Lung cancer, which is the leading cause of cancer-related death worldwide, is estimated to claim 1.4 million lives globally and 150,000 lives in the U.S. every year. This killer disease is very difficult to detect in its early stages and a majority of people have no symptoms until their lung cancer reaches an advanced stage.
The most common form of lung cancer is non-small cell lung cancer, or NSCLC, accounting for about 80% of all lung cancers, and the remaining 20% is made up by small cell lung cancer.
Targeted chemotherapy medicines like Tarceva that blocks a specific molecule -epidermal growth factor receptor, or EGFR, has been prescribed as a treatment for advanced NSCLC. However, eventually all patients develop resistance, rendering them unresponsive to Tarceva. Only half of the resistant cases are known to stem from secondary mutations within EGFR or amplification of c-Met, a receptor tyrosine kinase.
Scientists have been trying to understand for years the unknown mechanisms underlying resistance to Tarceva, a blockbuster cancer drug, co-marketed by Roche subsidiary Genentech and Astellas Pharma Inc.
A team of researchers at the University of California, San Francisco's Helen Diller Family Comprehensive Cancer Center has discovered a novel mechanism in which tumor cells develop resistance to Tarceva.
By using an inhibitor of a human protein called AXL in the experiments, Trever Bivona, assistant professor of hematology and oncology, University of California, San Francisco, and his colleagues have discovered that resistance to Tarceva involves over-expression of AXL, and that blocking this protein may prevent resistance to the cancer drug. AXL is also a receptor tyrosine kinase which has oncogenic potential.
Researchers expect that the new findings may lead to better treatments involving novel options "that would combine Tarceva with new drugs designed to block AXL".
The study findings were published online July 1 in Nature Genetics.
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by RTT Staff Writer
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