Does tumor mutational status correlate with clinical response to imatinib?
Michael C Heinrich* and Christopher L Corless
Correspondence *Department of Medicine, Oregon Health & Science University, R&D-19, 3710 SW US Veterans, Hospital Road, Portland, OR 97239, USA
Email heinrich@ohsu.edu
This article has no abstract so we have provided the first paragraph of the full text.
GISTs are intra-abdominal sarcomas that respond poorly to conventional chemotherapy. Most GISTs strongly express KIT (CD117), which serves as a convenient diagnostic marker but is also a treatment target. Recent clinical studies with the small molecule KIT inhibitor imatinib have provided important insights into GIST biology. Tumor response is not predicted by KIT expression per se, but rather by the presence and type of oncogenic KIT mutation.
Full text of this article is available with one of the following:
- Personal subscription Purchase your own personal subscription to this journal. Already a subscriber? Please log in for immediate access.
- 7 day single article pass for US$18 In order to purchase this article you must be a registered user. Please register or log in.
- Site licence Learn more about institutional site licences
Current Subscribers
Please log in to access the full text article using the login box at the top of the page.
MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated.

