RTK ligands secreted through paracrine, autocrine, and endocrine mechanisms in the tumor microenvironment are important determinants of therapeutic responses to anticancer kinase inhibitors. This limited primary response could be attributable to resistance inherent in the tumor cells rather than resistance acquired over the course of treatment. Citation 1 Although the remainder also responded, the response was only partial even though they too had TKI-sensitive EGFR mutations-either exon 19 deletions or the L858R missense mutation in exon 21. Despite the fact that treatment of these mutated NSCLCs with EGFR tyrosine kinase inhibitors (TKIs) has shown remarkable progress, a recent randomized Phase 3 clinical trial with erlotinib found tumor reduction greater than 90% in only 5% of patients. Approximately 14% of NSCLCs harbor mutations in the gene encoding epidermal growth factor receptor (EGFR), a receptor tyrosine kinase (RTK). Of the 2 major histologic types, small cell lung cancer and non-small cell lung cancer (NSCLC), the latter is by far the more prevalent (~85%). Lung cancer is the leading cause of cancer death in the US and other countries.
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