Besides VEGF (vascular endothelial growth factor), human lung cancers are known to express PDGFR (platelet-derived growth factor receptors). NSCLC, like most cancers, involves defects in signal transduction pathways. Receptor tyrosine kinases (RTKs) play a pivotal role in these signaling pathways, transmitting extracellular molecular signals into the cytoplasm and/or nucleus of a cell. Among such RTKs are the receptors for polypeptide growth factors such as epidermal growth factor (EGF), insulin, platelet-derived growth factor (PDGF), neurotrophins (i.e., NGF), and fibroblast growth factor (FGF). Phosphorylation of such RTKs activates their cytoplasmic domain kinase function, which in turns activates downstream signaling molecules. Thus, RTKs are key mediators of cellular signaling as well as oncogenesis resulting from over-expression and activation of such RTKs and their substrates. Due to their pivotal role in normal and aberrant signaling, RTKs are the subject of increasing focus as potential drug targets for the treatment of certain types of cancer. For example, Herceptin.RTM., an inhibitor of HER2/neu, is currently an approved therapy for a certain subset of breast cancer. Iressa.TM. (ZD1839) and Tarceva.TM. (OSI-774), both small-molecule inhibitors of EGFR, have been approved for the treatment of NSCLC.