More than 60 percent of breast cancer cases involve defects in the same biochemical chain of events within cancer cells– known as the PI3 kinase (PI3K) pathway–but efforts to develop therapies targeting this pathway have met with little success after hundreds of mostly failed clinical trials. And researchers still don’t understand why.
Now, using an innovative, unbiased laboratory method, UC San Francisco scientists may have finally cracked the case. The researchers identified a protein that cancer cells use as a shield to protect the PI3K pathway against targeted drugs, and showed that blocking this protein using a second drug (itself already in phase 2 clinical trials) allowed multiple previously ineffective therapies to slow cancer cell growth and shrink tumors. The researchers now plan to pursue clinical trials to determine if these combination therapies can extend the lives of patients with advanced, recurrent breast cancer.
“The failure of PI3 kinase drugs has been a huge mystery,” said senior author Sourav Bandyopadhyay, PhD, assistant professor of bioengineering and therapeutic sciences and a member of the UCSF Helen Diller Family Comprehensive Cancer Center. “Every pharma company in the cancer space has tried to target the PI3 kinase pathway, with little success. Now we may know
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