AI Article Synopsis
- Recent research shows that mutations in the epidermal growth factor receptor (EGF-R) can help predict how patients will respond to gefitinib, a targeted cancer therapy.
- This discovery allows for comparisons between different drug targets, highlighting the importance of molecular diagnostics to identify cancers that depend on specific oncogenes for survival.
- For common cancers with multiple genetic alterations, a dual approach is suggested: targeting essential life processes with non-specific drugs while also combining them with selective therapies for better effectiveness and specificity.
Article Abstract
Activating mutations in the epidermal growth factor receptor (EGF-R) predict response to gefitinib. How does this recent discovery affect our outlook on selective (targeted) cancer therapy? It allows us to compare mutant EGF-R with Bcr-Abl as anticancer drug targets and to discuss the nature of oncogene addiction. It emphasizes molecular diagnostics to identify oncogene-addictive cancers. It also re-enforces the notion that most cancers with multiple oncogenic alterations (common cancers) will unlikely respond to selective drugs alone. In such cancers, one strategy is targeting cancer-non-specific, universal and vital structures, essential for life of all cells: microtubules, topoisomerases, histone deacetylases, the proteasome. But in order to be cancer-selective, these chemotherapeutic agents need to be combined with selective agents. Such combinations can be effective and selective in common cancers.
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| http://dx.doi.org/10.4161/cbt.3.5.984 | DOI Listing |
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