Discovery leads to rapid mouse 'personalized trials' in breast cancer
One person's breast cancer is not the same as another person's, because the gene mutations differ in each tumor.
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Since: Dec 05
#1 Sep 5, 2009
The decoding of the human genome in 2000, sparked a new era of tailored cancer medicine.
However, uncovering the genetic differences that determine how a person responds to a drug, and developing tests, or biomarkers, for those differences, is proving more challenging than ever.
As a result, patients with cancer are still being prescribed medicines on a trial-and-error basis or one-size-fits-all.
In an issue of Nature, scientists reported that surveying the human genome has found that many more gene mutations drive the development of cancer than previously thought.
Genomics are far too limited in scope to encompass the vagaries and complexities of human cancer biology.
The human genome project will give way to the human epigenome project which will give way to the human proteome and human kinome project. The next generation of tests will be biosystematic.
What is needed is to measure the net effect of all processes within the cancer, acting with and against each other in real time, and test living cells actually exposed to drugs and drug combinations of interest.
The key to understanding the genome is understanding how cells work. How is the cell being killed regardless of the mechanism?
The core understanding is the cell, composed of hundreds of complex molecules that regulate the pathways necessary for vital cellular functions. If a targeted drug could perturb any of these pathways, it is important to examine the effects of drug combinations within the context of the cell.
Both genomics and proeomics can identify potential therapeutic targets, but these targets require the determination of cellular endpoints. You still need to measure the net effect of all processes, not just the individual molecular targets.
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