[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 1118
1. Kong KY, Williamson EA, Rogers JH, Tran T, Hromas R, Dahl R: Expression of Scl in mesoderm rescues hematopoiesis in the absence of Oct-4. Blood; 2009 Jul 2;114(1):60-3
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, hematopoiesis can be rescued in the absence of Oct-4 after mesoderm specification if the essential hematopoietic transcription factor stem cell leukemia is expressed.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Genet. 2000 Apr;24(4):372-6 [10742100.001]
  • [Cites] Development. 2000 Jun;127(11):2447-59 [10804185.001]
  • [Cites] Development. 2003 Jun;130(11):2505-12 [12702663.001]
  • [Cites] Genesis. 2003 Sep;37(1):18-24 [14502573.001]
  • [Cites] Nature. 1990 Mar 29;344(6265):435-9 [1690859.001]
  • [Cites] Nature. 1990 Jun 21;345(6277):686-92 [1972777.001]
  • [Cites] Stem Cells. 2006 Aug;24(8):1937-45 [16690781.001]
  • [Cites] Development. 1996 Mar;122(3):881-94 [8631266.001]
  • [Cites] Blood. 1997 Aug 15;90(4):1435-47 [9269761.001]
  • [Cites] Development. 1998 Feb;125(4):725-32 [9435292.001]
  • [Cites] Cell. 1998 Oct 30;95(3):379-91 [9814708.001]
  • [Cites] Biochem Cell Biol. 1998;76(6):947-56 [10392708.001]
  • [Cites] Genes Dev. 1999 Oct 1;13(19):2478-83 [10521392.001]
  • [Cites] Immunity. 1995 Dec;3(6):703-14 [8777716.001]
  • (PMID = 19321862.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102283; United States / NHLBI NIH HHS / HL / R01 HL075783; United States / NCI NIH HHS / CA / CA102283; United States / NHLBI NIH HHS / HL / HL075783
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Octamer Transcription Factor-3; 0 / Pou5f1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Recombinant Proteins; 0 / Tal1 protein, mouse
  • [Other-IDs] NLM/ PMC2710954
  •  go-up   go-down


2. Cossu F: Genetics of SCID. Ital J Pediatr; 2010;36:76
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


Advertisement
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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. (L)-Methionine .
  • Hazardous Substances Data Bank. L-Threonine .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


6. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


7. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • ZFIN. ZFIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


8. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYCLOSPORIN A .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


9. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


10. Park TS, Cheong JW, Song J, Choi JR: Therapy-related myelodysplastic syndrome with der(17)t(12;17)(q13;p13) as a new recurrent cytogenetic abnormality after treatment for chronic lymphocytic leukemia. Leuk Res; 2009 Jul;33(7):1001-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related myelodysplastic syndrome with der(17)t(12;17)(q13;p13) as a new recurrent cytogenetic abnormality after treatment for chronic lymphocytic leukemia.
  • He was initially diagnosed with chronic lymphocytic leukemia (CLL) and treated with six cycles of fludarabine, cyclophosphamide, and rituximab chemotherapy.
  • The chromosomal abnormality der(17)t(12;17)(q13;p13) is very rare in hematologic malignancies, and has been reported in only two patients with therapy-related acute myeloid leukemia (t-AML).
  • In addition, we suggest that der(17)t(12;17)(q13;p13) should be considered a new recurrent, nonrandom chromosomal abnormality in patients with t-MDS/AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics. Translocation, Genetic / genetics


11. Wandroo F, Bell A, Darbyshire P, Pratt G, Stankovic T, Gordon J, Lawson S, Moss P: ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia. Int J Lab Hematol; 2008 Apr;30(2):149-57
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia.
  • ZAP-70 is, however, expressed in adult B cell chronic lymphocytic leukemia where it correlates with a poor prognosis.
  • We wished to determine if ZAP-70 is also expressed in pediatric B cell malignancy.
  • A quantitative PCR assay for ZAP-70 expression was established and ZAP-70 expression in a range of human B cell lines was compared with expression in the Jurkat T cell line.
  • ZAP-70 expression was then determined in bone marrow lymphoblasts obtained from 12 patients with pre-B cell acute lymphoblastic leukemia (ALL).
  • ZAP-70 expression was not detected in mature B cell lines but was detected in pre-B cell lines at a level comparable to that seen in T cells.
  • ZAP-70 expression was strongly expressed in nine of the 12 cases of primary pre-B cell lymphoblastic leukemia.
  • The T cell-associated protein kinase ZAP-70 is highly expressed in pre-B lineage cells and most cases of pre-B acute lymphoblastic leukemia.
  • ZAP-70 expression may hold prognostic value for pre-B ALL and raises the prospect of a novel therapeutic target.
  • [MeSH-major] B-Lymphocytes / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cells, B-Lymphoid / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism
  • [MeSH-minor] Adolescent. Blotting, Western. Bone Marrow Cells / metabolism. Cell Line, Transformed. Cell Line, Tumor. Child. Child, Preschool. Female. Flow Cytometry. Gene Expression. Humans. Jurkat Cells. Male. Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18333847.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
  •  go-up   go-down


12. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TESTOSTERONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


13. Jacobs SA, Foon KA: Monoclonal antibody therapy of leukaemias and lymphomas. Expert Opin Biol Ther; 2005 Sep;5(9):1225-43
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Aminoglycosides / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia / drug therapy. Lymphoma / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antigens, CD / immunology. Antigens, CD20 / immunology. Antigens, Differentiation, Myelomonocytic / immunology. Antigens, Neoplasm / immunology. Glycoproteins / immunology. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Leukemia, T-Cell / drug therapy. Lymphoma, B-Cell / drug therapy. Lymphoma, Follicular / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Randomized Controlled Trials as Topic. Rituximab. Sialic Acid Binding Ig-like Lectin 3

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16120052.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, CD20; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / CD52 antigen; 0 / Glycoproteins; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / gemtuzumab; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 170
  •  go-up   go-down


14. Roecker AM, Allison JC, Kisor DF: Nelarabine: efficacy in the treatment of clinical malignancies. Future Oncol; 2006 Aug;2(4):441-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • COS Scholar Universe. author profiles.
  • SciCrunch. DrugBank: Data: Chemical .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


15. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


16. Tageja N, Mohammad M, Bentley G, Bishop C: Adult T-Cell Leukemia/Lymphoma with CLL-Like Morphology-A Case Report. Case Rep Med; 2010;2010:729790
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-Cell Leukemia/Lymphoma with CLL-Like Morphology-A Case Report.
  • Adult T-cell Leukemia/Lymphoma (ATL) is rarely seen in the U.S. and Europe, usually limited to African Americans from the southeastern U.S. and immigrants from HTLV-1 endemic areas.
  • Reaching an accurate and timely diagnosis of ATL in such nonendemic areas can be challenging, owing to limited exposure, diverse manifestations, and varying cell morphology.
  • We present a case of chronic adult T-cell leukemia (ATL) with Chronic Lymphocytic Leukemia- (CLL-) like morphology that remained untreated for ten years and then developed treatment refractory acute ATL crisis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 1994 Feb;86(2):383-5 [8199030.001]
  • [Cites] Br J Haematol. 1999 May;105(2):369-75 [10233406.001]
  • [Cites] J Clin Pathol. 2007 Dec;60(12):1373-7 [18042693.001]
  • [Cites] Leuk Lymphoma. 1993 Dec;12(1-2):123-30 [8161929.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] J Clin Pathol. 1989 Jun;42(6):567-84 [2738163.001]
  • [Cites] Eur J Haematol. 2008 Mar;80(3):185-96 [18081707.001]
  • (PMID = 20368783.001).
  • [ISSN] 1687-9635
  • [Journal-full-title] Case reports in medicine
  • [ISO-abbreviation] Case Rep Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2846349
  •  go-up   go-down


17. Xiong JW, Yu Q, Zhang J, Mably JD: An acyltransferase controls the generation of hematopoietic and endothelial lineages in zebrafish. Circ Res; 2008 May 9;102(9):1057-64
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The molecular pathway that regulates the specification of both cell lineages remains elusive.
  • We isolated lycat from the deletion interval of cloche, a zebrafish mutant that has dramatically reduced hematopoietic and endothelial cell lineages.
  • Reduction of lycat mRNA levels in wild-type zebrafish embryos decreases both endothelial and hematopoietic lineages.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • SciCrunch. ZFIN: Data: Gene Expression .
  • The Lens. Cited by Patents in .
  • ZFIN. ZFIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mech Dev. 2000 Feb;90(2):237-52 [10640707.001]
  • [Cites] Science. 2001 Sep 14;293(5537):2080-4 [11486055.001]
  • [Cites] Dev Cell. 2002 Jul;3(1):127-36 [12110173.001]
  • [Cites] Biochemistry. 2003 Apr 22;42(15):4311-20 [12693927.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2003 May 1;23(5):911-2 [12740225.001]
  • [Cites] Nature. 2003 May 22;423(6938):448-52 [12717451.001]
  • [Cites] Development. 2003 Dec;130(25):6187-99 [14602685.001]
  • [Cites] Development. 1995 Oct;121(10):3141-50 [7588049.001]
  • [Cites] Genes Dev. 1996 Dec 15;10(24):3116-28 [8985181.001]
  • [Cites] Development. 1996 Dec;123:285-92 [9007248.001]
  • [Cites] Development. 1997 Jan;124(2):381-9 [9053314.001]
  • [Cites] Dev Biol. 1997 Mar 1;183(1):37-48 [9119113.001]
  • [Cites] Development. 1997 Oct;124(20):4105-11 [9374406.001]
  • [Cites] Development. 1998 Feb;125(4):725-32 [9435292.001]
  • [Cites] Genes Dev. 1998 Mar 1;12(5):621-6 [9499398.001]
  • [Cites] Development. 1999 Nov;126(21):4691-701 [10518487.001]
  • [Cites] Nature. 2004 Dec 2;432(7017):625-30 [15577911.001]
  • [Cites] Dev Biol. 2005 Jan 15;277(2):522-36 [15617691.001]
  • [Cites] Dev Cell. 2005 Mar;8(3):389-400 [15737934.001]
  • [Cites] Blood. 2005 May 1;105(9):3502-11 [15644413.001]
  • [Cites] Dev Dyn. 2005 Jul;233(3):1163-72 [15937927.001]
  • [Cites] Blood. 2005 Jul 15;106(2):534-41 [15802528.001]
  • [Cites] Blood. 2005 Jul 15;106(2):521-30 [15827125.001]
  • [Cites] Development. 2005 Dec;132(23):5199-209 [16251212.001]
  • [Cites] Development. 2003 Nov;130(22):5297-305 [14530294.001]
  • [Cites] Cell. 2006 Jun 2;125(5):1003-13 [16751107.001]
  • [Cites] J Cell Sci. 2004 Feb 1;117(Pt 4):521-6 [14730009.001]
  • [Cites] J Biol Chem. 2004 Jul 23;279(30):31727-34 [15152008.001]
  • [Cites] Development. 2006 Sep;133(18):3641-50 [16914492.001]
  • [Cites] Nature. 2006 Sep 21;443(7109):337-9 [16988712.001]
  • [Cites] Dev Cell. 2006 Oct;11(4):519-33 [17011491.001]
  • [Cites] Dev Biol. 2007 Mar 15;303(2):772-83 [17125762.001]
  • [Cites] Blood. 2007 Apr 1;109(7):2679-87 [17148580.001]
  • [Cites] PLoS Biol. 2007 May;5(5):e132 [17472439.001]
  • [Cites] Nat Methods. 2007 Jun;4(6):501-9 [17486087.001]
  • [Cites] Blood. 2007 Nov 15;110(10):3601-9 [17675553.001]
  • [Cites] PLoS Biol. 2006 Jan;4(1):e10 [16336046.001]
  • [CommentIn] Circ Res. 2008 May 9;102(9):1005-7 [18467639.001]
  • (PMID = 18388326.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG019676-05; United States / NIA NIH HHS / AG / K01 AG019676; United States / NIA NIH HHS / AG / K01 AG019676-05; United States / NIA NIH HHS / AG / K01-AG19676
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Etsrp protein, zebrafish; 0 / Morpholines; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Recombinant Fusion Proteins; 0 / Zebrafish Proteins; 0 / tal1 protein, zebrafish; EC 2.3.- / Acyltransferases; EC 2.3.1.- / lysocardiolipin acyltransferase, mouse
  • [Other-IDs] NLM/ NIHMS46427; NLM/ PMC2405954
  •  go-up   go-down


18. DeAngelo DJ: The treatment of adolescents and young adults with acute lymphoblastic leukemia. Hematology Am Soc Hematol Educ Program; 2005;:123-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


19. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


20. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


21. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Cutaneous T-Cell Lymphoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


22. Hussein K, von Neuhoff N, Büsche G, Buhr T, Kreipe H, Bock O: Opposite expression pattern of Src kinase Lyn in acute and chronic haematological malignancies. Ann Hematol; 2009 Nov;88(11):1059-67
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Opposite expression pattern of Src kinase Lyn in acute and chronic haematological malignancies.
  • Lck/yes-related novel (Lyn) tyrosine kinase overexpression has been suggested to be important for leukaemic cell growth making it an attractive target for therapy.
  • We aimed to shed more light on Lyn's role in haematological neoplasm and systematically investigated Lyn expression in MPN, acute and chronic leukaemia subtypes (n = 236).
  • On top, B-cell chronic lymphocytic leukaemia (B-CLL) and chronic myeloid leukaemia significantly overexpressed Lyn when compared to de novo acute lymphoblastic leukaemia, de novo acute myeloid leukaemia (AML) and Philadelphia-chromosome-negative myeloproliferative neoplasms (p < 0.001).
  • Most of acute leukaemia subtypes showed a notable down-regulation of Lyn mRNA but anyhow individual cases were labelled for the active form of Lyn protein.
  • We conclude that tyrosine kinase Lyn contributes to the malignant phenotype in certain leukaemia subtypes and therefore attracts targeted therapy.
  • [MeSH-major] Leukemia / enzymology. Neoplasm Proteins / biosynthesis. src-Family Kinases / biosynthesis
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Bone Marrow / enzymology. Bone Marrow / pathology. Child. Child, Preschool. Chronic Disease. Female. Gene Expression Regulation, Leukemic. Humans. Janus Kinase 2 / genetics. Male. MicroRNAs / biosynthesis. MicroRNAs / genetics. Middle Aged. Neoplasms, Second Primary / enzymology. Neoplasms, Second Primary / genetics. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Receptors, Thrombopoietin / genetics. Young Adult

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19290526.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / Mirn337 microRNA, human; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Receptors, Thrombopoietin; 143641-95-6 / MPL protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.10.2 / lyn protein-tyrosine kinase; EC 2.7.10.2 / src-Family Kinases
  •  go-up   go-down


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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


24. Look AT: Investigator profile. An interview with A. Thomas Look, M.D. Interview by Vicki Glaser. Zebrafish; 2005;2(4):231-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18248181.001).
  • [ISSN] 1557-8542
  • [Journal-full-title] Zebrafish
  • [ISO-abbreviation] Zebrafish
  • [Language] eng
  • [Publication-type] Interview
  • [Publication-country] United States
  •  go-up   go-down


25. Kumagai T, Müller CI, Desmond JC, Imai Y, Heber D, Koeffler HP: Scutellaria baicalensis, a herbal medicine: anti-proliferative and apoptotic activity against acute lymphocytic leukemia, lymphoma and myeloma cell lines. Leuk Res; 2007 Apr;31(4):523-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Scutellaria baicalensis, a herbal medicine: anti-proliferative and apoptotic activity against acute lymphocytic leukemia, lymphoma and myeloma cell lines.
  • S.B inhibited the growth of ALL, lymphoma and myeloma cell lines by inducing apoptosis and cell cycle arrest at clinically achievable concentrations.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Apoptosis / drug effects. Cell Proliferation / drug effects. Drugs, Chinese Herbal / therapeutic use. Multiple Myeloma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Scutellaria baicalensis / chemistry
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Colony-Forming Units Assay. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Drug Screening Assays, Antitumor. Flavonoids / therapeutic use. Flow Cytometry. Humans. Membrane Potential, Mitochondrial / drug effects. Tumor Cells, Cultured / drug effects

  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17007926.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Drugs, Chinese Herbal; 0 / Flavonoids; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 347Q89U4M5 / baicalin
  •  go-up   go-down


31. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


32. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


33. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Multiple Sclerosis.
  • MedlinePlus Health Information. consumer health - Multiple Sclerosis.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FORMALDEHYDE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


35. Schetelig J, van Biezen A, Brand R, Caballero D, Martino R, Itala M, García-Marco JA, Volin L, Schmitz N, Schwerdtfeger R, Ganser A, Onida F, Mohr B, Stilgenbauer S, Bornhäuser M, de Witte T, Dreger P: Allogeneic hematopoietic stem-cell transplantation for chronic lymphocytic leukemia with 17p deletion: a retrospective European Group for Blood and Marrow Transplantation analysis. J Clin Oncol; 2008 Nov 1;26(31):5094-100
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic hematopoietic stem-cell transplantation for chronic lymphocytic leukemia with 17p deletion: a retrospective European Group for Blood and Marrow Transplantation analysis.
  • PURPOSE: Patients with chronic lymphocytic leukemia (CLL) and 17p deletion (17p-) have a poor prognosis.
  • Although allogeneic hematopoietic stem-cell transplantation (HCT) has the potential to cure patients with advanced CLL, it is not known whether this holds true for patients with 17p-CLL.
  • Acute, grade 2 to 4 graft-versus-host disease (GVHD) occurred in 43% of patients, and extensive chronic GVHD occurred in 53% of patients.
  • The cumulative incidence of progressive disease at 4 years was 34%.
  • CONCLUSION: Allogeneic HCT has the potential to induce long-term disease-free survival in patients with 17p-CLL.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 17. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cell Transplantation. Leukemia, Lymphocytic, Chronic, B-Cell / surgery
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Europe. Female. Graft vs Host Disease / etiology. Humans. Male. Middle Aged. Registries. Retrospective Studies. Surveys and Questionnaires. Time Factors. Transplantation, Homologous. Treatment Failure. Treatment Outcome

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18711173.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


36. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.
  • 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

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


37. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • SciCrunch. HGNC: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


38. Le Gouill S, Milpied N, Buzyn A, De Latour RP, Vernant JP, Mohty M, Moles MP, Bouabdallah K, Bulabois CE, Dupuis J, Rio B, Gratecos N, Yakoub-Agha I, Attal M, Tournilhac O, Decaudin D, Bourhis JH, Blaise D, Volteau C, Michallet M, Société Française de Greffe de Moëlle et de Thérapie Cellulaire: Graft-versus-lymphoma effect for aggressive T-cell lymphomas in adults: a study by the Société Francaise de Greffe de Moëlle et de Thérapie Cellulaire. J Clin Oncol; 2008 May 10;26(14):2264-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Graft-versus-lymphoma effect for aggressive T-cell lymphomas in adults: a study by the Société Francaise de Greffe de Moëlle et de Thérapie Cellulaire.
  • PURPOSE: Aggressive T-cell lymphomas (ATCLs) represent 10% to 15% of non-Hodgkin's lymphomas (NHLs) in adults.
  • ATCLs show a worse prognosis than B-cell lymphomas.
  • PATIENTS AND METHODS: On behalf of the Société Française de Greffe de Moëlle et de Thérapie Cellulaire, we conducted a retrospective analysis including 77 ATCL patients who underwent allogeneic stem-cell transplantation (alloSCT).
  • RESULTS: The different diagnosis included anaplastic large-cell lymphoma (ALCL; n = 27), peripheral T-cell lymphoma not otherwise specified (PTCL-NOS; n = 27), angioimmunoblastic T-cell lymphoma (AITL; n = 11), hepatosplenic gamma/delta lymphoma (HSL; n = 3), T-cell granular lymphocytic leukemia (T-GLL; n = 1), nasal natural killer (NK)/T-cell lymphoma (nasal-NK/L; n = 3) or non-nasal NK/T-cell lymphoma (non-nasal-NK/L; n = 2), enteropathy-type T-cell (n = 1), and human T-lymphotropic virus (HTLV)-1 lymphoma (n = 2).
  • Thirty-one patients were in complete remission (CR) at the time of alloSCT, whereas 26 were in partial response (PR).
  • In multivariate analysis, chemoresistant disease (stable, refractory, or progressing disease) at the time of alloSCT and the occurrence of severe grade 3 to 4 acute graft-versus-host disease (aGVHD) were the strongest adverse prognostic factors for OS (P = .03 and .03, respectively).
  • Disease status at transplantation significantly influenced the 5-year EFS (P = .003), and an HLA-mismatched donor increased TRM (P = .04).
  • [MeSH-major] Graft vs Tumor Effect / immunology. Lymphoma, T-Cell / immunology. Lymphoma, T-Cell / therapy. Stem Cell Transplantation
  • [MeSH-minor] Adolescent. Adult. Child. Disease-Free Survival. Female. Graft vs Host Disease / immunology. Humans. Male. Middle Aged. Retrospective Studies. Transplantation Conditioning. Transplantation, Homologous / immunology


39. Li AH, Qiu GQ, Gu WY, Ling Y, Weng KZ, Tan Q, Cao XS: [Expression of CD4+ CD25+ regulatory T cells in the patients with acute lymphocytic leukemia]. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi; 2007 May;23(5):439-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of CD4+ CD25+ regulatory T cells in the patients with acute lymphocytic leukemia].
  • AIM: To evaluate the proportion of CD4(+) CD25(+) Tregs in the peripheral blood of the patients suffering from acute lymphocytic leukemia (ALL) with or without chemotherapy and investigate whether the serum from patients could convert peripheral CD4(+) CD25(-) T cells to CD4(+) CD25(+) Tregs.
  • METHODS: The proportion of CD4(+) CD25(+) T cells in the peripheral blood of three groups of people (the patients with ALL before therapy, the patients with ALL who achieved partial remission (PR) or complete remission (CR) and the healthy donors) was evaluated by flow cytometry.
  • The serum derived from the patients with ALL can convert CD4(+) CD25(-) T cells to CD4(+) CD25(+) Tregs, which might be one of the important reasons for immunosuppression in ALL.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. T-Lymphocytes, Regulatory / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17488606.001).
  • [ISSN] 1007-8738
  • [Journal-full-title] Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
  • [ISO-abbreviation] Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Interleukin-2 Receptor alpha Subunit
  •  go-up   go-down


40. Hagemeijer A, Graux C: ABL1 rearrangements in T-cell acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2010 Apr;49(4):299-308
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


41. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


42. Terme JM, Mocquet V, Kuhlmann AS, Zane L, Mortreux F, Wattel E, Duc Dodon M, Jalinot P: Inhibition of the hTERT promoter by the proto-oncogenic protein TAL1. Leukemia; 2009 Nov;23(11):2081-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this report, we show that the basic helix-loop-helix factor, TAL1 (T-cell acute lymphoblastic leukemia 1), is a negative regulator of the hTERT promoter.
  • Considering the relationship recently established between TAL1 and the human T-cell leukemia virus type 1 (HTLV-1) Tax protein, which was confirmed in T lymphocyte clones derived from adult T-cell leukemia patients, we analyzed the effect of TAL1 with respect to the earlier characterized effects of Tax and HBZ (HTLV-1 basic leucine zipper) on hTERT expression.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Gene Expression Regulation, Leukemic / physiology. Leukemia, T-Cell / genetics. Proto-Oncogene Proteins / metabolism. Telomerase / genetics. Telomerase / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19587703.001).
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Proto-Oncogene Proteins; 0 / Sp1 Transcription Factor; 0 / Viral Proteins; 0 / tax protein, Human T-lymphotrophic virus 1; 135471-20-4 / TAL1 protein, human; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
  •  go-up   go-down


43. Aamot HV, Bjørnslett M, Delabie J, Heim S: t(14;22)(q32;q11) in non-Hodgkin lymphoma and myeloid leukaemia: molecular cytogenetic investigations. Br J Haematol; 2005 Sep;130(6):845-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] t(14;22)(q32;q11) in non-Hodgkin lymphoma and myeloid leukaemia: molecular cytogenetic investigations.
  • Two non-Hodgkin lymphomas (NHL), one chronic lymphocytic leukaemia/small lymphocytic lymphoma and one diffuse large B-cell lymphoma and three cases of myeloid leukaemia, two chronic (CML) and one acute (AML), showed, by G-banding analysis, apparently identical chromosomal translocations t(14;22)(q32;q11), in three of the cases as the sole abnormality.
  • A three-way variant translocation of the classical t(9;22)(q34;q11), t(9;22;14)(q34;q11;q32), involving both BCR and ABL, was unravelled by the molecular cytogenetic investigations in the three myeloid leukaemia cases; a similar variant translocation has previously been reported in seven CML.
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Myeloid / genetics. Lymphoma, Non-Hodgkin / genetics. Translocation, Genetic

  • Genetic Alliance. consumer health - Hodgkin lymphoma.
  • Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16156854.001).
  • [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 / Immunoglobulin Heavy Chains
  •  go-up   go-down


44. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


45. Taki T, Taniwaki M: Chromosomal translocations in cancer and their relevance for therapy. Curr Opin Oncol; 2006 Jan;18(1):62-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


46. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


47. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Peripheral T-cell lymphoma.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


48. Manola KN, Sambani C, Karakasis D, Kalliakosta G, Harhalakis N, Papaioannou M: Leukemias associated with Turner syndrome: report of three cases and review of the literature. Leuk Res; 2008 Mar;32(3):481-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemias associated with Turner syndrome: report of three cases and review of the literature.
  • Cases of leukemia associated with Turner syndrome (TS) are rare.
  • Here we report three TS patients with leukemia including one case of T-large granular lymphocyte leukemia (T-LGL), one rare case of coexistence of chronic lymphocytic leukemia (CLL) and idiopathic myelofibrosis (IMF) and one case of a patient with AML-M2 who received autologous stem cell transplantation (SCT).
  • T-LGL and coexistence of CLL and IMF associated with TS are reported for the first time while the last case represents the first report of SCT in a leukemia patient with TS.
  • Our cases and the limited data of previously reported leukemia patients with TS suggest that TS is not associated with a specific type of leukemia and that presentation, clinical course and response to treatment are similar to that of the non-TS leukemia patients.
  • Interestingly, in the mosaic TS patients, the abnormal clones were restricted to the monosomic 45,X cells, indicating that the leukemic clones possibly originate from the monosomic cell line.
  • Even in cases with no additional chromosome abnormalities, the ratio of X/XX cells in bone marrow cells was significantly increased compared to that in constitutional karyotype, indicating that monosomic cells possibly provide a survival advantage for leukemia cells or that reduced programmed cell death may be responsible for the expansion of the monosomic cells.
  • [MeSH-major] Leukemia / complications. Turner Syndrome / complications
  • [MeSH-minor] Adult. Female. Humans. Leukemia, Large Granular Lymphocytic / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Myeloid, Acute / complications. Middle Aged. Monosomy. Treatment Outcome

  • Genetic Alliance. consumer health - Turner syndrome.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Turner Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17669490.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 42
  •  go-up   go-down


49. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


50. Giles F, Fischer T, Cortes J, Garcia-Manero G, Beck J, Ravandi F, Masson E, Rae P, Laird G, Sharma S, Kantarjian H, Dugan M, Albitar M, Bhalla K: A phase I study of intravenous LBH589, a novel cinnamic hydroxamic acid analogue histone deacetylase inhibitor, in patients with refractory hematologic malignancies. Clin Cancer Res; 2006 Aug 1;12(15):4628-35
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: LBH589 is a novel histone deacetylase inhibitor that inhibits proliferation and induces apoptosis in tumor cell lines.
  • EXPERIMENTAL DESIGN: Fifteen patients (median age, 63 years; range, 42-87 years) with acute myeloid leukemia (13 patients), acute lymphocytic leukemia (1 patient), or myelodysplastic syndrome (1 patient) were treated with LBH589 at the following dose levels (mg/m(2)): 4.8 (3 patients), 7.2 (3 patients), 9.0 (1 patient), 11.5 (3 patient), and 14.0 (5 patients).
  • [MeSH-major] Enzyme Inhibitors / administration & dosage. Histone Deacetylase Inhibitors. Hydroxamic Acids / administration & dosage. Leukemia, Myeloid / drug therapy. Myelodysplastic Syndromes / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Acute Disease. Adult. Aged. Aged, 80 and over. Apoptosis / drug effects. Biomarkers, Tumor / antagonists & inhibitors. Biomarkers, Tumor / metabolism. Cell Proliferation / drug effects. Cinnamates / administration & dosage. Cinnamates / adverse effects. Dose-Response Relationship, Drug. Drug Administration Schedule. Follow-Up Studies. Histones / drug effects. Histones / metabolism. Humans. Indoles. Injections, Intravenous. Maximum Tolerated Dose. Middle Aged. Predictive Value of Tests. Structure-Activity Relationship. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16899611.001).
  • [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] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cinnamates; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Histones; 0 / Hydroxamic Acids; 0 / Indoles; 9647FM7Y3Z / panobinostat
  •  go-up   go-down


51. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Steroids.
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


52. Plastiras S, Kampessi O: Acute lymphocytic crisis following herpes simplex type 1 virus hepatitis in a nonimmunocompromised man: a case report. J Med Case Rep; 2009;3:7492
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute lymphocytic crisis following herpes simplex type 1 virus hepatitis in a nonimmunocompromised man: a case report.
  • INTRODUCTION: An increase in circulating lymphocytes can be seen following infections such as infectious mononucleosis and pertussis, or in lymphoproliferative disorders such as acute and chronic lymphocytic leukemia.
  • Acute lymphocytic crisis following herpes simplex virus hepatitis has not been described in the literature.
  • During the fifth day of hospitalization, the patient developed a lymphocytic crisis and, after further tests the patient was diagnosed as having herpes simplex virus hepatitis.
  • CONCLUSION: This case report shows that herpes simplex virus type 1 is a possible cause of an acute lymphocytic crisis similar to other well known infectious agents such as Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus, human herpes virus type 6, adenovirus, toxoplasma and human T-cell lymphotropic virus.
  • Furthermore, this case report expands the clinical spectrum of herpes simplex virus hepatitis, since it is reported in a nonimmunocompromised patient presenting with atypical acute lymphocytic syndrome.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Gastroenterol. 1999 Jun;28(4):386-9 [10372946.001]
  • [Cites] Clin Exp Immunol. 1974 Sep;18(1):1-11 [4549622.001]
  • [Cites] Clin Infect Dis. 1997 Mar;24(3):334-8 [9114181.001]
  • [Cites] Rev Cubana Med Trop. 1992;44(2):104-8 [9768198.001]
  • [Cites] J Hepatol. 1993 Jun;18(2):256-7 [8409342.001]
  • [Cites] Am J Clin Pathol. 1991 Jun;95(6):809-15 [2042590.001]
  • [Cites] N Engl J Med. 1991 Feb 14;324(7):444-9 [1988829.001]
  • [Cites] CMAJ. 1987 Apr 15;136(8):835-8 [3494497.001]
  • [Cites] Medicine (Baltimore). 1986 Mar;65(2):124-34 [3005799.001]
  • [Cites] Am J Hematol. 1988 Jan;27(1):49-55 [2833099.001]
  • [Cites] Arch Intern Med. 1981 Oct;141(11):1519-21 [7025779.001]
  • [Cites] Hum Pathol. 1978 Jan;9(1):51-61 [631844.001]
  • [Cites] Aust N Z J Med. 1976 Dec;6(6):588-90 [799503.001]
  • [Cites] Proc Natl Acad Sci U S A. 1968 Jan;59(1):94-101 [5242134.001]
  • [Cites] Leuk Lymphoma. 1998 May;29(5-6):491-8 [9643562.001]
  • (PMID = 19830209.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2737771
  •  go-up   go-down


53. Nowak AK, Lake RA, Robinson BW: Combined chemoimmunotherapy of solid tumours: improving vaccines? Adv Drug Deliv Rev; 2006 Oct 1;58(8):975-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


54. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


55. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


56. Malcovati L: Novel homeobox gene recombination in T-cell acute lymphoblastic leukemia. Haematologica; 2006 Mar;91(3):290A
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


57. Hu HB, Hu Q: [ID4 methylation patterns in childhood T line and B line lymphocytic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2010 Dec;12(12):940-2
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [ID4 methylation patterns in childhood T line and B line lymphocytic leukemia].
  • OBJECTIVE: To study the relationship of methylation of inhibitor of DNA binding 4 (ID4) gene core promoter region with childhood T line, B line and T/B acute lymphocytic leukemia (ALL).
  • Thirty-four hospitalized children with non-tumor disease served as the control group.
  • [MeSH-minor] Humans. Polymerase Chain Reaction. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21172127.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Inhibitor of Differentiation Proteins
  •  go-up   go-down


58. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Fanconi Anemia.
  • Genetic Alliance. consumer health - Anemia.
  • Genetic Alliance. consumer health - Pediatric T-cell leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


59. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Leukemia.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


60. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


61. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Multiple Sclerosis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


62. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


63. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Chronic Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


64. Hatoum HA, Mahfouz RA, Otrock ZK, Hudaib AR, Taher AT, Shamseddine AI: Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report. Am J Hematol; 2007 Jan;82(1):69-72
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myeloid leukemia with T-cell receptor gamma gene rearrangement occurring in a patient with chronic lymphocytic leukemia: a case report.
  • The association of chronic lymphocytic leukemia (CLL) and acute leukemia, either lymphoid or myeloid is a rare event.
  • Our review of the medical literature revealed only 6 cases of CLL transformation to acute myeloid leukemia (AML) (M0, M1 and M2) with no other associated malignancy.
  • We report a similar case but with occurrence of AML-M4 associated with normal cytogenetic analysis and molecular testing but with positive T-cell receptor gamma gene rearrangement rather than the usual Vbeta rearrangement.
  • [MeSH-major] Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


65. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


66. Qian W, Liu J, Jin J, Ni W, Xu W: Arsenic trioxide induces not only apoptosis but also autophagic cell death in leukemia cell lines via up-regulation of Beclin-1. Leuk Res; 2007 Mar;31(3):329-39
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arsenic trioxide induces not only apoptosis but also autophagic cell death in leukemia cell lines via up-regulation of Beclin-1.
  • Although recent data shows that arsenic trioxide (As2O3) is capable of inducing cell death via cell cycle arrest and apoptosis both in acute promyelocytic leukemia (APL) and in non-APL cells, the mechanisms of As2O3-mediated cell death are not fully understood.
  • In this study, we investigated the in vitro effects of As2O3 on cell growth inhibition and cell death in human T-lymphocytic leukemia and myelodysplastic syndrome (MDS) cell lines.
  • Autophagic cell death (programmed cell death type II) and apoptosis (programmed cell death type I) were activated together in leukemia cell lines after exposed to As2O3.
  • Furthermore, 3-methyladenine (an autophagy inhibitor) significantly reduced autophagic cell death and sequentially induced apoptosis.
  • Finally, leukemia cells treated with 4 microM As2O3 showed a considerable up-regulation of Beclin-1 (a Bcl-2-interacting protein) expression, which was independent of transcription of mRNA and required protein synthesis.
  • In addition, Molt-4 cells treated with As2O3 exhibited the down-regulation of Bax protein expression, suggesting that Bax may be involved in accumulating of Beclin-1 and triggering autophagic cell death in As2O3-treated leukemia cells.
  • These results may lead to a better understanding of the mechanism of action of As2O3, and provide a suggestion that As2O3 may be of therapeutic value for the treatment of patients with human T-lymphocytic leukemia and myelodysplastic syndrome.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Arsenicals / pharmacology. Leukemia, T-Cell / drug therapy. Membrane Proteins / metabolism. Myelodysplastic Syndromes / drug therapy. Oxides / pharmacology
  • [MeSH-minor] Cell Death / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / drug effects. Proto-Oncogene Proteins c-akt / metabolism. Structure-Activity Relationship. Up-Regulation / drug effects

  • MedlinePlus Health Information. consumer health - Myelodysplastic Syndromes.
  • Hazardous Substances Data Bank. ARSENIC TRIOXIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16882451.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Arsenicals; 0 / BECN1 protein, human; 0 / Membrane Proteins; 0 / Oxides; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; S7V92P67HO / arsenic trioxide
  •  go-up   go-down


67. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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


68. Ogilvy S, Ferreira R, Piltz SG, Bowen JM, Göttgens B, Green AR: The SCL +40 enhancer targets the midbrain together with primitive and definitive hematopoiesis and is regulated by SCL and GATA proteins. Mol Cell Biol; 2007 Oct;27(20):7206-19
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The SCL +40 enhancer targets the midbrain together with primitive and definitive hematopoiesis and is regulated by SCL and GATA proteins.
  • The SCL/Tal-1 gene encodes a basic helix-loop-helix transcription factor with key roles in hematopoietic and neural development.
  • SCL is expressed in, and required for, both primitive and definitive erythropoiesis.
  • Thus far, we have identified only one erythroid SCL enhancer.
  • Located 40 kb downstream of exon 1a, the +40 enhancer displays activity in primitive erythroblasts.
  • We demonstrate here that a 3.7-kb fragment containing this element also targets expression to the midbrain, a known site of endogenous SCL expression.
  • Although the 3.7-kb construct was active in primitive, but not definitive, erythroblasts, a larger 5.0-kb fragment, encompassing the 3.7-kb region, was active in both fetal and adult definitive hematopoietic cells.
  • This included Ter119+ erythroid cells along with fetal liver erythroid and myeloid progenitors.
  • Unlike two other SCL hematopoietic enhancers (+18/19 and -4), +40 enhancer transgenes were inactive in the endothelium.
  • A conserved 400-bp core region, essential for both hematopoietic and midbrain +40 enhancer activity in embryos, relied on two GATA/E-box motifs and was bound in vivo by GATA-1 and SCL in erythroid cells.
  • These results suggest a model in which the SCL +18/19 and/or -4 enhancers initiate SCL expression in early mesodermal derivatives capable of generating blood and endothelium, with subsequent activation of the +40 enhancer via an autoregulatory loop.

  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 2000 Jan;20(2):713-23 [10611250.001]
  • [Cites] Blood. 1999 Dec 1;94(11):3754-63 [10572089.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1652-5 [10688820.001]
  • [Cites] Development. 2001 Dec;128(23):4815-27 [11731461.001]
  • [Cites] EMBO J. 2002 Jun 17;21(12):3039-50 [12065417.001]
  • [Cites] J Biotechnol. 2002 Sep 25;98(2-3):145-60 [12141984.001]
  • [Cites] Nature. 2003 Jan 30;421(6922):547-51 [12540851.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):992-7 [12552125.001]
  • [Cites] Mol Cell Biol. 2003 Nov;23(21):7585-99 [14560005.001]
  • [Cites] Neuroscience. 2003;122(2):421-36 [14614907.001]
  • [Cites] Mol Cell Biol. 2004 Feb;24(4):1439-52 [14749362.001]
  • [Cites] Mol Cell Biol. 2004 Mar;24(5):1870-83 [14966269.001]
  • [Cites] Blood. 2004 May 1;103(9):3342-8 [14726374.001]
  • [Cites] EMBO J. 2004 Jul 21;23(14):2841-52 [15215894.001]
  • [Cites] J Immunol. 1973 Jun;110(6):1470-5 [4541304.001]
  • [Cites] Oncogene. 1992 Apr;7(4):653-60 [1565464.001]
  • [Cites] Nature. 1995 Feb 2;373(6513):432-4 [7830794.001]
  • [Cites] Blood. 1995 Aug 15;86(4):1502-14 [7632958.001]
  • [Cites] Cell. 1996 Jul 12;86(1):47-57 [8689686.001]
  • [Cites] EMBO J. 1996 Jul 15;15(14):3713-21 [8670875.001]
  • [Cites] EMBO J. 1996 Aug 15;15(16):4123-9 [8861941.001]
  • [Cites] EMBO J. 1997 Jun 2;16(11):3145-57 [9214632.001]
  • [Cites] Nucleic Acids Res. 1997 Nov 1;25(21):4400-7 [9336475.001]
  • [Cites] Blood. 1998 Jan 15;91(2):419-30 [9427694.001]
  • [Cites] J Biol Chem. 1998 Jun 5;273(23):14347-54 [9603943.001]
  • [Cites] Dev Biol. 1999 May 1;209(1):128-42 [10208748.001]
  • [Cites] Development. 1999 Jun;126(12):2799-811 [10331989.001]
  • [Cites] Dev Biol. 1999 Jun 15;210(2):305-21 [10357893.001]
  • [Cites] Development. 1999 Sep;126(17):3891-904 [10433917.001]
  • [Cites] Blood. 1999 Sep 15;94(6):1855-63 [10477714.001]
  • [Cites] Nucleic Acids Res. 2004;32(21):6454-67 [15590906.001]
  • [Cites] Mol Cell Biol. 2005 Feb;25(4):1215-27 [15684376.001]
  • [Cites] Blood. 2005 May 15;105(10):3871-4 [15677556.001]
  • [Cites] Mol Cell Biol. 2005 Jun;25(12):5215-25 [15923636.001]
  • [Cites] EMBO J. 2005 Jul 6;24(13):2354-66 [15920471.001]
  • [Cites] Int J Dev Neurosci. 2005 Aug;23(5):449-63 [16011889.001]
  • [Cites] Stem Cells. 2005 Oct;23(9):1378-88 [16051983.001]
  • [Cites] Nature. 2005 Nov 17;438(7066):360-3 [16292311.001]
  • [Cites] Eur J Neurosci. 2006 Apr;23(7):1677-89 [16623824.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1251-9 [16627757.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):840-5 [17213321.001]
  • [Cites] Nat Biotechnol. 2000 Feb;18(2):181-6 [10657125.001]
  • (PMID = 17709394.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [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 / GATA Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse
  • [Other-IDs] NLM/ PMC2168913
  •  go-up   go-down


69. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


70. Qiuping Z, Jie X, Youxin J, Qun W, Wei J, Chun L, Jin W, Yan L, Chunsong H, Mingzhen Y, Qingping G, Qun L, Kejian Z, Zhimin S, Junyan L, Jinquan T: Selectively frequent expression of CXCR5 enhances resistance to apoptosis in CD8(+)CD34(+) T cells from patients with T-cell-lineage acute lymphocytic leukemia. Oncogene; 2005 Jan 20;24(4):573-84
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selectively frequent expression of CXCR5 enhances resistance to apoptosis in CD8(+)CD34(+) T cells from patients with T-cell-lineage acute lymphocytic leukemia.
  • We investigated CD4(+)CD34(+), CD8(+)CD34(+), CD4(+)CD34(-), and CD8(+)CD34(-) T cells from cord blood and from typical patients with T-cell-lineage acute lymphocytic leukemia and T-cell-lineage chronic lymphocytic leukemia in terms of expression and functions of CXCR5/CXCL13.
  • We found that CXCR5 was selectively frequently expressed on T-cell-lineage acute (chronic) lymphocytic leukemia (T-ALL) CD8(+)CD34(+) T cells, but not on T-ALL CD4(+)CD34(+), CD4(+)CD34(-), and CD8(+)CD34(-) T cells.
  • A proliferation-inducing ligand expression in T-ALL CD8(+)CD34(+) T cells was upregulated by CXCL13/BCA-1 (B-cell attracting chemokine 1).
  • In this process, cell-cell contact in culture was necessary.
  • Normal lymphocytes, especially naive B and T cells, utilized CXCR5/CXCL13 for migration, homing, maturation, and cell homeostasis, as well as secondary lymphoid tissue organogenesis.
  • [MeSH-major] Antigens, CD34 / metabolism. Apoptosis. CD8-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptors, Cytokine / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Adaptor Proteins, Signal Transducing / metabolism. Cell Adhesion / drug effects. Cell Line. Cell Lineage / drug effects. Chemokine CXCL13. Chemokines, CXC / metabolism. Chemokines, CXC / pharmacology. Chemotaxis / drug effects. Humans. Inhibitor of Apoptosis Proteins. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Nuclear Proteins / pharmacology. Receptors, CXCR5. Receptors, Chemokine / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Up-Regulation / genetics

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [RetractionIn] Oncogene. 2011 Jun 16;30(24):2798 [21677655.001]
  • (PMID = 15580304.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ANP32B protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Antigens, CD34; 0 / BIRC7 protein, human; 0 / CXCL13 protein, human; 0 / CXCR5 protein, human; 0 / Chemokine CXCL13; 0 / Chemokines, CXC; 0 / Inhibitor of Apoptosis Proteins; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Receptors, CXCR5; 0 / Receptors, Chemokine; 0 / Receptors, Cytokine; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


71. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

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

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


72. Buie LW, Epstein SS, Lindley CM: Nelarabine: a novel purine antimetabolite antineoplastic agent. Clin Ther; 2007 Sep;29(9):1887-99
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • SciCrunch. DrugBank: Data: Chemical .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


73. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


74. Lu Y, Hou SX, Zhang LK, Li Y, He JY, Guo DD: [Transdermal and lymph targeting transfersomes of vincristine]. Yao Xue Xue Bao; 2007 Oct;42(10):1097-101
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Vincristine (VCR) is mainly used to treat acute lymphocytic leukemia, Hodgkin and non-Hodgkin lymphoma in clinic with definite therapeutic effect.
  • The in vitro transdermal research with modified Franz cell showed that VCR-T permeated through the skin in accordance with polynomial equation, and with an accumulation permeation percentage of 67.4% up to 12 h.

  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18229621.001).
  • [ISSN] 0513-4870
  • [Journal-full-title] Yao xue xue bao = Acta pharmaceutica Sinica
  • [ISO-abbreviation] Yao Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Liposomes; 0 / Surface-Active Agents; 5J49Q6B70F / Vincristine
  •  go-up   go-down


75. Strauss T, Metsuyanim S, Pessach I, Shuchan-Eisen I, Kuint J, Dekel B: Analysis of circulating hem-endothelial marker RNA levels in preterm infants. BMC Pediatr; 2009;9:42
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of circulating hem-endothelial marker RNA levels in preterm infants.
  • BACKGROUND: Circulating endothelial cells may serve as novel markers of angiogenesis.
  • These include a subset of hem-endothelial progenitor cells that play a vital role in vascular growth and repair.
  • The presence and clinical implications of circulating RNA levels as an expression for hematopoietic and endothelial-specific markers have not been previously evaluated in preterm infants.
  • This study aims to determine circulating RNA levels of hem-endothelial marker genes in peripheral blood of preterm infants and begin to correlate these findings with prenatal complications.
  • METHODS: Peripheral blood samples from seventeen preterm neonates were analyzed at three consecutive post-delivery time points (day 3-5, 10-15 and 30).
  • Using quantitative reverse transcription-polymerase chain reaction we studied the expression patterns of previously established hem-endothelial-specific progenitor-associated genes (AC133, Tie-2, Flk-1 (VEGFR2) and Scl/Tal1) in association with characteristics of prematurity and preterm morbidity.
  • RESULTS: Circulating Tie-2 and SCL/Tal1 RNA levels displayed an inverse correlation to gestational age (GA).
  • We observed significantly elevated Tie-2 levels in preterm infants born to mothers with amnionitis, and in infants with sustained brain echogenicity on brain sonography.
  • Other markers showed similar expression patterns yet we could not demonstrate statistically significant correlations.
  • CONCLUSION: These preliminary findings suggest that circulating RNA levels especially Tie2 and SCL decline with maturation and might relate to some preterm complication.
  • Further prospective follow up of larger cohorts are required to establish this association.
  • [MeSH-major] Endothelial Cells / cytology. Endothelium, Vascular / metabolism. Hematopoietic Stem Cells / cytology. Infant, Premature / blood. Neovascularization, Physiologic. RNA / blood. Stem Cells / cytology
  • [MeSH-minor] Antigens, CD / blood. Antigens, CD / genetics. Basic Helix-Loop-Helix Transcription Factors / blood. Basic Helix-Loop-Helix Transcription Factors / genetics. Birth Weight. Echoencephalography. Female. Gestational Age. Glycoproteins / blood. Glycoproteins / genetics. Humans. Infant, Newborn. Male. Peptides / blood. Peptides / genetics. Proto-Oncogene Proteins / blood. Proto-Oncogene Proteins / genetics. Receptor, TIE-2 / blood. Receptor, TIE-2 / genetics. Reverse Transcriptase Polymerase Chain Reaction. Vascular Endothelial Growth Factor Receptor-2 / blood. Vascular Endothelial Growth Factor Receptor-2 / genetics

  • MedlinePlus Health Information. consumer health - Premature Babies.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3422-7 [10725398.001]
  • [Cites] Pediatr Res. 2009 Feb;65(2):221-5 [18852688.001]
  • [Cites] Matrix Biol. 2001 Sep;20(5-6):319-25 [11566266.001]
  • [Cites] Am J Pathol. 2001 Dec;159(6):2271-80 [11733376.001]
  • [Cites] J Am Soc Nephrol. 2002 Feb;13(2):544-50 [11805186.001]
  • [Cites] Acta Haematol. 2001;106(4):157-61 [11815712.001]
  • [Cites] Circulation. 2002 Dec 10;106(24):3009-17 [12473544.001]
  • [Cites] N Engl J Med. 2003 Feb 13;348(7):593-600 [12584367.001]
  • [Cites] Ophthalmic Res. 2003 Jul-Aug;35(4):217-23 [12815197.001]
  • [Cites] Cancer Biol Ther. 2003 May-Jun;2(3):255-6 [12878859.001]
  • [Cites] Circulation. 2003 Nov 18;108(20):2511-6 [14581410.001]
  • [Cites] Blood Cells Mol Dis. 2004 Jan-Feb;32(1):168-75 [14757432.001]
  • [Cites] Cancer Res. 2004 Jun 15;64(12):4373-7 [15205354.001]
  • [Cites] Pediatrics. 1986 Dec;78(6):995-1006 [3537951.001]
  • [Cites] Genes Dev. 1994 Aug 15;8(16):1897-909 [7958865.001]
  • [Cites] Nature. 1995 Jul 6;376(6535):70-4 [7596437.001]
  • [Cites] Science. 1997 Feb 14;275(5302):964-7 [9020076.001]
  • [Cites] Blood. 1998 May 15;91(10):3527-61 [9572988.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2004 Dec;24(12):e192-6 [15486312.001]
  • [Cites] Surg Today. 2005;35(6):436-41 [15912289.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):4993-7 [15958538.001]
  • [Cites] N Engl J Med. 2005 Sep 8;353(10):999-1007 [16148285.001]
  • [Cites] Br J Cancer. 2005 Oct 3;93(7):793-8 [16160694.001]
  • [Cites] Circulation. 2005 Oct 18;112(16):2383-5 [16230495.001]
  • [Cites] Circulation. 2005 Oct 18;112(16):2477-86 [16230500.001]
  • [Cites] Stem Cells. 2006 May;24(5):1185-93 [16410390.001]
  • [Cites] Prog Neurobiol. 2007 Dec;83(6):349-62 [17884277.001]
  • [Cites] Stroke. 2008 Jan;39(1):69-74 [18063830.001]
  • [Cites] Lancet. 2008 Jan 5;371(9606):75-84 [18177778.001]
  • [Cites] Leukemia. 2008 Jan;22(1):103-13 [17898790.001]
  • [Cites] J Clin Invest. 2008 Feb;118(2):467-70 [18219388.001]
  • [Cites] Histol Histopathol. 2008 Jun;23(6):773-80 [18366015.001]
  • [Cites] Br J Ophthalmol. 2008 May;92(5):689-93 [18408080.001]
  • [Cites] Circ Res. 2001 Jul 6;89(1):E1-7 [11440984.001]
  • (PMID = 19555479.001).
  • [ISSN] 1471-2431
  • [Journal-full-title] BMC pediatrics
  • [ISO-abbreviation] BMC Pediatr
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC133 antigen; 0 / Antigens, CD; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Glycoproteins; 0 / Peptides; 0 / Proto-Oncogene Proteins; 135471-20-4 / TAL1 protein, human; 63231-63-0 / RNA; EC 2.7.10.1 / Receptor, TIE-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC2709108
  •  go-up   go-down


76. Tsukasaki K, Hermine O, Bazarbachi A, Ratner L, Ramos JC, Harrington W Jr, O'Mahony D, Janik JE, Bittencourt AL, Taylor GP, Yamaguchi K, Utsunomiya A, Tobinai K, Watanabe T: Definition, prognostic factors, treatment, and response criteria of adult T-cell leukemia-lymphoma: a proposal from an international consensus meeting. J Clin Oncol; 2009 Jan 20;27(3):453-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Definition, prognostic factors, treatment, and response criteria of adult T-cell leukemia-lymphoma: a proposal from an international consensus meeting.
  • Adult T-cell leukemia-lymphoma (ATL) is a distinct peripheral T-lymphocytic malignancy associated with a retrovirus designated human T-cell lymphotropic virus type I (HTLV-1).
  • The diversity in clinical features and prognosis of patients with this disease has led to its subclassification into the following four categories: acute, lymphoma, chronic, and smoldering types.
  • The chronic and smoldering subtypes are considered indolent and are usually managed with watchful waiting until disease progression, analogous to the management of some patients with chronic lymphoid leukemia (CLL) or other indolent histology lymphomas.
  • Patients with aggressive ATL generally have a poor prognosis because of multidrug resistance of malignant cells, a large tumor burden with multiorgan failure, hypercalcemia, and/or frequent infectious complications as a result of a profound T-cell immunodeficiency.
  • A set of response criteria specific for ATL reflecting a combination of those for lymphoma and CLL was proposed.
  • A treatment strategy based on the clinical subclassification and prognostic factors is suggested, including watchful waiting approach, chemotherapy, antiviral therapy, allogeneic hematopoietic stem-cell transplantation (alloHSCT), and targeted therapies.

  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 1999 Apr;17(4):1244 [10561185.001]
  • [Cites] J Clin Oncol. 2007 Dec 1;25(34):5458-64 [17968021.001]
  • [Cites] Oncogene. 2000 Oct 12;19(43):4954-60 [11042682.001]
  • [Cites] Blood. 2001 Jun 1;97(11):3612-20 [11369658.001]
  • [Cites] Br J Haematol. 2001 Jun;113(3):779-84 [11380470.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3875-81 [11389029.001]
  • [Cites] Leuk Lymphoma. 2001 Jan;40(3-4):287-94 [11426550.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1160-5 [11493465.001]
  • [Cites] Blood. 2002 May 1;99(9):3383-9 [11964307.001]
  • [Cites] Oncogene. 2002 Apr 11;21(16):2466-75 [11971181.001]
  • [Cites] Hematol J. 2002;3(6):276-82 [12522449.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4576-82 [12560223.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3625-34 [14506150.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1838-45 [14592824.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2474-9 [14645001.001]
  • [Cites] Hematol J. 2004;5(2):130-4 [15048063.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Lancet. 1987 Jul 11;2(8550):94-5 [2885585.001]
  • [Cites] Cancer. 1988 Feb 15;61(4):824-8 [3257406.001]
  • [Cites] J Clin Pathol. 1989 Jun;42(6):567-84 [2738163.001]
  • [Cites] Cancer. 1990 Jan 15;65(2):327-32 [2295055.001]
  • [Cites] Cancer. 1991 May 15;67(10):2605-9 [2015561.001]
  • [Cites] Leuk Res. 1991;15(2-3):81-90 [2016910.001]
  • [Cites] Leuk Res. 1991;15(2-3):99-103 [2016911.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Leuk Res. 1993 Feb;17(2):157-66 [8429692.001]
  • [Cites] Cancer. 1994 Jun 1;73(11):2753-8 [8194016.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1744-8 [7760890.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1749-51 [7760891.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996;13 Suppl 1:S186-90 [8797722.001]
  • [Cites] Blood. 1997 Feb 1;89(3):948-56 [9028326.001]
  • [Cites] J Clin Oncol. 1997 May;15(5):1778-85 [9164185.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 1996;67:1-424 [9190379.001]
  • [Cites] Blood. 1999 Jan 1;93(1):278-83 [9864171.001]
  • [Cites] Br J Haematol. 1999 May;105(2):369-75 [10233406.001]
  • [Cites] Lancet Oncol. 2004 Nov;5(11):664-72 [15522654.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):419-30 [15543232.001]
  • [Cites] Leukemia. 2005 May;19(5):829-34 [15744352.001]
  • [Cites] Blood. 2005 May 15;105(10):4143-5 [15665110.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6047-57 [16155611.001]
  • [Cites] Cancer Lett. 2006 Mar 28;234(2):249-55 [15896902.001]
  • [Cites] Int J Cancer. 2006 Jun 15;118(12):3054-61 [16425276.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4500-7 [16484591.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1021-9 [16569765.001]
  • [Cites] J Clin Oncol. 2007 Feb 10;25(5):579-86 [17242396.001]
  • [Cites] Blood. 2007 Apr 1;109(7):3060-8 [17138822.001]
  • [Cites] Leuk Res. 2007 Jun;31(6):751-7 [17188352.001]
  • [Cites] Leuk Res. 2007 Jul;31(7):915-20 [17123603.001]
  • [Cites] Am J Clin Pathol. 2007 Nov;128(5):875-82 [17951212.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2849-55 [11023521.001]
  • (PMID = 19064971.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Consensus Development Conference; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Number-of-references] 61
  • [Other-IDs] NLM/ PMC2737379
  •  go-up   go-down


77. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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


78. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Glucocorticoid Resistance.
  • MedlinePlus Health Information. consumer health - Steroids.
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


79. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


80. Belov L, Huang P, Chrisp JS, Mulligan SP, Christopherson RI: Screening microarrays of novel monoclonal antibodies for binding to T-, B- and myeloid leukaemia cells. J Immunol Methods; 2005 Oct 20;305(1):10-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Screening microarrays of novel monoclonal antibodies for binding to T-, B- and myeloid leukaemia cells.
  • We have developed a microarray (DotScan) that enables rapid immunophenotyping and classification of leukaemias and lymphomas by measuring the capture of cells by immobilized dots of 82 CD antibodies [Belov, L., de la Vega, O., dos Remedios, C.G., Mulligan, S.P., 2001.
  • Immunophenotyping of leukemia using a cluster of differentiation antibody microarray. Cancer Res.
  • Identification of repertoires of surface antigens on leukemias using an antibody microarray.
  • After blocking the remaining nitrocellulose surface, individual arrays were incubated with each of 7 cell types from a human leukaemia cell panel consisting of three cell lines, CCRF-CEM (a T-cell acute lymphocytic leukaemia), MEC-1 (derived from B-cell chronic lymphocytic leukaemia) and HL-60 (a promyelocytic leukaemia), and four leukaemias from patients: a T-cell prolymphocytic leukaemia, a B-cell chronic lymphocytic leukaemia, and two acute myeloid leukaemias.
  • Leukaemia cells were captured by those immobilized antibodies for which they expressed the corresponding surface molecule.
  • The data obtained show the unique expression profiles of the 7 cell types in the leukaemia cell panel obtained with the DotScan microarray, and the differential capture patterns for these 7 cell types screened against the 498 antibodies in the HLDA8 microarray constructed for this study.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antigens, CD / analysis. Leukemia / classification. Protein Array Analysis / methods
  • [MeSH-minor] Cell Line, Tumor. Collodion / chemistry. Flow Cytometry. Humans. Leukemia, B-Cell / classification. Leukemia, B-Cell / immunology. Leukemia, Myeloid / classification. Leukemia, Myeloid / immunology. Leukemia, T-Cell / classification. Leukemia, T-Cell / immunology

  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Nitrocellulose .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16125720.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 9004-70-0 / Collodion
  •  go-up   go-down


81. Malissen B, Luche H: Immunology: Egocentric pre-T-cell receptors. Nature; 2010 Oct 14;467(7317):793-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


82. Carney DA, Westerman DA, Tam CS, Milner A, Prince HM, Kenealy M, Wolf M, Januszewicz EH, Ritchie D, Came N, Seymour JF: Therapy-related myelodysplastic syndrome and acute myeloid leukemia following fludarabine combination chemotherapy. Leukemia; 2010 Dec;24(12):2056-62
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy-related myelodysplastic syndrome and acute myeloid leukemia following fludarabine combination chemotherapy.
  • Fludarabine combination chemotherapy achieves high response rates in chronic lymphocytic leukemia (CLL) and indolent lymphoma.
  • The aim of this study was to investigate the incidence and characteristics of treatment-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) after treatment with fludarabine in combination for lymphoproliferative disorders and identify risk factors for its development.
  • Median overall survival post-t-MDS/AML diagnosis was 11 months.
  • Patients developing t-MDS/AML included 11/54 with follicular lymphoma (FL) (crude rate 20.4%), 5/82 with CLL (6.1%) and 3/24 with Waldenstrom macroglobulinemia or marginal zone lymphoma (12.5%).
  • [MeSH-major] Antineoplastic Agents / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Myelodysplastic Syndromes / chemically induced. Neoplasms, Second Primary / chemically induced. Vidarabine / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged


83. McReynolds LJ, Gupta S, Figueroa ME, Mullins MC, Evans T: Smad1 and Smad5 differentially regulate embryonic hematopoiesis. Blood; 2007 Dec 1;110(12):3881-90
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Smad1 and Smad5 differentially regulate embryonic hematopoiesis.
  • The bone morphogenetic protein (BMP) signaling pathway regulates multiple steps of hematopoiesis, mediated through receptor-regulated Smads, including Smad1 and Smad5.
  • Here, we use loss-of-function approaches in zebrafish to compare the roles of Smad1 and Smad5 during embryonic hematopoiesis.
  • We show that knockdown of Smad1 or Smad5 generates distinct and even opposite hematopoietic phenotypes.
  • Embryos depleted for Smad1 have an increased number of primitive erythrocytes, but fail to produce mature embryonic macrophages.
  • In contrast, Smad5-depleted embryos are defective in primitive erythropoiesis, yet have normal numbers of macrophages.
  • Loss of either Smad1 or Smad5 causes a failure in the generation of definitive hematopoietic progenitors.
  • To investigate the mechanism behind these phenotypes, we used rescue experiments and found that Smad5 is unable to rescue the Smad1 loss-of-function phenotype, indicating that the 2 highly related proteins have inherently distinct activities.
  • Microarray experiments revealed that the 2 proteins redundantly regulate the key initiators of the hemato-vascular program, including scl, lmo2, and gfi1.
  • However, each also regulates a remarkably distinct genetic program, with Smad5 uniquely regulating the BMP signaling pathway itself.
  • Our results suggest that specificity of BMP signaling output, with respect to hematopoiesis, can be explained by differential functions of Smad1 and Smad5.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • SciCrunch. ZFIN: Data: Gene Expression .
  • ZFIN. ZFIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Dev Dyn. 1999 Nov;216(3):285-98 [10590480.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5208-14 [17327398.001]
  • [Cites] Development. 2000 Jan;127(2):343-54 [10603351.001]
  • [Cites] Development. 2000 Mar;127(5):957-67 [10662635.001]
  • [Cites] Development. 2001 Mar;128(6):849-58 [11222140.001]
  • [Cites] Development. 2001 Mar;128(6):859-69 [11222141.001]
  • [Cites] Development. 2001 Sep;128(18):3609-21 [11566864.001]
  • [Cites] Blood. 2001 Nov 15;98(10):3087-96 [11698295.001]
  • [Cites] Dev Biol. 2001 Dec 1;240(1):157-67 [11784053.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Dev Biol. 2002 Oct 15;250(2):263-79 [12376102.001]
  • [Cites] Blood. 2003 Jan 1;101(1):124-33 [12393578.001]
  • [Cites] Eur J Biochem. 2003 Feb;270(4):715-25 [12581211.001]
  • [Cites] Blood. 2003 Aug 1;102(3):906-15 [12702499.001]
  • [Cites] Blood. 2003 Nov 1;102(9):3196-205 [12855559.001]
  • [Cites] EMBO J. 2004 Feb 25;23(4):844-56 [14963489.001]
  • [Cites] Stem Cells. 2004;22(4):457-74 [15277693.001]
  • [Cites] Oncogene. 2004 Sep 20;23(43):7233-46 [15378083.001]
  • [Cites] Nucleic Acids Res. 1993 Mar 11;21(5):1087-95 [8464695.001]
  • [Cites] Genes Dev. 1995 Sep 1;9(17):2105-16 [7657163.001]
  • [Cites] Dev Dyn. 1995 Jul;203(3):253-310 [8589427.001]
  • [Cites] Development. 1996 Dec;123:67-80 [9007230.001]
  • [Cites] Development. 1996 Dec;123:81-93 [9007231.001]
  • [Cites] Development. 1997 Nov;124(22):4457-66 [9409664.001]
  • [Cites] Development. 1999 Apr;126(8):1571-80 [10079220.001]
  • [Cites] Development. 1999 Apr;126(8):1631-42 [10079226.001]
  • [Cites] Development. 1999 May;126(10):2149-59 [10207140.001]
  • [Cites] Mech Dev. 1999 Oct;88(1):73-88 [10525190.001]
  • [Cites] Annu Rev Cell Dev Biol. 2005;21:659-93 [16212511.001]
  • [Cites] Annu Rev Genet. 2005;39:481-501 [16285869.001]
  • [Cites] Genes Dev. 2005 Dec 1;19(23):2783-810 [16322555.001]
  • [Cites] Curr Biol. 2006 Mar 7;16(5):506-11 [16527746.001]
  • [Cites] Development. 2006 Jun;133(11):2177-87 [16672337.001]
  • [Cites] Dev Biol. 2006 Aug 1;296(1):104-18 [16765933.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3707-12 [16896158.001]
  • [Cites] Immunity. 2006 Dec;25(6):963-75 [17157041.001]
  • [Cites] Int J Dev Biol. 2007;51(1):79-84 [17183467.001]
  • [Cites] Blood. 2007 Jan 15;109(2):516-23 [16990609.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):840-5 [17213321.001]
  • [Cites] FASEB J. 1999 Dec;13(15):2105-24 [10593858.001]
  • (PMID = 17761518.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM056326; United States / NHLBI NIH HHS / HL / R01 HL056182; United States / NIGMS NIH HHS / GM / GM56326; United States / NHLBI NIH HHS / HL / HL056182; United States / NHLBI NIH HHS / HL / R37 HL056182; United States / NIGMS NIH HHS / GM / T32 GM007288; United States / NIGMS NIH HHS / GM / R56 GM056326
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Bone Morphogenetic Proteins; 0 / DNA-Binding Proteins; 0 / Gfi1 protein, zebrafish; 0 / LIM Domain Proteins; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins; 0 / Smad1 Protein; 0 / Smad5 Protein; 0 / Transcription Factors; 0 / Zebrafish Proteins; 0 / lmo2 protein, zebrafish; 0 / smad5 protein, zebrafish; 0 / tal1 protein, zebrafish
  • [Other-IDs] NLM/ PMC2200801
  •  go-up   go-down


84. Hensel M, Zoz M, Giesecke C, Benner A, Neben K, Jauch A, Stilgenbauer S, Ho AD, Krämer A: High rate of centrosome aberrations and correlation with proliferative activity in patients with untreated B-cell chronic lymphocytic leukemia. Int J Cancer; 2007 Sep 1;121(5):978-83
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High rate of centrosome aberrations and correlation with proliferative activity in patients with untreated B-cell chronic lymphocytic leukemia.
  • B-cell chronic lymphocytic leukemia (CLL) is characterized by a high rate of clonal genomic alterations and a low proliferative activity with cell cycle arrest in G(0)/G(1) phase.
  • To investigate whether centrosome aberrations do occur in CLL and whether they correlate with common prognostic factors and disease activity, we examined peripheral blood mononuclear cells (PBMC) from 70 patients with previously untreated CLL using an antibody to gamma-tubulin.
  • Accordingly, more centrosome aberrations were found in PHA-stimulated T lymphocytes from healthy individuals as well as in B cells from surgically removed tonsil tissue of patients with acute tonsillitis as compared to the peripheral blood B lymphocytes from the control group.
  • [MeSH-major] Cell Proliferation. Centrosome. Leukemia, Lymphocytic, Chronic, B-Cell / pathology

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17417785.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


85. Gran B, Yu S, Zhang GX, Rostami A: Accelerated thymocyte maturation in IL-12Rβ2-deficient mice contributes to increased susceptibility to autoimmune inflammatory demyelination. Exp Mol Pathol; 2010 Oct;89(2):126-34
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Accelerated maturation is observed in mice injected with anti-CD3 to mimic pre-T-cell receptor stimulation, and also in mice immunized with myelin oligodendrocyte glycoprotein (MOG) peptide to induce EAE.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • [Cites] Nature. 2003 Feb 13;421(6924):744-8 [12610626.001]
  • [Cites] Nat Immunol. 2003 Mar;4(3):255-60 [12577054.001]
  • [Cites] J Immunol. 1999 Oct 15;163(8):4349-59 [10510375.001]
  • [Cites] J Immunol. 2005 Jan 1;174(1):261-9 [15611248.001]
  • [Cites] J Immunol. 2005 Mar 1;174(5):2796-804 [15728489.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13574-9 [16174747.001]
  • [Cites] Semin Immunol. 2005 Dec;17(6):411-20 [16256363.001]
  • [Cites] J Immunol. 2006 Apr 1;176(7):4029-41 [16547238.001]
  • [Cites] J Immunol. 2006 Apr 1;176(7):4066-74 [16547242.001]
  • [Cites] J Immunol. 2006 Apr 15;176(8):4818-25 [16585576.001]
  • [Cites] Drug News Perspect. 2006 Mar;19(2):77-83 [16628262.001]
  • [Cites] Curr Med Chem. 2006;13(10):1149-56 [16719776.001]
  • [Cites] J Neuroimmunol. 2007 Apr;185(1-2):75-86 [17320975.001]
  • [Cites] Methods Mol Biol. 2007;380:377-90 [17876107.001]
  • [Cites] Mol Immunol. 2008 Feb;45(3):599-606 [17920446.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):2987-92 [18287049.001]
  • [Cites] Immunol Lett. 2008 Mar 15;116(2):104-10 [18243340.001]
  • [Cites] Prog Histochem Cytochem. 2008;43(2):73-120 [18555891.001]
  • [Cites] J Immunol. 2008 Jul 1;181(1):320-8 [18566397.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Aug 8;372(4):509-12 [18503756.001]
  • [Cites] Annu Rev Immunol. 2003;21:139-76 [12414722.001]
  • [Cites] J Exp Med. 2003 Jul 21;198(2):349-60 [12860933.001]
  • [Cites] J Exp Med. 2003 Sep 1;198(5):757-69 [12953095.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 11;100(23):13453-8 [14597717.001]
  • [Cites] Immunity. 2003 Nov;19(5):641-4 [14614851.001]
  • [Cites] J Exp Med. 2003 Dec 15;198(12):1951-7 [14662908.001]
  • [Cites] Cell Mol Life Sci. 2004 Feb;61(3):263-80 [14770292.001]
  • [Cites] J Immunol. 2004 Mar 1;172(5):2909-16 [14978093.001]
  • [Cites] Blood. 2004 Mar 15;103(6):1985-94 [14592827.001]
  • [Cites] Nat Immunol. 2004 Apr;5(4):418-25 [14991052.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 May 4;101(18):7058-63 [15118099.001]
  • [Cites] J Neuroimmunol. 2004 Nov;156(1-2):123-31 [15465603.001]
  • [Cites] J Immunol. 1990 Dec 15;145(12):4167-73 [2124236.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Jul 15;88(14):6323-7 [2068112.001]
  • [Cites] Cell Immunol. 1993 Jan;146(1):52-61 [8425230.001]
  • [Cites] J Immunol. 1994 Mar 15;152(6):2729-35 [7511624.001]
  • [Cites] Annu Rev Immunol. 1995;13:93-126 [7612239.001]
  • [Cites] J Exp Med. 1995 Oct 1;182(4):961-71 [7561699.001]
  • [Cites] J Exp Med. 1995 Nov 1;182(5):1377-88 [7595208.001]
  • [Cites] Immunity. 1997 Mar;6(3):245-55 [9075925.001]
  • [Cites] Annu Rev Immunol. 1998;16:495-521 [9597139.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1707-12 [10677522.001]
  • [Cites] J Immunol. 2000 Dec 1;165(11):6221-8 [11086056.001]
  • [Cites] Immunity. 2000 Nov;13(5):715-25 [11114383.001]
  • [Cites] Int Immunol. 2002 Aug;14(8):943-51 [12147631.001]
  • [Cites] J Clin Invest. 2002 Aug;110(4):493-7 [12189243.001]
  • [Cites] J Immunol. 2002 Dec 15;169(12):7104-10 [12471147.001]
  • [Cites] J Immunol. 2003 Feb 15;170(4):2153-60 [12574388.001]
  • [Cites] Eur J Immunol. 1999 Aug;29(8):2476-83 [10458761.001]
  • (PMID = 20599940.001).
  • [ISSN] 1096-0945
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI061818; United States / NINDS NIH HHS / NS / R01 NS048435; United States / NIAID NIH HHS / AI / U19 AI082726
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Mog protein, mouse; 0 / Myelin Proteins; 0 / Myelin-Associated Glycoprotein; 0 / Myelin-Oligodendrocyte Glycoprotein; 187348-17-0 / Interleukin-12
  • [Other-IDs] NLM/ NIHMS218212; NLM/ PMC2939283
  •  go-up   go-down


86. Yamasaki S, Saito T: Molecular basis for pre-TCR-mediated autonomous signaling. Trends Immunol; 2007 Jan;28(1):39-43
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular basis for pre-TCR-mediated autonomous signaling.
  • The pre-T-cell receptor (pre-TCR) is a multimeric complex composed of a nascent TCRbeta chain, an invariant pre-TCRalpha (pTalpha) chain and CD3 molecules, and is crucial for early T-cell development.
  • Despite its structural similarity to the mature alphabetaTCR, which requires MHC-antigen for receptor triggering, the pre-TCR is proposed to initiate signals in a ligand-independent manner.
  • In this review, we summarize current data relating to the molecular mechanism underlying the initiation of pre-TCR-mediated autonomous signaling.
  • [MeSH-major] Lymphoma / immunology. Membrane Glycoproteins / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology. Signal Transduction / immunology

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17126602.001).
  • [ISSN] 1471-4906
  • [Journal-full-title] Trends in immunology
  • [ISO-abbreviation] Trends Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / pre-T cell receptor alpha
  • [Number-of-references] 48
  •  go-up   go-down


87. Wang Z, Hu T, Cao LZ, Kang R, Zhao MY, Yu Y, Xu WQ: [Expression of WAVE1 in childhood acute lymphocytic leukemia and in the apoptosis of Jurkat cells induced by adriamycin]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Oct;10(5):620-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of WAVE1 in childhood acute lymphocytic leukemia and in the apoptosis of Jurkat cells induced by adriamycin].
  • OBJECTIVE: To investigate whether WASP/Verprolin homologous protein 1 (WAVE1) plays a role in the pathogenesis of childhood acute lymphoblastic leukemia (ALL).
  • The cell proliferation was detected with MTT.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Doxorubicin / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Wiskott-Aldrich Syndrome Protein Family / physiology
  • [MeSH-minor] Adolescent. Blotting, Western. Cell Proliferation / drug effects. Child. Child, Preschool. Female. Humans. Infant. Jurkat Cells. Male. RNA, Messenger / analysis

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18947485.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / RNA, Messenger; 0 / WASF1 protein, human; 0 / Wiskott-Aldrich Syndrome Protein Family; 80168379AG / Doxorubicin
  •  go-up   go-down


88. Ho AD, Hensel M: Pentostatin and purine analogs for indolent lymphoid malignancies. Future Oncol; 2006 Apr;2(2):169-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pentostatin has been shown to be active in a variety of B- and T-cell malignancies.
  • Early clinical trials indicated that this agent was highly active in acute lymphoblastic leukemias with high intracellular adenosine deaminase levels.
  • Through the efforts of a few investigators, better tolerated, low-dose regimens have been shown to be extremely active in lymphoproliferative diseases with very low intracellular adenosine deaminase levels such as hairy cell leukemia, B- and T-cell chronic leukemias, T-cell cutaneous lymphomas and low-grade non-Hodgkin lymphomas.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Leukemia, Hairy Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Prolymphocytic / drug therapy. Pentostatin / therapeutic use. Purine Nucleosides / therapeutic use

  • Hazardous Substances Data Bank. PENTOSTATIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16563086.001).
  • [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 / Adenosine Deaminase Inhibitors; 0 / Antibiotics, Antineoplastic; 0 / Purine Nucleosides; 395575MZO7 / Pentostatin
  • [Number-of-references] 92
  •  go-up   go-down


89. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

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