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BCR-ABL酪氨酸激酶抑制剂STI571的研究进展 被引量:1

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出处 《江苏医药》 CAS CSCD 北大核心 2002年第10期765-767,共3页 Jiangsu Medical Journal
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同被引文献31

  • 1Julia M Brain,Anuraag Saksena,Pierre Laneuville.The kinase inhibitor STI571 reverses the Bcr-Abl induced point mutation frequencies observed in pre-leukemic P190 Bcr-Abl transgenic mice[J].Leukemia Research,2002,26:1 011-1 016.
  • 2Isabelle Gaston,Paula E Stenberg,Arun Bhat,et al.Abl kinase but not PI3-kinase links to the cytoskeletal defects in Bcr-Abl transformed cells[J].Experimental Hematology,2000,28:77-86.
  • 3Michael E O'Dwayer,Brian J Druker.STI571:an inhibitor of the BCR-ABL tyrosine kinase for the treatment of chronic myelogenous leukaemia[J].Lancet Oncol,2000,(1):207-211.
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  • 5Druker B J,Talpaz M,Rasta D J,et al.Efficacy and safety of a specific inhibitor of the Bcr-Abl tyrosine kinase in chronic myeloid leukemia[J].The New England Journal of Medicine,2001,344:1 031-1 037.
  • 6Talpaz M,Silver R T,Durker B J,et al.Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia:results of a phase 2 study[J].Blood 2002,99:1 928-1 937.
  • 7Dorothea Gadzicki,Nils von Neuhoff,Doris Steinemann,et al.Bcr-Abl gene amplification and overexpression in a patient with chronic myeloid leukemia treated with imatinib[J].Cancer Genetics and Cytogenetics,2005,159:164-167.
  • 8Daniella Yeheskely-Hayon,Ronit Regev,Gera D Eytan,et al.The tyrosine kinase inhibitors imatinib and AG957 reverse multidrug resistance in a chronic myelogenous leukemia cell line[J].Leukemia Research,2005,29:793-802.
  • 9Darren R Veach,Mohammad Namavari,Tatiana Beresten,et al.Synthesis and in vitro examination of[124I]-,[125I]-and[131]-2-(4-iodophenylamino) pyrido[2,3-d] pyrimidin-7-one radiolabeled Abl kinase inhibitors[J].Article.Nuclear Medicine and Biology,2005,32:313-318.
  • 10Amie S Corbin,Elisabeth Buchdunger,Furet Pascal.Analysis of the Structural Basis of specificity of Inhibition of the Abl Kinase by STI571[J].The Journal of Biological Chemistry,2002,277(35):32 214-32 219.

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