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JNCI Journal of the National Cancer Institute 2003 95(4):252-253; doi:10.1093/jnci/95.4.252
© 2003 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 95, No. 4, 252-253, February 19, 2003
© 2003 Oxford University Press

EDITORIAL

AKT and the Phosphatidylinositol 3-Kinase/AKT Pathway: Important Molecular Targets for Lung Cancer Prevention and Treatment

James A. Crowell, Vernon E. Steele

Affiliation of authors: J. A. Crowell, V. E. Steele, Chemopreventive Agent Development Research Group, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD.

Correspondence to: James A. Crowell, Ph.D., Chemopreventive Agent Development Research Group, Division of Cancer Prevention, National Cancer Institute, EPN, Rm. 2117, MSC 7322, Bethesda, MD 20892 (e-mail: jc94h@nih.gov).

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The study by Chun et al. (1) in this issue of the Journal provides important evidence for both the involvement of the phosphatidylinositol 3-kinase (PI3K) signaling pathway in the early stages of lung carcinogenesis and the pharmacologic mechanism of deguelin in decreasing cancer-related increased AKT activity in the PI3K pathway. What makes these findings of great interest is the fact that there have been so few agents, natural or synthetic, tested to date that have shown potential to halt the progression of any form of lung cancer and that the authors have identified potential molecular targets for intervention in premalignant and malignant bronchial epithelial cells. As the . . . [Full Text of this Article]


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