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View the Table of Contents for the January 1 issue of Cancer Research.
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Paxillin is an important actin-binding protein that localizes to focal adhesions and interacts with the Src, BCR/ABL, and papilloma virus E6 oncoproteins. Jagadeeswaran and colleagues have now identified somatic mutations of paxillin in lung cancer. The most frequent mutation identified in paxillin, A127T, was found to enhance stress fiber formation and Bcl-2 association along with cell growth, survival, and invasion. Paxillin alterations were also found to affect angiogenesis in lung cancer xenografts. These findings suggest an important role for paxillin in the pathophysiology of lung cancer, also offering a possible therapeutic target for this disease.
Garlich et al. Page 206 The phosphoinositide 3-kinase (PI3K) signaling pathway is among the most frequently activated pathways in human cancer. Validation of PI3K as a therapeutic target remains incomplete in part because of the lack of a clinically viable small molecule inhibitor. Garlich and colleagues have described the engineering of a widely known pan PI3K inhibitor, LY294002, into a water-soluble, vascular-targeted, and clinically applicable prodrug termed SF1126. The results suggest that SF1126 may be applicable for phase I clinical trials. SF1126 may support a new paradigm for cancer treatment based upon the use of pan PI3K inhibitory prodrugs.
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