National Cancer Institute Stops Gene-based Clinical Trials – Part 2

Last week we discussed the National Cancer Institute’s suspension of three ongoing clinical trails using genomic platforms to select therapies for cancer patients. This week, we seek to answer the question: What went wrong?

The simple answer is that cancer isn’t simple.

Cancer dynamics are not linear. Cancer biology does not conform to the dictates of molecular biologists. Once again, we are forced to confront the realization that genotype does not equal phenotype.

In a nutshell, cancer cells utilize cross talk and redundancy to circumvent therapies. They back up, zig-zag and move in reverse, regardless of what the sign posts say. Using genomic signatures to predict response is like saying that Dr. Seuss and Shakespeare are truly the same because they use the same words. The building blocks of human biology are carefully construed into the complexities that we recognize as human beings. However appealing gene profiling may appear to those engaged in this field (such as Response Genetics, Caris, the group from Duke and many others) it will be years, perhaps decades, before these profiles can approximate the vagaries of human cancer.

Functional analyses like the EVA-PCD platform, which measure biological signals rather than DNA indicators, will continue to provide clinically validated information and play an important role in cancer drug selection. The data that support functional analyses is demonstrably greater and more compelling than any data currently generated from DNA analyses.