PLANNING AND LEADERSHIP FOR A BETTER WORLD
PLANNING AND LEADERSHIP FOR A BETTER WORLD
New drugs that specifically target the mutated genes responsible for cancer growth have shown great success in extending the lives of patients. And they offer far fewer side effects than conventional anti-cancer therapies. Unfortunately, many patients become resistant to these drugs due to secondary mutations.
To overcome this problem, a group of UCLA researchers has developed a "road map" of the complex signaling processes involved in cancer that could lead to new methods for diagnosing and overcoming such drug resistance.
The problem with targeted drug therapies is that cancer is a complicated mix of multiple, interconnected events gone awry through mutations. And while scientists have learned much about these individual events, they need a better understanding of how events function together, as a system, to cause malignancies.
"What we need is a big picture perspective," said Thomas Graeber, a professor of molecular and medical pharmacology and a researcher at UCLA's Crump Institute for Molecular Imaging, Jonsson Comprehensive Cancer Center and California NanoSystems Institute. In particular, he noted that there needs to be an understanding of the complex network of events in order to design new anti-cancer therapies that would simultaneously target the primary mutation while preventing the development of secondary, resistance-conferring mutations.
The future of molecular therapies, researchers say, relies on targeting multiple events simultaneously, making it exponentially more difficult for tumor cells to develop the mutations required to escape the effect of drug therapy. This is somewhat analogous to anti-HIV drug cocktail therapies that target the inhibition of multiple viral-replication steps.
In a study published March 29 in the journal "Science Signaling," Graeber and his team presented their use of proteomic experiments and mathematical analyses to build a systemwide view of how signaling mutations cause leukemia and to identify points of susceptibility that can be targeted by cocktail therapies to prevent drug resistance.
In their work, the UCLA team used technologies that concurrently measure hundreds of signaling events within cancer cells. This is done to try to learn more about how these events interconnect to determine how to target the cancer cells. These new approaches for sorting out the complexities of cancer cells involve building a wiring diagram of the interconnections, or "crosstalk," in cancer cells that will help scientists overcome drug resistances. Graeber likens this work to that of creating a better road map by identifying the bypass routes used by cancer cells to escape the inhibition caused by the drugs.
"We have the tourist information, but we need to discover the insider knowledge of the taxi driver to know how the cell gets around traffic jams rather than getting stuck in the traffic jam," he said.
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