A study by the University of Colorado Cancer Center published in the journal PLoS ONE and concurrent phase I clinical trial is examining a new strategy: targeting both important cancer-causing pathways simultaneously.
Genes make proteins and proteins tell your body's cells what to do: one talks to the next, which talks to the next, and to the next. Like a game of telephone, researchers call these "signaling pathways." Abnormalities in these signaling pathways can cause the growth and survival of cancer cells. Commonly, mutations or rearrangements of genes in the MAPK signaling pathway create cancer's fast growth, and alterations in the PI3K signaling pathway allow cancer cells to survive into virtual immortality.
Of course, researchers have extensively targeted these 2 signaling pathways, designing drugs that turn on or off genes in these pathways, thus interrupting the transmission of cancer-causing signals. Unfortunately, these pathways have proven difficult to drug and also it has been difficult to show the effectiveness of drugs that successfully interrupt the transmission of signals along these pathways.
A study by the University of Colorado Cancer Center published in the journal PLoS ONE and concurrent phase I clinical trial is examining a new strategy: targeting both these important cancer-causing pathways simultaneously.
"Well, these two pathways are mutated frequently in cancer. Why not hit both of them? It was as simplistic as that," says Todd Pitts, MS, research instructor in the Program for the Evaluation of Targeted Therapies, and the study's first author.
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