NDLI: Ph+ acute lymphoblastic leukemia resistant to the tyrosine kinase inhibitor STI571 has a unique BCR-ABL gene mutation

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Ph+ acute lymphoblastic leukemia resistant to the tyrosine kinase inhibitor STI571 has a unique BCR-ABL gene mutation

Content Provider	Scilit
Author	Hofmann, Wolf-K. Jones, Letetia C. Lemp, Nathan A. Vos, Sven De Gschaidmeier, Harald Hoelzer, Dieter Ottmann, Oliver G. Koeffler, H. Phillip
Copyright Year	2002
Description	The tyrosine kinase inhibitor STI571 is a promising agent for the treatment of advanced Philadelphia chromosome positive (Ph+) acute lymphoblastic leukemia (ALL), but resistance develops rapidly in most patients after an initial response. To identify mechanisms of resistance to STI571, 30 complementary DNAs (including 9 matched samples) obtained from the bone marrow of individuals with Ph+ ALL were analyzed by direct sequencing of a 714–base pair region of ABL encoding for the adenosine triphosphate (ATP)–binding site and the kinase activation loop. A single point mutation was found at nucleotide 1127 (GI6382056) resulting in Glu255Lys. This mutation occurred in 6 of 9 patients (67%) following their treatment with STI571 but not in the samples from patients before beginning treatment with STI571. Glu255Lys is within the motif important for forming the pocket of the ATP-binding site in ABL and it is highly conserved across species. In conclusion, Ph+ ALL samples resistant to STI571 have a unique mutation Glu255Lys of BCR-ABL.
Related Links	http://www.bloodjournal.org/content/bloodjournal/99/5/1860.full.pdf
Ending Page	1862
Page Count	3
Starting Page	1860
DOI	10.1182/blood.v99.5.1860
Journal	Blood
Issue Number	5
Volume Number	99
Language	English
Publisher	American Society of Hematology
Publisher Date	2002-03-01
Access Restriction	Open
Subject Keyword	Hematology Research and Experimental Medicine Treatment Bone Marrow Tyrosine Leukemia Inhibitor Kinase Lymphoblastic Sti571 Glu255lys Journal: Blood (Vol- 83, Issue- 5)
Content Type	Text
Resource Type	Article

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