This highly studied tumor or protein antigen's research history and newly discovered ability may lead to a discovery of new cancer-fighting drugs or treatment.
Rommie Amaro, a computational biologist at the University of California (UC), San Diego, studied the journey of the p53 to understand the effects of mutations that the gene for p53 is prone to.
Of the nearly 1.7 million people diagnosed with cancer each year in the United States alone, about half of those cancers have mutated versions of p53.
So Amaro decided to use supercomputers to study and watch the activities of these protein closely as she plugged in new x-ray snapshots of p53 fragments.
She discovered that four copies of p53 joined and wrapped themselves around a DNA strand. The protein went as far as getting more distorted and destabilized preventing it from binding to the DNA.
In that same observation, Amaro and her team noticed that once in a while, a small cleft forms in the core of the mutated protein. They decided to fire shots of virtual drug molecules into the samples. The compounds attached in the cleft, stabilized p53 just enough to allow it to resume its normal functions.
"A long-standing dream of cancer biology is to find small molecule drug compounds to restore the activity of p53," Amaro says.
Dozens of drugs in the development which target p53 work on the normal p53 but the current studies including Amaro's focus on making the sick p53 healthy.
Klas Wiman, a tumor cell biologist at the Karolinska Institute in Stockholm explained why big pharma don't go for the rescue approach. He said that restoring normal functions of these mutated proteins instead of just blocking them is difficult.
This method that's been used widely in the current research may have revolutionary results. It can even help prevent cancer even before it gets started.
See: CRISPR Gene-Edited Cells Tested for the First Time! Revolutionize Cancer Treatments!