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One example of the cross over from research of other initial cancer sites (because the same proteins and pathways are involved in many types of cancer), has been that KRAS gene variations or mutations are linked to ovarian cancer. Because many cancer cells use similar pathways, the same drug could be used to treat one person's lung cancer and another person's ovarian cancer, as long as each tumor contained similar targets.
The HER2 gene (typically known as the Herceptin gene) is also known as epidermal growth factor receptor (EGFR) type 2. The EGFR gene is found in a number of lung cancers. Herceptin may show clinical response with the presence of a mutation in the HER2 kinase domain in patients with lung cancer. You remember Tykerb? It is an inhibitor of the tyrosine kinase domains of HER1 and HER2. It has antitumor activity not only against HER1 (EGFR) but also HER2 (EGFR type 2).
Researchers have found that Herceptin (HER2-drug) can sensitize ovarian cancer cells to EGFR-targeted therapeutics. However, ovarian cancer cells that are not growth inhibited by Herceptin are still responsive to it. They found that responsiveness to alternative HER-targeted inhibitors, such as Iressa and Erbitux, is dramatically potentiated by long-term Herceptin treatment of ovarian cancer cells.
There are a lot of possibilities, but so far, I have only seen functional profiling conducted on human tumor samples, utilizing native microspheroids replete with vascular, stromal and inflammatory cells, that can analyze cellular responses in the context of the tumor microenvironment. This snapshot of cellular response recapitulates patient response to cytotoxic compounds, signal transduction inhibitors and growth factor antagonists in real time.
But you don't want me to get into that. It's as thick as pea soup!
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