While it may be nice to think that driver mutations are predictive of a response, sometimes the genetic signal may not be the driver mutation. Other signaling pathways, like passenger mutations, could be operative.
It turns out that most mutations in cancers are passengers. It had been thought by molecular scientists that driver mutations are the ones that cause cancer cells to grow, whereas passengers are co-travellers that make no contribution to cancer development.
However, buried among them are much larger numbers of driver mutations than was previously anticipated. This suggests that many more genes contribute to cancer development than was thought.
Cells speak to each other and the messages they send are interpreted via intracellular pathways. You wouldn't know this using analyte-based genomic and proteomic methodologies. However, functional (cytometric) profiling provides the window. It can test various cell-death signaling pathways downstream.
While most scientists use genomic or proteomic platforms to detect mutations in these pathways that might result in response to chemicals, functional (cytometric) profiling platforms have taken a different tack. By applying functional analysis, to measure the end result of pathway activation or deactivation, they can predict whether patients will actually respond.
The functional (cytometric) profiling platform has the capacity to measure genetic and epigenetic events as a functional, real-time adjunct to static genomic and proteomic platforms.
As virtually every presentation at the 2012 AACR meeting made obligatory reference to genomic analysis, almost every one of them then doubled back to metabolism as the principal driver of human cancer.
http://cancerfocus.org/forum/showthread.php?t=3675
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