From the Benz Lab
The Benz lab is making strides in improving treatment outcomes in breast cancer. Just before the break of New Year's Day 2012 (and after two years of preparation) the Benz lab submitted a new manuscript for publication describing a unique “phosphorylation code” embedded in the human estrogen receptor (ER), a protein whose overexpression drives the growth of about 70% of all breast cancers. Although the ER protein is targeted by all hormone-based therapies (e.g., tamoxifen and aromatase inhibitors) only about half of all ER-positive breast cancers respond to these treatments. There is no clear reason for this lack of response.
The Benz lab is one of several that has postulated that a specific pattern of ER phosphorylation determines whether tumors are treatment sensitive or resistant. (Phosphorylation is a biochemical process that involves the addition of phosphate to an organic compound; the activity is carried out by the action of enzymes called kinases.) To date this supposed ER phosphorylation code has remained undeciphered. The multidisciplinary team of Benz lab breast cancer scientists and Gibson lab protein chemists, using a powerful mass spectrometry approach pioneered at the Buck nearly 5 years ago, researchers in the Benz lab now believe that they’ve cracked the ER phosphorylation code.
The Benz lab is collaborating with a UK company, Proteome Sciences, which is interested in commercializing these lab findings. The goal is to develop personalized molecular tests that can predict how ER positive tumors will respond to various therapies. In addition, the Benz lab will explore new therapeutics (kinase inhibitors) capable of altering the ER phosphorylation pattern to restore treatment sensitivity to resistant ER breast cancers.