other clinical characteristics in TEL/AML1+ childhood B-acute lymphoblastic leukemia (B-ALL), immunophenotyping was performed with three-color flow cytometry, and the expression of TEL-AML1 fusion gene was detected with nested RT-PCR.
  • Diagnosis was made according to FAB and MIC criteria.
  • (2) compared with TEL-AML1- group, no significant difference was found in age, gender, white cell count and blasts count in peripheral blood of TEL-AML1+;.
  • (3) in TEL-AML1+ group, 21 out of 22 (95.5%) were common ALL, as compared with TEL-AML1- group, the positive rate of CD13 was higher (59.1%, 13/22) and the positive rate of CD20 was lower (22.7%, 5/22) than that in TEL-AML1- group, respectively (P < 0.05), and the mean fluorescence index of CD10 and HLA-DR significantly increased to 92.80 and 53.61, respectively (P < 0.05).
  • It is concluded that TEL-AML1 rearrangement is a frequent molecular abnormality in childhood ALL.
  • These characteristics may be useful in detection of minimal residual leukemia.

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  • (PMID = 16928306.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Core Binding Factor Alpha 2 Subunit; 0 / HLA-DR Antigens; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; EC 3.4.11.2 / Antigens, CD13
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93. Lee DS, Kim YR, Cho HK, Lee CK, Lee JH, Cho HI: The presence of TEL/AML1 rearrangement and cryptic deletion of the TEL gene in adult acute lymphoblastic leukemia (ALL). Cancer Genet Cytogenet; 2005 Oct 15;162(2):176-8
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  • [Title] The presence of TEL/AML1 rearrangement and cryptic deletion of the TEL gene in adult acute lymphoblastic leukemia (ALL).
  • TEL/AML1 (also known as ETV6/RUNX1) rearrangement is the most frequent genetic change in childhood B-acute lymphoblastic leukemia (ALL) and is associated with a favorable prognosis.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Deletion. Gene Rearrangement. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

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  • (PMID = 16213368.001).
  • [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 / 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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94. Kourti M, Vavatsi N, Gombakis N, Tzimagiorgis G, Sidi V, Koliouskas D, Athanassiadou F: Increased expression of multidrug resistance gene (MDR1) at relapse in a child with acute lymphoblastic leukemia. Pediatr Hematol Oncol; 2006 Sep;23(6):489-94
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  • [Title] Increased expression of multidrug resistance gene (MDR1) at relapse in a child with acute lymphoblastic leukemia.
  • Modern treatment protocols lead to complete remission in a high proportion of patients with childhood acute lymphoblastic leukemia (ALL).
  • Treatment failure in these patients is mainly attributable to de novo or acquired resistance to a wide variety of cytotoxic drugs, which is called multi drug resistance (MDR).
  • In order to contribute further information we present a rare case of a 15-month old girl with newly diagnosed CALLA positive pre-B acute lymphoblastic leukemia with favourable prognostic factors at diagnosis who experienced a relapse of the disease.
  • Using reverse transcriptase polymerase chain reaction method, m-RNA expression of the MDR1 gene upon relapse, was five-fold compared with that at diagnosis.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. P-Glycoprotein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Female. Humans. Infant. Neprilysin. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Messenger / analysis. Recurrence

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  • (PMID = 16849280.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / P-Glycoprotein; 0 / RNA, Messenger; EC 3.4.24.11 / Neprilysin
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95. Vieira L, Marques B, Cavaleiro C, Ambrósio AP, Jorge M, Neto A, Costa JM, Júnior EC, Boavida MG: Molecular cytogenetic characterization of rearrangements involving 12p in leukemia. Cancer Genet Cytogenet; 2005 Mar;157(2):134-9
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  • [Title] Molecular cytogenetic characterization of rearrangements involving 12p in leukemia.
  • Initially using conventional cytogenetic analysis, we characterized the chromosomal breakpoints of three leukemia patients (two with B-acute lymphoblastic leukemia and one with myelodysplastic/myeloproliferative disorder) presenting a t(5;12)(q13;p13), t(12;15)(p13;q22), and dic(9;12)(p11;p11), respectively, as the only structural abnormalities in the karyotype.
  • This report illustrates the chromosomal and molecular heterogeneity of rearrangements underlying 12p chromosome translocations in leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 12. DNA-Binding Proteins / genetics. Leukemia / genetics. Repressor Proteins / genetics

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  • (PMID = 15721634.001).
  • [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 / DNA-Binding Proteins; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
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96. Barbaric D, Wynne K, Aslanian S, Bond M, Reid GS: Immune evasion strategies of pediatric precursor-B acute lymphoblastic leukemia after allogeneic bone marrow transplantation-a case study. Leuk Res; 2005 Jun;29(6):711-4
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  • [Title] Immune evasion strategies of pediatric precursor-B acute lymphoblastic leukemia after allogeneic bone marrow transplantation-a case study.
  • Bone marrow transplantation (BMT) is the primary curative option for refractory/relapsed pediatric acute lymphoblastic leukemia.
  • In this study, we compared allogeneic T cell stimulation induced by sequentially obtained precursor-B acute lymphoblastic leukemia (ALL) samples from a single patient with overt graft versus leukemia (GVL) activity.
  • We observed a loss of T cell stimulatory capacity by post-transplantation relapse samples and changes in expression of MHC and the costimulatory molecule CD137 ligand.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Tumor Escape / immunology

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  • (PMID = 15863213.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD137; 0 / Receptors, Nerve Growth Factor; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF9 protein, human
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97. Pei SN, Kuo CY, Ma MC, Wang MC: Mediastinal mass and malignant pleural effusion in an aleukemic case with pre-B acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2009 Feb;31(2):139-41
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  • [Title] Mediastinal mass and malignant pleural effusion in an aleukemic case with pre-B acute lymphoblastic leukemia.
  • After a bone marrow examination, we diagnosed the patient with pre-B acute lymphoblastic leukemia (ALL).
  • This is the first reported case of a malignant pleural effusion and a mediastinal mass that preceded pre-B ALL.
  • [MeSH-major] Mediastinal Neoplasms / diagnosis. Pleural Effusion, Malignant / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • (PMID = 19194202.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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98. Hodge G, Davis S, Rice M, Tapp H, Saxon B, Revesz T: Garlic compounds selectively kill childhood pre-B acute lymphoblastic leukemia cells in vitro without reducing T-cell function: Potential therapeutic use in the treatment of ALL. Biologics; 2008 Mar;2(1):143-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Garlic compounds selectively kill childhood pre-B acute lymphoblastic leukemia cells in vitro without reducing T-cell function: Potential therapeutic use in the treatment of ALL.
  • Drugs used for remission induction therapy for childhood precursor-B acute lymphoblastic leukemia (ALL) are nonselective for malignant cells.
  • Apoptosis, lymphocyte proliferation and T-cell cytokine production were determined using multiparameter flow cytometry.
  • At concentrations of garlic compounds that did not result in significant increases in Annexin V and 7-AAD staining of normal lymphocytes, there was a significant increase in apoptosis of ALL cells with no alteration of T-cell proliferation as determined by CD25/CD69 upregulation or interferongamma, interleukin-2 or tumor necrosis factor-alpha intracellular cytokine production.
  • In contrast, the presence of chemotherapeutic agents resulted in nonselective increases in both lymphocyte and ALL apoptosis and a decrease in T-cell proliferation and cytokine production.
  • In conclusion, we show selective apoptosis of malignant cells by garlic compounds that do not alter T-cell immune function and indicate the potential therapeutic benefit of garlic compounds in the treatment of childhood ALL.

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  • [Cites] Blood. 2005 Jul 15;106(2):408-18 [15797997.001]
  • [Cites] Mycoses. 2005 Mar;48(2):95-100 [15743425.001]
  • [Cites] Clin Exp Immunol. 2005 Jan;139(1):159-64 [15606627.001]
  • [Cites] Mol Pharmacol. 1998 Mar;53(3):402-7 [9495804.001]
  • [Cites] Br J Haematol. 1993 Mar;83(3):419-27 [8485047.001]
  • [Cites] Annu Rev Immunol. 1992;10:411-52 [1590993.001]
  • [Cites] Antimicrob Agents Chemother. 1983 May;23(5):700-2 [6870217.001]
  • [Cites] Br J Biomed Sci. 2004;61(2):71-4 [15250668.001]
  • [Cites] J Antimicrob Chemother. 2004 May;53(5):832-6 [15044429.001]
  • [Cites] Blood. 2003 Dec 15;102(13):4541-6 [12920041.001]
  • [Cites] J Antimicrob Chemother. 2003 Mar;51(3):593-7 [12615859.001]
  • [Cites] Cytometry. 2002 Aug 1;48(4):209-15 [12210145.001]
  • [Cites] Cancer Treat Rev. 2001 Dec;27(6):327-37 [11908926.001]
  • [Cites] Jpn J Cancer Res. 2001 Nov;92(11):1157-65 [11714439.001]
  • [Cites] Br J Haematol. 2001 Nov;115(2):376-81 [11703339.001]
  • [Cites] Arch Neurol. 2001 Jan;58(1):91-7 [11176941.001]
  • [Cites] Cytokine. 2000 Dec;12(12):1763-8 [11097745.001]
  • (PMID = 19707437.001).
  • [ISSN] 1177-5475
  • [Journal-full-title] Biologics : targets & therapy
  • [ISO-abbreviation] Biologics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2727784
  • [Keywords] NOTNLM ; apoptosis / childhood precursor-B acute lymphoblastic leukemia / garlic / immune function / intracellular cytokines
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99. Sudhakar N, Nancy NK, Rajalekshmy KR, Rajkumar T: Diversity of T-cell receptor gene rearrangements in South Indian patients with common acute lymphoblastic leukemia. Iran J Immunol; 2009 Sep;6(3):141-6
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  • [Title] Diversity of T-cell receptor gene rearrangements in South Indian patients with common acute lymphoblastic leukemia.
  • BACKGROUND: Precursor B-Acute Lymphoblastic Leukemia (precursor B-ALL) occurs due to the uncontrolled proliferation of B-lymphoid precursors arrested at a particular stage of B-cell development.
  • Precursor-B-ALL is classified mainly into pro-B-ALL, common-ALL and pre-B-ALL.
  • The Common Acute Lymphoblastic Antigen CD10 is the marker for common-ALL.
  • OBJECTIVE: This study was aimed to examine the diversity of T-cell receptor Gamma (TCRG) and T-cell receptor Delta (TCRD) gene rearrangements in South Indian Common-ALL patients.
  • METHODS: Clonality of TCRG and TCRD was studied in 52 cases (pediatric=41 and adolescents and young adults=11) of common-ALL.
  • RESULTS: In pediatric common-ALL, clonal TCRG and TCRD gene rearrangements were detected in 19 (46.3%) and 18 (43.9%) cases respectively.
  • In the present study of common-ALL, the frequency of a TCRG rearrangement VII-J1.3/2.3 was significantly high in AYA compared to pediatric (36.3% vs 4.8%; p<0.025).
  • CONCLUSION: The reason for the high frequency of VII-J1.3/2.3 in AYA of common-ALL in South Indian population in connection with unknown infectious agents or environmental carcinogens needs to be evaluated further.
  • [MeSH-major] Gene Rearrangement, delta-Chain T-Cell Antigen Receptor. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell, gamma-delta / genetics

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  • (PMID = 19801787.001).
  • [ISSN] 1735-1383
  • [Journal-full-title] Iranian journal of immunology : IJI
  • [ISO-abbreviation] Iran J Immunol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Iran
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, gamma-delta
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100. Jeha S, Pei D, Raimondi SC, Onciu M, Campana D, Cheng C, Sandlund JT, Ribeiro RC, Rubnitz JE, Howard SC, Downing JR, Evans WE, Relling MV, Pui CH: Increased risk for CNS relapse in pre-B cell leukemia with the t(1;19)/TCF3-PBX1. Leukemia; 2009 Aug;23(8):1406-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased risk for CNS relapse in pre-B cell leukemia with the t(1;19)/TCF3-PBX1.
  • To evaluate the impact of contemporary therapy on the clinical outcome of children with pre-B acute lymphoblastic leukemia (ALL) and the t(1;19)/TCF3/PBX1, we analyzed 735 patients with B-cell precursor ALL treated in four successive protocols at St Jude Children's Research Hospital.
  • The 41 patients with the t(1;19) had a comparable event-free survival to that of the 694 patients with other B-cell precursor ALL (P=0.63; 84.2+/-7.1% (s.e.) vs 84.0+/-1.8% at 5 years).
  • [MeSH-major] Central Nervous System / pathology. Chromosomes, Human, Pair 1 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Leukemic Infiltration / epidemiology. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • [Cites] J Clin Oncol. 2003 Aug 15;21(16):3084-91 [12915598.001]
  • [Cites] Lancet Oncol. 2008 Mar;9(3):257-68 [18308251.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4674-81 [14581336.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] Blood. 1984 Mar;63(3):721-4 [6607758.001]
  • [Cites] Blood. 1986 Jun;67(6):1688-92 [2939898.001]
  • [Cites] Cancer. 1986 Nov 15;58(10):2239-43 [3463388.001]
  • [Cites] Blood. 1990 Jul 1;76(1):117-22 [2364165.001]
  • [Cites] Lancet. 1991 Jan 12;337(8733):61-6 [1670723.001]
  • [Cites] Leukemia. 1992 May;6(5):363-9 [1593901.001]
  • [Cites] J Clin Oncol. 1994 Dec;12(12):2601-6 [7989935.001]
  • [Cites] J Clin Oncol. 1998 Feb;16(2):527-35 [9469337.001]
  • [Cites] Blood. 1998 Jul 15;92(2):411-5 [9657739.001]
  • [Cites] Leukemia. 2006 Jan;20(1):35-41 [16307026.001]
  • [Cites] Haematologica. 2007 Nov;92(11):1561-4 [18024406.001]
  • [Cites] JAMA. 2003 Oct 15;290(15):2001-7 [14559953.001]
  • (PMID = 19282835.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA021765-30; United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / TCF3-PBX1 fusion protein, human
  • [Other-IDs] NLM/ NIHMS110407; NLM/ PMC2731684
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