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JNCI Journal of the National Cancer Institute 2004 96(15):1117-1119; doi:10.1093/jnci/djh244
© 2004 by Oxford University Press
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© 2004 Oxford University Press

EDITORIAL

Predicting Sensitivity of Non–Small-Cell Lung Cancer to Gefitinib: Is There a Role for P-Akt?

William Pao, Vincent A. Miller, Ennapadam Venkatraman, Mark G. Kris

Affiliations of authors: Program in Cancer Biology and Genetics (WP); Thoracic Oncology Service, Division of Solid Tumor Oncology, Department of Medicine (WP, VAM, MGK), and Department of Epidemiology and Biostatistics (EV), Memorial Sloan-Kettering Cancer Center, New York, NY; Weill Medical College of Cornell University, New York, NY

Correspondence to: Mark G. Kris, MD, Memorial Sloan-Kettering Cancer Center, 1275 York Ave., New York, NY 10021 (e-mail: krism@mskcc.org)

The first 10% of the full text of this article appears below.

The epidermal growth factor receptor (EGFR) is a tyrosine kinase receptor of the ErbB family that is abnormally activated in epithelial tumors (1). Receptor activation leads to recruitment and phosphorylation of downstream intracellular substrates. Multiple pathways are activated, including the phosphatidylinositol 3–kinase/Akt (PI3K/Akt) cascade implicated in cell survival and the RAS/RAF/mitogen-activated protein kinase (MAPK) cascade associated with cell proliferation (2,3). Aberrant signaling through EGFR can lead to tumor-promoting cellular activities.

EGFR is the target for cancer therapies such as gefitinib (4-quinazolinamine, N-[3-chloro-4-fluorophenylamino]-7-methoxy- 6-[3-(4-morpholinyl) propoxy]) (4,5), which inhibits the tyrosine kinase activity of EGFR by reversibly competing with adenosine triphosphate (ATP) at . . . [Full Text of this Article]


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