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JCI table of contents: Dec. 3, 2007
Date:12/3/2007

b.edu">mathar@uab.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=32481

ACCOMPANYING COMMENTARY
TITLE: Targeting mutant p53 shows promise for sunscreens and skin cancer

AUTHOR CONTACT:
Wafik S. El-Deiry
University of Pennsylvania School of Medicine,
Philadelphia, Pennsylvania, USA.
Phone: (215) 898-9015; Fax: (215) 573-9139; E-mail: wafik@mail.med.upenn.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=34251

EDITOR'S PICK: Modifying an anticancer drug makes it more specific

Imatinib (marketed as Gleevec in the US and Glivec in Europe and Australia) is used to treat various cancers, including chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GISTs). It can be used to treat these two distinct types of cancer because they are caused by related proteins tyrosine kinases. However, this lack of specificity for a single protein means that imatinib can also inhibit tyrosine kinases that mediate normal bodily functions and it has been reported that in some patients this causes a toxic effect on the heart. To address some of these problems, Ariel Fernndez and colleagues at Rice University, Houston, have engineered a modified form of imatinib (known as WBZ_4) that inhibited the tyrosine kinase behind GISTs (c-KIT) as effectively as imatinib did, and that neither inhibited the tyrosine kinase behind CML (BCR-Abl) nor had toxic effects on the heart when it was administered to mice. Importantly, WBZ_4 was as effective as imatinib at reducing tumor volume and weight in a mouse model of GISTs. As noted by George Demetri from the Dana-Farber Cancer Institute, Boston, in the accompanying commentary, this study gives hope that in the future it mig
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215-573-1850
Journal of Clinical Investigation
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