IMAGE: Joaquin Espinosa, PhD, and colleagues pinpoint new targets in known cancer-causing pathway view more
Credit: University of Colorado Cancer Center
A little p63 goes a long way in embryonic development – and flaws in p63 can result in birth defects like cleft palette, fused fingers or even missing limbs. But once this early work is done, p63 goes silent, sitting quietly in the genome from that point forward. Unless it is accidentally reactivated. When p63 comes back to life within the adult genome, the result can be cancer. More than half of all squamous cell carcinomas, often found in the skin, lung, breast, and head/neck, involve excess p63 activity.
Researchers have known that p63 drives squamous cell cancers. The question has been what to do about it. Unfortunately, it has been impossible to simply switch off p63. And so the question becomes how else can doctors and researchers interfere with the action of p63 to shield patients from its cancerous effects.
Today, a team of University of Colorado Cancer Center researchers working in the lab of Joaquin Espinosa, PhD, sheds light on p63 activity in squamous cell carcinoma of the lung, providing an actionable path forward to drug
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