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1. Webb TR, Slavish J, George RE, Look AT, Xue L, Jiang Q, Cui X, Rentrop WB, Morris SW: Anaplastic lymphoma kinase: role in cancer pathogenesis and small-molecule inhibitor development for therapy. Expert Rev Anticancer Ther; 2009 Mar;9(3):331-56
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  • [Title] Anaplastic lymphoma kinase: role in cancer pathogenesis and small-molecule inhibitor development for therapy.
  • Anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase in the insulin receptor superfamily, was initially identified in constitutively activated oncogenic fusion forms - the most common being nucleophosmin-ALK - in anaplastic large-cell lymphomas, and subsequent studies have identified ALK fusions in diffuse large B-cell lymphomas, systemic histiocytosis, inflammatory myofibroblastic tumors, esophageal squamous cell carcinomas and non-small-cell lung carcinomas.

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  • [Cites] Crit Rev Oncol Hematol. 2006 Dec;60(3):216-26 [16860997.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Dec 29;351(4):839-46 [17094947.001]
  • [Cites] Am J Surg Pathol. 2006 Dec;30(12):1502-12 [17122505.001]
  • [Cites] World J Gastroenterol. 2006 Nov 28;12(44):7104-12 [17131471.001]
  • [Cites] J Clin Invest. 2006 Dec;116(12):3171-82 [17111047.001]
  • [Cites] Ann Oncol. 2000 Jan;11(1):53-8 [10690387.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):793-8 [10706082.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2144-9 [10706887.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2603-8 [10706604.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Apr 21;270(3):936-41 [10772929.001]
  • [Cites] Am J Pathol. 2000 May;156(5):1711-21 [10793082.001]
  • [Cites] Br J Haematol. 2000 Jun;109(3):584-91 [10886208.001]
  • [Cites] Am J Pathol. 2000 Aug;157(2):377-84 [10934142.001]
  • [Cites] Science. 2000 Sep 15;289(5486):1938-42 [10988075.001]
  • [Cites] Curr Oncol Rep. 2002 Jul;4(4):317-24 [12044241.001]
  • [Cites] Br J Haematol. 2002 Jun;117(4):812-20 [12060115.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Aug;34(4):354-62 [12112524.001]
  • [Cites] Int J Cancer. 2002 Jul 1;100(1):49-56 [12115586.001]
  • [Cites] Genes Chromosomes Cancer. 2001 May;31(1):85-90 [11284039.001]
  • [Cites] Lab Invest. 2001 Mar;81(3):419-26 [11310834.001]
  • [Cites] Blood. 1999 Nov 15;94(10):3509-15 [10552961.001]
  • [Cites] Blood. 1997 Mar 1;89(5):1483-90 [9057627.001]
  • [Cites] Mol Cell Biol. 1997 Apr;17(4):2312-25 [9121481.001]
  • [Cites] J Biol Chem. 1997 Apr 4;272(14):9410-6 [9083079.001]
  • [Cites] Cancer Res. 1997 May 1;57(9):1814-9 [9135027.001]
  • [Cites] Cell. 2000 Oct 13;103(2):211-25 [11057895.001]
  • [Cites] Neuron. 2000 Dec;28(3):819-33 [11163269.001]
  • [Cites] Bull Cancer. 2000 Dec;87(12):873-6 [11174115.001]
  • [Cites] Ann Diagn Pathol. 2001 Feb;5(1):10-4 [11172201.001]
  • [Cites] Blood. 1994 Oct 15;84(8):2467-71 [7919366.001]
  • [Cites] J Biochem. 1994 Jun;115(6):1088-96 [7982887.001]
  • [Cites] Cancer Res. 1995 Apr 15;55(8):1792-7 [7712489.001]
  • [Cites] Cytogenet Cell Genet. 1995;70(1-2):143-4 [7736780.001]
  • [Cites] Ann N Y Acad Sci. 1995 Sep 7;766:442-58 [7486690.001]
  • [Cites] Cancer Res. 1996 Jan 1;56(1):100-4 [8548747.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):4181-6 [8633037.001]
  • [Cites] Cancer Res. 1996 Jun 1;56(11):2515-8 [8653688.001]
  • [Cites] J Biol Chem. 1996 Aug 30;271(35):21446-52 [8702927.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14753-8 [8962127.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14759-64 [8962128.001]
  • [Cites] Oncogene. 1997 Jan 30;14(4):439-49 [9053841.001]
  • [Cites] Blood. 1997 Feb 15;89(4):1394-404 [9028963.001]
  • [Cites] Cell Signal. 2007 Apr;19(4):740-7 [17110082.001]
  • [Cites] PLoS One. 2007;2(2):e255 [17327916.001]
  • [Cites] Mod Pathol. 2007 Mar;20(3):310-9 [17277765.001]
  • [Cites] Cell. 2007 Mar 9;128(5):961-75 [17350579.001]
  • [Cites] Oncogene. 1997 May 8;14(18):2175-88 [9174053.001]
  • [Cites] Biochim Biophys Acta. 1997 Dec 9;1333(3):F217-48 [9426205.001]
  • [Cites] Blood. 1998 Mar 15;91(6):2076-84 [9490693.001]
  • [Cites] Cancer Res. 1998 Mar 1;58(5):1057-62 [9500471.001]
  • [Cites] Leuk Lymphoma. 1998 Apr;29(3-4):249-56 [9684923.001]
  • [Cites] Am J Pathol. 1998 Sep;153(3):875-86 [9736036.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3591-8 [9808552.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):6951-61 [9819383.001]
  • [Cites] Am J Clin Pathol. 1999 Jan;111(1 Suppl 1):S56-67 [9894470.001]
  • [Cites] Blood. 1999 Apr 15;93(8):2697-706 [10194450.001]
  • [Cites] J Biol Chem. 1999 Apr 30;274(18):12474-9 [10212223.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3913-21 [10339500.001]
  • [Cites] Am J Pathol. 1999 Jun;154(6):1657-63 [10362790.001]
  • [Cites] Cancer Res. 1999 Jun 15;59(12):2776-80 [10383129.001]
  • [Cites] Blood. 1999 Jul 1;94(1):362-4 [10381534.001]
  • [Cites] N Engl J Med. 1999 Oct 14;341(16):1165-73 [10519894.001]
  • [Cites] J Med Chem. 2004 Dec 30;47(27):6658-61 [15615512.001]
  • [Cites] Clin Lung Cancer. 2004 Dec;6 Suppl 1:S20-3 [15638953.001]
  • [Cites] Cancer Sci. 2005 Jan;96(1):54-6 [15649256.001]
  • [Cites] Eur J Neurosci. 2005 Jan;21(2):513-21 [15673450.001]
  • [Cites] J Clin Pharmacol. 2005 Apr;45(4):394-403 [15778420.001]
  • [Cites] Oncogene. 2005 Apr 28;24(19):3206-15 [15735675.001]
  • [Cites] Cancer Lett. 2005 Jul 8;225(1):1-26 [15922853.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Jul 15;332(4):1146-52 [15949466.001]
  • [Cites] Am J Pathol. 2005 Jul;167(1):213-22 [15972965.001]
  • [Cites] Haematologica. 2005 Jul;90(7):988-90 [15996942.001]
  • [Cites] Methods Mol Med. 2005;115:271-94 [15998974.001]
  • [Cites] J Biol Chem. 2005 Jul 15;280(28):26039-48 [15886198.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):26953-64 [15908427.001]
  • [Cites] Pediatr Blood Cancer. 2005 Nov;45(6):796-801 [15602716.001]
  • [Cites] Semin Cancer Biol. 2005 Dec;15(6):506-14 [16154360.001]
  • [Cites] J Pediatr Surg. 2005 Oct;40(10):1581-6 [16226988.001]
  • [Cites] Int J Cancer. 2005 Dec 20;117(6):942-51 [15986444.001]
  • [Cites] Curr Mol Med. 2005 Nov;5(7):625-42 [16305489.001]
  • [Cites] Dev Genes Evol. 2006 Jan;216(1):10-8 [16220264.001]
  • [Cites] Int J Cancer. 2006 Mar 1;118(5):1181-6 [16161041.001]
  • [Cites] J Comp Neurol. 2006 Mar 10;495(2):202-12 [16435287.001]
  • [Cites] J Med Chem. 2006 Feb 9;49(3):1006-15 [16451066.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1617-23 [16254137.001]
  • [Cites] Cancer Lett. 2006 Feb 20;233(1):16-20 [15878231.001]
  • [Cites] Oncogene. 2006 May 25;25(22):3150-9 [16501609.001]
  • [Cites] Gene Expr Patterns. 2006 Jun;6(5):448-61 [16458083.001]
  • [Cites] J Med Chem. 2006 Sep 21;49(19):5759-68 [16970400.001]
  • [Cites] J Neural Transm (Vienna). 2006 Oct;113(10):1569-73 [16604305.001]
  • [Cites] J Biol Chem. 2006 Oct 13;281(41):30857-64 [16901907.001]
  • [Cites] Lancet. 2006 Oct 14;368(9544):1303-4 [17046443.001]
  • [Cites] Med Res Rev. 2008 May;28(3):372-412 [17694547.001]
  • [Cites] Exp Hematol. 2006 Dec;34(12):1670-9 [17157164.001]
  • [Cites] Hum Pathol. 2001 Apr;32(4):428-33 [11331960.001]
  • [Cites] Nature. 2001 May 17;411(6835):355-65 [11357143.001]
  • [Cites] J Biol Chem. 2001 May 18;276(20):16772-9 [11278720.001]
  • [Cites] Br J Haematol. 2001 May;113(2):275-95 [11380391.001]
  • [Cites] Am J Surg Pathol. 2001 Jun;25(6):761-8 [11395553.001]
  • [Cites] Mod Pathol. 2001 Jun;14(6):569-76 [11406658.001]
  • [Cites] Genes Cells. 2001 Jun;6(6):531-44 [11442633.001]
  • [Cites] Am J Pathol. 2001 Aug;159(2):411-5 [11485898.001]
  • [Cites] Am J Surg Pathol. 2001 Nov;25(11):1364-71 [11684952.001]
  • [Cites] Cell. 2001 Nov 2;107(3):387-98 [11701128.001]
  • [Cites] Lancet. 2001 Oct 27;358(9291):1421-3 [11705489.001]
  • [Cites] Clin Cancer Res. 2002 Jan;8(1):240-5 [11801565.001]
  • [Cites] N Engl J Med. 2002 Feb 28;346(9):645-52 [11870241.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1928-37 [11877262.001]
  • [Cites] J Biol Chem. 2002 Apr 19;277(16):14153-8 [11809760.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3314-33 [12032772.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10700-5 [12149456.001]
  • [Cites] Oncogene. 2002 Aug 29;21(38):5823-34 [12185581.001]
  • [Cites] J Biol Chem. 2002 Aug 30;277(35):32071-7 [12070152.001]
  • [Cites] J Biochem. 2002 Sep;132(3):359-71 [12204104.001]
  • [Cites] Mod Pathol. 2002 Sep;15(9):931-8 [12218210.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):35862-8 [12107166.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):35990-8 [12122009.001]
  • [Cites] Histopathology. 2002 Nov;41(5):461-7 [12405914.001]
  • [Cites] Ai Zheng. 2002 Jan;21(1):58-62 [12500399.001]
  • [Cites] Genes Chromosomes Cancer. 2003 May;37(1):98-105 [12661011.001]
  • [Cites] Pathol Oncol Res. 2003;9(1):13-9 [12704441.001]
  • [Cites] Br J Cancer. 2003 May 19;88(10):1522-6 [12771916.001]
  • [Cites] Eur J Neurosci. 2003 May;17(10):2127-34 [12786979.001]
  • [Cites] Science. 2003 Aug 8;301(5634):805-9 [12907793.001]
  • [Cites] Mod Pathol. 2003 Aug;16(8):828-32 [12920229.001]
  • [Cites] EMBO Rep. 2003 Aug;4(8):781-6 [12855999.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2638-41 [12750159.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2568-73 [12763927.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2642-4 [12816858.001]
  • [Cites] J Pediatr Surg. 2003 Sep;38(9):1296-304 [14523809.001]
  • [Cites] Nature. 2003 Oct 2;425(6957):507-12 [14523446.001]
  • [Cites] Nature. 2003 Oct 2;425(6957):512-6 [14523447.001]
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7345-55 [14612533.001]
  • [Cites] Science. 2003 Dec 5;302(5651):1760-5 [14615545.001]
  • [Cites] Nature. 2003 Dec 18;426(6968):789-96 [14685227.001]
  • [Cites] Cancer Lett. 2004 Feb 20;204(2):127-43 [15013213.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3256-64 [15126367.001]
  • [Cites] Hum Pathol. 2004 Jun;35(6):711-21 [15188137.001]
  • [Cites] Nature. 2004 Jul 15;430(6997):345-50 [15208641.001]
  • [Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]
  • [Cites] Brain Res Dev Brain Res. 2004 Sep 17;152(2):189-97 [15351507.001]
  • [Cites] J Cell Sci. 2004 Oct 15;117(Pt 22):5405-15 [15466886.001]
  • [Cites] Br J Haematol. 1989 Jan;71(1):31-6 [2917127.001]
  • [Cites] Blood. 1989 Feb 15;73(3):806-13 [2537120.001]
  • [Cites] Leukemia. 1989 Dec;3(12):866-70 [2555633.001]
  • [Cites] J Cell Biol. 1990 Mar;110(3):607-16 [1689730.001]
  • [Cites] Br J Haematol. 1990 Feb;74(2):161-8 [2156548.001]
  • [Cites] Am J Surg Pathol. 1990 Apr;14(4):305-16 [2157342.001]
  • [Cites] Science. 1990 Dec 21;250(4988):1690-4 [2270483.001]
  • [Cites] J Biol Chem. 1992 Feb 5;267(4):2582-7 [1733956.001]
  • [Cites] J Biol Chem. 1992 Jun 5;267(16):11408-16 [1597470.001]
  • [Cites] J Biol Chem. 1992 Dec 25;267(36):25889-97 [1464602.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):679-82 [8421705.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] J Biol Chem. 1994 Apr 29;269(17):12999-3004 [8175719.001]
  • [Cites] Oncogene. 1994 Jun;9(6):1567-74 [8183550.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3389-95 [18451166.001]
  • [Cites] Br J Cancer. 2008 May 6;98(9):1536-9 [18414414.001]
  • [Cites] Curr Opin Genet Dev. 2008 Feb;18(1):87-96 [18406132.001]
  • [Cites] Cancer Sci. 2008 Jul;99(7):1319-25 [18452557.001]
  • [Cites] Hum Pathol. 2008 Jun;39(6):846-56 [18400254.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Jul 25;372(2):351-5 [18501703.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5496-504 [18385450.001]
  • [Cites] Cancer Res. 2008 Jul 1;68(13):4971-6 [18593892.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4275-83 [18594010.001]
  • [Cites] Lung Cancer. 2008 Aug;61(2):163-9 [18242762.001]
  • [Cites] J Biol Chem. 2008 Sep 5;283(36):25036-45 [18599487.001]
  • [Cites] Blood. 2008 Oct 1;112(7):2965-8 [18660380.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):930-5 [18724359.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):967-70 [18923523.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):971-4 [18923524.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):975-8 [18923525.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19893-7 [19064915.001]
  • [Cites] Oncogene. 2008 Apr 24;27(19):2728-36 [17998938.001]
  • [Cites] Semin Radiat Oncol. 2007 Jan;17(1):62-9 [17185199.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 2;104(1):270-5 [17185414.001]
  • [Cites] J Neurochem. 2006 Dec;99(6):1470-9 [17230638.001]
  • [Cites] FEBS Lett. 2007 Feb 20;581(4):727-34 [17274988.001]
  • [Cites] Cancer Control. 2007 Apr;14(2):124-32 [17387297.001]
  • [Cites] Am J Surg Pathol. 2007 Apr;31(4):509-20 [17414097.001]
  • [Cites] Am J Clin Pathol. 2007 May;127(5):670-86 [17439828.001]
  • [Cites] Cancer Res. 2007 Apr 15;67(8):3529-34 [17440059.001]
  • [Cites] Nat Rev Cancer. 2007 May;7(5):345-56 [17457302.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4278-86 [17483340.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4408-17 [17483355.001]
  • [Cites] Leuk Lymphoma. 2007 May;48(5):1053-6 [17487757.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Jun 29;358(2):399-403 [17490616.001]
  • [Cites] Oncology (Williston Park). 2007 May;21(6):689-96; discussion 699-700, [17564326.001]
  • [Cites] Int J Biochem Cell Biol. 2007;39(7-8):1349-57 [17537667.001]
  • [Cites] J Mol Med (Berl). 2007 Aug;85(8):863-75 [17318615.001]
  • [Cites] Exp Hematol. 2007 Aug;35(8):1240-8 [17560012.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] Oncogene. 2007 Aug 16;26(38):5606-14 [17353907.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1621-30 [17416736.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Oct 12;362(1):5-10 [17706593.001]
  • [Cites] Ann Oncol. 2007 Sep;18 Suppl 10:x25-31 [17761720.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2600-9 [17537995.001]
  • [Cites] J Biol Chem. 2007 Sep 28;282(39):28683-90 [17681947.001]
  • [Cites] Nat Rev Drug Discov. 2007 Oct;6(10):834-48 [17853901.001]
  • [Cites] Cell Signal. 2007 Dec;19(12):2434-43 [17904822.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3374-83 [17690253.001]
  • [Cites] Nat Med. 2007 Nov;13(11):1341-8 [17922009.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):19936-41 [18077425.001]
  • [Cites] Cell. 2007 Dec 14;131(6):1190-203 [18083107.001]
  • [Cites] Mol Cancer Ther. 2007 Dec;6(12 Pt 1):3314-22 [18089725.001]
  • [Cites] Nat Rev Cancer. 2008 Jan;8(1):11-23 [18097461.001]
  • [Cites] J Thorac Oncol. 2008 Jan;3(1):13-7 [18166835.001]
  • [Cites] Nat Biotechnol. 2008 Jan;26(1):127-32 [18183025.001]
  • [Cites] Neuropsychopharmacology. 2008 Feb;33(3):685-700 [17487225.001]
  • [Cites] Recent Pat Anticancer Drug Discov. 2007 Jun;2(2):175-86 [18221061.001]
  • [Cites] Pediatr Clin North Am. 2008 Feb;55(1):97-120, x [18242317.001]
  • [Cites] Oncology (Williston Park). 2007 Dec;21(14):1696-706; discussion 1706-9, 1712, 1715 [18247017.001]
  • [Cites] Hum Pathol. 2008 Mar;39(3):410-9 [18261625.001]
  • [Cites] J Biol Chem. 2008 Feb 15;283(7):3743-50 [18070884.001]
  • [Cites] Curr Opin Oncol. 2008 Mar;20(2):162-75 [18300766.001]
  • [Cites] Leuk Res. 2008 Mar;32(3):383-93 [17720243.001]
  • [Cites] Neoplasia. 2008 Mar;10(3):298-302 [18320074.001]
  • [Cites] J Clin Oncol. 2008 Apr 1;26(10):1742-51 [18375904.001]
  • [Cites] J Clin Pathol. 2008 Apr;61(4):428-37 [17938159.001]
  • [Cites] Curr Opin Hematol. 2008 May;15(3):210-4 [18391787.001]
  • (PMID = 19275511.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA069129-10; United States / NCI NIH HHS / CA / R01 CA69129; United States / NCI NIH HHS / CA / R01 CA069129; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / R01 CA069129-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; 134034-50-7 / pleiotrophin; 137497-38-2 / midkine; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 304
  • [Other-IDs] NLM/ NIHMS105118; NLM/ PMC2780428
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2. Ardini E, Magnaghi P, Orsini P, Galvani A, Menichincheri M: Anaplastic Lymphoma Kinase: role in specific tumours, and development of small molecule inhibitors for cancer therapy. Cancer Lett; 2010 Dec 28;299(2):81-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anaplastic Lymphoma Kinase: role in specific tumours, and development of small molecule inhibitors for cancer therapy.
  • The Anaplastic Lymphoma Kinase (ALK) is a receptor tyrosine kinase first identified as the product of a gene rearrangement in Anaplastic Large Cell Lymphoma.
  • ALK has subsequently been found to be rearranged, mutated, or amplified in a further series of tumours including neuroblastoma, and Non-Small Cell Lung Cancer.
  • These observations have sparked the development of small molecule kinase inhibitors, the most advanced of which is currently in clinical testing and which has shown promising preliminary activity in the subset of lung cancer patients whose tumours harbour activated ALK.
  • In this review, we describe the various oncogenic forms of ALK, relevant clinical settings, and give a detailed overview of current drug discovery efforts in the field.
  • [MeSH-minor] Animals. Humans. Molecular Structure. Piperidines / chemistry. Piperidines / therapeutic use. Pyridines / chemistry. Pyridines / therapeutic use. Pyrimidines / chemistry. Pyrimidines / therapeutic use. Pyrroles / chemistry. Pyrroles / therapeutic use. Receptor Protein-Tyrosine Kinases

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  • [Copyright] Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20934803.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / GSK 1838705A; 0 / NVP-TAE684; 0 / PF-2341066; 0 / Piperidines; 0 / Pyridines; 0 / Pyrimidines; 0 / Pyrroles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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3. Palmer RH, Vernersson E, Grabbe C, Hallberg B: Anaplastic lymphoma kinase: signalling in development and disease. Biochem J; 2009 Jun 15;420(3):345-61
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  • [Title] Anaplastic lymphoma kinase: signalling in development and disease.
  • The ALK (anaplastic lymphoma kinase) RTK was originally identified as a member of the insulin receptor subfamily of RTKs that acquires transforming capability when truncated and fused to NPM (nucleophosmin) in the t(2;5) chromosomal rearrangement associated with ALCL (anaplastic large cell lymphoma).
  • Recent reports of the EML4 (echinoderm microtubule-associated protein like 4)-ALK oncoprotein in NSCLC (non-small cell lung cancer), together with the identification of activating point mutations in neuroblastoma, have highlighted ALK as a significant player and target for drug development in cancer.
  • [MeSH-minor] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Carcinoma, Non-Small-Cell Lung / pathology. Humans. Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / pathology. Models, Biological. Neuroblastoma / genetics. Neuroblastoma / metabolism. Neuroblastoma / pathology. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. Receptor Protein-Tyrosine Kinases

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • [Cites] Cancer Genet Cytogenet. 2007 Jul 15;176(2):107-14 [17656252.001]
  • [Cites] Exp Hematol. 2007 Aug;35(8):1240-8 [17560012.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1580-1 [15317731.001]
  • [Cites] J Cell Sci. 2004 Oct 15;117(Pt 22):5405-15 [15466886.001]
  • [Cites] Blood. 1985 Oct;66(4):848-58 [3876124.001]
  • [Cites] J Antibiot (Tokyo). 1989 Apr;42(4):571-6 [2656615.001]
  • [Cites] Eur J Biochem. 1989 Dec 22;186(3):733-40 [2558016.001]
  • [Cites] J Biol Chem. 1990 Jun 25;265(18):10765-70 [2355021.001]
  • [Cites] EMBO J. 1990 Jul;9(7):2279-87 [2357970.001]
  • [Cites] J Biol Chem. 1990 Oct 5;265(28):16721-4 [2170351.001]
  • [Cites] Biochem Biophys Res Commun. 1990 Oct 30;172(2):850-4 [1700712.001]
  • [Cites] Biochem Biophys Res Commun. 1990 Nov 30;173(1):246-51 [1701634.001]
  • [Cites] Biochem Biophys Res Commun. 1991 Oct 15;180(1):145-51 [1819274.001]
  • [Cites] Anat Embryol (Berl). 1992 Sep;186(4):387-406 [1416088.001]
  • [Cites] Biochem Int. 1992 Oct;28(1):1-9 [1445382.001]
  • [Cites] Trends Biochem Sci. 1993 Feb;18(2):40-1 [8387703.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] J Biol Chem. 1994 Apr 29;269(17):12999-3004 [8175719.001]
  • [Cites] Oncogene. 1994 Jun;9(6):1567-74 [8183550.001]
  • [Cites] Cancer. 1994 Sep 1;74(5):1584-90 [7520350.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Sep 15;203(2):1131-9 [8093031.001]
  • [Cites] Neurosci Lett. 1994 Sep 12;178(2):216-20 [7824199.001]
  • [Cites] Development. 1995 Jan;121(1):37-51 [7867507.001]
  • [Cites] Breast Cancer Res Treat. 1994;31(2-3):309-14 [7533562.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Mar 28;92(7):2558-62 [7708684.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jul 3;92(14):6334-8 [7603991.001]
  • [Cites] Am J Surg Pathol. 1995 Aug;19(8):859-72 [7611533.001]
  • [Cites] Blood. 1995 Sep 1;86(5):1954-60 [7655022.001]
  • [Cites] Nat Med. 1996 May;2(5):561-6 [8616716.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):4181-6 [8633037.001]
  • [Cites] Hum Pathol. 1996 Jun;27(6):590-4 [8666370.001]
  • [Cites] J Biol Chem. 1996 Aug 30;271(35):21446-52 [8702927.001]
  • [Cites] Oncogene. 1997 Jan 30;14(4):439-49 [9053841.001]
  • [Cites] Blood. 1997 Feb 15;89(4):1394-404 [9028963.001]
  • [Cites] Blood. 1997 Mar 1;89(5):1483-90 [9057627.001]
  • [Cites] Mol Cell Biol. 1997 Apr;17(4):2312-25 [9121481.001]
  • [Cites] J Biochem. 1997 Feb;121(2):197-205 [9089390.001]
  • [Cites] Oncogene. 1997 May 8;14(18):2175-88 [9174053.001]
  • [Cites] J Biol Chem. 1997 Jul 4;272(27):16733-6 [9201975.001]
  • [Cites] Nature. 1997 Aug 14;388(6643):691-3 [9262405.001]
  • [Cites] Blood. 1997 Oct 15;90(8):2901-10 [9376569.001]
  • [Cites] Science. 1998 Jan 23;279(5350):577-80 [9438854.001]
  • [Cites] Adv Exp Med Biol. 1998;431:221-6 [9598063.001]
  • [Cites] Mol Cell Biol. 1998 Dec;18(12):6951-61 [9819383.001]
  • [Cites] EMBO Rep. 2003 Aug;4(8):781-6 [12855999.001]
  • [Cites] Oncogene. 2003 Aug 21;22(35):5399-407 [12934099.001]
  • [Cites] Br J Haematol. 1998 Dec;103(4):1138-44 [9886332.001]
  • [Cites] Genes Cells. 1998 Dec;3(12):811-22 [10096022.001]
  • [Cites] Blood. 1999 Apr 15;93(8):2697-706 [10194450.001]
  • [Cites] Blood. 1999 May 1;93(9):3088-95 [10216106.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3913-21 [10339500.001]
  • [Cites] Cancer Res. 1999 Jun 15;59(12):2776-80 [10383129.001]
  • [Cites] J Thorac Surg. 1954 Jul;28(1):55-63 [13175281.001]
  • [Cites] Blood. 2005 Jan 15;105(2):827-9 [15374880.001]
  • [Cites] Nat Biotechnol. 2005 Jan;23(1):94-101 [15592455.001]
  • [Cites] Mutat Res. 2005 Feb 15;570(1):9-15 [15680399.001]
  • [Cites] Nat Med. 2005 Jun;11(6):623-9 [15895073.001]
  • [Cites] Biochemistry. 2005 Jun 14;44(23):8533-42 [15938644.001]
  • [Cites] Am J Pathol. 2005 Jul;167(1):213-22 [15972965.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Aug 5;333(3):714-21 [15985215.001]
  • [Cites] Haematologica. 2005 Jul;90(7):988-90 [15996942.001]
  • [Cites] J Biol Chem. 2005 Jul 15;280(28):26039-48 [15886198.001]
  • [Cites] Cell. 2005 Jul 15;122(1):45-57 [16009132.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):26953-64 [15908427.001]
  • [Cites] Leukemia. 2005 Jul;19(7):1128-34 [15902287.001]
  • [Cites] Anticancer Res. 2005 Sep-Oct;25(5):3191-6 [16101126.001]
  • [Cites] Hum Pathol. 2005 Sep;36(9):939-44 [16153455.001]
  • [Cites] Pediatr Blood Cancer. 2005 Nov;45(6):796-801 [15602716.001]
  • [Cites] Int J Cancer. 2005 Dec 20;117(6):942-51 [15986444.001]
  • [Cites] J Pharmacol Exp Ther. 2005 Dec;315(3):971-9 [16002463.001]
  • [Cites] Lab Invest. 2005 Dec;85(12):1544-54 [16170336.001]
  • [Cites] J Cell Sci. 2005 Dec 15;118(Pt 24):5811-23 [16317043.001]
  • [Cites] Dev Genes Evol. 2006 Jan;216(1):10-8 [16220264.001]
  • [Cites] Int J Cancer. 2006 Mar 1;118(5):1181-6 [16161041.001]
  • [Cites] Blood. 2006 Jan 15;107(2):689-97 [16189272.001]
  • [Cites] J Comp Neurol. 2006 Mar 10;495(2):202-12 [16435287.001]
  • [Cites] J Med Chem. 2006 Feb 9;49(3):1006-15 [16451066.001]
  • [Cites] Blood. 2006 Feb 15;107(4):1617-23 [16254137.001]
  • [Cites] J Clin Oncol. 2006 May 10;24(14):2137-50 [16682732.001]
  • [Cites] Gene Expr Patterns. 2006 Jun;6(5):448-61 [16458083.001]
  • [Cites] Lab Invest. 2006 Jul;86(7):645-53 [16619002.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6589-97 [16818631.001]
  • [Cites] Mol Cell Biol. 2006 Aug;26(16):6209-22 [16880530.001]
  • [Cites] Br J Haematol. 2006 Oct;135(1):26-32 [16939498.001]
  • [Cites] Blood. 2006 Oct 1;108(7):2407-15 [16763206.001]
  • [Cites] Blood. 2006 Oct 15;108(8):2796-803 [16825495.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Dec 29;351(4):839-46 [17094947.001]
  • [Cites] Genes Cells. 2006 Dec;11(12):1405-17 [17121547.001]
  • [Cites] World J Gastroenterol. 2006 Nov 28;12(44):7104-12 [17131471.001]
  • [Cites] J Clin Invest. 2006 Dec;116(12):3171-82 [17111047.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 2;104(1):270-5 [17185414.001]
  • [Cites] Oncogene. 2007 Feb 8;26(6):859-69 [16878150.001]
  • [Cites] Oncogene. 2007 Feb 8;26(6):813-21 [16909118.001]
  • [Cites] FEBS Lett. 2007 Feb 20;581(4):727-34 [17274988.001]
  • [Cites] Blood. 2007 Mar 1;109(5):2156-64 [17077326.001]
  • [Cites] Mod Pathol. 2007 Mar;20(3):310-9 [17277765.001]
  • [Cites] Cell. 2007 Mar 9;128(5):961-75 [17350579.001]
  • [Cites] Am J Surg Pathol. 2007 Apr;31(4):509-20 [17414097.001]
  • [Cites] Oncogene. 2007 May 3;26(20):2950-4 [17086210.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4278-86 [17483340.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4408-17 [17483355.001]
  • [Cites] J Exp Zool B Mol Dev Evol. 2007 May 15;308(3):269-82 [17285636.001]
  • [Cites] Hum Pathol. 2007 Jun;38(6):940-5 [17509395.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Jun 29;358(2):399-403 [17490616.001]
  • [Cites] Differentiation. 2007 Jun;75(5):418-26 [17286600.001]
  • [Cites] Lancet. 2007 Jun 23;369(9579):2106-20 [17586306.001]
  • [Cites] N Engl J Med. 2007 Jul 5;357(1):39-51 [17611206.001]
  • [Cites] J Mol Med (Berl). 2007 Aug;85(8):863-75 [17318615.001]
  • [Cites] Cancer Res. 2009 Mar 15;69(6):2550-8 [19244133.001]
  • [Cites] Blood. 2009 Mar 19;113(12):2776-90 [18845790.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] Oncogene. 2007 Aug 16;26(38):5606-14 [17353907.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1621-30 [17416736.001]
  • [Cites] Blood. 1999 Nov 1;94(9):3265-8 [10556217.001]
  • [Cites] Blood. 1999 Nov 15;94(10):3614-7 [10610119.001]
  • [Cites] J Biol Chem. 2000 Feb 25;275(8):5600-5 [10681541.001]
  • [Cites] Ann Oncol. 2000 Jan;11(1):53-8 [10690387.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):793-8 [10706082.001]
  • [Cites] Am J Pathol. 2000 Mar;156(3):781-9 [10702393.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2144-9 [10706887.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2603-8 [10706604.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Apr 21;270(3):936-41 [10772929.001]
  • [Cites] J Biol Chem. 2000 May 5;275(18):13564-70 [10788472.001]
  • [Cites] Am J Pathol. 2000 May;156(5):1711-21 [10793082.001]
  • [Cites] Blood. 2000 May 15;95(10):3204-7 [10807789.001]
  • [Cites] Dev Growth Differ. 2000 Apr;42(2):113-9 [10830434.001]
  • [Cites] Am J Pathol. 2000 Aug;157(2):377-84 [10934142.001]
  • [Cites] J Pharmacol Exp Ther. 2000 Oct;295(1):139-45 [10991971.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3681-95 [11090048.001]
  • [Cites] Blood. 2000 Dec 15;96(13):4319-27 [11110708.001]
  • [Cites] J Biol Chem. 2001 Mar 23;276(12):9526-31 [11121404.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1052-6 [11287975.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2194-9 [11280786.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2319-33 [11304786.001]
  • [Cites] Lab Invest. 2001 Mar;81(3):419-26 [11310834.001]
  • [Cites] J Biol Chem. 2001 May 18;276(20):16772-9 [11278720.001]
  • [Cites] Am J Pathol. 2001 Jun;158(6):2185-93 [11395396.001]
  • [Cites] Mod Pathol. 2001 Jun;14(6):569-76 [11406658.001]
  • [Cites] Genes Cells. 2001 Jun;6(6):531-44 [11442633.001]
  • [Cites] Am J Pathol. 2001 Aug;159(2):411-5 [11485898.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1209-16 [11493472.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6517-23 [11522649.001]
  • [Cites] Development. 2001 Sep;128(17):3331-8 [11546749.001]
  • [Cites] Am J Surg Pathol. 2001 Nov;25(11):1364-71 [11684952.001]
  • [Cites] Cell. 2001 Nov 2;107(3):387-98 [11701128.001]
  • [Cites] Lancet. 2001 Oct 27;358(9291):1421-3 [11705489.001]
  • [Cites] Mech Dev. 2002 Jan;110(1-2):85-96 [11744371.001]
  • [Cites] J Immunol. 2002 Jan 1;168(1):466-74 [11751994.001]
  • [Cites] Oncogene. 2002 Feb 7;21(7):1038-47 [11850821.001]
  • [Cites] Cancer Res. 2002 Mar 1;62(5):1559-66 [11888936.001]
  • [Cites] Am J Pathol. 2002 Apr;160(4):1487-94 [11943732.001]
  • [Cites] J Biol Chem. 2002 Apr 19;277(16):14153-8 [11809760.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4540-6 [12036886.001]
  • [Cites] Cell. 2002 May 31;109(5):639-49 [12062106.001]
  • [Cites] J Biol Chem. 2002 Jun 21;277(25):22231-9 [11919185.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Aug;34(4):354-62 [12112524.001]
  • [Cites] Int J Cancer. 2002 Jul 1;100(1):49-56 [12115586.001]
  • [Cites] N Engl J Med. 2002 Aug 15;347(7):472-80 [12181401.001]
  • [Cites] Oncogene. 2002 Aug 29;21(38):5823-34 [12185581.001]
  • [Cites] J Biochem. 2002 Sep;132(3):359-71 [12204104.001]
  • [Cites] Mod Pathol. 2002 Sep;15(9):931-8 [12218210.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):35862-8 [12107166.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):35990-8 [12122009.001]
  • [Cites] Histopathology. 2002 Nov;41(5):461-7 [12405914.001]
  • [Cites] Oncogene. 2003 Jan 30;22(4):517-27 [12555065.001]
  • [Cites] Blood. 2003 Mar 1;101(5):1919-27 [12424201.001]
  • [Cites] Nat Rev Cancer. 2003 Mar;3(3):203-16 [12612655.001]
  • [Cites] Exp Hematol. 2003 Mar;31(3):226-33 [12644020.001]
  • [Cites] Genes Chromosomes Cancer. 2003 May;37(1):98-105 [12661011.001]
  • [Cites] Clin Cancer Res. 2003 Jun;9(6):2213-20 [12796388.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Aug;37(4):427-32 [12800156.001]
  • [Cites] J Biol Chem. 2003 Aug 8;278(32):30028-36 [12748172.001]
  • [Cites] Cancer. 2009 Apr 15;115(8):1723-33 [19170230.001]
  • [Cites] Pediatr Dev Pathol. 2009 Jul-Aug;12(4):275-83 [18788887.001]
  • [Cites] Genes Chromosomes Cancer. 2003 Oct;38(2):187-90 [12939746.001]
  • [Cites] Lab Invest. 2003 Sep;83(9):1255-65 [13679433.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2638-41 [12750159.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2642-4 [12816858.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3692-9 [14506160.001]
  • [Cites] Nature. 2003 Oct 2;425(6957):507-12 [14523446.001]
  • [Cites] Nature. 2003 Oct 2;425(6957):512-6 [14523447.001]
  • [Cites] Am J Surg Pathol. 2003 Nov;27(11):1473-6 [14576483.001]
  • [Cites] Oncogene. 2003 Oct 30;22(49):7750-61 [14586401.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1464-71 [14563642.001]
  • [Cites] Development. 2004 Feb;131(4):743-54 [14757637.001]
  • [Cites] Cancer Lett. 2004 Feb 20;204(2):127-43 [15013213.001]
  • [Cites] Oncogene. 2004 Apr 8;23(15):2617-29 [14968112.001]
  • [Cites] J Cell Physiol. 2004 Jun;199(3):330-58 [15095281.001]
  • [Cites] J Clin Oncol. 2004 May 1;22(9):1682-8 [15117990.001]
  • [Cites] Blood. 2004 Jun 15;103(12):4622-9 [14962911.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] Hum Pathol. 2004 Jun;35(6):711-21 [15188137.001]
  • [Cites] Cancer. 2004 Jul 1;101(1):3-27 [15221985.001]
  • [Cites] J Cell Sci. 2004 Jul 1;117(Pt 15):3319-29 [15226403.001]
  • [Cites] Nature. 2004 Jul 15;430(6997):345-50 [15208641.001]
  • [Cites] Oncogene. 2004 Jul 15;23(32):5426-34 [15184887.001]
  • [Cites] Oncogene. 2004 Aug 12;23(36):6071-82 [15208656.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2259-67 [17519389.001]
  • [Cites] J Biol Chem. 2007 Sep 28;282(39):28683-90 [17681947.001]
  • [Cites] Cell Signal. 2007 Dec;19(12):2434-43 [17904822.001]
  • [Cites] Nat Med. 2007 Nov;13(11):1341-8 [17922009.001]
  • [Cites] Cell. 2007 Dec 14;131(6):1190-203 [18083107.001]
  • [Cites] Mol Cancer Ther. 2007 Dec;6(12 Pt 1):3314-22 [18089725.001]
  • [Cites] J Thorac Oncol. 2008 Jan;3(1):13-7 [18166835.001]
  • [Cites] Neuropsychopharmacology. 2008 Feb;33(3):685-700 [17487225.001]
  • [Cites] J Biol Chem. 2008 Feb 15;283(7):3743-50 [18070884.001]
  • [Cites] Annu Rev Physiol. 2008;70:431-57 [17850209.001]
  • [Cites] Neoplasia. 2008 Mar;10(3):298-302 [18320074.001]
  • [Cites] J Biochem. 2008 Apr;143(4):441-8 [18024471.001]
  • [Cites] PLoS Genet. 2008 Mar;4(3):e1000026 [18369445.001]
  • [Cites] J Clin Pathol. 2008 Apr;61(4):428-37 [17938159.001]
  • [Cites] Med Res Rev. 2008 May;28(3):372-412 [17694547.001]
  • [Cites] Oncogene. 2008 Apr 24;27(19):2728-36 [17998938.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3389-95 [18451166.001]
  • [Cites] Br J Cancer. 2008 May 6;98(9):1536-9 [18414414.001]
  • [Cites] Korean J Lab Med. 2008 Apr;28(2):89-94 [18458503.001]
  • [Cites] Hematol Oncol. 2008 Jun;26(2):108-13 [18220322.001]
  • [Cites] Nat Med. 2008 Jun;14(6):676-80 [18469826.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5496-504 [18385450.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4275-83 [18594010.001]
  • [Cites] Lung Cancer. 2008 Aug;61(2):163-9 [18242762.001]
  • [Cites] Curr Biol. 2008 Aug 5;18(15):1101-9 [18674914.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):930-5 [18724359.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):967-70 [18923523.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):971-4 [18923524.001]
  • [Cites] Nature. 2008 Oct 16;455(7215):975-8 [18923525.001]
  • [Cites] Cancer Res. 2008 Nov 1;68(21):8899-907 [18974134.001]
  • [Cites] Neuroreport. 2008 Nov 19;19(17):1733-8 [18849880.001]
  • [Cites] Biochem J. 2008 Dec 1;416(2):153-9 [18990089.001]
  • [Cites] Hum Pathol. 2009 Jan;40(1):75-82 [18755494.001]
  • [Cites] Blood. 2008 Dec 15;112(13):4808-17 [19064740.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19893-7 [19064915.001]
  • [Cites] Am J Pathol. 2009 Feb;174(2):361-70 [19131589.001]
  • [Cites] Am J Pathol. 2009 Feb;174(2):661-70 [19147828.001]
  • [Cites] Neoplasia. 2009 Feb;11(2):145-56 [19177199.001]
  • [Cites] Eur J Neurosci. 2009 Jan;29(2):275-86 [19200234.001]
  • (PMID = 19459784.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / EML4-ALK fusion protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
  • [Number-of-references] 237
  • [Other-IDs] NLM/ PMC2708929
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4. Milkiewicz KL, Ott GR: Inhibitors of anaplastic lymphoma kinase: a patent review. Expert Opin Ther Pat; 2010 Dec;20(12):1653-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitors of anaplastic lymphoma kinase: a patent review.
  • IMPORTANCE OF THE FIELD: Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase that belongs to the insulin receptor superfamily.
  • Aberrant ALK activity has been implicated in the oncogenesis of human cancers as a fusion protein in anaplastic large cell lymphoma, inflammatory myofibroblastic tumor, diffuse large B-cell lymphoma, systemic histiocytosis and NSCLC or through mutations in the full length protein in hereditary familial neuroblastoma.
  • AREAS COVERED IN THIS REVIEW: This manuscript provides a comprehensive review of the patent literature pertaining to ALK inhibitors and outlines their potential as anticancer therapeutic agents.
  • WHAT THE READER WILL GAIN: The reader will gain an understanding of the major structural classes of ALK inhibitors and insights into the future of this class of drugs.
  • The breadth of inhibitors combined with the recent discoveries of the involvement of ALK in lung, breast and colorectal cancers has kept the field advancing at a rapid pace.
  • [MeSH-major] Neoplasms / drug therapy. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm. Humans. Patents as Topic. Receptor Protein-Tyrosine Kinases

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  • (PMID = 20961208.001).
  • [ISSN] 1744-7674
  • [Journal-full-title] Expert opinion on therapeutic patents
  • [ISO-abbreviation] Expert Opin Ther Pat
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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5. Weiss J, Sos ML, Seidel D, Peifer M, Zander T, Heuckmann JM, Ullrich RT, Menon R, Maier S, Soltermann A, Moch H, Wagener P, Fischer F, Heynck S, Koker M, Schöttle J, Leenders F, Gabler F, Dabow I, Querings S, Heukamp LC, Balke-Want H, Ansén S, Rauh D, Baessmann I, Altmüller J, Wainer Z, Conron M, Wright G, Russell P, Solomon B, Brambilla E, Brambilla C, Lorimier P, Sollberg S, Brustugun OT, Engel-Riedel W, Ludwig C, Petersen I, Sänger J, Clement J, Groen H, Timens W, Sietsma H, Thunnissen E, Smit E, Heideman D, Cappuzzo F, Ligorio C, Damiani S, Hallek M, Beroukhim R, Pao W, Klebl B, Baumann M, Buettner R, Ernestus K, Stoelben E, Wolf J, Nürnberg P, Perner S, Thomas RK: Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer. Sci Transl Med; 2010 Dec 15;2(62):62ra93
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  • [Title] Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer.
  • Lung cancer remains one of the leading causes of cancer-related death in developed countries.
  • Although lung adenocarcinomas with EGFR mutations or EML4-ALK fusions respond to treatment by epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) inhibition, respectively, squamous cell lung cancer currently lacks therapeutically exploitable genetic alterations.
  • We conducted a systematic search in a set of 232 lung cancer specimens for genetic alterations that were therapeutically amenable and then performed high-resolution gene copy number analyses.
  • We identified frequent and focal fibroblast growth factor receptor 1 (FGFR1) amplification in squamous cell lung cancer (n = 155), but not in other lung cancer subtypes, and, by fluorescence in situ hybridization, confirmed the presence of FGFR1 amplifications in an independent cohort of squamous cell lung cancer samples (22% of cases).
  • Using cell-based screening with the FGFR inhibitor PD173074 in a large (n = 83) panel of lung cancer cell lines, we demonstrated that this compound inhibited growth and induced apoptosis specifically in those lung cancer cells carrying amplified FGFR1.
  • We validated the FGFR1 dependence of FGFR1-amplified cell lines by FGFR1 knockdown and by ectopic expression of an FGFR1-resistant allele (FGFR1(V561M)), which rescued FGFR1-amplified cells from PD173074-mediated cytotoxicity.
  • Thus, focal FGFR1 amplification is common in squamous cell lung cancer and associated with tumor growth and survival, suggesting that FGFR inhibitors may be a viable therapeutic option in this cohort of patients.
  • [MeSH-major] Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Receptor, Fibroblast Growth Factor, Type 1 / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Animals. Apoptosis / genetics. Apoptosis / physiology. Blotting, Western. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Line. Enzyme Inhibitors / therapeutic use. Gene Expression Regulation, Neoplastic / genetics. Humans. Male. Mice. Mice, Nude. Pyrimidines / therapeutic use. RNA Interference. Xenograft Model Antitumor Assays

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  • [Cites] Cancer Res. 2010 Mar 1;70(5):2085-94 [20179196.001]
  • [Cites] Nature. 2010 Feb 18;463(7283):899-905 [20164920.001]
  • [Cites] N Engl J Med. 2010 Oct 28;363(18):1693-703 [20979469.001]
  • [Cites] Chem Biol. 2010 Mar 26;17(3):285-95 [20338520.001]
  • [Cites] Cancer Res. 2010 Feb 1;70(3):868-74 [20103621.001]
  • [Cites] Nat Rev Cancer. 2010 Feb;10(2):116-29 [20094046.001]
  • [Cites] Cancer Biol Ther. 2009 Nov;8(21):2042-50 [19755855.001]
  • [Cites] Lung Cancer. 2001 Feb-Mar;31(2-3):139-48 [11165392.001]
  • [Cites] N Engl J Med. 2001 Mar 15;344(11):783-92 [11248153.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4342-9 [14645423.001]
  • [Cites] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073.001]
  • [Cites] Chem Biol. 2004 May;11(5):691-701 [15157880.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11 [15329413.001]
  • [Cites] EMBO J. 1998 Oct 15;17(20):5896-904 [9774334.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5561-70 [15994928.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9625-30 [15983384.001]
  • [Cites] Clin Cancer Res. 2006 Nov 15;12(22):6652-62 [17121884.001]
  • [Cites] N Engl J Med. 2006 Dec 14;355(24):2542-50 [17167137.001]
  • [Cites] Nature. 2007 Mar 8;446(7132):153-8 [17344846.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] Nature. 2007 Dec 6;450(7171):893-8 [17982442.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):19936-41 [18077425.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20007-12 [18077431.001]
  • [Cites] Cell. 2007 Dec 14;131(6):1190-203 [18083107.001]
  • [Cites] J Pathol. 2009 Jan;217(1):65-72 [18932182.001]
  • [Cites] Mol Pharmacol. 2009 Jan;75(1):196-207 [18849352.001]
  • [Cites] Cancer Res. 2009 May 1;69(9):3937-46 [19366796.001]
  • [Cites] Lancet. 2009 May 2;373(9674):1525-31 [19410716.001]
  • [Cites] J Clin Invest. 2009 Jun;119(6):1727-40 [19451690.001]
  • [Cites] N Engl J Med. 2009 Sep 3;361(10):947-57 [19692680.001]
  • [Cites] Nat Genet. 2009 Nov;41(11):1238-42 [19801978.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Oct 27;106(43):18351-6 [19805051.001]
  • [CommentIn] Sci Transl Med. 2010 Dec 15;2(62):62ps56 [21160076.001]
  • [CommentIn] Nat Rev Drug Discov. 2011 Feb;10(2):98-9 [21283102.001]
  • [ErratumIn] Sci Transl Med. 2012 Apr 18;4(130):130er2
  • [ErratumIn] Sci Transl Med. 2011 Jan 19;3(66):66er2
  • (PMID = 21160078.001).
  • [ISSN] 1946-6242
  • [Journal-full-title] Science translational medicine
  • [ISO-abbreviation] Sci Transl Med
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE25016
  • [Grant] United States / NCI NIH HHS / CA / K08 CA097980; United States / NCI NIH HHS / CA / P01 CA129243; United States / NCI NIH HHS / CA / R01 CA121210
  • [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 / Enzyme Inhibitors; 0 / PD 173074; 0 / Pyrimidines; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; Adenocarcinoma of lung
  • [Other-IDs] NLM/ NIHMS569992; NLM/ PMC3990281
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6. Kelleher FC, McDermott R: The emerging pathogenic and therapeutic importance of the anaplastic lymphoma kinase gene. Eur J Cancer; 2010 Sep;46(13):2357-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The emerging pathogenic and therapeutic importance of the anaplastic lymphoma kinase gene.
  • The anaplastic lymphoma kinase gene (ALK) is a gene on chromosome 2p23 that has expression restricted to the brain, testis and small intestine but is not expressed in normal lymphoid tissue.
  • This gene was originally established as being implicated in the pathogenesis of rare diseases including inflammatory myofibroblastic tumour (IMT) and ALK-positive anaplastic large cell lymphoma, which is a subtype of non-Hodgkin's lymphoma.
  • In 2007, an inversion of chromosome 2 involving ALK and a fusion partner gene in a subset of non-small cell lung cancer was discovered.
  • This has been described in ALK-positive anaplastic large cell lymphoma in which ALK is fused to NPM (nucleolar protein gene) and in non-small cell lung cancer where ALK is fused to EML4 (Echinoderm microtubule-associated protein 4).
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / therapy. Drug Synergism. Gene Amplification. Humans. Lung Neoplasms / genetics. Lung Neoplasms / therapy. Lymphoma, Large-Cell, Anaplastic / genetics. Lymphoma, Large-Cell, Anaplastic / therapy. Mutation / genetics. Neuroblastoma / genetics. Neuroblastoma / therapy. Pyrimidines / therapeutic use. Pyrroles / therapeutic use. Receptor Protein-Tyrosine Kinases. Receptor, IGF Type 1 / antagonists & inhibitors

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  • [Copyright] Copyright 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20451371.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / GSK 1838705A; 0 / Pyrimidines; 0 / Pyrroles; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / anaplastic lymphoma kinase
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7. Rikova K, Guo A, Zeng Q, Possemato A, Yu J, Haack H, Nardone J, Lee K, Reeves C, Li Y, Hu Y, Tan Z, Stokes M, Sullivan L, Mitchell J, Wetzel R, Macneill J, Ren JM, Yuan J, Bakalarski CE, Villen J, Kornhauser JM, Smith B, Li D, Zhou X, Gygi SP, Gu TL, Polakiewicz RD, Rush J, Comb MJ: Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. Cell; 2007 Dec 14;131(6):1190-203
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  • [Title] Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer.
  • Despite the success of tyrosine kinase-based cancer therapeutics, for most solid tumors the tyrosine kinases that drive disease remain unknown, limiting our ability to identify drug targets and predict response.
  • Here we present the first large-scale survey of tyrosine kinase activity in lung cancer.
  • Using a phosphoproteomic approach, we characterize tyrosine kinase signaling across 41 non-small cell lung cancer (NSCLC) cell lines and over 150 NSCLC tumors.
  • Profiles of phosphotyrosine signaling are generated and analyzed to identify known oncogenic kinases such as EGFR and c-Met as well as novel ALK and ROS fusion proteins.
  • By focusing on activated cell circuitry, the approach outlined here provides insight into cancer biology not available at the chromosomal and transcriptional levels and can be applied broadly across all human cancers.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Phosphotyrosine / metabolism. Protein-Tyrosine Kinases / metabolism. Signal Transduction / genetics
  • [MeSH-minor] Cell Line, Tumor. Enzyme Activation. Gene Fusion. Humans. Models, Biological. Molecular Sequence Data. Phosphorylation. Receptor Protein-Tyrosine Kinases. Receptor, Platelet-Derived Growth Factor alpha / metabolism


8. Seidemann K, Tiemann M, Schrappe M, Yakisan E, Simonitsch I, Janka-Schaub G, Dörffel W, Zimmermann M, Mann G, Gadner H, Parwaresch R, Riehm H, Reiter A: Short-pulse B-non-Hodgkin lymphoma-type chemotherapy is efficacious treatment for pediatric anaplastic large cell lymphoma: a report of the Berlin-Frankfurt-Münster Group Trial NHL-BFM 90. Blood; 2001 Jun 15;97(12):3699-706
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  • [Title] Short-pulse B-non-Hodgkin lymphoma-type chemotherapy is efficacious treatment for pediatric anaplastic large cell lymphoma: a report of the Berlin-Frankfurt-Münster Group Trial NHL-BFM 90.
  • Anaplastic large-cell lymphoma (ALCL) accounts for approximately 10% of pediatric non-Hodgkin lymphoma (NHL).
  • Previous experience from NHL-Berlin-Frankfurt-Münster (BFM) trials indicated that the short-pulse B-NHL-type treatment strategy may also be efficacious for ALCL.
  • The purpose of this study was to test the efficacy of this protocol for treatment of childhood ALCL in a large prospective multicenter trial and to define risk factors.
  • Immunophenotype was T-cell in 40 patients, B-cell in 5, null in 31, and not determined in 13.
  • Stages were as follows: I, n = 8; II, n = 20; III, n = 55; IV, n = 6.
  • Extranodal manifestations were as follows: mediastinum, n = 28; lung, n = 13; skin, n = 16; soft tissue, n = 13; bone, n = 14; central nervous system, n = 1; bone marrow, n = 5.
  • After a cytoreductive prephase, treatment was stratified into 3 branches: patients in K1 (stage I and II resected) received three 5-day courses (methotrexate [MTX] 0.5 g/m(2), dexamethasone, oxazaphorins, etoposide, cytarabine, doxorubicin, and intrathecal therapy); patients in K2 (stage II nonresected and stage III) received 6 courses; patients in K3 (stage IV or multifocal bone disease) received 6 intensified courses including MTX 5 g/m(2), high-dose cytarabine/etoposide.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lymphoma, Large-Cell, Anaplastic / drug therapy
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Disease-Free Survival. Female. Germany. Humans. Immunophenotyping. Infant. Lymphoma, B-Cell / drug therapy. Male. Prospective Studies. Protein-Tyrosine Kinases / metabolism. Receptor Protein-Tyrosine Kinases. Recurrence. Risk Factors. Treatment Failure


9. Rodig SJ, Shapiro GI: Crizotinib, a small-molecule dual inhibitor of the c-Met and ALK receptor tyrosine kinases. Curr Opin Investig Drugs; 2010 Dec;11(12):1477-90
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  • Crizotinib (PF-02341066), under development by Pfizer, is an orally bioavailable, ATP-competitive, small-molecule inhibitor of the receptor tyrosine kinases (RTKs) c-Met (also known as hepatocyte growth factor receptor) and anaplastic lymphoma kinase (ALK), for the potential treatment of cancers dependent on these oncogenic kinases for growth and survival.
  • Since the first published characterizations of crizotinib only a few years ago, the drug has been extensively validated as a highly specific inhibitor of c-Met and ALK among > 120 different RTKs surveyed.
  • In preclinical tumor xenograft studies, crizotinib inhibited the growth and survival of cell lines dependent upon c-Met or ALK enzymatic activity.
  • Crizotinib has been particularly effective against anaplastic large cell lymphoma and non-small cell lung cancer (NSCLC) cell lines that harbor ALK translocations resulting in expression of oncogenic ALK fusion proteins.
  • At the time of publication, an ongoing phase III clinical trial is comparing crizotinib with standard second-line chemotherapy in previously treated patients with NSCLC harboring ALK rearrangement, and a phase III trial comparing crizotinib with standard chemotherapy in the first-line setting in non-squamous lung cancer is planned.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-met / antagonists & inhibitors. Pyrazoles / therapeutic use. Pyridines / therapeutic use. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line, Tumor. Clinical Trials as Topic. Drug Approval. Drug Evaluation, Preclinical. Humans

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  • (PMID = 21154129.001).
  • [ISSN] 2040-3429
  • [Journal-full-title] Current opinion in investigational drugs (London, England : 2000)
  • [ISO-abbreviation] Curr Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Pyrazoles; 0 / Pyridines; 53AH36668S / crizotinib; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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10. Neal JW, Sequist LV: Exciting new targets in lung cancer therapy: ALK, IGF-1R, HDAC, and Hh. Curr Treat Options Oncol; 2010 Jun;11(1-2):36-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exciting new targets in lung cancer therapy: ALK, IGF-1R, HDAC, and Hh.
  • The anaplastic lymphoma kinase (ALK) inhibitor crizotinib will become an integral addition to the treatment of patients with non-small cell lung cancer (NSCLC) harboring genetic ALK translocations.
  • The insulin-like growth factor receptor (IGF-1R) monoclonal antibody figitumumab, while initially promising, appears to increase toxicity and death in combination with chemotherapy in the treatment of patients with NSCLC of squamous histology; therefore, clinical development of this class of agents will need to proceed with caution.
  • The histone deacetylation (HDAC) inhibitor vorinostat did not demonstrate an improvement in overall survival (OS) compared with placebo in a large randomized trial, but other agents in this class may have greater selectivity and efficacy.
  • Inhibitors of the hedgehog (Hh) signaling pathways have some early clinical promise in both NSCLC and small cell lung cancer (SCLC), and larger studies using these agents are eagerly anticipated.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hedgehog Proteins / antagonists & inhibitors. Histone Deacetylases / chemistry. Lung Neoplasms / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor, IGF Type 1 / antagonists & inhibitors

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  • [Cites] Nature. 2008 Sep 18;455(7211):406-10 [18754008.001]
  • [Cites] J Clin Oncol. 2009 May 20;27(15):2516-22 [19380445.001]
  • [Cites] J Clin Oncol. 2007 Jul 20;25(21):3109-15 [17577020.001]
  • [Cites] J Natl Cancer Inst. 2002 Jul 17;94(14):1099-106 [12122101.001]
  • [Cites] Mol Cell Biol. 2004 Dec;24(24):10826-34 [15572685.001]
  • [Cites] Endocr Relat Cancer. 2006 Jun;13(2):583-92 [16728584.001]
  • [Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]
  • [Cites] J Thorac Oncol. 2009 Nov;4(11):1397-403 [19745765.001]
  • [Cites] J Clin Oncol. 2010 Jan 1;28(1):56-62 [19933908.001]
  • [Cites] Exp Cell Res. 2001 May 1;265(2):195-202 [11302684.001]
  • [Cites] Clin Cancer Res. 2010 Mar 1;16(5):1561-71 [20179225.001]
  • [Cites] Clin Cancer Res. 2006 Jul 15;12(14 Pt 2):4392s-4395s [16857816.001]
  • [Cites] Oncogene. 2007 Feb 15;26(7):1046-55 [16909105.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Aug 18;106(33):14132-7 [19666565.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2002 Nov;11(11):1413-8 [12433720.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):944-50 [16424029.001]
  • [Cites] Br J Dermatol. 2005 Jan;152(1):43-51 [15656799.001]
  • [Cites] Nat Genet. 1996 Sep;14 (1):78-81 [8782823.001]
  • [Cites] J Thorac Oncol. 2009 Apr;4(4):522-6 [19347984.001]
  • [Cites] Lancet Oncol. 2010 Feb;11(2):129-35 [20036194.001]
  • [Cites] N Engl J Med. 2009 Sep 17;361(12 ):1173-8 [19726761.001]
  • [Cites] N Engl J Med. 2009 Sep 17;361(12 ):1164-72 [19726763.001]
  • [Cites] Nat Chem Biol. 2009 Mar;5(3):154-6 [19151731.001]
  • [Cites] Clin Cancer Res. 2009 Aug 15;15(16):5117-25 [19671857.001]
  • [Cites] Nature. 2003 Mar 20;422(6929):313-7 [12629553.001]
  • [Cites] Med Res Rev. 2008 May;28(3):372-412 [17694547.001]
  • [Cites] Clin Cancer Res. 2008 Oct 15;14(20):6618-24 [18927303.001]
  • [Cites] Nat Rev Cancer. 2008 Dec;8(12):915-28 [19029956.001]
  • [Cites] Mol Cell. 2005 May 27;18(5):601-7 [15916966.001]
  • [Cites] J Thorac Oncol. 2009 Feb;4(2):161-6 [19179890.001]
  • [Cites] Oncogene. 1997 May 8;14 (18):2175-88 [9174053.001]
  • [Cites] Lung Cancer. 2006 Jun;52(3):281-90 [16616798.001]
  • [Cites] J Biol Chem. 2004 Jan 9;279(2):1197-205 [14555646.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 10;100(12 ):7331-6 [12777630.001]
  • [Cites] Genet Med. 2004 Nov-Dec;6(6):530-9 [15545751.001]
  • [Cites] Nature. 2009 Apr 9;458(7239):776-9 [19169242.001]
  • [Cites] Nature. 1998 Jan 1;391(6662):90-2 [9422511.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2259-67 [17519389.001]
  • [Cites] J Clin Oncol. 2009 Sep 10;27(26):4247-53 [19667264.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4275-83 [18594010.001]
  • [Cites] Oncogene. 1997 Jan 30;14(4):439-49 [9053841.001]
  • [Cites] Clin Cancer Res. 2007 Jun 15;13(12):3605-10 [17510206.001]
  • [Cites] Cancer Cell. 2009 Aug 4;16(2):126-36 [19647223.001]
  • [Cites] Clin Cancer Res. 2009 Aug 15;15(16):5216-23 [19671850.001]
  • [Cites] Bioessays. 2004 Dec;26(12):1351-62 [15551269.001]
  • [Cites] Nat Rev Cancer. 2004 Jul;4(7):505-18 [15229476.001]
  • [Cites] Cell. 1997 Aug 22;90(4):595-606 [9288740.001]
  • [Cites] Genes Dev. 2002 Nov 1;16(21):2743-8 [12414725.001]
  • [Cites] Lung Cancer. 2007 Mar;55(3):279-86 [17134788.001]
  • [Cites] Nature. 2007 Aug 2;448(7153):561-6 [17625570.001]
  • [Cites] J Clin Invest. 2008 Jul;118(7):2609-19 [18568074.001]
  • [Cites] Clin Cancer Res. 2009 Jun 15;15(12):3947-57 [19509170.001]
  • (PMID = 20676809.001).
  • [ISSN] 1534-6277
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hedgehog Proteins; 0 / Histone Deacetylase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / anaplastic lymphoma kinase; EC 3.5.1.98 / Histone Deacetylases
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11. Le Deley MC, Rosolen A, Williams DM, Horibe K, Wrobel G, Attarbaschi A, Zsiros J, Uyttebroeck A, Marky IM, Lamant L, Woessmann W, Pillon M, Hobson R, Mauguen A, Reiter A, Brugières L: Vinblastine in children and adolescents with high-risk anaplastic large-cell lymphoma: results of the randomized ALCL99-vinblastine trial. J Clin Oncol; 2010 Sep 1;28(25):3987-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vinblastine in children and adolescents with high-risk anaplastic large-cell lymphoma: results of the randomized ALCL99-vinblastine trial.
  • PURPOSE: The impact of adding vinblastine to a 4-month chemotherapy regimen, based on the Non-Hodgkin's Lymphoma Berlin-Frankfurt-Münster 90 protocol, in childhood high-risk anaplastic large-cell lymphoma (ALCL) was assessed.
  • PATIENTS AND METHODS: Children and adolescents with high-risk ALCL, defined by mediastinal, lung, liver, spleen, or skin involvement, were eligible for the trial.
  • [MeSH-minor] Adolescent. Child. Disease-Free Survival. Humans. Lymphoma, Large-Cell, Anaplastic / drug therapy

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  • [CommentIn] J Clin Oncol. 2011 Feb 1;29(4):e90-1; author reply e92-3 [21172896.001]
  • (PMID = 20679620.001).
  • [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 Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5V9KLZ54CY / Vinblastine
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12. Ong C, Sullivan J, Hertzberg M, Stapleton K: Stage IV CD30+ anaplastic large cell lymphoma: response to acitretin and interferon-alpha. Australas J Dermatol; 2002 Aug;43(3):207-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Stage IV CD30+ anaplastic large cell lymphoma: response to acitretin and interferon-alpha.
  • Retinoids and interferon (IFN)-alpha induce differentiation, affect cell proliferation and alter various immune parameters.
  • We present a 53-year-old woman with stage IV CD30+ anaplastic large cell lymphoma with brain, lung and skin involvement.
  • After a combination of oral acitretin 50 mg daily and IFN-alpha 3 million units subcutaneously 3 times per week, the skin lesions cleared within 2 months, lung lesions by 5 months and brain lesions by 7 months.
  • Although we cannot exclude that methotrexate played a role in the development of this lymphoma and that its withdrawal contributed to the clearance of lesions, we propose that the patient's disease responded to the combination of acitretin and IFN-alpha.
  • [MeSH-major] Acitretin / administration & dosage. Interferon-alpha / administration & dosage. Lymphoma, Large-Cell, Anaplastic / drug therapy. Lymphoma, Large-Cell, Anaplastic / pathology. Skin Ulcer / drug therapy. Skin Ulcer / pathology
  • [MeSH-minor] Administration, Oral. Antigens, CD30 / analysis. Antineoplastic Agents / administration & dosage. Arm. Biopsy, Needle. Drug Therapy, Combination. Female. Follow-Up Studies. Humans. Immunohistochemistry. Infusions, Intravenous. Keratolytic Agents / administration & dosage. Magnetic Resonance Imaging. Middle Aged. Neoplasm Staging. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 12121400.001).
  • [ISSN] 0004-8380
  • [Journal-full-title] The Australasian journal of dermatology
  • [ISO-abbreviation] Australas. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Antineoplastic Agents; 0 / Interferon-alpha; 0 / Keratolytic Agents; LCH760E9T7 / Acitretin
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13. Ambrosini V, Quarta C, Zinzani PL, Nanni C, Fini M, Torricelli P, Giavaresi G, D'Errico-Grigioni A, Malvi D, Franchi R, Fanti S: 18[F]FDG small animal PET study of sorafenib efficacy in lymphoma preclinical models. Q J Nucl Med Mol Imaging; 2010 Dec;54(6):689-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 18[F]FDG small animal PET study of sorafenib efficacy in lymphoma preclinical models.
  • AIM: Kinase inhibitors have been proposed as novel therapeutic agents in different forms of solid tumours.
  • The Food and Drug Administration (FDA) approved the use of Sorafenib, an oral multikinase inhibitor, for advanced renal carcinoma and unresectable hepatocellular carcinoma.
  • On-going studies are investigating the efficacy of Sorafenib in other solid tumours such as melanoma and non-small cells lung carcinoma and pre-clinical models showed the efficacy of treatment with Sorafenib in murine models of renal cells carcinoma, breast cancer, colon carcinoma and melanoma.
  • To our knowledge, Sorafenib has never been employed in human lymphoma.
  • The aim of the present study was to assess the efficacy of Sorafenib in murine models of human anaplastic large cells lymphoma (ALCL) and Hodgkin lymphoma (HD).
  • Tumour bearing animals were randomly selected to receive treatment with Sorafenib or no treatment.
  • Caspase-3 production showed a dose-dependent trend reaching significantly higher values for 0.046 mg/L and 0.465 mg/L drug concentrations in both cell lines.
  • CONCLUSION: Sorafenib showed a good cytotoxic effect in vitro especially on human HD cell line, but these findings were not confirmed in vivo.
  • Factors influencing drug availability at tumour site or differences in the downstream pathways may be responsible for the scarse effect of treatment.
  • [MeSH-major] Benzenesulfonates / therapeutic use. Fluorodeoxyglucose F18. Lymphoma / drug therapy. Lymphoma / radionuclide imaging. Positron-Emission Tomography / veterinary. Pyridines / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Drug Evaluation, Preclinical / methods. Drug Evaluation, Preclinical / veterinary. Humans. Mice. Niacinamide / analogs & derivatives. Phenylurea Compounds. Prognosis. Radiopharmaceuticals. Treatment Outcome

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  • (PMID = 20639808.001).
  • [ISSN] 1824-4785
  • [Journal-full-title] The quarterly journal of nuclear medicine and molecular imaging : official publication of the Italian Association of Nuclear Medicine (AIMN) [and] the International Association of Radiopharmacology (IAR), [and] Section of the Society of Radiopharmaceutical Chemistry and Biology
  • [ISO-abbreviation] Q J Nucl Med Mol Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Pyridines; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib
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14. Senderowicz AM: Novel direct and indirect cyclin-dependent kinase modulators for the prevention and treatment of human neoplasms. Cancer Chemother Pharmacol; 2003 Jul;52 Suppl 1:S61-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Abnormalities in the cell cycle are responsible for the majority of human neoplasias.
  • Most abnormalities occur due to hyperphosphorylation of the tumor suppressor gene Rb by the key regulators of the cell cycle, the cyclin-dependent kinases (CDKs).
  • Thus, a pharmacological CDK inhibitor may be useful in the prevention and/or treatment of human neoplasms.
  • Antitumor activity was observed in some patients with non-Hodgkin's lymphoma and renal, colon, and prostate cancers.
  • Concentrations between 300 and 500 n M-necessary to inhibit CDK-were achieved safely.
  • Phase II/III trials using this 1-h schedule in several tumor types including non-small-cell lung cancer, chronic lymphocytic leukemia, mantle cell lymphoma, and head and neck cancer are being conducted worldwide.
  • (2) it promotes cell-cycle arrest by accumulation in p21/p27;.
  • The last of these represents a novel strategy to combine UCN-01 with DNA-damaging agents.
  • Another patient with refractory anaplastic large-cell lymphoma had no evidence of disease at >4 years.
  • A question that remains unanswered is "Which is the best schedule for combination with standard antitumor agents?
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclin-Dependent Kinases / antagonists & inhibitors. Enzyme Inhibitors / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Alkaloids / administration & dosage. Animals. Cell Cycle / drug effects. Clinical Trials as Topic. Flavonoids / administration & dosage. Humans. Piperidines / administration & dosage. Staurosporine / analogs & derivatives. Tumor Cells, Cultured


15. Kruczynski A, Mayer P, Marchand A, Vispé S, Fournier E, Annereau JP, Brel V, Barret JM, Delsol G, Imbert T, Fahy J, Bailly C: Antitumor activity of pyridoisoquinoline derivatives F91873 and F91874, novel multikinase inhibitors with activity against the anaplastic lymphoma kinase. Anticancer Drugs; 2009 Jun;20(5):364-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor activity of pyridoisoquinoline derivatives F91873 and F91874, novel multikinase inhibitors with activity against the anaplastic lymphoma kinase.
  • The anaplastic lymphoma kinase (ALK) is a validated target for the therapy of different malignancies.
  • Aberrant expression of constitutively active ALK chimeric proteins has been implicated in the pathogenesis of anaplastic large-cell lymphoma (ALCL) and has been detected in other cancers such as inflammatory myofibroblastic tumors, diffuse large B-cell lymphomas, certain non-small-cell lung cancers, rhabdomyosarcomas, neuroblastomas and glioblastomas.
  • F91873 and F91874 also inhibited nucleophosmin-ALK and signal transducer and activator of transcription 3 phosphorylation in the ALCL cell line COST with the same potency.
  • Both F91873 and F91874 behaved as ATP noncompetitive inhibitors and inhibited cell proliferation of the ALK(+) ALCL cell lines COST, PIO, and Karpas299 ALCL.
  • This growth inhibition effect was associated with a G1-phase cell cycle arrest.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Lymphoma, Large-Cell, Anaplastic / drug therapy. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Quinolizines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Animals. Carcinoma, Non-Small-Cell Lung / enzymology. Carcinoma, Non-Small-Cell Lung / pathology. Cell Line, Tumor / drug effects. Cell Line, Tumor / enzymology. Female. G1 Phase / drug effects. Lung Neoplasms / enzymology. Lung Neoplasms / pathology. Mice. Mice, Inbred ICR. Mice, SCID. Ovarian Neoplasms / enzymology. Ovarian Neoplasms / pathology. Protein Structure, Tertiary. Receptor Protein-Tyrosine Kinases. Recombinant Fusion Proteins / antagonists & inhibitors. Xenograft Model Antitumor Assays

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  • (PMID = 19322071.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / F 91873; 0 / F 91874; 0 / Protein Kinase Inhibitors; 0 / Quinolizines; 0 / Recombinant Fusion Proteins; 0 / Thiazoles; EC 2.7.1.- / p80(NPM-ALK) protein; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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16. Settleman J: Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK). Semin Oncol; 2009 Apr;36(2 Suppl 1):S36-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK).
  • The clinical success of drugs such as imatinib, erlotinib, and lapatinib, together with findings demonstrating the important relationship between specific tumor genotypes and clinical response to these agents, also has brought to the forefront the concept of "personalized cancer medicine."
  • The potential broader significance of this relationship has been further highlighted in preclinical studies using tumor-derived cell lines as a model system that can faithfully recapitulate the association of specific genotypes with drug sensitivity, suggesting the utility of cancer cell lines to identify novel candidate biomarkers for predicting clinically responsive patient subsets for newly developed anticancer agents.
  • The case of the anaplastic lymphoma kinase (ALK) nicely exemplifies this, and cell line profiling has revealed that ALK mutations present in a subset of anaplastic large cell lymphomas (ALCLs), non-small cell lung cancers (NSCLCs), and neuroblastomas appear to sensitize cancer cells to treatment with selective ALK kinase inhibitors.
  • [MeSH-major] Neoplasms / drug therapy. Oncogene Proteins, Fusion / drug effects. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Cells, Cultured. Drug Design. Humans. Receptor Protein-Tyrosine Kinases

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  • (PMID = 19393834.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / anaplastic lymphoma kinase
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17. Cheng M, Ott GR: Anaplastic lymphoma kinase as a therapeutic target in anaplastic large cell lymphoma, non-small cell lung cancer and neuroblastoma. Anticancer Agents Med Chem; 2010 Mar;10(3):236-49
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  • [Title] Anaplastic lymphoma kinase as a therapeutic target in anaplastic large cell lymphoma, non-small cell lung cancer and neuroblastoma.
  • Anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase in the insulin receptor superfamily, was originally identified as the oncogenic NPM (nucleophosmin)-ALK fusion protein due to a t (2;5) chromosomal translocation in anaplastic large cell lymphomas.
  • The recent reports of EML4 (echinoderm microtubule-associated protein-like 4)-ALK oncogenic proteins in non-small cell lung cancer (NSCLC) and the identification of ALK activating point mutations and gene amplification in neuroblastoma have indicated ALK as a potential major therapeutic target for human cancers.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Lymphoma, Large-Cell, Anaplastic / drug therapy. Neuroblastoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Antineoplastic Agents / chemistry. Antineoplastic Agents / therapeutic use. Drug Evaluation, Preclinical. Drug Screening Assays, Antitumor. Enzyme Inhibitors / chemistry. Enzyme Inhibitors / therapeutic use. Humans. Oncogene Proteins, Fusion / metabolism. Receptor Protein-Tyrosine Kinases


18. McDermott U, Iafrate AJ, Gray NS, Shioda T, Classon M, Maheswaran S, Zhou W, Choi HG, Smith SL, Dowell L, Ulkus LE, Kuhlmann G, Greninger P, Christensen JG, Haber DA, Settleman J: Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors. Cancer Res; 2008 May 1;68(9):3389-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors.
  • Whereas these agents can elicit dramatic clinical responses in some settings, their activity is generally limited to a subset of treated patients whose tumor cells harbor a specific genetic lesion.
  • We have established an automated platform for examining the sensitivity to various molecularly targeted inhibitors across a large panel of human tumor-derived cell lines to identify additional genotype-correlated responses that may be clinically relevant.
  • Among the inhibitors tested in a panel of 602 cell lines derived from a variety of human cancers, we found that a selective inhibitor of the anaplastic lymphoma kinase (ALK) potently suppressed growth of a small subset of tumor cells.
  • This subset included lines derived from anaplastic large cell lymphomas, non-small-cell lung cancers, and neuroblastomas.
  • ALK is a receptor tyrosine kinase that was first identified as part of a protein fusion derived from a chromosomal translocation detected in the majority of anaplastic large cell lymphoma patients, and has recently been implicated as an oncogene in a small fraction of non-small-cell lung cancers and neuroblastomas.
  • Significantly, sensitivity in these cell lines was well correlated with specific ALK genomic rearrangements, including chromosomal translocations and gene amplification.
  • Moreover, in such cell lines, ALK kinase inhibition can lead to potent suppression of downstream survival signaling and an apoptotic response.
  • These findings suggest that a subset of lung cancers, lymphomas, and neuroblastomas that harbor genomic ALK alterations may be clinically responsive to pharmacologic ALK inhibition.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Lymphoma / drug therapy. Neuroblastoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Pyrimidines / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Benzimidazoles / therapeutic use. Cell Line, Tumor. Cytogenetic Analysis. Drug Evaluation, Preclinical. Gene Amplification / physiology. Genomic Instability / drug effects. Humans. Mutation. Protein Kinase Inhibitors / therapeutic use. Pyridones / therapeutic use. Receptor Protein-Tyrosine Kinases. Translocation, Genetic


19. Palumbo G, Grana CM, Cocca F, De Santis R, Del Principe D, Baio SM, Mei R, Paganelli G: Pretargeted antibody-guided radioimmunotherapy in a child affected by resistant anaplastic large cell lymphoma. Eur J Haematol; 2007 Sep;79(3):258-62
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  • [Title] Pretargeted antibody-guided radioimmunotherapy in a child affected by resistant anaplastic large cell lymphoma.
  • Anaplastic large cell lymphoma (ALCL) is characterized by preferential paracortical and intrasinusoidal lymph node involvement by large anaplastic tumor cells expressing the CD30 antigen.
  • Up to 80% of pediatric patients with ALCL can be cured with multi-agent chemotherapeutic regimens.
  • In these cases, the highly aggressive clinical course of ALCL, associated with systemic symptoms and extranodal involvement, has been treated with different approaches in various cooperative trials, including conventional chemotherapy and human stem cell transplantation (HSCT).
  • More recently, radioimmunotherapy has been studied with encouraging results in cancer patients, including non-Hodgkin's lymphoma.
  • [MeSH-major] Antibodies, Neoplasm / therapeutic use. Lymphoma, Large-Cell, Anaplastic / radionuclide imaging. Radioimmunotherapy / methods
  • [MeSH-minor] Child. Female. Hematopoietic Stem Cell Transplantation. Humans. Lung Neoplasms / secondary. Salvage Therapy / methods


20. Sabbatini P, Korenchuk S, Rowand JL, Groy A, Liu Q, Leperi D, Atkins C, Dumble M, Yang J, Anderson K, Kruger RG, Gontarek RR, Maksimchuk KR, Suravajjala S, Lapierre RR, Shotwell JB, Wilson JW, Chamberlain SD, Rabindran SK, Kumar R: GSK1838705A inhibits the insulin-like growth factor-1 receptor and anaplastic lymphoma kinase and shows antitumor activity in experimental models of human cancers. Mol Cancer Ther; 2009 Oct;8(10):2811-20
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  • [Title] GSK1838705A inhibits the insulin-like growth factor-1 receptor and anaplastic lymphoma kinase and shows antitumor activity in experimental models of human cancers.
  • GSK1838705A blocks the in vitro proliferation of cell lines derived from solid and hematologic malignancies, including multiple myeloma and Ewing's sarcoma, and retards the growth of human tumor xenografts in vivo.
  • GSK1838705A also inhibits the anaplastic lymphoma kinase (ALK), which drives the aberrant growth of anaplastic large-cell lymphomas, some neuroblastomas, and a subset of non-small cell lung cancers.
  • GSK1838705A is therefore a promising antitumor agent for therapeutic use in human cancers.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Protein Kinase Inhibitors / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / pharmacology. Pyrroles / pharmacology. Receptor, IGF Type 1 / antagonists & inhibitors. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Cell Proliferation / drug effects. Enzyme Activation / drug effects. Humans. Mice. Phosphorylation / drug effects. Receptor Protein-Tyrosine Kinases. Receptor, Insulin / metabolism. Signal Transduction / drug effects


21. Zhou X, Sun C, Wang J, Mao J, Guo H: Rapid fatal pulmonary complications in a Chinese patient after bortezomib treatment for ALK-negative anaplastic large-cell lymphoma. Clin Lymphoma Myeloma Leuk; 2010 Apr;10(2):152-4
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  • [Title] Rapid fatal pulmonary complications in a Chinese patient after bortezomib treatment for ALK-negative anaplastic large-cell lymphoma.
  • Herein, we present a case of rapid fatal pulmonary complications in a patient with ALK-negative anaplastic large-cell lymphoma after receiving a treatment with bortezomib.
  • [MeSH-major] Boronic Acids. Pyrazines
  • [MeSH-minor] Aged. Asian Continental Ancestry Group. Bortezomib. Enzyme Inhibitors / therapeutic use. Fatal Outcome. Hematologic Neoplasms / chemically induced. Hematologic Neoplasms / enzymology. Humans. Lung / enzymology. Lung / metabolism. Lymphoma, Large B-Cell, Diffuse / chemically induced. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large-Cell, Anaplastic / chemically induced. Lymphoma, Large-Cell, Anaplastic / enzymology. Male

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  • (PMID = 20371451.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
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