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1. Ren SY, Xue F, Feng J, Skorski T: Intrinsic regulation of the interactions between the SH3 domain of p85 subunit of phosphatidylinositol-3 kinase and the protein network of BCR/ABL oncogenic tyrosine kinase. Exp Hematol; 2005 Oct;33(10):1222-8
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  • OBJECTIVE: BCR/ABL fusion tyrosine kinase is responsible for the initiation and maintenance of the Philadelphia chromosome-positive chronic myelogenous leukemia (CML) and a cohort of acute lymphocytic leukemias.
  • RESULTS: We show here that the SH3 domain of p85alpha (p85alpha-SH3) pulls down the p210BCR/ABL kinase from hematopoietic cell lysates.
  • [MeSH-minor] Amino Acid Substitution. Animals. Cell Line, Tumor. Fusion Proteins, bcr-abl. Hematopoietic Stem Cells / metabolism. Humans. Immunoprecipitation / methods. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Mice. Mutagenesis, Site-Directed. Point Mutation / genetics. Protein Binding

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  • (PMID = 16219545.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA83700
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protein Subunits; 0 / Proto-Oncogene Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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2. Cossu F: Genetics of SCID. Ital J Pediatr; 2010;36:76
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  • Human SCID (Severe Combined Immunodeficiency) is a prenatal disorder of T lymphocyte development, that depends on the expression of numerous genes.
  • The knowledge of the genetic basis of SCID is essential for diagnosis (e.g., clinical phenotype, lymphocyte profile) and treatment (e.g., use and type of pre-hematopoietic stem cell transplant conditioning).Over the last years novel genetic defects causing SCID have been discovered, and the molecular and immunological mechanisms of SCID have been better characterized.
  • Distinct forms of SCID show both common and peculiar (e.g., absence or presence of nonimmunological features) aspects, and they are currently classified into six groups according to prevalent pathophysiological mechanisms: impaired cytokine-mediated signaling; pre-T cell receptor defects; increased lymphocyte apoptosis; defects in thymus embryogenesis; impaired calcium flux; other mechanisms.This review is the updated, extended and largely modified translation of the article "Cossu F: Le basi genetiche delle SCID", originally published in Italian language in the journal "Prospettive in Pediatria" 2009, 156:228-238.
  • [MeSH-minor] Genetic Therapy. Genotype. Hematopoietic Stem Cell Transplantation. Humans. Infant, Newborn. Neonatal Screening. T-Lymphocytes / pathology

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  • [Cites] J Pediatr. 2005 Jan;146(1):137-40 [15644840.001]
  • [Cites] Immunol Rev. 2005 Feb;203:110-26 [15661025.001]
  • [Cites] Immunol Rev. 2005 Feb;203:127-42 [15661026.001]
  • [Cites] Bone Marrow Transplant. 2005 Mar;35(6):537-47 [15665844.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4179-86 [15731174.001]
  • [Cites] J Clin Invest. 2005 Nov;115(11):2974-6 [16276411.001]
  • [Cites] Mol Genet Metab. 2005 Dec;86(4):427-30 [16260163.001]
  • [Cites] J Immunol. 2002 Jun 15;168(12):6323-9 [12055248.001]
  • [Cites] Br J Haematol. 2002 Dec;119(3):765-8 [12437656.001]
  • [Cites] Nat Rev Cancer. 2003 Jul;3(7):477-88 [12835668.001]
  • [Cites] J Allergy Clin Immunol. 2004 Apr;113(4):734-41 [15100681.001]
  • [Cites] Ann Hum Genet. 2004 May;68(Pt 3):265-8 [15180707.001]
  • [Cites] Lancet. 2004 Jun 19;363(9426):2051-4 [15207958.001]
  • [Cites] Pediatr Res. 1977 Jan;11(1 Pt 2):63-89 [401538.001]
  • [Cites] Pediatr Res. 1984 Aug;18(8):723-8 [6332299.001]
  • [Cites] N Engl J Med. 1985 May 2;312(18):1151-9 [2984567.001]
  • [Cites] Cell. 1993 Apr 9;73(1):147-57 [8462096.001]
  • [Cites] J Allergy Clin Immunol. 1994 Feb;93(2):543-50 [8120281.001]
  • [Cites] Am J Med Genet. 1996 Oct 16;65(2):167-70 [8911612.001]
  • [Cites] J Pediatr. 1997 Mar;130(3):345-6 [9063405.001]
  • [Cites] J Pediatr Hematol Oncol. 2006 Jan;28(1):53-6 [16394896.001]
  • [Cites] Cell. 2006 Jan 27;124(2):287-99 [16439204.001]
  • [Cites] J Pediatr. 2006 Feb;148(2):272-4 [16492442.001]
  • [Cites] Trends Immunol. 2006 Mar;27(3):146-53 [16423560.001]
  • [Cites] J Allergy Clin Immunol. 2006 Apr;117(4):897-903 [16630949.001]
  • [Cites] Nat Rev Immunol. 2006 Oct;6(10):728-40 [16998507.001]
  • [Cites] Orphanet J Rare Dis. 2006;1:34 [16959034.001]
  • [Cites] Hum Mutat. 2006 Dec;27(12):1174-84 [16960852.001]
  • [Cites] Nat Genet. 2007 Jan;39(1):86-92 [17187068.001]
  • [Cites] J Immunol. 2007 Feb 15;178(4):2556-64 [17277165.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3198-206 [17170122.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3595-602 [17185467.001]
  • [Cites] J Allergy Clin Immunol. 2007 Aug;120(2):423-8 [17481714.001]
  • [Cites] Nat Rev Immunol. 2007 Sep;7(9):690-702 [17703229.001]
  • [Cites] Lancet. 2007 Oct 20;370(9596):1443-52 [17950858.001]
  • [Cites] J Obstet Gynaecol Can. 2007 Nov;29(11):927-44 [17977497.001]
  • [Cites] J Clin Invest. 1998 Jul 15;102(2):421-9 [9664084.001]
  • [Cites] Clin Genet. 2008 Apr;73(4):380-4 [18339010.001]
  • [Cites] Annu Rev Immunol. 2008;26:355-88 [18304000.001]
  • [Cites] Annu Rev Immunol. 2008;26:233-59 [18304005.001]
  • [Cites] J Allergy Clin Immunol. 2008 Apr;121(4):1056-8 [18243287.001]
  • [Cites] Blood. 2008 Apr 15;111(8):4209-19 [18218852.001]
  • [Cites] Clin Exp Immunol. 2008 Jul;153(1):75-80 [18505430.001]
  • [Cites] Nat Rev Immunol. 2008 Jul;8(7):545-58 [18551129.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3143-50 [18688286.001]
  • [Cites] Nat Immunol. 2008 Nov;9(11):1307-15 [18836449.001]
  • [Cites] J Immunol. 2008 Nov 1;181(9):5815-6 [18941168.001]
  • [Cites] Blood. 2008 Nov 1;112(9):3594-600 [18669893.001]
  • [Cites] Curr Opin Allergy Clin Immunol. 2008 Dec;8(6):510-4 [18978464.001]
  • [Cites] Curr Opin Allergy Clin Immunol. 2008 Dec;8(6):534-9 [18978468.001]
  • [Cites] Eur J Pediatr. 2009 Jan;168(1):87-93 [18509675.001]
  • [Cites] Science. 2008 Dec 5;322(5907):1562-5 [19056990.001]
  • [Cites] J Allergy Clin Immunol. 2008 Dec;122(6):1219-20 [18845326.001]
  • [Cites] J Allergy Clin Immunol. 2008 Dec;122(6):1082-6 [18992930.001]
  • [Cites] Nat Genet. 2009 Jan;41(1):106-11 [19043416.001]
  • [Cites] Nat Genet. 2009 Jan;41(1):101-5 [19043417.001]
  • [Cites] J Inherit Metab Dis. 2009 Aug;32(4):459-71 [19585268.001]
  • [Cites] Adv Exp Med Biol. 2009;650:46-58 [19731800.001]
  • [Cites] Immunol Res. 2009;45(1):37-45 [19238335.001]
  • [Cites] Blood. 2009 Oct 8;114(15):3216-26 [19633200.001]
  • [Cites] Blood. 2009 Oct 22;114(17):3524-32 [19638621.001]
  • [Cites] Nat Rev Immunol. 2009 Nov;9(11):811-6 [19809471.001]
  • [Cites] Curr Opin Allergy Clin Immunol. 2009 Dec;9(6):496-502 [19779332.001]
  • [Cites] Curr Opin Allergy Clin Immunol. 2009 Dec;9(6):503-9 [19823081.001]
  • [Cites] Curr Opin Allergy Clin Immunol. 2009 Dec;9(6):489-95 [19841578.001]
  • [Cites] Clin Immunol. 2009 Dec;133(3):287-94 [19740703.001]
  • [Cites] Pediatrics. 2000 Mar;105(3):E39 [10699141.001]
  • [Cites] Int Immunol. 2000 Apr;12(4):449-57 [10744646.001]
  • [Cites] Curr Opin Immunol. 2000 Aug;12(4):468-73 [10899029.001]
  • [Cites] J Immunol. 2001 Jan 15;166(2):1308-13 [11145714.001]
  • [Cites] Bone Marrow Transplant. 2001 Aug;28(3):227-33 [11535989.001]
  • [Cites] N Engl J Med. 2009 Jan 29;360(5):447-58 [19179314.001]
  • [Cites] Immunol Rev. 2009 Mar;228(1):41-57 [19290920.001]
  • [Cites] Immunol Rev. 2009 Mar;228(1):273-87 [19290934.001]
  • [Cites] Annu Rev Immunol. 2009;27:199-227 [19302039.001]
  • [Cites] Pediatr Transplant. 2009 Mar;13(2):244-50 [18822103.001]
  • [Cites] Immunol Res. 2009;43(1-3):223-42 [18979075.001]
  • [Cites] Clin Immunol. 2009 Apr;131(1):24-30 [19097825.001]
  • [Cites] Clin Immunol. 2009 May;131(2):179-88 [19217351.001]
  • [Cites] Blood. 2009 Apr 23;113(17):4114-24 [19168787.001]
  • [Cites] Pediatrics. 2009 May;123(5):e871-7 [19403480.001]
  • [Cites] Annu Rev Immunol. 2009;27:591-619 [19132916.001]
  • [Cites] Int J Mol Sci. 2009 Apr;10(4):1729-72 [19468337.001]
  • [Cites] Acta Paediatr. 2009 Jun;98(6):1062-4 [19243569.001]
  • [Cites] Immunol Res. 2009;44(1-3):4-17 [18592143.001]
  • [Cites] Immunol Res. 2009;44(1-3):61-70 [19066739.001]
  • [Cites] Br J Haematol. 2009 Apr;145(2):164-72 [19208095.001]
  • [Cites] Nat Rev Immunol. 2009 Jul;9(7):480-90 [19543225.001]
  • [Cites] Blood. 2009 Jul 2;114(1):105-8 [19414857.001]
  • [Cites] Eur J Med Genet. 2009 Nov-Dec;52(6):373-8 [19467349.001]
  • [Cites] Gene Ther. 2009 Nov;16(11):1285-91 [19776764.001]
  • [Cites] J Pediatr. 2009 Dec;155(6):834-840.e1 [19818451.001]
  • [Cites] Nat Rev Immunol. 2009 Dec;9(12):823-32 [19935802.001]
  • [Cites] Eur J Pediatr. 2010 Mar;169(3):311-4 [19657670.001]
  • [Cites] N Engl J Med. 2010 Jan 28;362(4):314-9 [20107217.001]
  • [Cites] J Allergy Clin Immunol. 2010 Jan;125(1):209-16 [20109747.001]
  • [Cites] Immunol Allergy Clin North Am. 2010 Feb;30(1):103-24 [20113889.001]
  • [Cites] Immunol Allergy Clin North Am. 2010 Feb;30(1):125-42 [20113890.001]
  • [Cites] Nat Rev Mol Cell Biol. 2010 Mar;11(3):171-81 [20125188.001]
  • [Cites] Clin Immunol. 2010 May;135(2):183-92 [20172764.001]
  • [Cites] Clin Immunol. 2010 May;135(2):169-82 [20189884.001]
  • [Cites] Clin Immunol. 2010 May;135(2):236-46 [20236866.001]
  • [Cites] Nat Immunol. 2010 Jun;11(6):457-60 [20485269.001]
  • [Cites] Immunol Allergy Clin North Am. 2010 May;30(2):173-8 [20493394.001]
  • [Cites] Immunol Allergy Clin North Am. 2010 May;30(2):221-36 [20493398.001]
  • [Cites] Public Health Rep. 2010 May-Jun;125 Suppl 2:88-95 [20518449.001]
  • [Cites] MMWR Morb Mortal Wkly Rep. 2010 Jun 11;59(22):687-8 [20535093.001]
  • [Cites] Proc Natl Acad Sci U S A. 2010 Jun 1;107(22):10097-102 [20479256.001]
  • [Cites] Immunology. 2010 Jun;130(2):166-71 [20557575.001]
  • [Cites] Am J Med Genet A. 2010 Aug;152A(8):ix [20662017.001]
  • [Cites] N Engl J Med. 2010 Jul 22;363(4):355-64 [20660403.001]
  • [Cites] Pediatrics. 2010 Aug;126(2):e465-9 [20603253.001]
  • [Cites] Blood. 2010 Aug 12;116(6):900-8 [20457870.001]
  • [Cites] J Allergy Clin Immunol. 2010 Sep;126(3):602-10.e1-11 [20673987.001]
  • [Cites] Nature. 2010 Sep 16;467(7313):318-22 [20844535.001]
  • [Cites] J Allergy Clin Immunol. 2010 Nov;126(5):1073-4 [20933257.001]
  • [Cites] Blood. 2007 Dec 15;110(13):4198-205 [17785587.001]
  • [Cites] Nature. 1999 Apr 8;398(6727):473-4 [10206641.001]
  • [Cites] J Clin Immunol. 1999 Mar;19(2):87-97 [10226883.001]
  • [Cites] J Pediatr Surg. 2004 Nov;39(11):1607-15 [15547821.001]
  • (PMID = 21078154.001).
  • [ISSN] 1824-7288
  • [Journal-full-title] Italian journal of pediatrics
  • [ISO-abbreviation] Ital J Pediatr
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2999594
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3. Garbe AI, Krueger A, Gounari F, Zúñiga-Pflücker JC, von Boehmer H: Differential synergy of Notch and T cell receptor signaling determines alphabeta versus gammadelta lineage fate. J Exp Med; 2006 Jun 12;203(6):1579-90
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  • [Title] Differential synergy of Notch and T cell receptor signaling determines alphabeta versus gammadelta lineage fate.
  • Thymic precursors expressing the pre-T cell receptor (TCR), the gammadeltaTCR, or the alphabetaTCR can all enter the CD4+ 8+ alphabeta lineage, albeit with different efficacy.
  • In particular, in alphabeta lineage commitment, the pre-TCR synergizes more efficiently with Notch signals than the other two TCRs, whereas gammadeltaTCR-expressing cells can survive and expand in the absence of Notch signals, even though Notch signaling enhances their proliferation.
  • These observations suggest a new model of alphabeta versus gammadelta lineage choice in which lineage fate is determined by the extent of synergy between TCR and Notch signaling and in which the evolutionarily recent advent of the cell-autonomously signaling pre-TCR increased the efficacy of alphabeta T cell generation.

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  • [Cites] Blood. 2006 Jul 1;108(1):305-10 [16507772.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 May 14;93(10):4683-7 [8643464.001]
  • [Cites] Nature. 1995 Jun 29;375(6534):795-8 [7596413.001]
  • [Cites] Immunity. 2006 Jul;25(1):105-16 [16814577.001]
  • [Cites] Cell. 1996 Jul 26;86(2):243-51 [8706129.001]
  • [Cites] Nature. 2000 Aug 3;406(6795):524-7 [10952314.001]
  • [Cites] J Immunol. 2000 Nov 15;165(10):5566-72 [11067911.001]
  • [Cites] J Exp Med. 2000 Aug 21;192(4):537-48 [10952723.001]
  • [Cites] J Immunol. 2001 Mar 1;166(5):3184-93 [11207271.001]
  • [Cites] Immunity. 2001 Jul;15(1):71-82 [11485739.001]
  • [Cites] Nat Rev Immunol. 2001 Dec;1(3):193-9 [11905828.001]
  • [Cites] Nat Immunol. 2002 May;3(5):483-8 [11927911.001]
  • [Cites] Immunity. 2002 Dec;17(6):749-56 [12479821.001]
  • [Cites] EMBO J. 2003 Nov 3;22(21):5780-92 [14592976.001]
  • [Cites] J Exp Med. 2004 Mar 1;199(5):607-15 [14993248.001]
  • [Cites] J Immunol. 2004 May 1;172(9):5230-9 [15100261.001]
  • [Cites] Immunity. 2004 May;20(5):611-22 [15142529.001]
  • [Cites] Adv Immunol. 2004;84:201-38 [15246254.001]
  • [Cites] Nature. 1985 Mar 7-13;314(6006):103-7 [2983227.001]
  • [Cites] Nature. 1985 May 16-22;315(6016):232-3 [3873615.001]
  • [Cites] Nature. 1987 Jun 25-Jul 1;327(6124):677-82 [2439914.001]
  • [Cites] Nature. 1988 Sep 15;335(6187):229-33 [2970593.001]
  • [Cites] J Exp Med. 1989 Mar 1;169(3):795-806 [2494291.001]
  • [Cites] Nature. 1989 Apr 13;338(6216):591-3 [2784545.001]
  • [Cites] Nature. 1989 Dec 21-28;342(6252):931-4 [2480528.001]
  • [Cites] EMBO J. 1991 Jan;10(1):93-100 [1703490.001]
  • [Cites] Cell. 1993 Oct 22;75(2):283-94 [8402912.001]
  • [Cites] Science. 1994 Nov 18;266(5188):1208-12 [7973703.001]
  • [Cites] Immunity. 1995 Jun;2(6):617-27 [7796295.001]
  • [Cites] Immunity. 1996 Oct;5(4):343-52 [8885867.001]
  • [Cites] J Immunol. 1997 Jan 1;158(1):65-75 [8977176.001]
  • [Cites] Cell. 1997 Mar 21;88(6):833-43 [9118226.001]
  • [Cites] J Exp Med. 1997 May 5;185(9):1541-7 [9151891.001]
  • [Cites] Immunity. 1997 Jul;7(1):83-95 [9252122.001]
  • [Cites] Immunity. 1998 Apr;8(4):427-38 [9586633.001]
  • [Cites] J Exp Med. 1998 Oct 19;188(8):1465-71 [9782123.001]
  • [Cites] Eur J Immunol. 1998 Nov;28(11):3456-67 [9842888.001]
  • [Cites] Immunity. 1998 Nov;9(5):649-55 [9846486.001]
  • [Cites] Immunol Rev. 1998 Oct;165:111-9 [9850856.001]
  • [Cites] Immunity. 1999 May;10(5):547-58 [10367900.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1440-7 [15486060.001]
  • [Cites] Immunity. 2005 May;22(5):583-93 [15894276.001]
  • [Cites] Immunity. 2005 May;22(5):595-606 [15894277.001]
  • [Cites] Nat Immunol. 2005 Sep;6(9):881-8 [16056227.001]
  • [Cites] Immunity. 2005 Oct;23(4):431-43 [16226508.001]
  • [Cites] Nat Immunol. 2006 Jan;7(1):67-75 [16327787.001]
  • [Cites] Immunity. 2006 Jan;24(1):53-64 [16413923.001]
  • (PMID = 16754723.001).
  • [ISSN] 0022-1007
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI045846; United States / NCI NIH HHS / CA / P01 CA10990; United States / NIAID NIH HHS / AI / R01 AI47281; United States / NIAID NIH HHS / AI / R01 AI047281; United States / NIAID NIH HHS / AI / R01 AI45846
  • [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 / Homeodomain Proteins; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / Receptors, Notch; 128559-51-3 / RAG-1 protein
  • [Other-IDs] NLM/ PMC2118312
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4. Derré L, Bruyninx M, Baumgaertner P, Ferber M, Schmid D, Leimgruber A, Zoete V, Romero P, Michielin O, Speiser DE, Rufer N: Distinct sets of alphabeta TCRs confer similar recognition of tumor antigen NY-ESO-1157-165 by interacting with its central Met/Trp residues. Proc Natl Acad Sci U S A; 2008 Sep 30;105(39):15010-5
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  • Here, we studied T cell receptor (TCR) primary structure and function of 605 HLA-A*0201/NY-ESO-1(157-165)-specific CD8 T cell clones derived from five melanoma patients.
  • All remaining T cell clones belong to two additional sets expressing BV1 or BV13 TCRs, associated with alpha-chains with highly diverse VJ usage, CDR3 amino acid sequence, and length.
  • Yet, all T cell clonotypes recognize tumor antigen with similar functional avidity.
  • Two residues, Met-160 and Trp-161, located in the middle region of the NY-ESO-1(157-165) peptide, are critical for recognition by most of the T cell clonotypes.
  • [MeSH-major] Neoplasm Proteins / immunology. Peptide Fragments / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology

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  • [Cites] Cancer Res. 2000 Aug 15;60(16):4499-506 [10969798.001]
  • [Cites] Protein Eng Des Sel. 2007 Aug;20(8):397-403 [17644531.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3 Suppl):766s-772s [11300471.001]
  • [Cites] J Immunol. 2002 Apr 15;168(8):4231-40 [11937585.001]
  • [Cites] J Exp Med. 2002 Apr 15;195(8):991-1001 [11956290.001]
  • [Cites] Eur J Immunol. 2002 Nov;32(11):3181-90 [12555663.001]
  • [Cites] Annu Rev Immunol. 2003;21:659-84 [12615890.001]
  • [Cites] J Immunol. 2003 May 15;170(10):5103-9 [12734356.001]
  • [Cites] Nat Immunol. 2003 Jul;4(7):657-63 [12796775.001]
  • [Cites] Nat Rev Immunol. 2004 Feb;4(2):123-32 [15040585.001]
  • [Cites] Nature. 1974 Apr 19;248(5450):701-2 [4133807.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Oct 15;88(20):8987-90 [1833769.001]
  • [Cites] J Mol Biol. 1993 Dec 5;234(3):779-815 [8254673.001]
  • [Cites] J Exp Med. 1994 Dec 1;180(6):2335-40 [7964506.001]
  • [Cites] J Immunol. 1994 Dec 15;153(12):5586-92 [7527444.001]
  • [Cites] J Exp Med. 1998 May 18;187(10):1647-57 [9584143.001]
  • [Cites] J Exp Med. 2004 Dec 20;200(12):1547-57 [15596521.001]
  • [Cites] Immunity. 2005 Jan;22(1):117-29 [15664164.001]
  • [Cites] Nat Immunol. 2005 Mar;6(3):239-45 [15716973.001]
  • [Cites] J Exp Med. 2005 Apr 18;201(8):1243-55 [15837811.001]
  • [Cites] J Immunother. 2005 May-Jun;28(3):252-7 [15838382.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):1912-6 [16488988.001]
  • [Cites] Annu Rev Immunol. 2006;24:419-66 [16551255.001]
  • [Cites] J Immunol. 2006 Nov 15;177(10):6804-14 [17082594.001]
  • [Cites] Eur J Immunol. 2007 Mar;37(3):838-48 [17323415.001]
  • [Cites] J Immunol. 2007 Aug 15;179(4):2368-79 [17675498.001]
  • [Cites] J Mol Biol. 2007 Sep 14;372(2):535-48 [17658550.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2047-54 [11280765.001]
  • (PMID = 18809922.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Peptide Fragments; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / peptide NY-ESO-1 157-165; 2ZD004190S / Threonine; AE28F7PNPL / Methionine
  • [Other-IDs] NLM/ PMC2567484
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5. Martínez-Delgado B, Cuadros M, Honrado E, Ruiz de la Parte A, Roncador G, Alves J, Castrillo JM, Rivas C, Benítez J: Differential expression of NF-kappaB pathway genes among peripheral T-cell lymphomas. Leukemia; 2005 Dec;19(12):2254-63
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  • [Title] Differential expression of NF-kappaB pathway genes among peripheral T-cell lymphomas.
  • Nuclear factor kappa B (NF-kappaB) is one important pathway in T-cell proliferation and survival.
  • In a previously reported microarray study, we found NF-kappaB pathway genes differentially expressed between peripheral (PTCL) and lymphoblastic lymphomas.
  • This distinction was found among all T-cell lymphoma categories analyzed (PTCL unspecified, angioimmunoblastic, cutaneous and natural killer/T lymphomas) with the exception of anaplastic lymphomas (ALCL), which were characterized by reduced NF-kappaB expression in anaplastic cells.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, T-Cell, Peripheral / genetics. NF-kappa B / genetics

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  • (PMID = 16270046.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B
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6. Strick R, Zhang Y, Emmanuel N, Strissel PL: Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias. Hum Genet; 2006 Jun;119(5):479-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.
  • The t(9;22) BCR/ABL fusion is associated with over 90% of chronic myelogenous and 25% of acute lymphocytic leukemia.
  • Chromosome 11q23 translocations in acute myeloid and lymphoid leukemia cells demonstrate myeloid lymphoid leukemia (MLL) fusions with over 40 gene partners, like AF9 and AF4 on chromosomes 9 and 4, respectively.
  • Therapy-related leukemia is associated with the above gene rearrangements following the treatment with topoisomerase II (topo II) inhibitors.
  • In this report, using cell lines and primary cells, chromatin structural elements were analyzed in BCR, ABL and AF4 and, for comparison, in MLL2, which is a homolog to MLL, but not associated with chromosome translocations.
  • Although MLL2 was expressed in all cell lines tested, except for the presence of one DNAse I site in the promoter, no other structural elements were found in MLL2.
  • A NHR model presented demonstrates the importance of chromatin structure in chromosome translocations involved with leukemia.
  • [MeSH-major] Chromatin / chemistry. Chromosome Breakage. Chromosomes, Human / genetics. Leukemia / genetics. Leukemia / metabolism. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Cell Line, Tumor. Cells, Cultured. Chronic Disease. Humans. K562 Cells. Proto-Oncogene Proteins c-bcr / chemistry. Proto-Oncogene Proteins c-bcr / genetics. Recombination, Genetic

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  • [Cites] Biochemistry. 1997 May 20;36(20):5934-9 [9166762.001]
  • [Cites] Cell. 1985 May;41(1):127-32 [2986841.001]
  • [Cites] Gene. 2002 May 29;291(1-2):251-7 [12095698.001]
  • [Cites] EMBO J. 1990 Apr;9(4):1319-27 [2323342.001]
  • [Cites] Science. 1994 Jan 28;263(5146):515-8 [8290959.001]
  • [Cites] Curr Biol. 2000 Jul 27-Aug 10;10(15):923-6 [10959840.001]
  • [Cites] Leukemia. 1996 Feb;10(2):372-7 [8637251.001]
  • [Cites] J Cell Biochem. 2001;82(2):299-309 [11527155.001]
  • [Cites] Genomics. 1995 May 1;27(1):67-82 [7665185.001]
  • [Cites] Annu Rev Biochem. 1989;58:351-75 [2549853.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jun 21;91(13):6236-9 [8016145.001]
  • [Cites] Oncogene. 1989 May;4(5):559-67 [2657572.001]
  • [Cites] Oncogene. 1990 Nov;5(11):1669-73 [2267134.001]
  • [Cites] Oncogene. 2001 May 24;20(23):2900-7 [11420702.001]
  • [Cites] J Cell Biol. 2001 Dec 10;155(6):899-910 [11739403.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):331-45 [11921269.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4790-5 [10758153.001]
  • [Cites] EMBO J. 2002 Oct 1;21(19):5269-80 [12356743.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Oct;32(2):144-54 [11550282.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Apr;36(4):393-401 [12619163.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2076-80 [2832845.001]
  • [Cites] Nucleic Acids Res. 1997 Feb 1;25(3):511-7 [9016589.001]
  • [Cites] Cancer Res. 1999 Jul 15;59(14 ):3357-62 [10416593.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Aug 14;98 (17 ):9802-7 [11493704.001]
  • [Cites] Oncogene. 1998 Dec 3;17(22):2921-31 [9879998.001]
  • [Cites] J Cell Sci. 2004 Sep 1;117(Pt 19):4583-90 [15331666.001]
  • [Cites] Nucleic Acids Res. 1988 Jun 24;16(12):5533-56 [2838820.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Jul;86(14):5497-501 [2546156.001]
  • [Cites] Cell. 1995 Dec 29;83(7):1137-48 [8548801.001]
  • [Cites] J Cell Biochem Suppl. 2000;Suppl 35:3-22 [11389527.001]
  • [Cites] Hum Mol Genet. 1998 May;7(5):767-76 [9536079.001]
  • [Cites] Hum Mol Genet. 2000 Jul 1;9(11):1671-9 [10861294.001]
  • [Cites] Mol Cell Biol. 1991 Oct;11(10):4973-84 [1656219.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14535-40 [10588740.001]
  • [Cites] Cell Mol Life Sci. 2002 Feb;59(2):373-85 [11915950.001]
  • [Cites] Mol Cell Biol. 1997 Jul;17(7):4070-9 [9199342.001]
  • [Cites] Biochem J. 1994 Nov 1;303 ( Pt 3):681-95 [7980433.001]
  • [Cites] Blood. 1996 Apr 1;87(7):2649-58 [8639880.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 May 15;90(10 ):4631-5 [8506309.001]
  • [Cites] Hum Mol Genet. 2002 Jun 1;11(12):1391-7 [12023981.001]
  • [Cites] J Biol Chem. 2002 Jun 14;277(24):21458-67 [11940566.001]
  • [Cites] Hum Mutat. 2003 Sep;22(3):229-44 [12938088.001]
  • [Cites] Cell. 1992 Nov 13;71(4):701-8 [1423625.001]
  • [Cites] Oncogene. 1998 Dec 10;17 (23 ):3035-44 [9881706.001]
  • [Cites] Genomics. 1999 Jul 15;59(2):187-92 [10409430.001]
  • [Cites] Leuk Res. 2002 Aug;26(8):713-20 [12191565.001]
  • [Cites] Br J Haematol. 1999 Apr;105(1):256-64 [10233389.001]
  • [Cites] Blood. 2000 Feb 1;95(3):738-43 [10648381.001]
  • [Cites] Oncogene. 1999 Dec 23;18(56):7975-84 [10637508.001]
  • [Cites] Cancer Res. 1995 Jan 1;55(1):34-8 [7805037.001]
  • [Cites] Cancer Res. 1996 Apr 15;56(8):1855-62 [8620504.001]
  • [Cites] Blood. 1996 Mar 1;87(5):1912-22 [8634439.001]
  • [Cites] Nature. 2001 Sep 27;413(6854):435-8 [11574892.001]
  • [Cites] Cancer Lett. 2003 Apr 10;193(1):1-9 [12691817.001]
  • [Cites] Leukemia. 1997 Sep;11(9):1571-4 [9305614.001]
  • [Cites] Chromosoma. 1996 Aug;105(2):122-33 [8753702.001]
  • [Cites] Leukemia. 1999 Dec;13(12):2107-13 [10602437.001]
  • [Cites] Cancer Res. 1993 Oct 1;53(19):4489-92 [8402620.001]
  • [Cites] Mol Cell Biol. 1999 Apr;19(4):2986-97 [10082566.001]
  • [Cites] Hum Genet. 2003 Jul;113(1):80-91 [12665971.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3793-803 [9808573.001]
  • [Cites] Genomics. 1998 Jan 15;47(2):217-29 [9479494.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3778-83 [11739186.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3237-42 [11751629.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Sep;35(1):92-6 [12203795.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4550-5 [11389089.001]
  • [Cites] Blood. 1990 Aug 1;76(3):597-601 [2198962.001]
  • [Cites] Genetics. 2002 Apr;160(4):1363-73 [11973293.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):9882-7 [12114534.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Nov;41(3):257-65 [15334549.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4411-3 [10781030.001]
  • [Cites] FASEB J. 2004 Jan;18(1):173-5 [14630694.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Apr;33(4):362-78 [11921271.001]
  • [Cites] Mol Pharmacol. 1998 Jul;54(1):78-85 [9658192.001]
  • [Cites] Cancer Res. 2004 Apr 15;64(8):2656-62 [15087374.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):3070-5 [11867721.001]
  • [Cites] Semin Hematol. 1999 Oct;36(4 Suppl 7):59-72 [10595755.001]
  • [Cites] Chromosoma. 1991 Feb;100(2):97-102 [1849068.001]
  • [Cites] Leukemia. 1998 Mar;12(3):346-52 [9529129.001]
  • [Cites] Leukemia. 1995 Aug;9(8):1305-12 [7643617.001]
  • (PMID = 16572268.001).
  • [ISSN] 0340-6717
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chromatin; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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7. Corcoran M, Parker A, Orchard J, Davis Z, Wirtz M, Schmitz OJ, Oscier D: ZAP-70 methylation status is associated with ZAP-70 expression status in chronic lymphocytic leukemia. Haematologica; 2005 Aug;90(8):1078-88
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ZAP-70 methylation status is associated with ZAP-70 expression status in chronic lymphocytic leukemia.
  • BACKGROUND AND OBJECTIVES: ZAP-70 expression is a recognized prognostic marker in chronic lymphocytic leukemia (CLL).
  • DESIGN AND METHODS: Patients with CLL (n=87), acute lymphoblastic leukemia (n=13), mantle cell leukemia (n=13) and splenic marginal zone lymphoma (n=14) of known immunoglobulin gene mutation (IgVH) status were studied.
  • [MeSH-major] DNA Methylation. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. ZAP-70 Protein-Tyrosine Kinase / genetics
  • [MeSH-minor] 5' Untranslated Regions / genetics. Conserved Sequence. Dinucleoside Phosphates / genetics. Humans. Introns. Leukemia / genetics. Reference Values. Restriction Mapping

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  • [CommentIn] Haematologica. 2005 Aug;90(8):1012 [16079094.001]
  • (PMID = 16079107.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / 5' Untranslated Regions; 0 / Dinucleoside Phosphates; 2382-65-2 / cytidylyl-3'-5'-guanosine; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase
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8. Sakai M, Takeyama H, Kojima Y, Shimokawa T: [Treatment results of acute leukemia in elderly patients: analysis of 61 consecutive patients in a single institution]. Gan To Kagaku Ryoho; 2008 Feb;35(2):239-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment results of acute leukemia in elderly patients: analysis of 61 consecutive patients in a single institution].
  • In order to investigate the clinical characteristics and management of elderly patients with acute leukemia, we retrospectively analyzed treatment results for 61 acute leukemia patients aged 65 years or more (median age 72) admitted to our department between October 1995 and September 2006.
  • There were 6 elderly patients with ALL (acute lymphocytic leukemia) and 55 patients with AML (acute myelogenous leukemia).
  • The intensive chemotherapy group and the de novo leukemia group showed a significantly higher CR rate and longer survival.
  • Intensive chemotherapy was effective for 65-74-year-old patients with de novo AML.
  • In future, we consider that the prognosis for elderly patients with acute leukemia will improve, if made-to-order treatment is given, depending on evidence-based stratification of patients with organs having low reserve capacity.
  • [MeSH-major] Leukemia, Lymphoid / drug therapy. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Acute Disease. Age Distribution. Aged. Aged, 80 and over. Female. Humans. Male. Retrospective Studies. Survival Rate


9. Kode J, Dudhal N, Banavali S, Chiplunkar S: T-cell receptor gamma and delta junctional gene rearrangements as diagnostic and prognostic biomarker for T-cell acute lymphoblastic leukemia. Leuk Lymphoma; 2006 Apr;47(4):769-70
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  • [Title] T-cell receptor gamma and delta junctional gene rearrangements as diagnostic and prognostic biomarker for T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Biomarkers, Tumor. Gene Rearrangement. Leukemia, T-Cell / diagnosis. Leukemia, T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell, gamma-delta / metabolism

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  • (PMID = 16886283.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Antigen, T-Cell, gamma-delta
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10. Frazer JK, Meeker ND, Rudner L, Bradley DF, Smith AC, Demarest B, Joshi D, Locke EE, Hutchinson SA, Tripp S, Perkins SL, Trede NS: Heritable T-cell malignancy models established in a zebrafish phenotypic screen. Leukemia; 2009 Oct;23(10):1825-35
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  • [Title] Heritable T-cell malignancy models established in a zebrafish phenotypic screen.
  • T-cell neoplasias are common in pediatric oncology, and include acute lymphoblastic leukemia (T-ALL) and lymphoblastic lymphoma (T-LBL).
  • These cancers have worse prognoses than their B-cell counterparts, and their treatments carry significant morbidity.
  • Although many pediatric malignancies have characteristic translocations, most T-lymphocyte-derived diseases lack cytogenetic hallmarks.
  • Although dysregulation of the NOTCH1 pathway occurs in a substantial fraction of cases, many other genetic lesions of T-cell malignancy have not yet been determined.
  • Using transgenic fish with T-lymphocyte-specific expression of enhanced green fluorescent protein (EGFP), we performed chemical mutagenesis, screened animals for GFP(+) tumors, and identified multiple lines with a heritable predisposition to T-cell malignancy.
  • T-cell receptor analyses confirmed their clonality.
  • Malignancies were transplantable and contained leukemia-initiating cells, like their human correlates.
  • In summary, we have identified multiple zebrafish mutants that recapitulate human T-cell neoplasia and show heritable transmission.

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  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Leukemia. 2002 Jul;16(7):1259-66 [12094249.001]
  • [Cites] Rev Clin Exp Hematol. 2002 Jun;6(2):91-113; discussion 200-2 [12196211.001]
  • [Cites] Science. 2003 Feb 7;299(5608):887-90 [12574629.001]
  • [Cites] Curr Opin Hematol. 2003 Jul;10(4):290-6 [12799535.001]
  • [Cites] J Clin Oncol. 2003 Oct 1;21(19):3616-22 [14512392.001]
  • [Cites] Nat Immunol. 2003 Dec;4(12):1238-46 [14608381.001]
  • [Cites] Blood Cells Mol Dis. 2004 Jan-Feb;32(1):246-61 [14757442.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Immunity. 2004 Apr;20(4):367-79 [15084267.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 11;101(19):7369-74 [15123839.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1298-305 [15142873.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Ann Intern Med. 1975 Oct;83(4):534-52 [126656.001]
  • [Cites] Scand J Haematol. 1975 Sep;15(2):117-31 [1188315.001]
  • [Cites] Nature. 1981 May 28;291(5813):293-6 [7248006.001]
  • [Cites] Blood. 1989 Apr;73(5):1247-58 [2467704.001]
  • [Cites] Genetics. 1994 Apr;136(4):1401-20 [8013916.001]
  • [Cites] J Natl Cancer Inst. 1994 Nov 2;86(21):1600-8 [7932824.001]
  • [Cites] Development. 1996 Dec;123:1-36 [9007226.001]
  • [Cites] Leukemia. 1997 Aug;11(8):1347-59 [9264391.001]
  • [Cites] Blood. 1998 Sep 1;92(5):1556-64 [9716583.001]
  • [Cites] Curr Opin Hematol. 1998 Jul;5(4):292-301 [9747636.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3278-85 [15618471.001]
  • [Cites] Ultrastruct Pathol. 2005 May-Aug;29(3-4):175-202 [16036874.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6306-15 [16155013.001]
  • [Cites] Best Pract Res Clin Haematol. 2006;19(2):269-79 [16516124.001]
  • [Cites] Leukemia. 2006 Sep;20(9):1496-510 [16826225.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 10;103(41):15166-71 [17015828.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] BMC Genomics. 2007;8:11 [17212827.001]
  • [Cites] Leukemia. 2007 Mar;21(3):462-71 [17252014.001]
  • [Cites] J Med Genet. 2007 Jul;44(7):e83 [17601929.001]
  • [Cites] Development. 2007 Dec;134(23):4147-56 [17959717.001]
  • [Cites] WormBook. 2006;:1-6 [18050456.001]
  • [Cites] Dev Comp Immunol. 2008;32(7):745-57 [18222541.001]
  • [Cites] Oncogene. 2008 Jul 10;27(30):4242-8 [18345029.001]
  • [Cites] Dev Dyn. 2008 Sep;237(9):2575-84 [18729230.001]
  • [Cites] Br J Haematol. 2008 Nov;143(3):378-82 [18729850.001]
  • [Cites] Semin Hematol. 2009 Jan;46(1):33-8 [19100366.001]
  • [Cites] Dev Biol. 1999 Dec 1;216(1):1-15 [10588859.001]
  • [Cites] Science. 2000 Mar 17;287(5460):2032-6 [10720333.001]
  • [Cites] Semin Hematol. 2000 Oct;37(4):381-95 [11071360.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2223-33 [11187913.001]
  • [Cites] Curr Opin Hematol. 2001 Jul;8(4):189-91 [11561153.001]
  • (PMID = 19516274.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / K08 HD053350-03; United States / NCI NIH HHS / CA / P30-CA042014; United States / NICHD NIH HHS / HD / K08-HD53350; United States / NICHD NIH HHS / HD / R21 HD060310; United States / NICHD NIH HHS / HD / R21 HD060310-01; United States / NIDDK NIH HHS / DK / T32-DK007115; United States / NIDDK NIH HHS / DK / T32 DK007115; United States / NICHD NIH HHS / HD / K08 HD053350; United States / NIAID NIH HHS / AI / R21-AI079784; United States / NICHD NIH HHS / HD / K12 HD001410; United States / NICHD NIH HHS / HD / K12-HD001410; United States / NICHD NIH HHS / HD / K08 HD053350-02; United States / NCI NIH HHS / CA / P30 CA042014
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins
  • [Other-IDs] NLM/ NIHMS112911; NLM/ PMC2761994
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11. Medyouf H, Alcalde H, Berthier C, Guillemin MC, dos Santos NR, Janin A, Decaudin D, de Thé H, Ghysdael J: Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia. Nat Med; 2007 Jun;13(6):736-41
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  • [Title] Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia.
  • In the T-cell lineage, calcineurin activation is important for pre-T-cell receptor (TCR) signaling, TCR-mediated positive selection of thymocytes into mature T cells, and many aspects of the immune response.
  • We observed sustained calcineurin activation in human B- and T-cell lymphomas and in all mouse models of lymphoid malignancies analyzed.
  • In intracellular NOTCH1 (ICN1)- and TEL-JAK2-induced T-cell lymphoblastic leukemia, two mouse models relevant to human malignancies, in vivo inhibition of calcineurin activity by CsA or FK506 induced apoptosis of leukemic cells and rapid tumor clearance, and substantially prolonged mouse survival.
  • In contrast, ectopic expression of a constitutively activated mutant of calcineurin favored leukemia progression.
  • Moreover, CsA treatment induced apoptosis in human lymphoma and leukemia cell lines.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Calcineurin / metabolism. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / enzymology
  • [MeSH-minor] Animals. Calcineurin Inhibitors. Cell Line, Tumor. Cyclosporine / pharmacology. Disease Models, Animal. Enzyme Activation / drug effects. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / enzymology. Lymphoma, B-Cell / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Oncogene Proteins, Fusion / deficiency. Oncogene Proteins, Fusion / genetics. Receptor, Notch1 / physiology. Tacrolimus / pharmacology

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  • [CommentIn] Nat Med. 2007 Jun;13(6):669-71 [17554330.001]
  • (PMID = 17515895.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Calcineurin Inhibitors; 0 / NOTCH1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; 0 / TEL-JAK2 fusion protein, mouse; 83HN0GTJ6D / Cyclosporine; EC 3.1.3.16 / Calcineurin; WM0HAQ4WNM / Tacrolimus
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12. Osmond RI, Das S, Crouch MF: Development of cell-based assays for cytokine receptor signaling, using an AlphaScreen SureFire assay format. Anal Biochem; 2010 Aug;403(1-2):94-101
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  • [Title] Development of cell-based assays for cytokine receptor signaling, using an AlphaScreen SureFire assay format.
  • The signal transducers and activators of transcription (STAT) proteins are a small family of signaling proteins that are crucial for cytokine and growth factor receptor-mediated signaling in various blood cell types.
  • Despite their central role in immune and hematopoietic cellular regulation, there are relatively few options for monitoring receptor-mediated JAK/STAT signaling events in a cell-based format, without the need for cellular transfections or labor intensive methodology.
  • With three different cell lines (human acute monocytic leukemia THP-1 cells, human erythroleukemic TF-1 cells, and human T lymphocytic Jurkat cells), we have optimized a rapid and homogeneous methodology for monitoring endogenous, receptor-mediated signaling via STAT 1, STAT 3, or STAT 5 phosphorylation, in response to several agonists.
  • [MeSH-minor] Biochemistry / methods. Blotting, Western. Cell Line, Tumor. Humans. Jurkat Cells. Phosphorylation. STAT1 Transcription Factor / metabolism. STAT3 Transcription Factor / metabolism. STAT5 Transcription Factor / metabolism

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20382104.001).
  • [ISSN] 1096-0309
  • [Journal-full-title] Analytical biochemistry
  • [ISO-abbreviation] Anal. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Cytokine; 0 / STAT Transcription Factors; 0 / STAT1 Transcription Factor; 0 / STAT3 Transcription Factor; 0 / STAT5 Transcription Factor
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13. Iversen PO, Sørensen DR, Tronstad KJ, Gudbrandsen OA, Rustan AC, Berge RK, Drevon CA: A bioactively modified fatty acid improves survival and impairs metastasis in preclinical models of acute leukemia. Clin Cancer Res; 2006 Jun 1;12(11 Pt 1):3525-31
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  • [Title] A bioactively modified fatty acid improves survival and impairs metastasis in preclinical models of acute leukemia.
  • PURPOSE: Polyunsaturated fatty acids (PUFA) and the sulfur-substituted fatty acid tetradecylthioacetic acid (TTA) inhibit proliferation and induce apoptosis in lymphoma and leukemic cell lines, but it is unknown if they can modify leukemogenesis in the intact organism.
  • EXPERIMENTAL DESIGN: We now examined the effects of PUFA and TTA in rats transplanted with either acute promyelocytic leukemia or acute T-cell leukemia.
  • RESULTS: Whereas TTA prolonged survival (P < 0.05) in both types of rat leukemia, n-3 PUFA had no significant effect compared with controls.
  • CONCLUSIONS: Dietary intake of TTA, but not of n-3 PUFA, in rats with acute leukemia, prolonged their survival.
  • TTA intake was also associated with reduced leukemic cell burden as well as diminished extramedullar dissemination.
  • TTA represents a modified fatty acid that exerts unique effects on malignant hematopoietic cells, and the present study indicates that TTA may have a therapeutic potential in patients with acute leukemias.
  • [MeSH-major] Fatty Acids, Unsaturated / administration & dosage. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Sulfides / administration & dosage
  • [MeSH-minor] Animals. Apoptosis / drug effects. Diet. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Humans. Leukemic Infiltration / diagnosis. Matrix Metalloproteinases / drug effects. Neoplasm Metastasis. Rats. Structure-Activity Relationship. Survival Rate. Transplantation, Heterologous. Xenograft Model Antitumor Assays

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  • (PMID = 16740779.001).
  • [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 / Fatty Acids, Unsaturated; 0 / Sulfides; 2921-20-2 / 1-(carboxymethylthio)tetradecane; EC 3.4.24.- / Matrix Metalloproteinases
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14. van Anders SM, Hamilton LD, Schmidt N, Watson NV: Associations between testosterone secretion and sexual activity in women. Horm Behav; 2007 Apr;51(4):477-82
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  • On three separate nights, they provided pre-activity, post-activity, and next-morning saliva samples and completed brief questionnaires at the last two timepoints.
  • Women's T was higher pre-intercourse than pre-control activity.
  • Women's T was also higher post-intercourse than post-control activity, though the percent change in T from pre- to post-activity was highest for cuddling, then intercourse, then exercise.

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  • (PMID = 17320881.001).
  • [ISSN] 0018-506X
  • [Journal-full-title] Hormones and behavior
  • [ISO-abbreviation] Horm Behav
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 3XMK78S47O / Testosterone
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15. Patterson LJ, Gering M, Eckfeldt CE, Green AR, Verfaillie CM, Ekker SC, Patient R: The transcription factors Scl and Lmo2 act together during development of the hemangioblast in zebrafish. Blood; 2007 Mar 15;109(6):2389-98
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  • Thus, expression of these critical regulators is dependent on continued expression of upstream regulators, which may include cell-extrinsic signals.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cell Line. DNA / metabolism. Embryo, Nonmammalian / cytology. Embryo, Nonmammalian / embryology. Embryo, Nonmammalian / metabolism. Endothelial Cells / cytology. Endothelial Cells / metabolism. Erythroid Cells / cytology. Erythroid Cells / metabolism. Gene Expression Regulation, Developmental. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. LIM Domain Proteins. Mice. Myeloid Cells / cytology. Myeloid Cells / metabolism. Phenotype. Protein Binding. Transcription Factors

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  • (PMID = 17090656.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM63904; United Kingdom / Medical Research Council / / MC/ U137981013; United States / NCI NIH HHS / CA / P01CA65493; United States / NIGMS NIH HHS / GM / R01 GM063904-01; United States / NIGMS NIH HHS / GM / R01 GM063904
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / Zebrafish Proteins; 0 / lmo2 protein, zebrafish; 0 / tal1 protein, zebrafish; 9007-49-2 / DNA
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16. Roecker AM, Allison JC, Kisor DF: Nelarabine: efficacy in the treatment of clinical malignancies. Future Oncol; 2006 Aug;2(4):441-8
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  • Nelarabine is indicated for the treatment of adult and pediatric patients with T-cell acute lymphoblastic leukemia or T-cell lymphoblastic lymphoma whose disease has not responded to, or has relapsed after treatment with, at least two chemotherapy regimens.
  • [MeSH-major] Arabinonucleosides / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16922610.001).
  • [ISSN] 1479-6694
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Arabinonucleosides; 60158CV180 / nelarabine
  • [Number-of-references] 22
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17. Hager-Theodorides AL, Dessens JT, Outram SV, Crompton T: The transcription factor Gli3 regulates differentiation of fetal CD4- CD8- double-negative thymocytes. Blood; 2005 Aug 15;106(4):1296-304
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  • Analysis of null mutants showed that Gli3 is involved at the transitions from DN1 to CD44+ CD25+ DN (DN2) cell and from DN to CD4+ CD8+ double-positive (DP) cell.
  • Gli3 is required for differentiation from DN to DP thymocyte, after pre-T-cell receptor (TCR) signaling but is not necessary for pre-TCR-induced proliferation or survival.
  • The effect of Gli3 was dose dependent, suggesting its direct involvement in the transcriptional regulation of genes controlling T-cell differentiation during fetal development.
  • [MeSH-major] Antigens, CD / analysis. Cell Differentiation. DNA-Binding Proteins / physiology. Nerve Tissue Proteins / physiology. T-Lymphocytes / cytology. Thymus Gland / cytology. Transcription Factors / physiology
  • [MeSH-minor] Animals. Antigens, CD4. Antigens, CD8. Cell Lineage. Embryo, Mammalian / cytology. Embryo, Mammalian / immunology. Gene Expression Regulation, Developmental. Kruppel-Like Transcription Factors. Mice. Mice, Inbred C57BL. Mice, Mutant Strains


18. Meijerink JP: Genetic rearrangements in relation to immunophenotype and outcome in T-cell acute lymphoblastic leukaemia. Best Pract Res Clin Haematol; 2010 Sep;23(3):307-18
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  • [Title] Genetic rearrangements in relation to immunophenotype and outcome in T-cell acute lymphoblastic leukaemia.
  • Mutually exclusive oncogenic rearrangements may delineate specific T-cell acute lymphoblastic leukaemia (T-ALL) subgroups, and so far at least 4 molecular-cytogenetic subgroups have been identified, i.e. the TAL/LMO, the TLX1/HOX11, the TLX3/HOX11L2 and the HOXA subgroups.
  • A fifth group with an immature immunophenotype that can be predicted by an early T-cell precursor signature has also been identified, and has been associated with poor outcome.
  • The association of these subgroups with the expression of specific immunophenotypic markers reflecting arrest at specific T-cell developmental stages will be reviewed.
  • [MeSH-major] Gene Rearrangement. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Signal Transduction

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21112032.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 135471-20-4 / TAL1 protein, human
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19. DeAngelo DJ: The treatment of adolescents and young adults with acute lymphoblastic leukemia. Hematology Am Soc Hematol Educ Program; 2005;:123-30
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  • [Title] The treatment of adolescents and young adults with acute lymphoblastic leukemia.
  • Intensive chemotherapy regimens for children with acute lymphoblastic leukemia (ALL) have greatly improved, and the majority of children with precursor B-cell ALL are able to achieve a complete remission (CR), with an induction rate approaching 98% and a 5-year estimated event-free survival rate (EFS) of approximately 80%.
  • In addition, new insights into the molecular pathogenesis of T cell ALL have led to new therapeutic strategies.

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  • (PMID = 16304369.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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20. Huang YF, Shangguan D, Liu H, Phillips JA, Zhang X, Chen Y, Tan W: Molecular assembly of an aptamer-drug conjugate for targeted drug delivery to tumor cells. Chembiochem; 2009 Mar 23;10(5):862-8
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  • In this study, we covalently link the antitumor agent doxorubicin (Dox) to the DNA aptamer sgc8c, which was selected by the cell-SELEX method.
  • In doing so, we expected that this sgc8c-Dox conjugate would specifically kill the target CCRF-CEM (T-cell acute lymphoblastic leukemia, T-cell ALL) cells, but with minimal toxicity towards nontarget cells.
  • Cell viability tests demonstrate that the sgc8c-Dox conjugates not only possess potency similar to unconjugated Dox, but also have the required molecular specificity that is lacking in most current targeted drug delivery strategies.
  • Furthermore, we found that nonspecific uptake of membrane-permeable Dox to nontarget cell lines could also be inhibited by linking the drug with the aptamer; thus, the conjugates are selective for cells that express higher amounts of target proteins.

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  • [Cites] J Biol Chem. 2001 May 11;276(19):16464-8 [11279054.001]
  • [Cites] Bioconjug Chem. 1993 Nov-Dec;4(6):521-7 [7508268.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15416-21 [14676325.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Apr;80(8):2258-62 [6300903.001]
  • [Cites] Cancer Chemother Pharmacol. 1986;18(3):185-97 [2948729.001]
  • [Cites] Science. 1990 Aug 3;249(4968):505-10 [2200121.001]
  • [Cites] Nature. 1990 Aug 30;346(6287):818-22 [1697402.001]
  • [Cites] Bioorg Med Chem. 1995 Oct;3(10):1305-12 [8564396.001]
  • [Cites] Anal Chem. 2005 Apr 15;77(8):2281-7 [15828758.001]
  • [Cites] Expert Opin Drug Deliv. 2006 May;3(3):311-24 [16640493.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):5989-92 [16778167.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 8;103(32):11838-43 [16873550.001]
  • [Cites] Nat Biotechnol. 2006 Aug;24(8):1005-15 [16823371.001]
  • [Cites] Angew Chem Int Ed Engl. 2006 Dec 11;45(48):8149-52 [17099918.001]
  • [Cites] Chembiochem. 2007 Apr 16;8(6):603-6 [17373017.001]
  • [Cites] Clin Chem. 2007 Jun;53(6):1153-5 [17463173.001]
  • [Cites] Acc Chem Res. 2008 Jan;41(1):98-107 [17705444.001]
  • [Cites] Anal Chem. 2008 Feb 1;80(3):721-8 [18177018.001]
  • [Cites] Chemistry. 2008;14(6):1769-75 [18092308.001]
  • [Cites] Bioconjug Chem. 2008 Feb;19(2):525-31 [18163537.001]
  • [Cites] J Proteome Res. 2008 May;7(5):2133-9 [18363322.001]
  • [Cites] Cancer J. 2008 May-Jun;14(3):154-69 [18536555.001]
  • [Cites] ChemMedChem. 2008 Jun;3(6):991-1001 [18338423.001]
  • [Cites] Cancer Cell. 2003 Mar;3(3):207-12 [12676579.001]
  • (PMID = 19253922.001).
  • [ISSN] 1439-7633
  • [Journal-full-title] Chembiochem : a European journal of chemical biology
  • [ISO-abbreviation] Chembiochem
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM079359; United States / NIGMS NIH HHS / GM / R01 GM079359-01; None / None / / R01 GM079359-01; United States / NIGMS NIH HHS / GM / R01 GM079359-02; United States / NIGMS NIH HHS / GM / R01 GM079359-03; None / None / / R01 GM079359-02; None / None / / R01 GM079359-01S1; United States / NIGMS NIH HHS / GM / R01 GM079359-01S1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Aptamers, Nucleotide; 0 / Drug Carriers; 0 / Immunoconjugates; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ NIHMS149610; NLM/ PMC2992821
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21. Ohnuki K, Watanabe Y, Takahashi Y, Kobayashi S, Watanabe S, Ogawa S, Kotani M, Kozono H, Tanabe K, Abe R: Antigen-specific CD4+ effector T cells: analysis of factors regulating clonal expansion and cytokine production: clonal expansion and cytokine production by CD4+ effector T cells. Biochem Biophys Res Commun; 2009 Mar 20;380(4):742-7
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  • In order to fully understand T cell-mediated immunity, the mechanisms that regulate clonal expansion and cytokine production by CD4(+) antigen-specific effector T cells in response to a wide range of antigenic stimulation needs clarification.
  • For this purpose, panels of antigen-specific CD4(+) T cell clones with different thresholds for antigen-induced proliferation were generated by repeated stimulation with high- or low-dose antigen.
  • There was no significant difference in antigen-dependent cytokine production by TG40 cells transfected with TCR obtained from either high- or low-dose-responding T cell clones, suggesting that the affinity of TCRs for their ligands is not primary determinant of T cell antigen reactivity.
  • The proliferative responses of all T cell clones to both peptide stimulation and to TCRbeta crosslinking revealed parallel dose-response curves.
  • Finally, the antigen responses of high- and low-peptide-responding T cell clones reveal that clonal expansion and cytokine production of effector T cells occur independently of antigen concentration.
  • [MeSH-minor] Animals. Cell Adhesion Molecules / metabolism. Clone Cells. Flow Cytometry. Mice. Mice, Inbred BALB C. Ovalbumin / immunology. Peptide Fragments / immunology. Receptors, Antigen, T-Cell / metabolism

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  • (PMID = 19338745.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / OVA 323-339; 0 / Peptide Fragments; 0 / Receptors, Antigen, T-Cell; 9006-59-1 / Ovalbumin
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22. Braun FK, Fecker LF, Schwarz C, Walden P, Assaf C, Dürkop H, Sterry W, Eberle J: Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-cell lymphoma cells. J Invest Dermatol; 2007 Oct;127(10):2425-37
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  • [Title] Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-cell lymphoma cells.
  • Control of apoptosis via death ligands plays a basic role for lymphocyte homeostasis and lymphoma development.
  • In this study, cutaneous T-cell lymphoma (CTCL) cell lines revealed pronounced resistance to death ligands as compared to cell lines of T-cell acute lymphoblastic leukemia (T-ALL).
  • The proapoptotic activity of tumor necrosis factor (TNF)-alpha was blocked, sensitivity to TNF-related apoptosis-inducing ligand was significantly reduced, and 1/4 CTCL cell lines was resistant to CD95 activation.
  • No indication for a responsibility of typical downstream regulators of apoptosis was obtained, but loss of CD95 was found in 1/4, loss of TNF-R1 in 3/4, loss of caspase-10 in 2/4, loss of Bid in 1/4, and overexpression of cellular flice inhibitory protein was found in 4/4 CTCL cell lines.
  • [MeSH-major] Apoptosis / physiology. Lymphoma, T-Cell, Cutaneous / pathology. Receptors, Death Domain / antagonists & inhibitors. Signal Transduction / physiology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antigens, CD95 / physiology. BH3 Interacting Domain Death Agonist Protein / physiology. CASP8 and FADD-Like Apoptosis Regulating Protein / physiology. Caspase 10 / physiology. Cell Line, Tumor. Female. Humans. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Male. Middle Aged. TNF-Related Apoptosis-Inducing Ligand / antagonists & inhibitors. TNF-Related Apoptosis-Inducing Ligand / physiology. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 17495957.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / Receptors, Death Domain; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / Caspase 10
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23. Dzhagalov I, Dunkle A, He YW: The anti-apoptotic Bcl-2 family member Mcl-1 promotes T lymphocyte survival at multiple stages. J Immunol; 2008 Jul 1;181(1):521-8
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  • Genetic studies have demonstrated that the Bcl-2 family member Mcl-1 is an important anti-apoptotic protein in the development of multiple cell types including T lymphocytes.
  • In this study, we examined the expression pattern of Mcl-1 in different populations of T cells at the single-cell level and found that Mcl-1 protein is constitutively expressed in all T cell populations and up-regulated upon TCR stimulation.
  • We then investigated the role of Mcl-1 in the survival of these different populations by conditionally deleting Mcl-1 at various T cell stages.

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
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  • [Cites] J Immunol. 1993 Jul 1;151(1):83-91 [8326141.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3516-20 [7682708.001]
  • [Cites] Science. 1993 Sep 17;261(5128):1584-8 [8372353.001]
  • [Cites] Cell. 1993 Oct 22;75(2):229-40 [8402909.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Oct 25;91(22):10685-9 [7938012.001]
  • [Cites] J Exp Med. 1994 Nov 1;180(5):1955-60 [7964471.001]
  • [Cites] Science. 1995 Mar 10;267(5203):1506-10 [7878471.001]
  • [Cites] J Exp Med. 1995 Apr 1;181(4):1519-26 [7699333.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 May 23;92(11):4763-7 [7761398.001]
  • [Cites] Immunity. 1995 Jul;3(1):87-98 [7621080.001]
  • [Cites] EMBO J. 1995 Oct 2;14(19):4641-53 [7588594.001]
  • [Cites] J Exp Med. 1995 Dec 1;182(6):1973-83 [7500043.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Dec 19;92(26):12070-4 [8618846.001]
  • [Cites] Science. 1996 Jun 28;272(5270):1947-50 [8658169.001]
  • [Cites] Cell. 1997 Jun 27;89(7):1033-41 [9215626.001]
  • [Cites] Immunity. 1997 Jul;7(1):147-54 [9252127.001]
  • [Cites] Immunity. 1999 Mar;10(3):323-32 [10204488.001]
  • [Cites] Annu Rev Immunol. 1999;17:781-828 [10358774.001]
  • [Cites] Science. 2005 Feb 18;307(5712):1101-4 [15718471.001]
  • [Cites] J Exp Med. 2005 Feb 21;201(4):603-14 [15728238.001]
  • [Cites] Semin Immunol. 2005 Jun;17(3):183-91 [15826823.001]
  • [Cites] J Immunol. 2005 Jun 1;174(11):6967-73 [15905539.001]
  • [Cites] Genes Dev. 2005 Jun 1;19(11):1294-305 [15901672.001]
  • [Cites] Cell Res. 2005 Oct;15(10):749-69 [16246265.001]
  • [Cites] J Exp Med. 2005 Dec 5;202(11):1471-6 [16314438.001]
  • [Cites] Blood. 2007 Feb 15;109(4):1620-6 [17062731.001]
  • [Cites] J Exp Med. 2007 Jul 9;204(7):1665-75 [17591857.001]
  • [Cites] J Exp Med. 2007 Oct 29;204(11):2513-20 [17908937.001]
  • [Cites] Science. 1999 Nov 26;286(5445):1735-8 [10576740.001]
  • [Cites] Nature. 1999 Nov 18;402(6759):255-62 [10580495.001]
  • [Cites] Genes Dev. 2000 Jan 1;14(1):23-7 [10640272.001]
  • [Cites] J Immunol. 2000 Apr 15;164(8):3950-4 [10754284.001]
  • [Cites] J Immunol. 2001 Jan 15;166(2):795-9 [11145652.001]
  • [Cites] Immunity. 2001 Nov;15(5):763-74 [11728338.001]
  • [Cites] Immunity. 2002 Jun;16(6):759-67 [12121658.001]
  • [Cites] Science. 2003 Nov 7;302(5647):1036-8 [14500851.001]
  • [Cites] Nature. 2003 Dec 11;426(6967):671-6 [14668867.001]
  • [Cites] Biochim Biophys Acta. 2004 Mar 1;1644(2-3):179-88 [14996502.001]
  • [Cites] J Immunol. 1993 Sep 1;151(5):2546-54 [8360476.001]
  • (PMID = 18566418.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI074754; United States / NIAID NIH HHS / AI / AI054658-05; United States / NCI NIH HHS / CA / R01 CA092123; United States / NCI NIH HHS / CA / CA092123-05; United States / NIAID NIH HHS / AI / R01 AI054658-05; United States / NIAID NIH HHS / AI / AI54683; United States / NCI NIH HHS / CA / R01 CA092123-05; United States / NCI NIH HHS / CA / CA92123; United States / NIAID NIH HHS / AI / R01 AI054658
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein
  • [Other-IDs] NLM/ NIHMS66462; NLM/ PMC2561902
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24. Look AT: Investigator profile. An interview with A. Thomas Look, M.D. Interview by Vicki Glaser. Zebrafish; 2005;2(4):231-6
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  • Work in Dr. Look's laboratory focuses on the molecular pathogenesis of leukemia.
  • His group has been credited with the identification and functional analysis of several chimeric oncogenes activated by chromosomal translocations, including the E2A-HLF transcription factor, which was shown to act through an evolutionarily conserved genetic pathway to promote leukemia cell survival.
  • Their efforts in human T-cell acute lymphoblastic leukemia have revealed key multistep mutational pathways that drive the pathogenesis of this disease and demonstrated that NOTCH1 receptors are mutationally activated in a majority of these cases.
  • Look's laboratory developed the first transgenic model of leukemia in the zebrafish, opening the way for chemical and genome-wide genetic modifier screens in a vertebrate disease model.

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  • (PMID = 18248181.001).
  • [ISSN] 1557-8542
  • [Journal-full-title] Zebrafish
  • [ISO-abbreviation] Zebrafish
  • [Language] eng
  • [Publication-type] Interview
  • [Publication-country] United States
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25. Gläsker S, Li J, Xia JB, Okamoto H, Zeng W, Lonser RR, Zhuang Z, Oldfield EH, Vortmeyer AO: Hemangioblastomas share protein expression with embryonal hemangioblast progenitor cell. Cancer Res; 2006 Apr 15;66(8):4167-72
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  • [Title] Hemangioblastomas share protein expression with embryonal hemangioblast progenitor cell.
  • Hemangioblastomas are central nervous system (CNS) tumors of unknown histogenesis, which can occur sporadically or in von Hippel-Lindau disease.
  • Failure to specify the cytologic origin of the stromal cell has precluded the development of nonsurgical therapies and limits understanding of its basic biology.
  • We report that the stromal cells express proteins (Scl, brachyury, Csf-1R, Gata-1, Flk-1, and Tie-2) that characterize embryonic progenitor cells with hemangioblastic differentiation potential and conclude that embryonic progenitors with hemangioblast potential represent a possible cytologic equivalent of the stromal cell.

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  • (PMID = 16618738.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiopoietin-1; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Brachyury protein; 0 / Fetal Proteins; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Proto-Oncogene Proteins; 0 / T-Box Domain Proteins; 135471-20-4 / TAL1 protein, human; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, TIE-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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26. Isoda T, Ito S, Kajiwara M, Nagasawa M: Successful high-dose methotrexate chemotherapy in a patient with acute lymphocytic leukemia who developed acute renal failure during the initial treatment. Pediatr Int; 2007 Dec;49(6):1018-9
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  • [Title] Successful high-dose methotrexate chemotherapy in a patient with acute lymphocytic leukemia who developed acute renal failure during the initial treatment.
  • Methotrexate (MTX) is a key drug in the chemotherapy for childhood acute lymphocytic leukemia (ALL).
  • [MeSH-major] Acute Kidney Injury / chemically induced. Antimetabolites, Antineoplastic / adverse effects. Methotrexate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18045317.001).
  • [ISSN] 1328-8067
  • [Journal-full-title] Pediatrics international : official journal of the Japan Pediatric Society
  • [ISO-abbreviation] Pediatr Int
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
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27. Verbeek WH, Van De Water JM, Al-Toma A, Oudejans JJ, Mulder CJ, Coupé VM: Incidence of enteropathy--associated T-cell lymphoma: a nation-wide study of a population-based registry in The Netherlands. Scand J Gastroenterol; 2008;43(11):1322-8
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  • [Title] Incidence of enteropathy--associated T-cell lymphoma: a nation-wide study of a population-based registry in The Netherlands.
  • OBJECTIVE: Enteropathy-associated T-cell lymphomas (EATLs) are T-cell non-Hodgkin lymphomas of the small bowel, which are specifically associated with coeliac disease (CD).
  • We included all T-cell lymphomas detected between January 2000 and December 2006 that initially presented in the small bowel.
  • Finally, the distribution of characteristics such as the localization, the Marsh classification and method of diagnosis are described.
  • Most EATLs were localized in the proximal small intestine and the diagnosis was made by surgical resection in the majority of cases.
  • CONCLUSIONS: EATL is a rare disease with an incidence of 0.10 per 100,000 inhabitants per year, occurring in older age, with a peak incidence in the 7th decade.
  • [MeSH-major] Celiac Disease / epidemiology. Lymphoma, T-Cell / epidemiology

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  • (PMID = 18618372.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
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28. Shapira T, Pereg D, Lishner M: How I treat acute and chronic leukemia in pregnancy. Blood Rev; 2008 Sep;22(5):247-59
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  • [Title] How I treat acute and chronic leukemia in pregnancy.
  • The prevalence of pregnancy associated leukemia is approximately 1 case out of 10,000 pregnancies.
  • The treatment of a pregnant woman with leukemia may be associated with severe adverse fetal outcome including death and malformations, and therefore poses a difficult challenge for both the patient and the attending physician.
  • When acute leukemia is diagnosed during the 1st trimester, patients should be treated promptly similar to non-pregnant patients.
  • When the diagnosis is made later in pregnancy standard chemotherapy regimen should be considered and usually pregnancy termination is not mandatory.
  • Pregnancy associated chronic myelogenous leukemia (CML) can be treated with interferon throughout pregnancy with no apparent increase in adverse fetal outcome.
  • In the very rare case of chronic lymphocytic leukemia (CLL) during pregnancy treatment can usually be delayed until after delivery.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia / drug therapy. Pregnancy Complications, Neoplastic / drug therapy. Prenatal Exposure Delayed Effects


29. Yu Q, Sharma A, Sen JM: TCF1 and beta-catenin regulate T cell development and function. Immunol Res; 2010 Jul;47(1-3):45-55
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  • [Title] TCF1 and beta-catenin regulate T cell development and function.
  • T cell factor-1 (TCF1) critically regulates T cell development.
  • We have genetically manipulated the beta-catenin gene and generated mutant mice that have shown an essential role for beta-catenin and TCF1 during pre-T cell receptor (TCR) and TCR-dependent stages of T cell development.
  • [MeSH-major] Cell Differentiation. Gene Expression Regulation. T Cell Transcription Factor 1 / metabolism. T-Lymphocytes / cytology. T-Lymphocytes / immunology. beta Catenin / metabolism
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Humans. Mice. Receptors, Antigen, T-Cell / genetics. Receptors, Antigen, T-Cell / metabolism. Signal Transduction

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  • [Cites] Nat Med. 2009 Jul;15(7):808-13 [19525962.001]
  • [Cites] Nat Immunol. 2009 Sep;10(9):992-9 [19648923.001]
  • [Cites] J Immunol. 2009 Sep 15;183(6):3873-84 [19717519.001]
  • [Cites] Cell. 1994 Jan 28;76(2):229-39 [8293461.001]
  • [Cites] Genes Dev. 2000 Jul 15;14(14):1693-711 [10898785.001]
  • [Cites] Genes Dev. 2000 Aug 1;14(15):1837-51 [10921899.001]
  • [Cites] Eur J Immunol. 2001 Jan;31(1):285-93 [11265645.001]
  • [Cites] Nat Immunol. 2001 Aug;2(8):691-7 [11477404.001]
  • [Cites] Nat Immunol. 2001 Sep;2(9):863-9 [11526403.001]
  • [Cites] Eur J Immunol. 2002 Apr;32(4):967-71 [11920562.001]
  • [Cites] J Immunol. 2002 May 1;168(9):4268-71 [11970965.001]
  • [Cites] Nat Rev Immunol. 2002 May;2(5):309-22 [12033737.001]
  • [Cites] Mol Cell. 2002 Sep;10(3):563-71 [12408824.001]
  • [Cites] Mol Cell. 2002 Sep;10(3):573-84 [12408825.001]
  • [Cites] Nat Rev Immunol. 2002 Dec;2(12):933-44 [12461566.001]
  • [Cites] J Exp Med. 2003 Feb 17;197(4):475-87 [12591905.001]
  • [Cites] Eur J Immunol. 2003 Jan;33(1):12-8 [12594827.001]
  • [Cites] Annu Rev Immunol. 2003;21:139-76 [12414722.001]
  • [Cites] Nat Immunol. 2003 Dec;4(12):1177-82 [14608382.001]
  • [Cites] Int Immunol. 2003 Dec;15(12):1485-94 [14645157.001]
  • [Cites] J Exp Med. 2004 Jan 19;199(2):221-9 [14718516.001]
  • [Cites] Am J Physiol Cell Physiol. 2004 Apr;286(4):C747-56 [14613891.001]
  • [Cites] Nat Rev Immunol. 2004 Jul;4(7):529-40 [15229472.001]
  • [Cites] EMBO J. 1991 Jan;10(1):123-32 [1989880.001]
  • [Cites] J Exp Med. 1994 Apr 1;179(4):1349-53 [8145047.001]
  • [Cites] J Immunol. 1994 Jul 1;153(1):53-62 [8207255.001]
  • [Cites] Immunol Today. 1994 Aug;15(8):362-6 [7916949.001]
  • [Cites] Nature. 1995 Mar 2;374(6517):70-4 [7870176.001]
  • [Cites] Annu Rev Immunol. 1995;13:93-126 [7612239.001]
  • [Cites] Curr Opin Immunol. 1995 Apr;7(2):188-95 [7546378.001]
  • [Cites] Immunity. 1998 Jan;8(1):11-20 [9462507.001]
  • [Cites] Mol Cell Biol. 1998 Jun;18(6):3495-501 [9584189.001]
  • [Cites] J Immunol. 1998 Oct 15;161(8):3984-91 [9780167.001]
  • [Cites] Nature. 1998 Oct 8;395(6702):608-12 [9783587.001]
  • [Cites] Curr Opin Genet Dev. 1999 Feb;9(1):15-21 [10072352.001]
  • [Cites] Int Immunol. 1999 Mar;11(3):317-23 [10221643.001]
  • [Cites] Mol Cell Biol. 1999 Jun;19(6):4503-15 [10330189.001]
  • [Cites] Nat Immunol. 2005 Aug;6(8):800-9 [16025118.001]
  • [Cites] J Immunol. 2005 Dec 15;175(12):7981-8 [16339534.001]
  • [Cites] Immunol Rev. 2006 Feb;209:159-69 [16448541.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3322-6 [16492759.001]
  • [Cites] Annu Rev Immunol. 2006;24:607-56 [16551261.001]
  • [Cites] J Immunol. 2006 Apr 15;176(8):4880-7 [16585583.001]
  • [Cites] Nature. 2006 May 11;441(7090):235-8 [16648838.001]
  • [Cites] Immunol Res. 2006;34(2):117-32 [16760572.001]
  • [Cites] Scand J Immunol. 2006 Aug;64(2):93-6 [16867153.001]
  • [Cites] Eur J Immunol. 2006 Sep;36(9):2376-83 [16897815.001]
  • [Cites] Immunity. 2007 Feb;26(2):227-39 [17306568.001]
  • [Cites] J Immunol. 2007 Apr 15;178(8):5028-34 [17404285.001]
  • [Cites] Curr Opin Immunol. 2007 Jun;19(3):281-6 [17433650.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5463-72 [17317856.001]
  • [Cites] J Immunol. 2007 Jul 1;179(1):126-31 [17579030.001]
  • [Cites] Cancer Cell. 2007 Dec;12(6):528-41 [18068630.001]
  • [Cites] Cell. 2007 Dec 14;131(6):1204 [18083108.001]
  • [Cites] Blood. 2008 Jan 1;111(1):160-4 [17855627.001]
  • [Cites] Blood. 2008 Jan 1;111(1):142-9 [17906078.001]
  • [Cites] Nat Med. 2008 Feb;14(2):162-9 [18246080.001]
  • [Cites] Mol Cell Biol. 2008 Mar;28(5):1713-23 [18160717.001]
  • [Cites] Immunity. 2008 Apr;28(4):445-53 [18400187.001]
  • [Cites] Int Immunol. 2008 Jul;20(7):925-35 [18511409.001]
  • [Cites] Nat Rev Immunol. 2008 Aug;8(8):581-93 [18617885.001]
  • [Cites] Nat Rev Immunol. 2008 Oct;8(10):788-801 [18802443.001]
  • [Cites] J Immunol. 2009 Jan 15;182(2):751-8 [19124717.001]
  • [Cites] J Immunol. 2009 Jan 15;182(2):759-65 [19124718.001]
  • [Cites] Blood. 2009 Jan 15;113(3):546-54 [18832654.001]
  • [Cites] Curr Opin Immunol. 2009 Jun;21(3):274-80 [19524429.001]
  • (PMID = 20082155.001).
  • [ISSN] 1559-0755
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 AG000768-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell; 0 / T Cell Transcription Factor 1; 0 / beta Catenin
  • [Other-IDs] NLM/ NIHMS172600; NLM/ PMC2891409
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30. Hwang C, Jang S, Choi DK, Kim S, Lee JH, Lee Y, Kim CD, Lee JH: The role of nkx2.5 in keratinocyte differentiation. Ann Dermatol; 2009 Nov;21(4):376-81
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  • BACKGROUND: Nkx2.5 is a homeodomain-containing nuclear transcription protein that has been associated with acute T-lymphoblastic leukemia.
  • In addition, the expression of Nkx2.5 was significantly increased in psoriasis and squamous cell carcinoma, but was barely detected in atopic dermatitis and basal cell carcinoma.
  • CONCLUSION: These results suggest that Nkx2.5 may play a role in the change from proliferation to differentiation of keratinocytes and in the pathogenesis of skin disease with aberrant keratinocyte differentiation.

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  • [Cites] Exp Mol Med. 1999 Mar 31;31(1):5-19 [10231017.001]
  • [Cites] J Cell Sci Suppl. 1993;17:197-208 [7511614.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5329-34 [14500364.001]
  • [Cites] J Am Coll Cardiol. 2003 Nov 5;42(9):1650-5 [14607454.001]
  • [Cites] Mol Cell Biol. 2003 Dec;23(24):9222-32 [14645532.001]
  • [Cites] Gene Expr Patterns. 2004 Nov;5(1):129-34 [15533828.001]
  • [Cites] Pharmacol Ther. 2005 Aug;107(2):252-68 [15925411.001]
  • [Cites] Haematologica. 2006 Mar;91(3):317-21 [16531254.001]
  • [Cites] J Rheumatol. 2006 Nov;33(11):2167-72 [16981296.001]
  • [Cites] Arch Med Res. 2007 Jan;38(1):64-9 [17174725.001]
  • [Cites] Br J Dermatol. 2007 Feb;156(2):271-6 [17223866.001]
  • [Cites] Cell. 1977 Jun;11(2):417-22 [890737.001]
  • [Cites] PLoS One. 2008;3(6):e2301 [18523683.001]
  • [Cites] J Biol Chem. 1995 Jul 28;270(30):17702-11 [7543090.001]
  • [Cites] Dev Biol. 1996 Sep 15;178(2):203-16 [8812123.001]
  • [Cites] J Biol Chem. 1997 Jan 17;272(3):2021-30 [8999895.001]
  • [Cites] Cancer Res. 2007 Feb 15;67(4):1461-71 [17308084.001]
  • [Cites] J Am Acad Dermatol. 2007 Aug;57(2):347-54 [17433490.001]
  • [Cites] Bioessays. 2002 Sep;24(9):789-800 [12210515.001]
  • (PMID = 20523827.001).
  • [ISSN] 2005-3894
  • [Journal-full-title] Annals of dermatology
  • [ISO-abbreviation] Ann Dermatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2861273
  • [Keywords] NOTNLM ; Keratinocyte differentiation / Nkx2.5 / Transcription factor
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31. Chen W, Wang E, Lu Y, Gaal KK, Huang Q: Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review. Am J Clin Pathol; 2010 Jan;133(1):75-82
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  • [Title] Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review.
  • Therapy-related acute lymphoblastic leukemia (t-ALL) is a rare secondary leukemia following chemotherapy and/or radiotherapy for primary malignancies.
  • Chromosomal 11q23 abnormality, frequently detected in therapy-related acute myeloid leukemia, is the most common cytogenetic alteration in t-ALL.
  • However, t-ALL cases without 11q23 abnormality have been rarely described.
  • In the 48 cases, an 11q23 abnormality involving the MLL gene locus was the predominant chromosomal aberration (32 [67%]), followed by t(9;22) (6 [13%]) and a normal karyotype (4 [8%]).
  • Compared with t-ALL cases with an 11q23 abnormality, cases without an 11q23 abnormality had a relatively longer latency period (median, 36 vs 19 months) and a different primary malignancy spectrum.
  • The t(8;14)(q11.2;q32), a rare, nonrandom, balanced chromosomal translocation differing from the more common translocation involving c-MYC on chromosome 8q24, was seen in 1 adult t-ALL case, which may suggest another possible pathogenesis of this disease.
  • [MeSH-major] Chromosomes, Human, Pair 11. Combined Modality Therapy / adverse effects. Neoplasms / therapy. Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • (PMID = 20023261.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 42
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32. Brewer JL, Ericson SG: An improved methodology to detect human T cell receptor beta variable family gene expression patterns. J Immunol Methods; 2005 Jul;302(1-2):54-67
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  • [Title] An improved methodology to detect human T cell receptor beta variable family gene expression patterns.
  • Comprehensive gene expression analysis of the T cell receptor repertoire of an individual can be very useful in evaluating the immune response in a variety of conditions.
  • Antibody-based analysis methods can detect approximately 60% of the human T cell receptor beta variable (TCRBV) proteins, while gene expression analysis, primarily through employment of the polymerase chain reaction (PCR), has had somewhat greater success in the detection of additional TCRBV families.
  • We describe here a real-time reverse transcription polymerase chain reaction-based method, which allows efficient automation and integration of amplification, detection, and analysis with sequence-specific detection of all T cell receptor beta variable gene families, subfamilies, and alleles.
  • [MeSH-major] Gene Expression Profiling / methods. Multigene Family. Receptors, Antigen, T-Cell, alpha-beta / biosynthesis. Receptors, Antigen, T-Cell, alpha-beta / genetics
  • [MeSH-minor] DNA Primers. Fluorometry / methods. Genetic Variation. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / metabolism. Humans. Polymerase Chain Reaction / methods. RNA, Messenger / biosynthesis

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  • (PMID = 16038929.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 5 P20 RR16440-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / Receptors, Antigen, T-Cell, alpha-beta
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33. Yu C, Friday BB, Lai JP, Yang L, Sarkaria J, Kay NE, Carter CA, Roberts LR, Kaufmann SH, Adjei AA: Cytotoxic synergy between the multikinase inhibitor sorafenib and the proteasome inhibitor bortezomib in vitro: induction of apoptosis through Akt and c-Jun NH2-terminal kinase pathways. Mol Cancer Ther; 2006 Sep;5(9):2378-87
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  • Multiple tumor cell lines of varying histiotypes, including A549 (lung adenocarcinoma), 786-O (renal cell carcinoma), HeLa (cervical carcinoma), MDA-MB-231 (breast), K562 (chronic myelogenous leukemia), Jurkat (acute T-cell leukemia), MEC-2 (B-chronic lymphocytic leukemia), and U251 and D37 (glioma), as well as cells derived from primary human glioma tumors that are likely a more clinically relevant model were treated with sorafenib or bortezomib alone or in combination.
  • Sorafenib and bortezomib synergistically induced a marked increase in mitochondrial injury and apoptosis, reflected by cytochrome c release, caspase-3 cleavage, and poly(ADP-ribose) polymerase degradation in a broad range of solid tumor and leukemia cell lines.
  • These findings were accompanied by several biochemical changes, including decreased phosphorylation of vascular endothelial growth factor receptor-2, platelet-derived growth factor receptor-beta, and Akt and increased phosphorylation of stress-related c-Jun NH2-terminal kinase (JNK).
  • These findings show that sorafenib interacts synergistically with bortezomib to induce apoptosis in a broad spectrum of neoplastic cell lines and show an important role for the Akt and JNK pathways in mediating synergism.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Bortezomib. Cell Line, Tumor. Drug Synergism. Humans. Jurkat Cells. K562 Cells. MAP Kinase Signaling System / drug effects. Niacinamide / analogs & derivatives. Phenylurea Compounds. Proteasome Endopeptidase Complex / metabolism

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  • (PMID = 16985072.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Boronic Acids; 0 / Phenylurea Compounds; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 69G8BD63PP / Bortezomib; 9ZOQ3TZI87 / sorafenib; EC 2.7.11.1 / Oncogene Protein v-akt; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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34. Geurts JJ, Blezer EL, Vrenken H, van der Toorn A, Castelijns JA, Polman CH, Pouwels PJ, Bö L, Barkhof F: Does high-field MR imaging improve cortical lesion detection in multiple sclerosis? J Neurol; 2008 Feb;255(2):183-91
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  • [Title] Does high-field MR imaging improve cortical lesion detection in multiple sclerosis?
  • OBJECTIVE: Cortical lesions in multiple sclerosis (MS) are notoriously difficult to visualize with standard MR imaging (MRI) techniques.
  • However, the use of higher field-strengths with intrinsically higher signal-to-noise, which can partly be used to increase spatial resolution, may improve cortical lesion detection.
  • Therefore, in this post mortem study, the sensitivity of high field-strength MRI (4.7 T) for cortical lesions was investigated, and compared to that of standard field-strength (1.5 T).
  • Proteolipid protein (PLP)-stained tissue sections (10 microm) of the same brain slices were matched to the corresponding MR images, and cortical lesions were scored on all three MR sequences (blinded to histology) and in tissue sections (blinded to MRI).
  • Sensitivity of the sequences for four cortical lesion types was calculated.
  • RESULTS: Sensitivity for purely intracortical lesions (histological lesion types II, III, and IV; n = 128) was below 10 % for both 1.5 T and 4.7 T MRI, while mixed gray matter-white matter (type I) lesions (n = 5) were detected in four out of five cases.
  • CONCLUSIONS: MRI sensitivity for post mortem detection of cortical lesions is low, even when a higher field-strength was used.
  • It varies, however, for different subtypes of cortical lesions.

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  • [Cites] Brain. 2004 May;127(Pt 5):1101-7 [14998914.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 1962 Nov;25:315-20 [14016083.001]
  • [Cites] Neurology. 2003 Apr 8;60(7):1157-62 [12682324.001]
  • [Cites] Ital J Neurol Sci. 1992 Dec;13(9 Suppl 14):97-103 [1345748.001]
  • [Cites] Arch Neurol. 2007 Jan;64(1):76-80 [17210812.001]
  • [Cites] Neurology. 2004 Feb 24;62(4):586-90 [14981175.001]
  • [Cites] Mult Scler. 2003 Aug;9(4):323-31 [12926836.001]
  • [Cites] Ann Neurol. 2001 Jul;50(1):121-7 [11456302.001]
  • [Cites] Brain. 2001 Aug;124(Pt 8):1635-45 [11459754.001]
  • [Cites] Neuropathol Appl Neurobiol. 2004 Apr;30(2):106-17 [15043708.001]
  • [Cites] J Neurol Sci. 1987 Oct;81(1):67-77 [3681342.001]
  • [Cites] AJNR Am J Neuroradiol. 2005 Mar;26(3):572-7 [15760868.001]
  • [Cites] AJNR Am J Neuroradiol. 1999 Nov-Dec;20(10):1956-62 [10588125.001]
  • [Cites] Ann Neurol. 2001 Sep;50(3):389-400 [11558796.001]
  • [Cites] Mult Scler. 2000 Aug;6(4):280-5 [10962549.001]
  • [Cites] Brain. 2005 Nov;128(Pt 11):2705-12 [16230320.001]
  • [Cites] Neurology. 2006 Sep 26;67(6):960-7 [17000961.001]
  • [Cites] Acta Radiol. 1999 Nov;40(6):593-7 [10598845.001]
  • [Cites] Epilepsia. 2001 Jan;42(1):72-9 [11207788.001]
  • [Cites] J Neuropathol Exp Neurol. 2005 Dec;64(12):1101-7 [16319720.001]
  • [Cites] J Neuropathol Exp Neurol. 2005 Feb;64(2):147-55 [15751229.001]
  • [Cites] AJNR Am J Neuroradiol. 2001 Mar;22(3):470-5 [11237968.001]
  • [Cites] Curr Opin Neurol. 2002 Jun;15(3):239-45 [12045719.001]
  • [Cites] Med Phys. 1985 Mar-Apr;12(2):232-3 [4000083.001]
  • [Cites] J Neuropathol Exp Neurol. 2003 Jul;62(7):723-32 [12901699.001]
  • [Cites] AJNR Am J Neuroradiol. 2002 Jun-Jul;23(6):985-8 [12063230.001]
  • [Cites] AJNR Am J Neuroradiol. 2000 Feb;21(2):402-8 [10696031.001]
  • [Cites] Radiology. 2005 Jul;236(1):254-60 [15987979.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2004 Jul;75(7):998-1002 [15201359.001]
  • [Cites] Ann Neurol. 2004 Sep;56(3):407-15 [15349868.001]
  • [Cites] Neurobiol Dis. 2005 Dec;20(3):953-60 [16039866.001]
  • [Cites] AJNR Am J Neuroradiol. 2005 Aug;26(7):1824-31 [16091537.001]
  • [Cites] Acta Neurol Scand Suppl. 2006;183:48-50 [16637929.001]
  • [Cites] J Magn Reson Imaging. 2006 May;23(5):628-36 [16565955.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2001 Mar;70(3):311-7 [11181851.001]
  • [Cites] Brain. 1997 Nov;120 ( Pt 11):2059-69 [9397021.001]
  • (PMID = 18231704.001).
  • [ISSN] 0340-5354
  • [Journal-full-title] Journal of neurology
  • [ISO-abbreviation] J. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fixatives; 1HG84L3525 / Formaldehyde
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35. Hurren R, Beheshti Zavareh R, Dalili S, Wood T, Rose D, Chang H, Jamal N, Messner H, Batey RA, Schimmer AD: A novel diquinolonium displays preclinical anti-cancer activity and induces caspase-independent cell death. Apoptosis; 2008 Jun;13(6):748-55
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  • [Title] A novel diquinolonium displays preclinical anti-cancer activity and induces caspase-independent cell death.
  • Q(2 )induced cell death in leukemia, myeloma, and solid tumor cell lines with LD50s in the low to submicromolar range.
  • Moreover, Q(2) induced cell death in primary acute myeloid leukemia (AML) cells preferentially over normal hematopoietic cells.
  • In a mouse model of leukemia, Q(2) delayed tumor growth.
  • Mechanistically, Q(2) induced cell death through caspase independent mechanisms.
  • Potentially consistent with the induction of autophagic cell death, Q(2) treatment led to a punctate distribution of LC3 and increased MDC staining.
  • Thus, Q(2) is a novel quinolinium with preclinical activity in malignancies such as leukemia and myeloma and warrants further investigation.
  • [MeSH-major] Cell Death / drug effects. Quinolinium Compounds / pharmacology
  • [MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Animals. Autophagy / drug effects. Caspases / physiology. Cell Line, Tumor. Cell Survival / drug effects. HeLa Cells. Humans. Jurkat Cells. Lethal Dose 50. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Mice. Mice, Inbred DBA. Tumor Cells, Cultured. U937 Cells

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  • (PMID = 18415680.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-methyl-2-(3-(1-methyl-1,2-dihydroquinolin-2-yliden)prop-1-enyl)quinolinium iodide; 0 / Amino Acid Chloromethyl Ketones; 0 / Quinolinium Compounds; 0 / benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone; EC 3.4.22.- / Caspases
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36. Ismailoglu I, Yeamans G, Daley GQ, Perlingeiro RC, Kyba M: Mesodermal patterning activity of SCL. Exp Hematol; 2008 Dec;36(12):1593-603
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  • Consistent with this, the early pulse of SCL expression also expanded hematopoietic colony-forming cell numbers, while concomitantly repressing expression of paraxial and cardiac markers, and inhibited development of beating cardiomyocytes.
  • By mixing the inducible embryonic stem cells with fluorescently labeled wild-type cells in chimeric embryoid bodies, we show that these effects of SCL are cell autonomous.
  • [MeSH-minor] Animals. Antigens, Differentiation / biosynthesis. Antigens, Differentiation / genetics. Cell Line. Colony-Forming Units Assay. Endothelium, Vascular / cytology. Endothelium, Vascular / embryology. Mice. Myocytes, Cardiac / cytology. Myocytes, Cardiac / metabolism. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor alpha / metabolism. Time Factors. Transgenes / physiology. Vascular Endothelial Growth Factor Receptor-2 / genetics. Vascular Endothelial Growth Factor Receptor-2 / metabolism

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  • (PMID = 18809240.001).
  • [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 / Antigens, Differentiation; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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37. Ghinassi B, Verrucci M, Jelicic K, Di Noia A, Migliaccio G, Migliaccio AR: Interleukin-3 and erythropoietin cooperate in the regulation of the expression of erythroid-specific transcription factors during erythroid differentiation. Exp Hematol; 2007 May;35(5):735-47
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  • OBJECTIVE: To characterize how interleukin-3 and erythropoietin regulate cell fate by modulating the expression of lineage-specific transcription factors.
  • METHODS: This study analyzed mRNA and protein levels, gene transcription rates, and mRNA and protein stabilities of erythroid-specific transcription factors in lineage-restricted cells derived from the 32D cell line cultured either in interleukin-3 or erythropoietin.
  • Switching the erythroid cells to erythropoietin induced cell maturation (within 48 hours) and reduced expression of Gata-2 and Idl (in 24 hours) but did not alter the expression of Gata-1.
  • [MeSH-minor] Animals. Cell Differentiation / drug effects. Cell Differentiation / genetics. Cell Line. Gene Expression Profiling. Mice. Phenotype. RNA, Messenger / drug effects. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Structure-Activity Relationship. T-Cell Acute Lymphocytic Leukemia Protein 1. Time Factors

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  • (PMID = 17577923.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01-CA108671-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Erythroid-Specific DNA-Binding Factors; 0 / Idb1 protein, mouse; 0 / Inhibitor of Differentiation Protein 1; 0 / Interleukin-3; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / T-Cell Acute Lymphocytic Leukemia Protein 1; 0 / Tal1 protein, mouse; 11096-26-7 / Erythropoietin
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38. Tosello V, Mansour MR, Barnes K, Paganin M, Sulis ML, Jenkinson S, Allen CG, Gale RE, Linch DC, Palomero T, Real P, Murty V, Yao X, Richards SM, Goldstone A, Rowe J, Basso G, Wiernik PH, Paietta E, Pieters R, Horstmann M, Meijerink JP, Ferrando AA: WT1 mutations in T-ALL. Blood; 2009 Jul 30;114(5):1038-45
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  • The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.
  • This analysis showed that diagnosis and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at diagnosis, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at diagnosis.
  • [MeSH-major] Genes, Wilms Tumor. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Child. Chromosome Aberrations. Clone Cells / chemistry. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Genes, Homeobox. Humans. Kaplan-Meier Estimate. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Oncogenes. Polymorphism, Single Nucleotide. Prognosis. Recurrence. WT1 Proteins / chemistry. WT1 Proteins / genetics. Zinc Fingers / genetics

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  • [Cites] Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):6010-4 [1321431.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Hum Mol Genet. 1993 Mar;2(3):259-64 [8388765.001]
  • [Cites] Blood. 1994 May 15;83(10):2922-30 [8180387.001]
  • [Cites] Hum Mol Genet. 1995 Mar;4(3):351-8 [7795587.001]
  • [Cites] Blood. 1996 Mar 15;87(6):2171-9 [8630376.001]
  • [Cites] Hum Mutat. 1997;9(3):209-25 [9090524.001]
  • [Cites] Nucleic Acids Res. 1997 Jun 15;25(12):2532-4 [9171110.001]
  • [Cites] Eur J Haematol. 1997 May;58(5):346-9 [9222290.001]
  • [Cites] Blood. 1998 Apr 15;91(8):2961-8 [9531607.001]
  • [Cites] Kidney Int. 1998 Jun;53(6):1512-8 [9607183.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Pediatr Blood Cancer. 2006 Jan;46(1):18-25 [15929133.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Haematologica. 2006 Sep;91(9):1212-21 [16956820.001]
  • [Cites] Leukemia. 2007 Mar;21(3):550-1; author reply 552 [17205055.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Nat Genet. 2007 May;39(5):593-5 [17435759.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1258-66 [17443227.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9006-12 [17909001.001]
  • [Cites] Oncogene. 2007 Oct 15;26(47):6838-49 [17934490.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):6964-9 [18056171.001]
  • [Cites] J Exp Med. 2007 Dec 24;204(13):3059-66 [18070937.001]
  • [Cites] Leukemia. 2008 Jan;22(1):124-31 [17928886.001]
  • [Cites] Nat Rev Cancer. 2008 Feb;8(2):83-93 [18094723.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] Leukemia. 2008 Apr;22(4):762-70 [18185524.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):380-90 [18421304.001]
  • [Cites] Blood. 2008 May 1;111(9):4668-80 [18299449.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 May 6;105(18):6708-13 [18458336.001]
  • [Cites] Blood. 2008 Aug 1;112(3):733-40 [18411416.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]
  • [Cites] J Clin Oncol. 2008 Nov 20;26(33):5429-35 [18591546.001]
  • [Cites] Science. 2008 Nov 28;322(5906):1377-80 [19039135.001]
  • [Cites] Semin Hematol. 2000 Oct;37(4):381-95 [11071360.001]
  • [Cites] Genome Biol. 2001;2(8):RESEARCH0032 [11532216.001]
  • [Cites] Leukemia. 2001 Oct;15(10):1495-504 [11587205.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Oct;23(7):416-9 [11878574.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Nat Genet. 2004 Oct;36(10):1084-9 [15361874.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Clin Nephrol. 1985 Dec;24(6):269-78 [3000666.001]
  • [Cites] Genomics. 1989 Nov;5(4):685-93 [2556343.001]
  • [Cites] Cell. 1990 Jun 29;61(7):1257-69 [2163761.001]
  • [Cites] FEBS Lett. 1993 Feb 8;317(1-2):39-43 [8381368.001]
  • (PMID = 19494353.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE15931
  • [Grant] United States / NCI NIH HHS / CA / CA114737; United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA120196-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC2721784
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39. Romana SP, Radford-Weiss I, Ben Abdelali R, Schluth C, Petit A, Dastugue N, Talmant P, Bilhou-Nabera C, Mugneret F, Lafage-Pochitaloff M, Mozziconacci MJ, Andrieu J, Lai JL, Terre C, Rack K, Cornillet-Lefebvre P, Luquet I, Nadal N, Nguyen-Khac F, Perot C, Van den Akker J, Fert-Ferrer S, Cabrol C, Charrin C, Tigaud I, Poirel H, Vekemans M, Bernard OA, Berger R, Groupe Francophone de Cytogénétique Hématologique: NUP98 rearrangements in hematopoietic malignancies: a study of the Groupe Francophone de Cytogénétique Hématologique. Leukemia; 2006 Apr;20(4):696-706
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  • [Title] NUP98 rearrangements in hematopoietic malignancies: a study of the Groupe Francophone de Cytogénétique Hématologique.
  • In order to gain additional clinico-hematological data and to identify new partners of NUP98, the Groupe Francophone de Cytogénétique Hématologique (GFCH) collected cases of hematological malignancies where a 11p15 rearrangement was detected.
  • Genes of the HOXA cluster and the nuclear-receptor set domain (NSD) genes were frequently fused to NUP98, mainly in de novo myeloid malignancies whereas the DDX10 and TOP1 genes were equally rearranged in de novo and in therapy-related myeloid proliferations.
  • Involvement of ADD3 and C6ORF80 genes were detected, respectively, in myeloid disorders and in T-cell acute lymphoblastic leukemia (T-ALL), whereas the RAP1GDS1 gene was fused to NUP98 in T-ALL.

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  • (PMID = 16467868.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Receptors, Cytoplasmic and Nuclear; 157907-48-7 / HoxA protein
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40. Jagani Z, Song K, Kutok JL, Dewar MR, Melet A, Santos T, Grassian A, Ghaffari S, Wu C, Yeckes-Rodin H, Ren R, Miller K, Khosravi-Far R: Proteasome inhibition causes regression of leukemia and abrogates BCR-ABL-induced evasion of apoptosis in part through regulation of forkhead tumor suppressors. Cancer Res; 2009 Aug 15;69(16):6546-55
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  • [Title] Proteasome inhibition causes regression of leukemia and abrogates BCR-ABL-induced evasion of apoptosis in part through regulation of forkhead tumor suppressors.
  • BCR-ABL plays an essential role in the pathogenesis of chronic myeloid leukemia (CML) and some cases of acute lymphocytic leukemia (ALL).
  • Although ABL kinase inhibitors have shown great promise in the treatment of CML, the persistence of residual disease and the occurrence of resistance have prompted investigations into the molecular effectors of BCR-ABL.
  • As several downstream mediators of BCR-ABL are regulated by the proteasome degradation pathway, we also show that inhibition of this pathway, using bortezomib, causes regression of CML-like disease.
  • Our data delineate the involvement of FoxO proteins in BCR-ABL-induced evasion of apoptosis and provide evidence that bortezomib is a candidate therapeutic in the treatment of BCR-ABL-induced leukemia.

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  • [Cites] EMBO J. 1997 Oct 15;16(20):6151-61 [9321394.001]
  • [Cites] Blood. 1995 Jul 15;86(2):726-36 [7606002.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3829-40 [9808576.001]
  • [Cites] Cell. 1999 Mar 19;96(6):857-68 [10102273.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7421-6 [10377430.001]
  • [Cites] Haematologica. 2004 Dec;89(12):1428-33 [15590391.001]
  • [Cites] J Clin Oncol. 2005 Jan 20;23(3):630-9 [15659509.001]
  • [Cites] Cancer Cell. 2005 Feb;7(2):129-41 [15710326.001]
  • [Cites] Nat Rev Cancer. 2005 Mar;5(3):172-83 [15719031.001]
  • [Cites] Cancer Cell. 2005 Mar;7(3):227-38 [15766661.001]
  • [Cites] Oncogene. 2005 Mar 31;24(14):2317-29 [15688014.001]
  • [Cites] Mol Cancer Ther. 2005 Apr;4(4):686-92 [15827343.001]
  • [Cites] Blood. 2005 May 15;105(10):4021-7 [15665113.001]
  • [Cites] J Immunol. 2006 Apr 15;176(8):4757-65 [16585569.001]
  • [Cites] J Immunol. 2006 May 15;176(10):6302-12 [16670342.001]
  • [Cites] Blood. 2006 May 15;107(10):4063-70 [16424391.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6304-11 [16778207.001]
  • [Cites] Cell. 2007 Jan 26;128(2):309-23 [17254969.001]
  • [Cites] Cell. 2007 Jan 26;128(2):325-39 [17254970.001]
  • [Cites] Nat Rev Cancer. 2007 May;7(5):345-56 [17457302.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Jun;8(6):440-50 [17522590.001]
  • [Cites] Blood. 2007 Jul 1;110(1):345-53 [17374740.001]
  • [Cites] Curr Oncol Rep. 2007 Sep;9(5):391-8 [17706168.001]
  • [Cites] Oncology (Williston Park). 2007 Jun;21(7):785-92; discussion 798-800 [17722741.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2562-9 [17710227.001]
  • [Cites] Acta Physiol (Oxf). 2008 Jan;192(1):19-28 [18171426.001]
  • [Cites] Expert Opin Investig Drugs. 2008 Jun;17(6):865-78 [18491988.001]
  • [Cites] Blood. 1997 Dec 15;90(12):4947-52 [9389713.001]
  • [Cites] Mol Cell Biol. 2000 Feb;20(4):1179-86 [10648603.001]
  • [Cites] Curr Biol. 2000 Oct 5;10(19):1201-4 [11050388.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3343-56 [11071626.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] Curr Oncol Rep. 2001 May;3(3):228-37 [11296133.001]
  • [Cites] Science. 2001 Aug 3;293(5531):876-80 [11423618.001]
  • [Cites] Blood. 2001 Nov 15;98(10):2948-57 [11698276.001]
  • [Cites] Semin Oncol. 2001 Dec;28(6):613-9 [11740819.001]
  • [Cites] Trends Mol Med. 2002;8(4 Suppl):S49-54 [11927288.001]
  • [Cites] Cancer Cell. 2002 Aug;2(2):117-25 [12204532.001]
  • [Cites] J Biol Chem. 2002 Dec 6;277(49):47928-37 [12351634.001]
  • [Cites] J Biol Chem. 2003 Apr 4;278(14):12361-6 [12517744.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 May 27;100(11):6523-8 [12750477.001]
  • [Cites] J Cell Biol. 2003 Aug 18;162(4):613-22 [12913110.001]
  • [Cites] J Biol Chem. 2003 Sep 19;278(38):35959-67 [12857750.001]
  • [Cites] Leuk Res. 2004 May;28 Suppl 1:S21-8 [15036938.001]
  • [Cites] Cell. 2004 Apr 16;117(2):225-37 [15084260.001]
  • [Cites] Oncogene. 2004 Apr 22;23(19):3338-49 [14981546.001]
  • [Cites] Blood. 2004 Jun 15;103(12):4622-9 [14962911.001]
  • [Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]
  • [Cites] Science. 1990 Feb 16;247(4944):824-30 [2406902.001]
  • [Cites] Mol Cell Biol. 1991 Feb;11(2):1107-13 [1846663.001]
  • [ErratumIn] Cancer Res. 2009 Sep 1;69(17):7130. Rodin, Heather Yeckes [corrected to Yeckes-Rodin, Heather]
  • (PMID = 19654305.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL080192-05; United States / NHLBI NIH HHS / HL / HL080192; United States / NHLBI NIH HHS / HL / R01 HL080192; United States / NCI NIH HHS / CA / R01 CA131664; United States / NHLBI NIH HHS / HL / R01 HL080192-05; United States / NCI NIH HHS / CA / P30CA6516; United States / NCI NIH HHS / CA / R01 CA105306-05; United States / NCI NIH HHS / CA / R01 CA105306; United States / NCI NIH HHS / CA / CA105306; United States / NCI NIH HHS / CA / P30 CA006516; United States / NCI NIH HHS / CA / CA105306-05; United States / NCI NIH HHS / CA / CA131664
  • [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 / Antineoplastic Agents; 0 / Benzamides; 0 / Boronic Acids; 0 / Cysteine Proteinase Inhibitors; 0 / Forkhead Transcription Factors; 0 / Piperazines; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / Pyrimidines; 0 / Tumor Suppressor Proteins; 69G8BD63PP / Bortezomib; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Other-IDs] NLM/ NIHMS123965; NLM/ PMC2763358
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41. Bruenke J, Barbin K, Kunert S, Lang P, Pfeiffer M, Stieglmaier K, Niethammer D, Stockmeyer B, Peipp M, Repp R, Valerius T, Fey GH: Effective lysis of lymphoma cells with a stabilised bispecific single-chain Fv antibody against CD19 and FcgammaRIII (CD16). Br J Haematol; 2005 Jul;130(2):218-28
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  • [Title] Effective lysis of lymphoma cells with a stabilised bispecific single-chain Fv antibody against CD19 and FcgammaRIII (CD16).
  • A recombinant bispecific single-chain fragment variable antibody (bsscFv), directed against the B-cell antigen CD19 and the low affinity Fc-receptor FcgammaRIII (CD16), was designed for use in the treatment of patients with leukaemias and lymphomas.
  • In antibody-dependent cellular cytotoxicity experiments, ds[CD19 x CD16] mediated specific lysis of both CD19-positive malignant human B-lymphoid cell lines and primary tumour cells from patients with B-cell chronic lymphocytic leukaemia or B-cell acute lymphoblastic leukaemia.
  • Natural killer cells, mononuclear cells (MNCs) from healthy donors and, in some instances, MNCs isolated from patients after allogeneic stem cell transplantation, were used as effectors.
  • [MeSH-major] Antibodies, Bispecific / immunology. Antibody-Dependent Cell Cytotoxicity / immunology. Antigens, CD19 / immunology. Lymphoma, B-Cell / immunology. Receptors, IgG / immunology
  • [MeSH-minor] Antibody Specificity. Antigens, Neoplasm / immunology. Burkitt Lymphoma / immunology. Burkitt Lymphoma / pathology. Child. Dose-Response Relationship, Immunologic. Humans. Immunoglobulin Variable Region / immunology. Killer Cells, Natural / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Recombinant Fusion Proteins / immunology. Tumor Cells, Cultured

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  • (PMID = 16029450.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Bispecific; 0 / Antigens, CD19; 0 / Antigens, Neoplasm; 0 / Immunoglobulin Variable Region; 0 / Receptors, IgG; 0 / Recombinant Fusion Proteins
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42. Hagemeijer A, Graux C: ABL1 rearrangements in T-cell acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2010 Apr;49(4):299-308
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  • [Title] ABL1 rearrangements in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is the result of multiple oncogenic insults of thymocytes.
  • [MeSH-major] Gene Rearrangement. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-abl / genetics

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  • (PMID = 20073070.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
  • [Number-of-references] 60
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43. Nahimana A, Attinger A, Aubry D, Greaney P, Ireson C, Thougaard AV, Tjørnelund J, Dawson KM, Dupuis M, Duchosal MA: The NAD biosynthesis inhibitor APO866 has potent antitumor activity against hematologic malignancies. Blood; 2009 Apr 2;113(14):3276-86
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  • APO866 inhibits nicotinamide phosphoribosyltransferase (NMPRTase), a key enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis from the natural precursor nicotinamide.
  • Intracellular NAD is essential for cell survival, and NAD depletion resulting from APO866 treatment elicits tumor cell death.
  • Here, we determine the in vitro and in vivo sensitivities of hematologic cancer cells to APO866 using a panel of cell lines (n = 45) and primary cells (n = 32).
  • Most cancer cells (acute myeloid leukemia [AML], acute lymphoblastic leukemia [ALL], mantle cell lymphoma [MCL], chronic lymphocytic leukemia [CLL], and T-cell lymphoma), but not normal hematopoietic progenitor cells, were sensitive to low concentrations of APO866 as measured in cytotoxicity and clonogenic assays.
  • The NAD depletion led to cell death.
  • At 96 hours, APO866-mediated cell death occurred in a caspase-independent mode, and was associated with mitochondrial dysfunction and autophagy.
  • Further, in vivo administration of APO866 as a single agent prevented and abrogated tumor growth in animal models of human AML, lymphoblastic lymphoma, and leukemia without significant toxicity to the animals.
  • [MeSH-minor] Animals. Cell Death / drug effects. Dose-Response Relationship, Drug. HL-60 Cells. Humans. Jurkat Cells. K562 Cells. Mice. Mice, Inbred BALB C. Mice, Nude. Tumor Cells, Cultured. U937 Cells. Xenograft Model Antitumor Assays

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  • [CommentIn] Blood. 2009 Jun 4;113(23):6035-7; author reply 6037-8 [19498032.001]
  • (PMID = 19196867.001).
  • [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 / Acrylamides; 0 / Antineoplastic Agents; 0 / Cytokines; 0 / N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide; 0 / Piperidines; 0U46U6E8UK / NAD; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human
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44. Horino S, Rikiishi T, Niizuma H, Abe H, Watanabe Y, Onuma M, Hoshi Y, Sasahara Y, Yoshinari M, Kazama T, Hayashi Y, Kumaki S, Tsuchiya S: Refractory chronic immune thrombocytopenic purpura in a child with acute lymphoblastic leukemia. Int J Hematol; 2009 Nov;90(4):483-5
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  • [Title] Refractory chronic immune thrombocytopenic purpura in a child with acute lymphoblastic leukemia.
  • Immune thrombocytopenic purpura (ITP) has been associated with several hematologic malignancies such as Hodgkin and non-Hodgkin lymphomas and chronic lymphocytic leukemia, but it is rare in children with acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Purpura, Thrombocytopenic, Idiopathic / complications. Purpura, Thrombocytopenic, Idiopathic / surgery
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Chronic Disease. Female. Humans. Splenectomy. Treatment Outcome

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  • [Cites] Pediatr Blood Cancer. 2006 Mar;46(3):372-6 [15700256.001]
  • [Cites] J Pediatr. 1979 Mar;94(3):408-9 [284111.001]
  • [Cites] J Thromb Haemost. 2003 Jul;1(7):1587-92 [12871295.001]
  • [Cites] Am J Med. 2005 Sep;118(9):1026-33 [16164890.001]
  • [Cites] Eur J Haematol. 2007 Feb;78(2):139-43 [17328716.001]
  • [Cites] J Pediatr Hematol Oncol. 2005 Jul;27(7):397-9 [16012332.001]
  • [Cites] Cell. 2000 May 26;101(5):455-8 [10850488.001]
  • [Cites] Eur J Haematol. 1993 Oct;51(4):259-61 [7694874.001]
  • [Cites] Haematologica. 1998 Jul;83(7):669-70 [9718878.001]
  • [Cites] Eur J Immunol. 2004 Feb;34(2):336-44 [14768038.001]
  • [Cites] J Pediatr Hematol Oncol. 1998 Jan-Feb;20(1):44-8 [9482412.001]
  • [Cites] J Pediatr Hematol Oncol. 2006 Mar;28(3):170-2 [16679943.001]
  • [Cites] Br J Haematol. 1997 Mar;96(3):477-83 [9054651.001]
  • [Cites] Semin Oncol. 2006 Apr;33(2):230-9 [16616070.001]
  • [Cites] Neth J Med. 2006 Nov;64(10):356-63 [17122451.001]
  • [Cites] Pediatr Hematol Oncol. 2000 Dec;17(8):719-20 [11127406.001]
  • (PMID = 19816666.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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45. Chiarini F, Grimaldi C, Ricci F, Tazzari PL, Evangelisti C, Ognibene A, Battistelli M, Falcieri E, Melchionda F, Pession A, Pagliaro P, McCubrey JA, Martelli AM: Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia. Cancer Res; 2010 Oct 15;70(20):8097-107
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  • [Title] Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia.
  • Recent findings have highlighted that constitutively active phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling is a common feature of T-cell acute lymphoblastic leukemia (T-ALL), where it upregulates cell proliferation, survival, and drug resistance.
  • Here, we have analyzed the therapeutic potential of the novel dual PI3K/mTOR inhibitor NVP-BEZ235, an orally bioavailable imidazoquinoline derivative, which has entered clinical trials for solid tumors, on both T-ALL cell lines and patient samples.
  • NVP-BEZ235 was cytotoxic to a panel of T-ALL cell lines as determined by MTT assays.
  • NVP-BEZ235 treatment resulted in cell cycle arrest and apoptosis.
  • Remarkably, NVP-BEZ235 targeted the side population of both T-ALL cell lines and patient lymphoblasts, which might correspond to leukemia-initiating cells, and synergized with chemotherapeutic agents (cyclophosphamide, cytarabine, dexamethasone) currently used for treating T-ALL patients.
  • Taken together, our findings indicate that longitudinal inhibition at two nodes of the PI3K/Akt/mTOR network with NVP-BEZ235, either alone or in combination with chemotherapeutic drugs, may be an efficient treatment of those T-ALLs that have aberrant upregulation of this signaling pathway for their proliferation and survival.
  • [MeSH-major] Imidazoles / therapeutic use. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Quinolines / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Autophagy / drug effects. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Coculture Techniques. Flow Cytometry. Humans. Jurkat Cells / drug effects. Mice. Stromal Cells / drug effects


46. Chan WY, Follows GA, Lacaud G, Pimanda JE, Landry JR, Kinston S, Knezevic K, Piltz S, Donaldson IJ, Gambardella L, Sablitzky F, Green AR, Kouskoff V, Göttgens B: The paralogous hematopoietic regulators Lyl1 and Scl are coregulated by Ets and GATA factors, but Lyl1 cannot rescue the early Scl-/- phenotype. Blood; 2007 Mar 1;109(5):1908-16
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  • However, despite coregulation of Scl and Lyl1 by the same Ets and GATA factors, Scl expression was initiated prior to Lyl1 in embryonic stem (ES) cell differentiation assays.
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Cell Line. Conserved Sequence. Embryo, Mammalian / embryology. Embryo, Mammalian / metabolism. Endothelial Cells / metabolism. Gene Expression. Humans. Mice. Mice, Knockout. Molecular Sequence Data. Phenotype. Promoter Regions, Genetic / genetics. Sequence Alignment. Time Factors

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  • (PMID = 17053063.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / GATA2 Transcription Factor; 0 / Gata2 protein, mouse; 0 / Lyl1 protein, mouse; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Protein c-ets-1; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse
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47. De Keersmaecker K, Rocnik JL, Bernad R, Lee BH, Leeman D, Gielen O, Verachtert H, Folens C, Munck S, Marynen P, Fornerod M, Gilliland DG, Cools J: Kinase activation and transformation by NUP214-ABL1 is dependent on the context of the nuclear pore. Mol Cell; 2008 Jul 11;31(1):134-42
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  • We show that NUP214-ABL1 displays attenuated transforming capacity as compared to BCR-ABL1 and that NUP214-ABL1 preferentially transforms T cells, which is in agreement with its unique occurrence in T cell acute lymphoblastic leukemia.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Nuclear Pore / enzymology. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Animals. Cell Line. Enzyme Activation. Humans. Mice. Nuclear Pore Complex Proteins / metabolism

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  • (PMID = 18614052.001).
  • [ISSN] 1097-4164
  • [Journal-full-title] Molecular cell
  • [ISO-abbreviation] Mol. Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA8484
  • [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 / NUP214-ABL1 fusion protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases
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48. Taki T, Taniwaki M: Chromosomal translocations in cancer and their relevance for therapy. Curr Opin Oncol; 2006 Jan;18(1):62-8
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  • Observation of high frequencies of mutations in NOTCH1, NPM and JAK2 in T-cell acute lymphoblastic leukemia, acute myeloid leukemia with normal karyotype and myeloproliferative disorders (polycythemia vera, essential thrombocythemia and idiopathic myelofibrosis) have provided important suggestions for a better understanding of chromosomal translocations.

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  • (PMID = 16357566.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 46
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49. Carulli G, Marini A, Baccelli E, Lambelet P, Lari T, Azzarà A: Association of B-chronic lymphocytic leukemia and acute myeloid leukemia. J Exp Clin Cancer Res; 2007 Sep;26(3):421-4
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  • [Title] Association of B-chronic lymphocytic leukemia and acute myeloid leukemia.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Neoplasms, Multiple Primary / diagnosis


50. Beesley AH, Firth MJ, Ford J, Weller RE, Freitas JR, Perera KU, Kees UR: Glucocorticoid resistance in T-lineage acute lymphoblastic leukaemia is associated with a proliferative metabolism. Br J Cancer; 2009 Jun 16;100(12):1926-36
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  • [Title] Glucocorticoid resistance in T-lineage acute lymphoblastic leukaemia is associated with a proliferative metabolism.
  • Glucocorticoids (GCs) are among the most important drugs for acute lymphoblastic leukaemia (ALL), yet despite their clinical importance, the exact mechanisms involved in GC cytotoxicity and the development of resistance remain uncertain.
  • We examined the baseline profile of a panel of T-ALL cell lines to determine factors that contribute to GC resistance without prior drug selection.
  • The data also provide the first evidence that altered expression of wild-type MLL may contribute to GC-resistant phenotypes.
  • [MeSH-major] Cell Proliferation / drug effects. Dexamethasone / pharmacology. Drug Resistance, Neoplasm. Methylprednisolone / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Signal Transduction / drug effects


51. Shimizu D, Taki T, Utsunomiya A, Nakagawa H, Nomura K, Matsumoto Y, Nishida K, Horiike S, Taniwaki M: Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma. Int J Hematol; 2007 Apr;85(3):212-8
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  • [Title] Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma.
  • We analyzed NOTCH1 gene mutation in 53 adults with mature T-cell leukemia/lymphoma: 21 patients with adult T-cell leukemia (ATL), 25 with T-cell non-Hodgkin's lymphoma (T-NHL), and 7 with T-cell prolymphocytic leukemia.
  • We detected a nonsense mutation, C7249T (resulting in Q2417X, where X is a termination codon) in the PEST domain of NOTCH1 in an ATL patient and detected a 3-bp deletion (positions 7234-7236) that resulted in deletion of a proline codon at codon 2412 in the PEST domain of NOTCH1 in a patient with a T-NHL, peripheral T-cell lymphoma-unspecified (PTCL-u).
  • These findings suggest that nonsense mutation in the PEST domain in the ATL case was associated with NOTCH1 signaling through a pathway different from that for T-cell acute lymphoblastic leukemia (T-ALL).
  • Although NOTCH1 mutation occurs infrequently in mature T-cell leukemia/lymphoma, NOTCH1 may be involved in leukemogenesis associated with various forms of T-cell leukemia/lymphoma rather than only with T-ALL.
  • [MeSH-major] Codon, Nonsense. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell, Peripheral / genetics. Receptor, Notch1 / genetics

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  • [Cites] Blood. 2004 Sep 15;104(6):1696-702 [15187027.001]
  • [Cites] Blood. 2002 May 1;99(9):3398-403 [11964309.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] J Biol Chem. 2001 Sep 14;276(37):34371-8 [11425854.001]
  • [Cites] Mol Cell Biol. 2000 Oct;20(20):7505-15 [11003647.001]
  • [Cites] Virchows Arch. 2005 Apr;446(4):416-20 [15756589.001]
  • [Cites] Int J Hematol. 2005 Nov;82(4):277-84 [16298815.001]
  • [Cites] Ann Oncol. 2004 Jul;15(7):1091-6 [15205204.001]
  • [Cites] Int J Hematol. 2005 Nov;82(4):295-301 [16298817.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):655-64 [12509463.001]
  • [Cites] Leukemia. 2006 Mar;20(3):537-9 [16424867.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1255-64 [16210342.001]
  • [Cites] Leukemia. 2005 Oct;19(10):1841-3 [16079893.001]
  • [Cites] Blood. 2000 Sep 1;96(5):1906-13 [10961893.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2540-3 [16282337.001]
  • [Cites] Immunity. 1999 Sep;11(3):299-308 [10514008.001]
  • [Cites] Blood. 2006 Jan 15;107(2):781-5 [16166587.001]
  • [Cites] Science. 1999 Apr 30;284(5415):770-6 [10221902.001]
  • [Cites] Br J Haematol. 1999 Sep;106(3):702-5 [10468859.001]
  • [Cites] Blood. 2004 Dec 1;104(12 ):3697-704 [15292061.001]
  • [Cites] Nat Immunol. 2005 Jul;6(7):680-8 [15991363.001]
  • [Cites] Nature. 2005 Sep 8;437(7056):270-4 [16025100.001]
  • [Cites] Blood. 1994 Jan 15;83(2):505-11 [8286748.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3097-105 [15251982.001]
  • [Cites] Electrophoresis. 2001 Oct;22(18):4016-22 [11700735.001]
  • [Cites] Pathol Int. 2000 Sep;50(9):696-702 [11012982.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(12):4642-51 [16738328.001]
  • [Cites] Cell. 1997 Mar 21;88(6):833-43 [9118226.001]
  • [Cites] Blood. 2004 Jul 15;104(2):328-35 [15044256.001]
  • [Cites] Mol Cell Biol. 2000 Jun;20(11):3928-41 [10805736.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Feb;117(1):71-9 [10700871.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3898-906 [16118316.001]
  • [Cites] Trends Biochem Sci. 1996 Jul;21(7):267-71 [8755249.001]
  • [Cites] Cell. 2004 May 14;117(4):515-26 [15137944.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Blood. 1997 Jun 1;89(11):3909-18 [9166827.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):3043-9 [16707600.001]
  • [Cites] Leukemia. 2003 Apr;17(4):738-45 [12682631.001]
  • [Cites] Cell. 1996 Nov 1;87(3):483-92 [8898201.001]
  • [Cites] Leukemia. 2001 Oct;15(10):1627-32 [11587222.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(21):9265-73 [15485896.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3793-9 [11739188.001]
  • (PMID = 17483057.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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52. Dohda T, Maljukova A, Liu L, Heyman M, Grandér D, Brodin D, Sangfelt O, Lendahl U: Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-cell acute lymphoblastic leukemia cell lines. Exp Cell Res; 2007 Aug 15;313(14):3141-52
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  • [Title] Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-cell acute lymphoblastic leukemia cell lines.
  • In T-cell acute lymphoblastic leukemia (T-ALL) NOTCH 1 receptors are frequently mutated.
  • This leads to aberrantly high Notch signaling, but how this translates into deregulated cell cycle control and the transformed cell type is poorly understood.
  • Notch activity, measured immediately downstream of the NOTCH 1 receptor, is high, but expression of the canonical downstream Notch response genes HES 1 and HEY 2 is low both in primary cells from T-ALL patients and in T-ALL cell lines.
  • We show that in T-ALL cell lines, recruitment of NOTCH 1 intracellular domain (ICD) to the SKP2 promoter was accompanied by high SKP2 and low p27Kip1 protein levels.
  • T-ALL cells show a rapid G1-S cell cycle transition, while blocked Notch signaling resulted in G0/G1 cell cycle arrest, also observed by transfection of p27Kip1 or, to a smaller extent, a dominant negative SKP2 allele.
  • Collectively, our data suggest that the aberrantly high Notch signaling in T-ALL maintains SKP2 at a high level and reduces p27Kip1, leading to more rapid cell cycle progression.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptor, Notch1 / metabolism. S-Phase Kinase-Associated Proteins / metabolism. Signal Transduction / physiology. T-Lymphocytes / metabolism
  • [MeSH-minor] Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / metabolism. Cell Cycle / physiology. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Child. Cyclin-Dependent Kinase Inhibitor p27. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. Repressor Proteins / genetics. Repressor Proteins / metabolism

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  • (PMID = 17560996.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / HEY1 protein, human; 0 / HEY2 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Repressor Proteins; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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53. Akiyama S, Dhavan D, Yi T: PRL-2 increases Epo and IL-3 responses in hematopoietic cells. Blood Cells Mol Dis; 2010 Apr 15;44(4):209-14
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  • Dual specificity protein tyrosine phosphatase PRL-2 is overexpressed in pediatric acute myeloid leukemia (AML) and is located at human chromosome 1p35, a region often rearranged or amplified in malignant lymphoma and B-cell chronic lymphocytic leukemia (B-CLL).
  • Herein we demonstrated that ectopic expression of PRL-2 in murine pre-B-cell line Baf3ER and mouse bone marrow cells induced key features associated with malignant progression and metastasis.
  • PRL-2-transfected Baf3ER cells had augmented growth responses to hematopoietic growth factors Epo or IL-3 with shortened cell cycle, reduced requirement (5x) for Epo in cell survival, increased cell migration (3x), reduced cell adhesion (5x), and conversion to an immature cell morphology in association with increased expression (3x) of stem cell marker Bmi-1.

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  • [Cites] Blood. 1998 Feb 15;91(4):1216-24 [9454751.001]
  • [Cites] Cancer Lett. 1996 Dec 20;110(1-2):49-55 [9018080.001]
  • [Cites] Blood. 1998 May 15;91(10):3927-34 [9573031.001]
  • [Cites] EMBO J. 1998 Sep 15;17(18):5321-33 [9736611.001]
  • [Cites] Clin Cancer Res. 2004 Nov 1;10(21):7318-28 [15534108.001]
  • [Cites] Leukemia. 2005 Jan;19(1):77-82 [15510210.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Mar 25;328(4):1163-9 [15707999.001]
  • [Cites] Mol Cell Biol. 2005 Mar;25(6):2395-405 [15743832.001]
  • [Cites] Ann Hematol. 2005 Jul;84(7):474-6 [15700138.001]
  • [Cites] Clin Cancer Res. 2005 Oct 1;11(19 Pt 1):6835-9 [16203771.001]
  • [Cites] Mol Cancer Ther. 2005 Nov;4(11):1653-61 [16275986.001]
  • [Cites] Blood. 2006 Jan 1;107(1):305-8 [16160010.001]
  • [Cites] Cell Mol Life Sci. 2006 Feb;63(4):449-68 [16416030.001]
  • [Cites] Br J Cancer. 2006 Aug 7;95(3):347-54 [16832410.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Sep 15;348(1):229-37 [16875667.001]
  • [Cites] Nature. 1990 Feb 22;343(6260):762-4 [2154701.001]
  • [Cites] Oncogene. 2000 May 15;19(21):2612-8 [10851060.001]
  • [Cites] Histopathology. 2001 Apr;38(4):285-306 [11318894.001]
  • [Cites] Cancer Genet Cytogenet. 2001 Apr 1;126(1):45-51 [11343778.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3896-901 [11389032.001]
  • [Cites] J Immunol. 2001 Sep 15;167(6):3391-7 [11544330.001]
  • [Cites] Science. 2001 Nov 9;294(5545):1343-6 [11598267.001]
  • [Cites] Mol Cancer Ther. 2002 Dec;1(14):1255-64 [12516958.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3109-17 [12406872.001]
  • [Cites] Mol Cell. 2003 Apr;11(4):905-14 [12718877.001]
  • [Cites] Cancer Res. 2003 Jun 1;63(11):2716-22 [12782572.001]
  • [Cites] Mol Med. 2003 Mar-Apr;9(3-4):85-95 [12865944.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1849-56 [12738660.001]
  • [Cites] Br J Haematol. 2003 Sep;122(5):745-59 [12930384.001]
  • [Cites] Cancer Lett. 2003 Dec 30;202(2):201-11 [14643450.001]
  • [Cites] Clin Cancer Res. 2003 Nov 15;9(15):5607-15 [14654542.001]
  • [Cites] Am J Pathol. 2004 Jun;164(6):2039-54 [15161639.001]
  • [Cites] Pathobiology. 2004;71(4):176-84 [15263806.001]
  • [Cites] J Cancer Res Clin Oncol. 2004 Sep;130(9):521-6 [15133662.001]
  • [Cites] Leuk Res. 2004 Dec;28(12):1341-5 [15475076.001]
  • [Cites] Mol Cell Biol. 1991 Jan;11(1):381-90 [1986233.001]
  • [Cites] Mol Cell Biol. 1994 Jun;14(6):3752-62 [8196618.001]
  • [Cites] Blood. 1995 Jan 1;85(1):203-16 [7803794.001]
  • [Cites] Blood. 1996 Aug 15;88(4):1437-44 [8695864.001]
  • [Cites] Biochem Biophys Res Commun. 1998 Mar 17;244(2):421-7 [9514946.001]
  • (PMID = 20226699.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102481-03; United States / NCI NIH HHS / CA / R01 CA096636; United States / NCI NIH HHS / CA / R01 CA102481; United States / NCI NIH HHS / CA / R01 CA096636-05; United States / NCI NIH HHS / CA / CA102481-03; United States / NCI NIH HHS / CA / CA096636-05
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-3; 0 / Recombinant Fusion Proteins; 0 / Recombinant Proteins; 0 / STAT5 Transcription Factor; 11096-26-7 / Erythropoietin; 64FS3BFH5W / Epoetin Alfa; EC 3.1.3.48 / PTP4A2 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatases
  • [Other-IDs] NLM/ NIHMS182540; NLM/ PMC2847026
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54. Kreitman RJ: Recombinant immunotoxins for the treatment of chemoresistant hematologic malignancies. Curr Pharm Des; 2009;15(23):2652-64
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  • No agents of this class are approved yet for medical use, although a related molecule, denileukin diftitox, composed of interleukin-2 fused to truncated diphtheria toxin, is approved for relapsed/refractory cutaneous T-cell lymphoma.
  • Major responses were observed with LMB-2 in adult T-cell leukemia, chronic lymphocytic leukemia (CLL), cutaneous T-cell lymphoma, Hodgkin's disease, and hairy cell leukemia (HCL).
  • HA22, an improved version of BL22 with higher affinity to CD22, is now undergoing phase I testing in HCL, CLL, non-Hodgkin's lymphoma, and pediatric acute lymphoblastic leukemia.

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  • (PMID = 19689336.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Diphtheria Toxin; 0 / Immunotoxins; 0 / Leukocidins; 0 / Pseudomonas aeruginosa Cytotoxins; 0 / Recombinant Proteins; 0 / Toxins, Biological
  • [Number-of-references] 190
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55. Xu W, Li JY, Qian SX, Wu HX, Lu H, Chen LJ, Zhang SJ, Lu RL, Sheng RL: Outcome of treatment with Hyper-CVAD regimen in Chinese patients with acute lymphocytic leukemia. Leuk Res; 2008 Jun;32(6):930-5
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  • [Title] Outcome of treatment with Hyper-CVAD regimen in Chinese patients with acute lymphocytic leukemia.
  • Modern intensive chemotherapy regimens have improved the prognosis for adult patients with acute lymphocytic leukemia (ALL).
  • With these regimens, the complete response (CR) rates are approximately 75% and long-term disease-free survival (DFS) rates are about 20-35%.
  • However, patients with mediastinal disease had lower CR rates (P<0.05), with the presence of hepatomegaly and t(9;22) abnormalities had poor survival (P<0.05).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18061665.001).
  • [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] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
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56. Rapanotti MC, Caruso R, Ammatuna E, Zaza S, Trotta L, Divona M, Cicconi L, Funaro D, Federici G, Amadori S, De Rossi G, Lo-Coco F: Molecular characterization of paediatric idiopathic hypereosinophilia. Br J Haematol; 2010 Dec;151(5):440-6
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  • Early identification of pHES that may evolve towards a lymphomyeloproliferative disease is relevant in light of prognostic and therapeutic implications.
  • Molecular features of 10 pHES patients were analysed at presentation and during their clinical course, including analysis of BCR-ABL1 and FIP1L1/PDGFRA fusion genes, quantitation of WT1 gene copy number and clonality of T-cell receptor (TCR) and immunoglobulin heavy chain (IGH).
  • Five children showed IGH clonality at presentation: of these, two developed a B non-Hodgkin lymphoma and a B-lineage acute lymphocytic leukaemia at six and 12 months respectively, two spontaneously reverted to a polyclonal IGH profile during the follow-up, and the last one persisted with pHES without B-clonal evolution after 19 months.
  • IGH rearrangement was observed to be a frequent molecular feature of pHES and may precede B-cell clonal expansion and evolution into B-cell malignancies in children.
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Follow-Up Studies. Gene Rearrangement. Humans. Immunoglobulin Heavy Chains / genetics. Immunophenotyping. Infant. Lymphoma, B-Cell / etiology. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Prognosis

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20955401.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [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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57. Ngamphaiboon N, Sweeney R, Wetzler M, Wang ES: Pyridoxine treatment of vincristine-induced cranial polyneuropathy in an adult patient with acute lymphocytic leukemia: Case report and review of the literature. Leuk Res; 2010 Aug;34(8):e194-6
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  • [Title] Pyridoxine treatment of vincristine-induced cranial polyneuropathy in an adult patient with acute lymphocytic leukemia: Case report and review of the literature.
  • [MeSH-major] Cranial Nerve Diseases / chemically induced. Cranial Nerve Diseases / drug therapy. Polyneuropathies / chemically induced. Polyneuropathies / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyridoxine / therapeutic use. Vincristine / adverse effects

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  • (PMID = 20167372.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 12001-76-2 / Vitamin B Complex; 5J49Q6B70F / Vincristine; KV2JZ1BI6Z / Pyridoxine
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58. Spokoini R, Kfir-Erenfeld S, Yefenof E, Sionov RV: Glycogen synthase kinase-3 plays a central role in mediating glucocorticoid-induced apoptosis. Mol Endocrinol; 2010 Jun;24(6):1136-50
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  • It is still unclear how glucocorticoids (GCs) induce apoptosis of thymocytes and T lymphoma cells.
  • Emergence of GC-resistant lymphoma cells is a major obstacle in GC therapy, emphasizing the need for novel strategies that maintain the sensitivity of lymphoma cells to the proapoptotic effects of GC.
  • Chemical inhibition of GSK3 by SB216763, BIO-Acetoxime, or LiCl and GSK3 inhibition using a dominant-negative mutant of GSK3 impede this cell death process, indicating that GSK3 is involved in transmitting the apoptotic signal.
  • GC resistance in lymphoma cells can be relieved by inhibiting the phosphatidylinositol-3 kinase-Akt survival pathway, which inactivates GSK3.
  • Notch1, a transcription factor frequently activated in T acute lymphoblastic leukemia cells, confers GC resistance through activation of Akt.
  • [MeSH-minor] Animals. Apoptosis Regulatory Proteins / metabolism. Bcl-2-Like Protein 11. Cell Line. Dexamethasone / pharmacology. Drug Resistance, Neoplasm / drug effects. Enzyme Activation / drug effects. Glycogen Synthase Kinase 3 beta. Humans. Ligands. Membrane Proteins / metabolism. Mice. Models, Biological. Protein Binding / drug effects. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptors, Glucocorticoid / metabolism. Receptors, Notch / metabolism

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  • [Cites] J Exp Med. 2006 Jan 23;203(1):189-201 [16390935.001]
  • [Cites] Cell Cycle. 2006 May;5(10):1017-26 [16687934.001]
  • [Cites] Cell Cycle. 2007 Dec 15;6(24):3086-96 [18073527.001]
  • [Cites] Mol Endocrinol. 2005 Jun;19(6):1569-83 [15817653.001]
  • [Cites] Cell Cycle. 2007 Apr 15;6(8):927-30 [17404512.001]
  • [Cites] Front Neuroendocrinol. 2008 May;29(2):273-91 [18054070.001]
  • [Cites] J Exp Med. 1995 Aug 1;182(2):367-77 [7629499.001]
  • [Cites] Drug Resist Updat. 2007 Feb-Apr;10(1-2):13-29 [17303468.001]
  • [Cites] Mol Cell Biol. 2008 Dec;28(24):7309-22 [18838540.001]
  • [Cites] Cell Signal. 2002 Jun;14(6):557-62 [11897496.001]
  • [Cites] Mol Cell. 2004 Feb 13;13(3):329-40 [14967141.001]
  • [Cites] Mol Cell. 2005 Jul 22;19(2):159-70 [16039586.001]
  • [Cites] Mol Endocrinol. 2007 Jul;21(7):1552-68 [17440046.001]
  • [Cites] Cell Cycle. 2007 Sep 15;6(18):2236-40 [17881896.001]
  • [Cites] Mol Cell Endocrinol. 2006 Feb 26;246(1-2):142-6 [16388891.001]
  • [Cites] J Immunol. 2006 Feb 1;176(3):1695-702 [16424199.001]
  • [Cites] J Cell Biochem. 2006 Aug 15;98(6):1391-407 [16619268.001]
  • [Cites] Carcinogenesis. 2008 Mar;29(3):544-51 [18174237.001]
  • [Cites] BMC Cell Biol. 2006 Feb 28;7:10 [16507111.001]
  • [Cites] J Clin Invest. 2004 Feb;113(4):619-27 [14966571.001]
  • [Cites] J Natl Cancer Inst Monogr. 2001;(28):30-7 [11158204.001]
  • [Cites] Nat Cell Biol. 2002 May;4(5):E131-6 [11988758.001]
  • [Cites] Eur J Immunol. 2003 Apr;33(4):913-9 [12672057.001]
  • [Cites] Science. 1999 Nov 26;286(5445):1735-8 [10576740.001]
  • [Cites] J Biol Chem. 2003 Jun 27;278(26):23861-7 [12676946.001]
  • [Cites] Eur J Immunol. 2001 Sep;31(9):2702-8 [11536168.001]
  • [Cites] Exp Hematol. 2006 Nov;34(11):1542-52 [17046574.001]
  • [Cites] Neuron. 2003 Jun 19;38(6):899-914 [12818176.001]
  • [Cites] EMBO J. 1998 Dec 15;17(24):7209-18 [9857178.001]
  • [Cites] J Neurosci. 2004 Nov 3;24(44):9993-10002 [15525785.001]
  • [Cites] Blood. 1999 Apr 1;93(7):2282-96 [10090938.001]
  • [Cites] Adv Cancer Res. 2008;101:127-248 [19055945.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):331-42 [17010674.001]
  • [Cites] Cell Immunol. 2004 Jan;227(1):12-23 [15051511.001]
  • [Cites] Mol Endocrinol. 2008 Aug;22(8):1754-66 [18483179.001]
  • [Cites] Cell Death Differ. 2002 May;9(5):505-12 [11973609.001]
  • [Cites] Immunity. 1998 Dec;9(6):777-86 [9881968.001]
  • [Cites] Prog Neurobiol. 2006 Jul;79(4):173-89 [16935409.001]
  • [Cites] Cell Death Differ. 2002 Jan;9(1):6-19 [11803370.001]
  • [Cites] J Leukoc Biol. 2004 Jul;76(1):7-14 [15075361.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2941-8 [15598814.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10545-54 [16288047.001]
  • [Cites] EMBO J. 2003 Nov 17;22(22):6035-44 [14609950.001]
  • [Cites] Curr Opin Hematol. 2004 Nov;11(6):426-33 [15548998.001]
  • [Cites] FEBS Lett. 2006 Jun 12;580(14 ):3539-44 [16730715.001]
  • [Cites] Oncogene. 1999 Nov 18;18(48):6733-40 [10597281.001]
  • [Cites] Cell Death Differ. 2005 Aug;12 (8):1008-14 [15947788.001]
  • [Cites] Science. 2003 Mar 21;299(5614):1859-63 [12649474.001]
  • [Cites] Mol Cell Biol. 1997 Jul;17(7):3947-54 [9199329.001]
  • [Cites] J Biol Chem. 2004 Jan 23;279(4):2937-44 [14583609.001]
  • [Cites] J Exp Med. 1997 May 19;185(10):1827-36 [9151708.001]
  • [Cites] J Biol Chem. 2006 Jul 28;281(30):21353-61 [16714293.001]
  • [Cites] Oncogene. 2001 Sep 20;20(42):5991-6000 [11593406.001]
  • [Cites] J Biol Chem. 1999 Jul 23;274(30):21395-401 [10409701.001]
  • [Cites] Cell Res. 2005 Jan;15(1):36-42 [15686625.001]
  • [Cites] Exp Cell Res. 2006 Feb 1;312(3):322-30 [16309671.001]
  • [Cites] J Immunol. 2003 Mar 1;170(5):2469-78 [12594272.001]
  • [Cites] J Biol Chem. 2004 May 14;279(20):20858-65 [14996839.001]
  • [Cites] J Biol Chem. 2002 Mar 1;277(9):7610-8 [11751859.001]
  • [Cites] Blood. 2003 Jan 15;101(2):585-93 [12393559.001]
  • [Cites] J Biol Chem. 2003 Aug 22;278(34):32227-35 [12794074.001]
  • [Cites] Mol Endocrinol. 2008 Jun;22(6):1331-44 [18337589.001]
  • [Cites] J Biol Chem. 1998 Jun 5;273(23):14315-21 [9603939.001]
  • [Cites] Mol Cell Biol. 2007 Jul;27(14):5079-89 [17485443.001]
  • [Cites] Clin Cancer Res. 2002 Jun;8(6):1681-94 [12060604.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2766-73 [11289160.001]
  • [Cites] Eur J Immunol. 2004 Jan;34(1):119-25 [14971037.001]
  • [Cites] Apoptosis. 2007 Feb;12(2):271-91 [17191112.001]
  • [Cites] Nat Immunol. 2002 Oct;3(10):932-9 [12244308.001]
  • [Cites] Biochim Biophys Acta. 2004 Jul 23;1693(1):57-72 [15276325.001]
  • [Cites] Ann N Y Acad Sci. 2004 Jun;1024:86-101 [15265775.001]
  • [Cites] EMBO J. 2001 Dec 17;20(24):7108-16 [11742987.001]
  • [Cites] Biochem Soc Trans. 2006 Dec;34(Pt 6):1018-23 [17073741.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Cancer Cell Int. 2007 Mar 28;7:3 [17391526.001]
  • [Cites] J Biol Chem. 2004 Dec 31;279(53):55809-17 [15509554.001]
  • [Cites] Curr Drug Targets. 2006 Nov;7(11):1377-88 [17100578.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3138-47 [15070696.001]
  • [Cites] Cancer Lett. 2005 Jan 20;217(2):129-38 [15617830.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2305-13 [16489035.001]
  • [Cites] Mol Cell. 2006 Mar 17;21(6):749-60 [16543145.001]
  • [Cites] J Biol Chem. 1998 Aug 7;273(32):19929-32 [9685326.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):201-5 [12161751.001]
  • [Cites] Eur J Immunol. 2004 Oct;34(10):2781-90 [15368294.001]
  • [Cites] Oncogene. 1997 Aug 14;15(7):837-43 [9266970.001]
  • [Cites] Apoptosis. 2003 Oct;8(5):481-95 [12975579.001]
  • [Cites] J Biol Chem. 2006 Sep 1;281(35):25215-22 [16818494.001]
  • (PMID = 20371704.001).
  • [ISSN] 1944-9917
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BCL2L11 protein, human; 0 / Bcl-2-Like Protein 11; 0 / Bcl2l11 protein, mouse; 0 / Glucocorticoids; 0 / Ligands; 0 / Membrane Proteins; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Receptors, Glucocorticoid; 0 / Receptors, Notch; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.1 / GSK3B protein, human; EC 2.7.11.1 / Glycogen Synthase Kinase 3 beta; EC 2.7.11.1 / Gsk3b protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 2.7.11.26 / glycogen synthase kinase 3 alpha
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59. Nowak AK, Lake RA, Robinson BW: Combined chemoimmunotherapy of solid tumours: improving vaccines? Adv Drug Deliv Rev; 2006 Oct 1;58(8):975-90
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  • It is now clear that the way a chemotherapeutic drug kills a tumour cell determines how that dying cell interacts with the immune system and whether the interaction leads to an immune response.
  • Furthermore, lymphodepletion triggers homeostatic T cell reconstitution, creating new populations of pre-T cells that need education in the thymic environment.

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  • (PMID = 17005292.001).
  • [ISSN] 0169-409X
  • [Journal-full-title] Advanced drug delivery reviews
  • [ISO-abbreviation] Adv. Drug Deliv. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cancer Vaccines
  • [Number-of-references] 105
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60. Zhang Y, Payne KJ, Zhu Y, Price MA, Parrish YK, Zielinska E, Barsky LW, Crooks GM: SCL expression at critical points in human hematopoietic lineage commitment. Stem Cells; 2005 Jun-Jul;23(6):852-60
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  • The stem cell leukemia (SCL or tal-1) gene was initially identified as a translocation partner in a leukemia that possessed both lymphoid and myeloid differentiation potential.
  • Mice that lacked SCL expression showed a complete block in hematopoiesis; thus, SCL was associated with hematopoietic stem cell (HSC) function.
  • Using recently defined surface immunophenotypes, we fluorescence-activated cell-sorted (FACS) highly purified populations of primary human hematopoietic progenitors for reverse transcription-polymerase chain reaction (RT-PCR) analysis of SCL expression.
  • SCL expression was undetectable in immature cells of nonerythroid lineages, including pro-B cells, early thymic progenitors, and myeloid precursors expressing the M-CSF receptor.
  • [MeSH-minor] Animals. Antigens, CD34 / biosynthesis. Basic Helix-Loop-Helix Transcription Factors. Bone Marrow Cells / cytology. Cell Differentiation. Cell Line. Cell Lineage. Cell Separation. Cells, Cultured. Down-Regulation. Flow Cytometry. Humans. Immunophenotyping. Mice. Models, Biological. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells / cytology. Thymus Gland / metabolism. Time Factors

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  • (PMID = 15917481.001).
  • [ISSN] 1066-5099
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K01 DK066163; United States / NCI NIH HHS / CA / P01CA59318; United States / NHLBI NIH HHS / HL / P50HL54850; United States / NHLBI NIH HHS / HL / R01HL77912
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
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61. Dourado M, Sarmento AB, Pereira SV, Alves V, Silva T, Pinto AM, Rosa MS: CD26/DPPIV expression and 8-azaguanine response in T-acute lymphoblastic leukaemia cell lines in culture. Pathophysiology; 2007 May;14(1):3-10
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  • [Title] CD26/DPPIV expression and 8-azaguanine response in T-acute lymphoblastic leukaemia cell lines in culture.
  • Dipeptidyl peptidase IV, a cell membrane surface protease also known as CD26 (CD26/DPPIV), is known to play multiple functions in human organism, where it is largely expressed, for instance, in the development of human cancer and metastasis as well as in chemotherapy response.
  • The objective of this work was to study the CD26 membrane expression and DPPIV activity in T-acute leukaemia cell lines (CEM and MOLT3) in culture, in order to observe the modification of its expression under the 8-azaguanine treatment.
  • Cell line samples were incubated, some without different azaguanine concentration and others with, ranging from 10 to 100muM.
  • Cell surface CD26 expression has been identified by flow cytometry and DPPIV activity, in cultured medium, was fluorimetrically measured.
  • Results we have observed showed that 8-azaguanine induced a decrease in cell viability in a dose, time and cell type dependent manner with MOLT3 cells being the most sensitive to 8-azaguanine citotoxic effects (24h IC50: +/-10muM) when compared with CEM cells (24h IC50: +/-100muM).
  • In the same experimental conditions, MOLT3 cell treated with 8-azaguanine shows an increase in CD26 expression (MIF) compared with that of CEM cell submitted to the same conditions (65.4+/-1.3 versus 18.7+/-1.7).

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  • (PMID = 17055708.001).
  • [ISSN] 0928-4680
  • [Journal-full-title] Pathophysiology : the official journal of the International Society for Pathophysiology
  • [ISO-abbreviation] Pathophysiology
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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62. Santamaría-Quesada C, Vargas M, Venegas P, Calvo M, Obando C, Valverde B, Cartín W, Carrillo JM, Jimenez R, González M: Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica. J Pediatr Hematol Oncol; 2009 Feb;31(2):131-5
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  • [Title] Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica.
  • In Central America, nearly 70% of pediatric cancer is related to hemato-oncologic disorders, especially acute lymphoblastic leukemia (ALL).
  • Preliminary studies have described a high incidence of childhood leukemia in these countries; however, no molecular analyses of these malignancies have yet been carried out.
  • We studied diagnostic samples from 84 patients from the National Children's Hospital in San Jose, Costa Rica (65 precursor B-ALL, 5 T-cell ALL, and 14 acute myeloblastic leukemia).
  • The observed rate of leukemia was 52.2 cases per million children per year.
  • Twelve out of 65 (18.4%) precursor B-ALL tested positive for TEL-AML1 and 3 cases for BCR-ABL (4.6%).
  • None of the T-cell ALL cases were positive for either SIL-TAL1 or HOX11L2.
  • Within 14 acute myeloblastic leukemia patients, we confirmed 2 cases with FLT3-internal tandem duplication+, 1 patient with AML1-ETO, and only 1 case carrying a PML-RARalpha rearrangement.
  • The present study confirms the relatively high incidence of pediatric leukemia in Costa Rica and constitutes the first report regarding the incidence of the main molecular alterations of childhood leukemia in our region.
  • [MeSH-major] Leukemia / epidemiology. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Child. Costa Rica / epidemiology. Cytogenetic Analysis. Gene Rearrangement. Humans. Mutation. Oncogene Proteins, Fusion / analysis

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  • (PMID = 19194200.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion
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63. Malcovati L: Novel homeobox gene recombination in T-cell acute lymphoblastic leukemia. Haematologica; 2006 Mar;91(3):290A
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  • [Title] Novel homeobox gene recombination in T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Genes, Homeobox / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Recombination, Genetic / genetics

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  • [CommentOn] Haematologica. 2006 Mar;91(3):317-21 [16531254.001]
  • (PMID = 16531247.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] Italy
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64. Borriello A, Locasciulli A, Bianco AM, Criscuolo M, Conti V, Grammatico P, Cappellacci S, Zatterale A, Morgese F, Cucciolla V, Delia D, Della Ragione F, Savoia A: A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2007 Jan;21(1):72-8
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  • [Title] A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia.
  • Fanconi anemia (FA) is an autosomal recessive disease characterized by pancitopenia, congenital malformations, predisposition to cancers and chromosomal instability.
  • We report the clinical and molecular features of a patient initially identified as a potential FA case only because of chemotherapy toxicity during the treatment of a T-lineage acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Fanconi Anemia Complementation Group D2 Protein / genetics. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation
  • [MeSH-minor] Amino Acid Substitution. Antigens, CD. Antigens, CD13. Antigens, Differentiation, Myelomonocytic. Child. Chromosomal Instability. Disease Progression. Fanconi Anemia / genetics. Humans. Infection / etiology. Infection / genetics. Male. Pancytopenia / chemically induced. Pancytopenia / genetics. Remission Induction. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 17096012.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] Italy / Telethon / / TGM06S01
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / FANCD2 protein, human; 0 / Fanconi Anemia Complementation Group D2 Protein; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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65. Nishimura S, Takahashi S, Kamikatahira H, Kuroki Y, Jaalouk DE, O'Brien S, Koivunen E, Arap W, Pasqualini R, Nakayama H, Kuniyasu A: Combinatorial targeting of the macropinocytotic pathway in leukemia and lymphoma cells. J Biol Chem; 2008 Apr 25;283(17):11752-62
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  • [Title] Combinatorial targeting of the macropinocytotic pathway in leukemia and lymphoma cells.
  • Ligand-directed delivery of agents to leukemia and lymphoma cells has the potential to yield new mechanistic disease insights and targeted therapies.
  • From the screening of acute T-lymphoblastic leukemia Molt-4 cells with a random phage-display peptide library, we isolated a phage displaying the sequence CAYHRLRRC.
  • This peptide contains a lymph node-homing motif (Cys-Ala-Tyr) and a cell-penetrating motif (Arg-Leu-Arg-Arg).
  • Binding of this ligand-directed phage to a large panel of leukemia/lymphoma cells and to patient-derived samples was much higher than to non-leukemia control cells.
  • Flow cytometry with fluorescein-labeled peptide and endocytosis blocking with specific inhibitors revealed that CAYHRLRRC is indeed taken up through macropinocytosis in Molt-4 and K562 human leukemia cells.
  • Unexpectedly, the cell surface receptor for the CAYHRLRRC peptide is not a heparan sulfate proteoglycan as it would be predicted for other cell-penetrating peptides.
  • Confirming this interpretation, a CAYHRLRRC-directed peptidomimetic-induced cell death in all the leukemia and lymphoma cells was evaluated, whereas a control transactivator of transcription protein (tat)-directed proapoptotic peptidomimetic was non-selective.
  • In summary, the targeting peptide CAYHRLRRC is selectively internalized through macropinocytosis in leukemia and lymphoma cells and has potential as a drug lead for ligand-directed anti-leukemia therapies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Gene Expression Regulation, Leukemic. Leukemia / metabolism. Lymphoma / metabolism
  • [MeSH-minor] Catalysis. Cell Line, Tumor. Cell Survival. Chemistry, Pharmaceutical / methods. Drug Design. Humans. K562 Cells. Ligands. Peptide Library. Peptides / chemistry. Pinocytosis

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  • [Cites] Pharmacol Rev. 2006 Mar;58(1):32-45 [16507881.001]
  • [Cites] Nat Rev Drug Discov. 2007 Oct;6(10):834-48 [17853901.001]
  • [Cites] Exp Hematol. 2006 Apr;34(4):443-52 [16569591.001]
  • [Cites] Mol Biol Cell. 2000 Oct;11(10):3341-52 [11029040.001]
  • [Cites] Cancer Res. 2000 Dec 1;60(23):6551-6 [11118031.001]
  • [Cites] J Biol Chem. 2001 Feb 23;276(8):5836-40 [11084031.001]
  • [Cites] J Cell Biol. 2001 May 28;153(5):905-16 [11381078.001]
  • [Cites] Curr Opin Chem Biol. 2001 Jun;5(3):308-13 [11479123.001]
  • [Cites] Nat Med. 2001 Nov;7(11):1249-53 [11689892.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8110-2 [11719437.001]
  • [Cites] Nat Med. 2002 Feb;8(2):121-7 [11821895.001]
  • [Cites] Cancer Res. 2002 Feb 1;62(3):867-74 [11830545.001]
  • [Cites] J Cell Sci. 2002 Jul 15;115(Pt 14):2953-62 [12082155.001]
  • [Cites] Nat Rev Cancer. 2002 Jul;2(7):521-8 [12094238.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):13055-60 [12242328.001]
  • [Cites] J Biol Chem. 2003 Jan 3;278(1):585-90 [12411431.001]
  • [Cites] Int J Med Microbiol. 2002 Feb;291(6-7):487-94 [11890548.001]
  • [Cites] Nat Rev Immunol. 2003 Jan;3(1):23-35 [12511873.001]
  • [Cites] Nature. 2003 Mar 6;422(6927):37-44 [12621426.001]
  • [Cites] J Urol. 2003 Apr;169(4):1535-40 [12629410.001]
  • [Cites] J Control Release. 2003 Aug 28;91(1-2):45-51 [12932636.001]
  • [Cites] Nat Biotechnol. 2003 Sep;21(9):1040-6 [12897791.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5213-7 [14500347.001]
  • [Cites] Cancer Res. 2004 Jan 15;64(2):435-9 [14744752.001]
  • [Cites] Nat Med. 2004 Mar;10(3):310-5 [14770178.001]
  • [Cites] Cancer Cell. 2004 Feb;5(2):151-62 [14998491.001]
  • [Cites] Nature. 2004 May 20;429(6989):309-14 [15152255.001]
  • [Cites] Nat Med. 2004 Jun;10(6):625-32 [15133506.001]
  • [Cites] Cancer Cell. 2004 Sep;6(3):275-84 [15380518.001]
  • [Cites] J Cell Biol. 1986 Apr;102(4):1312-9 [3485637.001]
  • [Cites] J Cell Biol. 1994 Mar;124(5):689-703 [8120092.001]
  • [Cites] J Biol Chem. 1994 Dec 9;269(49):30745-8 [7982998.001]
  • [Cites] J Cell Biol. 1996 Dec;135(5):1249-60 [8947549.001]
  • [Cites] J Biol Chem. 1997 Jun 20;272(25):16010-7 [9188504.001]
  • [Cites] Science. 1998 Jan 16;279(5349):377-80 [9430587.001]
  • [Cites] Nat Biotechnol. 1999 Aug;17(8):768-74 [10429241.001]
  • [Cites] Nat Med. 1999 Sep;5(9):1032-8 [10470080.001]
  • [Cites] Mol Ther. 2004 Dec;10(6):1011-22 [15564133.001]
  • [Cites] J Control Release. 2005 Jan 20;102(1):247-53 [15653149.001]
  • [Cites] Adv Drug Deliv Rev. 2005 Feb 28;57(4):579-96 [15722165.001]
  • [Cites] J Biol Chem. 2005 Apr 15;280(15):15300-6 [15687490.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1154-63 [15870183.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):34-40 [16397212.001]
  • [Cites] Biochemistry. 2006 Jan 31;45(4):1116-27 [16430208.001]
  • [Cites] J Biol Chem. 2006 Feb 10;281(6):3544-51 [16326716.001]
  • [Cites] Cell. 2006 Apr 21;125(2):385-98 [16630824.001]
  • [Cites] J Biol Chem. 2006 Jun 9;281(23):15757-62 [16606620.001]
  • [Cites] Blood. 2006 Jun 15;107(12):4930-7 [16497970.001]
  • [Cites] Lancet. 2006 Nov 25;368(9550):1894-907 [17126723.001]
  • [Cites] Adv Drug Deliv Rev. 2006 Dec 30;58(15):1622-54 [17123658.001]
  • [Cites] Methods Mol Biol. 2007;357:385-406 [17172704.001]
  • [Cites] Biochemistry. 2007 Jan 16;46(2):492-501 [17209559.001]
  • [Cites] Nat Rev Drug Discov. 2007 Feb;6(2):149-65 [17268486.001]
  • [Cites] Leukemia. 2007 Mar;21(3):411-20 [17252013.001]
  • [Cites] Biochem J. 2007 Apr 15;403(2):335-42 [17217340.001]
  • [Cites] Adv Drug Deliv Rev. 2007 Mar 30;59(2-3):134-40 [17451840.001]
  • [Cites] Mol Pharm. 2007 May-Jun;4(3):435-47 [17373820.001]
  • [Cites] Biochem Soc Trans. 2007 Aug;35(Pt 4):784-7 [17635148.001]
  • [Cites] Biochem Soc Trans. 2007 Aug;35(Pt 4):788-93 [17635149.001]
  • [Cites] Trends Cardiovasc Med. 2006 Apr;16(3):80-8 [16546688.001]
  • (PMID = 18292083.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ligands; 0 / Peptide Library; 0 / Peptides
  • [Other-IDs] NLM/ PMC3762554
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66. Cox CV, Martin HM, Kearns PR, Virgo P, Evely RS, Blair A: Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia. Blood; 2007 Jan 15;109(2):674-82
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  • [Title] Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia.
  • A significant proportion of children with T-cell acute lymphoblastic leukemia (T-ALL) continue to fail therapy.
  • Consequently, characterization of the cells that proliferate to maintain the disease should provide valuable information on the most relevant therapeutic targets.
  • The majority of cells capable of long-term proliferation in vitro were derived from the CD34+/CD4- and CD34+/CD7- subfractions.
  • The immunophenotype and genotype of the original leukemia cells were preserved with serial passage in the NOD/SCID mice.
  • These data demonstrate the long-term repopulating ability of the CD34+/CD4- and CD34+/CD7- subfractions in T-ALL and suggest that a cell with a more primitive phenotype was the target for leukemic transformation in these cases.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Stem Cells / immunology. Stem Cells / pathology
  • [MeSH-minor] Adolescent. Animals. Cell Culture Techniques. Cell Proliferation. Cell Separation. Cells, Cultured. Child. Child, Preschool. Female. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor / genetics. Genotype. Humans. Immunophenotyping. Infant. Male. Mice. Mice, Inbred NOD. Mice, SCID. Xenograft Model Antitumor Assays


67. Te Boekhorst PA, Lamers CH, Schipperus MR, Hintzen RQ, van der Holt B, Cornelissen JJ, Löwenberg B, Gratama JW: T-lymphocyte reconstitution following rigorously T-cell-depleted versus unmodified autologous stem cell transplants. Bone Marrow Transplant; 2006 Apr;37(8):763-72
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  • [Title] T-lymphocyte reconstitution following rigorously T-cell-depleted versus unmodified autologous stem cell transplants.
  • We compared the kinetics of T-cell recovery after extensive ex vivo and in vivo T-cell depleted autologous stem cell transplantation (SCT) for multiple sclerosis (MS; n=8) with unmodified SCT for hematological malignancies (HM; n=39).
  • Unexpectedly, the kinetics of T-cell recovery between 3 and 12 months post transplant was similar in T-depleted and unmodified SCT.
  • Before SCT, the HM patients showed lymphopenia of all T-cell subsets, upregulated HLA-DR and CD95 expression and increased cytokine responses.
  • We suggest that the similar kinetics of T-cell recovery in the two patient groups may be explained by the susceptibility to apoptosis of the activated CD4(+) T-cells in the autografts of the HM patients.
  • This susceptibility to apoptosis would interfere with a swift and sustained CD4(+) T-cell regeneration post SCT.
  • [MeSH-major] Multiple Sclerosis / blood. Multiple Sclerosis / therapy. Stem Cell Transplantation / methods. T-Lymphocytes / metabolism. Transplantation, Autologous / methods

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  • (PMID = 16518423.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD27; 0 / Antigens, CD3; 0 / Antigens, CD4; 0 / Antigens, CD95; 0 / Cytokines; 0 / Interleukin-2; 126880-86-2 / L-Selectin; 82115-62-6 / Interferon-gamma; EC 3.1.3.48 / Antigens, CD45
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68. Ratei R, Karawajew L, Lacombe F, Jagoda K, Del Poeta G, Kraan J, De Santiago M, Kappelmayer J, Björklund E, Ludwig WD, Gratama J, Orfao A, European Working Group of Clinical Cell Analysis (EWGCCA): Normal lymphocytes from leukemic samples as an internal quality control for fluorescence intensity in immunophenotyping of acute leukemias. Cytometry B Clin Cytom; 2006 Jan;70(1):1-9
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  • [Title] Normal lymphocytes from leukemic samples as an internal quality control for fluorescence intensity in immunophenotyping of acute leukemias.
  • BACKGROUND: Multiparametric flow cytometry has become an indispensable but complex tool for the diagnosis of acute leukemias.
  • METHODS: Eight laboratories participated in the study and recruited a total of 151 individuals including 29 patients with B-cell precursor acute lymphoblastic leukemia (BCP-ALL), 77 with acute myeloid leukemia (AML), 10 with T-cell precursor acute lymphoblastic leukemia (T-ALL), and 35 normal bone marrow donors.
  • CONCLUSION: Residual normal lymphocytes can serve as internal quality control for studies addressing fluorescence intensity in the setting of immunophenotyping of acute leukemias.
  • [MeSH-major] Flow Cytometry / methods. Immunophenotyping / methods. Leukemia. Lymphocytes / cytology. Lymphocytes / metabolism
  • [MeSH-minor] Acute Disease. Case-Control Studies. Fluorescence. Humans. Quality Control. Reference Standards

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16278833.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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69. Mustjoki S, Ekblom M, Arstila TP, Dybedal I, Epling-Burnette PK, Guilhot F, Hjorth-Hansen H, Höglund M, Kovanen P, Laurinolli T, Liesveld J, Paquette R, Pinilla-Ibarz J, Rauhala A, Shah N, Simonsson B, Sinisalo M, Steegmann JL, Stenke L, Porkka K: Clonal expansion of T/NK-cells during tyrosine kinase inhibitor dasatinib therapy. Leukemia; 2009 Aug;23(8):1398-405
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  • Fifteen patients had a cytotoxic T-cell and seven patients had an NK-cell phenotype.
  • All T-cell expansions were clonal.
  • Responses to dasatinib were good and included complete, unexpectedly long-lasting remissions in patients with advanced leukemia.
  • In a phase II clinical study on 46 Philadelphia chromosome-positive acute lymphoblastic leukemia, patients with lymphocytosis had superior survival compared with patients without lymphocytosis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Killer Cells, Natural / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Lymphocytosis / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. T-Lymphocyte Subsets / drug effects. T-Lymphocytes, Cytotoxic / drug effects. Thiazoles / pharmacology

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  • [CommentIn] Acta Haematol. 2016;136(4):219-228 [27656875.001]
  • (PMID = 19295545.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
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70. Asnafi V, Buzyn A, Thomas X, Huguet F, Vey N, Boiron JM, Reman O, Cayuela JM, Lheritier V, Vernant JP, Fiere D, Macintyre E, Dombret H: Impact of TCR status and genotype on outcome in adult T-cell acute lymphoblastic leukemia: a LALA-94 study. Blood; 2005 Apr 15;105(8):3072-8
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  • [Title] Impact of TCR status and genotype on outcome in adult T-cell acute lymphoblastic leukemia: a LALA-94 study.
  • Patients with T-cell acute lymphoblastic leukemias (T-ALLs) within the Leucemies Aigues Lymphoblastiques de l'Adulte-94 (LALA-94) prospective trial were treated with a 4-drug per 4-week induction, with intermediate-dose cytarabine and mitoxantrone salvage treatment for patients not achieving complete remission (CR) in 1 course.
  • Representative patients with T-ALL (91 patients) were classified into surface T-cell receptor (TCR)-expressing T-ALL patients (TCRalphabeta+ or TCRgammadelta+), pre-alphabeta T-ALL patients (cTCRbeta+, TCR-), and immature (IM) cTCRbeta-, TCR- T-ALL patients; 81 patients underwent genotyping for SIL-TAL1, CALM-AF10, HOX11, and HOX11L2.
  • Once CR was obtained, cumulative relapse rates were similar for IM, pre-alphabeta, and TCR+ T-ALL patients (P = .51), but were higher in HOX11L2 (83%) and SIL-TAL1 (82%) T-ALL patients compared with other genetic subgroups (48%; P = .05).
  • This was associated with an inferior OS for HOX11L2 T-ALLs (13% vs 47% in HOX11L2-T-ALLs; P = .009).
  • Both TCR and genotypic stratification can therefore contribute to risk-adapted management of adult T-ALLs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics

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  • (PMID = 15637138.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Receptors, Antigen, T-Cell; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
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71. Malani AK, Gupta C, Rangineni R, Singh J, Ammar H: Concomitant presentation of acute myeloid leukemia with T-cell large granular lymphocytic leukemia. Acta Oncol; 2007;46(2):247-9
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  • [Title] Concomitant presentation of acute myeloid leukemia with T-cell large granular lymphocytic leukemia.
  • T-cell large granular lymphocyte leukemia (T-LGL) also known as T-cell chronic lymphocytic leukemia is rare and comprises a small minority of all small lymphocytic leukemias.
  • The concomitant presentation of T-LGL with acute myeloid leukemia (AML) has not been previously reported.
  • We present an elderly gentleman with concomitant T-LGL and AML (non-M3) diagnosed by a combination of morphologic evaluation, immunophenotyping by flow cytometry, and T-cell gene rearrangement studies.
  • He remains alive and well seven months after initial diagnosis.
  • [MeSH-major] Leukemia, Myeloid / diagnosis. Leukemia, Prolymphocytic, T-Cell / diagnosis
  • [MeSH-minor] Acute Disease. Aged, 80 and over. Antigens, CD / analysis. Flow Cytometry. Humans. Male

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  • (PMID = 17453377.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Antigens, CD
  • [Number-of-references] 17
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72. Perseghin P, Terruzzi E, Dassi M, Baldini V, Parma M, Coluccia P, Accorsi P, Confalonieri G, Tavecchia L, Verga L, Ravagnani F, Iacone A, Pogliani EM, Pioltelli P: Management of poor peripheral blood stem cell mobilization: incidence, predictive factors, alternative strategies and outcome. A retrospective analysis on 2177 patients from three major Italian institutions. Transfus Apher Sci; 2009 Aug;41(1):33-7
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  • [Title] Management of poor peripheral blood stem cell mobilization: incidence, predictive factors, alternative strategies and outcome. A retrospective analysis on 2177 patients from three major Italian institutions.
  • Patients' characteristics, including age, sex, stage of the underlying disease (complete or partial remission), diagnosis, previously administered radio/chemotherapy regimens, time-lapse from last chemotherapy before mobilization and mobilization schedule (including dose of GF) were considered as possibly predictive of poor or failed mobilization.
  • Therefore, a patient who fails a first mobilization (and when an HLA-compatible related on unrelated donor is not available) could undergo a second attempt either with different mobilization schedule or by using different GF, such as stem cell factor, growth hormone (GH), or more recently newly introduced drugs such as AMD3100, alone or in combination with rHuG- or -rHuGM-CSF.
  • [MeSH-major] Neoplasms / surgery. Peripheral Blood Stem Cell Transplantation / methods
  • [MeSH-minor] Adult. Antigens, CD34 / blood. Follow-Up Studies. Hematopoiesis. Hematopoietic Stem Cell Mobilization / methods. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / surgery. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / surgery. Leukemia, Myeloid, Acute / surgery. Lymphoma, Non-Hodgkin / surgery. Multiple Myeloma / surgery. Retrospective Studies. Survival Analysis

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  • (PMID = 19540167.001).
  • [ISSN] 1473-0502
  • [Journal-full-title] Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis
  • [ISO-abbreviation] Transfus. Apher. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34
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73. Rolny C, Lu L, Agren N, Nilsson I, Roe C, Webb GC, Welsh M: Shb promotes blood vessel formation in embryoid bodies by augmenting vascular endothelial growth factor receptor-2 and platelet-derived growth factor receptor-beta signaling. Exp Cell Res; 2005 Aug 15;308(2):381-93
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  • [Title] Shb promotes blood vessel formation in embryoid bodies by augmenting vascular endothelial growth factor receptor-2 and platelet-derived growth factor receptor-beta signaling.
  • To elucidate a possible role of Shb in embryonic vascular development, wild-type and SH2 domain mutated (R522K) Shb were overexpressed in murine embryonic stem (ES) cells.
  • This response may be the consequence of an increased number of VEGFR-2 positive cells at an early stage of EB development, a finding corroborated by both immunostaining and real-time RT-PCR.
  • The findings suggest that Shb may play a crucial role during early ES cell differentiation to vascular structures by transducing VEGFR-2 and PDGFR-beta signals.
  • [MeSH-major] Blood Vessels / embryology. Blood Vessels / metabolism. Neovascularization, Physiologic / physiology. Pluripotent Stem Cells / metabolism. Proto-Oncogene Proteins / metabolism. Receptor, Platelet-Derived Growth Factor beta / metabolism. Up-Regulation / physiology. Vascular Endothelial Growth Factor Receptor-2 / metabolism
  • [MeSH-minor] Animals. Antigens, CD31 / metabolism. Basic Helix-Loop-Helix Transcription Factors. Cell Differentiation / physiology. Cell Line. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Embryo Culture Techniques. Endothelial Cells / cytology. Endothelial Cells / metabolism. Gene Expression Profiling. Gene Expression Regulation, Developmental / physiology. Mice. Mutation / genetics. Oligonucleotide Array Sequence Analysis. Phenotype. Platelet Membrane Glycoprotein IIb / genetics. Platelet Membrane Glycoprotein IIb / metabolism. RNA, Messenger / metabolism. Signal Transduction / physiology. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 15919073.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Platelet Membrane Glycoprotein IIb; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Shb protein, mouse; 0 / Tal1 protein, mouse; 0 / Transcription Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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74. Leung KT, Li KK, Sun SS, Chan PK, Ooi VE, Chiu LC: Activation of the JNK pathway promotes phosphorylation and degradation of BimEL--a novel mechanism of chemoresistance in T-cell acute lymphoblastic leukemia. Carcinogenesis; 2008 Mar;29(3):544-51
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  • [Title] Activation of the JNK pathway promotes phosphorylation and degradation of BimEL--a novel mechanism of chemoresistance in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemias (T-ALLs) are highly malignant tumors with 20% of patients continues to fail therapy, in part due to chemoresistance of T-ALL cells via largely unknown mechanisms.
  • Here, we showed that lack of Bcl-2-interacting mediator of cell death (Bim)(EL) protein expression, a BH3-only member of the Bcl-2 family proteins, conferred resistance of a T-ALL cell line, Sup-T1, to etoposide-induced apoptosis.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Drug Resistance, Neoplasm. Leukemia-Lymphoma, Adult T-Cell / metabolism. MAP Kinase Kinase 4 / metabolism. Membrane Proteins / metabolism. Proto-Oncogene Proteins / metabolism


75. Van Vlierberghe P, Homminga I, Zuurbier L, Gladdines-Buijs J, van Wering ER, Horstmann M, Beverloo HB, Pieters R, Meijerink JP: Cooperative genetic defects in TLX3 rearranged pediatric T-ALL. Leukemia; 2008 Apr;22(4):762-70
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  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.
  • [MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion
  • [MeSH-minor] Cell Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics

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  • (PMID = 18185524.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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76. Seegmiller AC, Kroft SH, Karandikar NJ, McKenna RW: Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia. Am J Clin Pathol; 2009 Dec;132(6):940-9
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  • [Title] Characterization of immunophenotypic aberrancies in 200 cases of B acute lymphoblastic leukemia.
  • Morphologic distinction of leukemic lymphoblasts in B acute lymphoblastic leukemia (B-ALL) from their nonneoplastic counterparts in bone marrow (hematogones) can be difficult.
  • 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.
  • [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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77. Donahue RE, Jin P, Bonifacino AC, Metzger ME, Ren J, Wang E, Stroncek DF: Plerixafor (AMD3100) and granulocyte colony-stimulating factor (G-CSF) mobilize different CD34+ cell populations based on global gene and microRNA expression signatures. Blood; 2009 Sep 17;114(12):2530-41
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  • [Title] Plerixafor (AMD3100) and granulocyte colony-stimulating factor (G-CSF) mobilize different CD34+ cell populations based on global gene and microRNA expression signatures.
  • Three peripheral blood stem cell concentrates were collected from 3 macaques treated with G-CSF, plerixafor, or plerixafor plus G-CSF.
  • Plerixafor-mobilized cells were enriched for B cells, T cells, and mast cell genes, and G-CSF-mobilized cells were enriched for neutrophils and mononuclear phagocyte genes.
  • Two hematopoietic progenitor cell miR, miR-10 and miR-126, and a dendritic cell miR, miR-155, were up-regulated in G-CSF-mobilized CD34(+) cells.
  • A pre-B-cell acute lymphocytic leukemia miR, miR-143-3p, and a T-cell miR, miR-143-5p, were up-regulated in plerixafor plus G-CSF-mobilized cells.
  • Plerixafor-mobilized CD34(+) cells include more B-, T-, and mast cell precursors, whereas G-CSF-mobilized cells have more neutrophil and mononuclear phagocyte precursors.
  • [MeSH-major] Antigens, CD34 / metabolism. Gene Expression Profiling. Gene Expression Regulation / drug effects. Granulocyte Colony-Stimulating Factor / pharmacology. Hematopoietic Stem Cell Mobilization. Heterocyclic Compounds / pharmacology. MicroRNAs / genetics

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  • [Cites] Exp Hematol. 2006 Aug;34(8):1052-9 [16863911.001]
  • [Cites] Blood. 2006 May 1;107(9):3772-8 [16439684.001]
  • [Cites] Biol Blood Marrow Transplant. 2007 Apr;13(4):398-411 [17382247.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):1007-11 [17581586.001]
  • [Cites] PLoS One. 2007;2(10):e1020 [17925868.001]
  • [Cites] J Immunol. 2008 Jun 1;180(11):7358-67 [18490735.001]
  • [Cites] Blood. 2008 Aug 15;112(4):990-8 [18426988.001]
  • [Cites] J Transl Med. 2008;6:39 [18647411.001]
  • [Cites] Blood. 2008 Sep 1;112(5):2092-100 [18523146.001]
  • [Cites] Sci Signal. 2009 Jan 6;2(52):pe1 [19126861.001]
  • [Cites] Cell Stem Cell. 2009 Jan 9;4(1):62-72 [19128793.001]
  • [Cites] Pediatr Hematol Oncol. 2009 Jan;26(1):1-10 [19206004.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2735-40 [19193853.001]
  • [Cites] J Cell Biochem. 2006 Oct 15;99(3):690-705 [16888804.001]
  • [Cites] J Clin Invest. 2000 Dec;106(11):1331-9 [11104786.001]
  • [Cites] Genome Biol. 2003;4(5):P3 [12734009.001]
  • [Cites] Blood. 2003 Oct 15;102(8):2728-30 [12855591.001]
  • [Cites] J Clin Oncol. 2004 Mar 15;22(6):1095-102 [15020611.001]
  • [Cites] Blood. 1996 Feb 15;87(4):1644-53 [8608259.001]
  • [Cites] Blood. 1997 May 15;89(10):3522-8 [9160656.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] Science. 1999 Feb 5;283(5403):845-8 [9933168.001]
  • [Cites] Transfus Apher Sci. 2004 Dec;31(3):233-43 [15556471.001]
  • [Cites] Transfusion. 2005 Mar;45(3):295-300 [15752146.001]
  • [Cites] J Exp Med. 2005 Apr 18;201(8):1307-18 [15837815.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1867-74 [15890685.001]
  • [Cites] Blood. 2005 Dec 1;106(12):4002-8 [16105977.001]
  • [Cites] Blood. 2006 Feb 1;107(3):870-9 [16204315.001]
  • [Cites] Bone. 2006 Apr;38(4):497-508 [16337237.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5078-83 [16549775.001]
  • [CommentIn] Blood. 2010 Jan 28;115(4):916-7 [20110438.001]
  • (PMID = 19602709.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Antigens, CD34; 0 / Biomarkers; 0 / Drug Combinations; 0 / Heterocyclic Compounds; 0 / MicroRNAs; 0 / RNA, Messenger; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 155148-31-5 / JM 3100
  • [Other-IDs] NLM/ PMC2746476
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78. Szczepański T, Harrison CJ, van Dongen JJ: Genetic aberrations in paediatric acute leukaemias and implications for management of patients. Lancet Oncol; 2010 Sep;11(9):880-9
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  • [Title] Genetic aberrations in paediatric acute leukaemias and implications for management of patients.
  • The process of malignant transformation in paediatric acute leukaemias is complex, requiring at least two deleterious events resulting in DNA damage.
  • In this review we summarise the most common genetic aberrations for the three main subtypes of paediatric acute leukaemia: B-cell-precursor acute lymphoblastic leukaemia, T-cell acute lymphoblastic leukaemia and acute myeloid leukaemia.
  • Some genetic aberrations represent sensitive targets for molecular detection of minimal residual disease.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Chromosome Aberrations. Leukemia / genetics

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20435517.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 76
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79. Buie LW, Epstein SS, Lindley CM: Nelarabine: a novel purine antimetabolite antineoplastic agent. Clin Ther; 2007 Sep;29(9):1887-99
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Nelarabine was approved by the US Food and Drug Administration (FDA) in October 2005 for the treatment of T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL) that has not responded to or has relapsed after treatment with at least 2 chemotherapy regimens.
  • Nelarabine has activity in T-cell malignancies, as evaluated in 2 Phase I and 5 Phase II studies.
  • In PGAA 2001, patients with T-ALL in first relapse (n = 33) had an objective response rate of 55% (16 with a complete response [CR] and 2 with a partial response [PR]), and those with T-ALL in second relapse (n = 30) had an objective response rate of 27% (7 CR and 1 PR).
  • Among patients with central nervous system-positive T-ALL or T-cell non-Hodgkins lymphoma (T-NHL) (n = 21), 33% had an objective response (5 CR and 2 PR); among patients with T-ALL or T-NHL with extramedullary relapse (n = 22), 14% had a PR.
  • CALGB 19801 included 39 adult patients with T-cell malignancies, of whom 7 (18%) had a CR and an additional 2 (5%) had a CR without full hematologic recovery.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Arabinonucleosides / therapeutic use. Hematologic Neoplasms / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Lymphoma, T-Cell / drug therapy. Purine Nucleosides / therapeutic use

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  • (PMID = 18035189.001).
  • [ISSN] 0149-2918
  • [Journal-full-title] Clinical therapeutics
  • [ISO-abbreviation] Clin Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Arabinonucleosides; 0 / Purine Nucleosides; 60158CV180 / nelarabine
  • [Number-of-references] 29
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80. Seror E, Coquerel B, Gautheret-Dejean A, Ballerini P, Landman-Parker J, Leverger G, Schneider P, Vannier JP: Quantitation of Human herpes virus 6 genome in children with acute lymphoblastic leukemia. J Med Virol; 2008 Apr;80(4):689-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantitation of Human herpes virus 6 genome in children with acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia is the main type of leukemia in children.
  • The potential role of HHV-6 in the pathogenesis of pediatric acute lymphoblastic leukemia was investigated.
  • HHV-6 genome copy number was measured by quantitative real-time PCR (RQ-PCR) in bone marrow or peripheral blood samples obtained from 36 children (median age = 4 years) with B acute lymphoblastic leukemia (n = 31) and T acute lymphoblastic leukemia (n = 5) at diagnosis and during complete remission.
  • A total of 24.7% of samples were positive for HHV-6 genome: 13.9% were leukemia samples and 34.1% were complete remission samples.
  • Viral load was low with values lower at diagnosis (median viral copy number = 22.9) than at complete remission (median copy number = 60.1).
  • These results argue against a role of HHV6 infection in the development of pediatric acute lymphoblastic leukemia.
  • [MeSH-major] DNA, Viral / analysis. Herpesvirus 6, Human / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / virology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / virology. Roseolovirus Infections / complications. Roseolovirus Infections / virology

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  • (PMID = 18297709.001).
  • [ISSN] 0146-6615
  • [Journal-full-title] Journal of medical virology
  • [ISO-abbreviation] J. Med. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral
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81. Lin YW, Beharry ZM, Hill EG, Song JH, Wang W, Xia Z, Zhang Z, Aplan PD, Aster JC, Smith CD, Kraft AS: A small molecule inhibitor of Pim protein kinases blocks the growth of precursor T-cell lymphoblastic leukemia/lymphoma. Blood; 2010 Jan 28;115(4):824-33
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  • [Title] A small molecule inhibitor of Pim protein kinases blocks the growth of precursor T-cell lymphoblastic leukemia/lymphoma.
  • We demonstrate that SMI-4a, a novel benzylidene-thiazolidine-2, 4-dione small molecule inhibitor of the Pim kinases, kills a wide range of both myeloid and lymphoid cell lines with precursor T-cell lymphoblastic leukemia/lymphoma (pre-T-LBL/T-ALL) being highly sensitive.
  • Incubation of pre-T-LBL cells with SMI-4a induced G1 phase cell-cycle arrest secondary to a dose-dependent induction of p27(Kip1), apoptosis through the mitochondrial pathway, and inhibition of the mammalian target of rapamycin C1 (mTORC1) pathway based on decreases in phospho-p70 S6K and phospho-4E-BP1, 2 substrates of this enzyme.
  • In addition, treatment of these cells with SMI-4a was found to induce phosphorylation of extracellular signal-related kinase1/2 (ERK1/2), and the combination of SMI-4a and a mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor was highly synergistic in killing pre-T-LBL cells.
  • In immunodeficient mice carrying subcutaneous pre-T-LBL tumors, treatment twice daily with SMI-4a caused a significant delay in the tumor growth without any change in the weight, blood counts, or chemistries.
  • Our data suggest that inhibition of the Pim protein kinases may be developed as a therapeutic strategy for the treatment of pre-T-LBL.


82. Chiu PP, Jiang H, Dick JE: Leukemia-initiating cells in human T-lymphoblastic leukemia exhibit glucocorticoid resistance. Blood; 2010 Dec 9;116(24):5268-79
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  • [Title] Leukemia-initiating cells in human T-lymphoblastic leukemia exhibit glucocorticoid resistance.
  • T-cell acute lymphoblastic leukemia (T-ALL) is associated with a significant risk of disease relapse, but the biological basis for relapse is poorly understood.
  • Here, we identify leukemiainitiating cells (L-ICs) on the basis of functional assays and prospective isolation and report a role for L-ICs in T-ALL disease and relapse.
  • Long-term proliferation in response to NOTCH1 activating signals in OP9-DL1 coculture system or capacity to initiate leukemia in xenografts by the CD7(+)CD1a(-) subset of primary T-ALL samples was superior to other subsets, refining the identity of T-ALL L-ICs.
  • T-ALL engraftment was improved in nonobese diabetic/severe combined immunodeficiency (NOD/scid)IL2Rγ(null) (NSG) mice compared with NOD/scid with anti-CD122 treatment (NS122), but both showed changes in leukemia immunophenotype.
  • Our results establish that primary CD1a(-) T-ALL cells are functionally distinct from CD1a(+) cells and that the CD7(+)CD1a(-) subset is enriched for L-IC activity that may be involved in mediating disease relapse after therapy.
  • [MeSH-minor] Animals. Antigens, CD1. Antigens, CD7. Antineoplastic Agents, Hormonal / pharmacology. Cell Proliferation. Clone Cells / pathology. Coculture Techniques. Dexamethasone / pharmacology. Humans. Immunophenotyping. Mice. Mice, SCID. Receptor, Notch1 / metabolism. Recurrence. Transplantation, Heterologous

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  • (PMID = 20810926.001).
  • [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 / Antigens, CD1; 0 / Antigens, CD7; 0 / Antineoplastic Agents, Hormonal; 0 / CD1a antigen; 0 / Glucocorticoids; 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; 7S5I7G3JQL / Dexamethasone
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83. Choi J, Foss F: Efficacy of low dose clofarabine in refractory precursor T- acute lymphoblastic leukemia. Yale J Biol Med; 2006 Dec;79(3-4):169-72
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  • [Title] Efficacy of low dose clofarabine in refractory precursor T- acute lymphoblastic leukemia.
  • Refractory T-lymphoblastic leukemia in adults has a poor prognosis in patients who relapse after allogeneic stem cell transplantation, and relatively few new agents have demonstrated activity.
  • We used low dose clofarabine and induced a remission in a patient who relapsed in the skin and marrow after allogeneic transplant and was refractory to nelarabine and report a near complete response, suggesting significant activity for low intermittent dose clofarabine in patients with relapsed T-cell leukemias.
  • [MeSH-major] Adenine Nucleotides / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Adult. Bone Marrow Neoplasms / drug therapy. Bone Marrow Neoplasms / secondary. Clinical Trials as Topic. Drug Administration Schedule. Drug Resistance, Neoplasm. Humans. Immunophenotyping. Male. Recurrence. Skin Neoplasms / drug therapy. Skin Neoplasms / secondary. Stem Cell Transplantation. Transplantation, Homologous. Treatment Outcome

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  • [Cites] J Clin Oncol. 2004 Oct 15;22(20):4075-86 [15353542.001]
  • [Cites] Nat Rev Drug Discov. 2006 Oct;5(10):855-63 [17016426.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3396-403 [15908652.001]
  • [Cites] Mol Pharmacol. 2006 Jan;69(1):346-53 [16234483.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] J Clin Oncol. 2006 Apr 20;24(12):1917-23 [16622268.001]
  • [Cites] Cancer Res. 1991 May 1;51(9):2386-94 [1707752.001]
  • [Cites] J Clin Oncol. 2003 Mar 15;21(6):1167-73 [12637486.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2379-86 [12791647.001]
  • [Cites] Blood. 2004 Feb 1;103(3):784-9 [14551141.001]
  • (PMID = 17940627.001).
  • [ISSN] 1551-4056
  • [Journal-full-title] The Yale journal of biology and medicine
  • [ISO-abbreviation] Yale J Biol Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Arabinonucleosides; 60158CV180 / nelarabine; 762RDY0Y2H / clofarabine
  • [Other-IDs] NLM/ PMC1994805
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84. Gong H, Liu WL, Zhou JF, Xu HZ: [Expression of mitosis checkpoint gene CHFR in acute leukemia]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1085-8
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  • [Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].
  • OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.
  • METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
  • The cell cycle was examined by flow cytometric analysis.
  • (1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
  • CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.
  • Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 16029562.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
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85. Malissen B, Luche H: Immunology: Egocentric pre-T-cell receptors. Nature; 2010 Oct 14;467(7317):793-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunology: Egocentric pre-T-cell receptors.
  • [MeSH-major] Protein Multimerization. Receptors, Antigen, T-Cell, alpha-beta / chemistry. Receptors, Antigen, T-Cell, alpha-beta / metabolism

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  • [CommentOn] Nature. 2010 Oct 14;467(7317):844-8 [20944746.001]
  • (PMID = 20944732.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] eng
  • [Publication-type] Comment; News
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta
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86. Ikezoe T, Yang Y, Bandobashi K, Saito T, Takemoto S, Machida H, Togitani K, Koeffler HP, Taguchi H: Oridonin, a diterpenoid purified from Rabdosia rubescens, inhibits the proliferation of cells from lymphoid malignancies in association with blockade of the NF-kappa B signal pathways. Mol Cancer Ther; 2005 Apr;4(4):578-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This study found that oridonin, a natural diterpenoid purified from Rabdosia rubescens, inhibited growth of multiple myeloma (MM; U266, RPMI8226), acute lymphoblastic T-cell leukemia (Jurkat), and adult T-cell leukemia (MT-1) cells with an effective dose that inhibited 50% of target cells (ED50) ranging from 0.75 to 2.7 microg/mL.
  • Of note, oridonin decreased survival of freshly isolated adult T-cell leukemia (three samples), acute lymphoblastic leukemia (one sample), chronic lymphocytic leukemia (one sample), non-Hodgkin's lymphoma (three samples), and MM (four samples) cells from patients in association with inhibition of NF-kappa B DNA-binding activity.
  • Taken together, oridonin might be useful as adjunctive therapy for individuals with lymphoid malignancies, including the lethal disease adult T-cell leukemia.
  • [MeSH-major] Cell Proliferation / drug effects. Diterpenes / pharmacology. Isodon / metabolism. NF-kappa B / metabolism. Phytotherapy / methods. Plant Extracts / pharmacology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Apoptosis. Blotting, Western. Cell Line. Cell Line, Tumor. Diterpenes, Kaurane. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Female. Genes, Reporter. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / metabolism. Humans. In Situ Nick-End Labeling. Jurkat Cells. Leukemia / drug therapy. Leukemia / pathology. Lipopolysaccharides / metabolism. Male. Mice. Middle Aged. Models, Chemical. Multiple Myeloma / drug therapy. Multiple Myeloma / pathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction. T-Lymphocytes / metabolism. T-Lymphocytes / virology. Thymidine / chemistry. Thymidine / metabolism. Time Factors. Transfection. Trypan Blue / pharmacology. bcl-X Protein

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  • (PMID = 15827331.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / Diterpenes; 0 / Diterpenes, Kaurane; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein; 0APJ98UCLQ / oridonin; I2ZWO3LS3M / Trypan Blue; VC2W18DGKR / Thymidine
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87. Maruo T, Namikawa K, Kunihiro A, Lynch J, Shida T, Kishikawa S: Large granular lymphocytic leukaemia complicated with histiocytic sarcoma in a dog. J S Afr Vet Assoc; 2009 Dec;80(4):261-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Large granular lymphocytic leukaemia complicated with histiocytic sarcoma in a dog.
  • Based on these findings this case was diagnosed as LGL leukaemia.
  • Shortly after diagnosis, the dog developed sudden onset of central nervous system signs and died on day 270.
  • A common outcome of canine LGL is the development of acute blast crisis or lymphoma.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Histiocytic Sarcoma / veterinary. Leukemia, Large Granular Lymphocytic / veterinary

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