07 Jul Unexpected link between most common cancer drivers may yield more effective drugs
From left, Vincent Cryns, Mo Chen and Richard A. Anderson. PHOTO BY TIANMU WEN
Two of the most common genetic changes that cause cells to become cancerous, which were previously thought to be separate and regulated by different cellular signals, are working in concert, according to new research from the University of Wisconsin–Madison.
To date, researchers have focused on finding drugs that block one or the other to treat cancer. Understanding their cooperative effects may lead to more effective treatments.
Cells muster a protein, called p53, which acts inside the cell nucleus to respond to stress, but mutations of the gene that produces p53 are the most frequent genetic abnormalities in cancer. Mutations activating a cellular pathway called PI3K/Akt, located on the surface of cells, are also often implicated in runaway cell growth in cancer.
Cellular signaling pathways allow cells to accomplish important communications tasks that maintain healthy cell functions. The process is a bit like sending mail, which requires a specific series of steps and appropriate stamps and marks on the envelope to deliver a letter to the correct address.
A team led by UW–Madison cancer researchers Richard A. Anderson and Vincent Cryns has discovered a direct link between the p53 and PI3K/Akt pathways. The findings, published today in the journal Nature Cell Biology, identified links in the pathways that make promising targets for new cancer treatments.