BOSTON, Jan. 29 (UPI) -- Researchers at Harvard University found that blocking specific signaling enzymes that contribute to common benign skin lesions called seborrheic keratoses, or SKs, cause them die, according to a new study.
The researchers, who work at Massachusetts General Hospital, were investigating why the lesions, which have genetic similarities to cancer, grow but never turn cancerous.
Previous research has identified genes thought to be involved with differentiation between skin cells and skin cancer development. Two genes that code for proteins activating the Akt kinase enzyme, known to block cell-death related pathways, leading researchers to see what happens when the kinase is blocked.
"Understanding why SKs never become malignant, even though they have mutations in classic oncogenes, was the primary question we wanted to address when we started studying this skin lesion," said Dr. Victor Neel, director of dermatologic surgery at Massachusetts General Hospital, in a press release. "Finding a novel inhibitor of SKs was a serendipitous byproduct of that inquiry."
For the study, published in the Journal of Investigative Dermatology, researchers exposed SK cell cultures to an Akt inhibitor called A44, which induced death in the cells. They also found that applying A44 to intact lesions taken from patients' skin died by the same process as the cultured cells.
The researchers said they have already filed a patent application based on the study but that further work with A44 and other compounds is necessary before a clinical trial can be conducted.
"Inhibition of this enzyme in SK cells causes rapid cell death while having no effect on normal skin cells. We are confident that this paper heralds the development of an effective, topical treatment for SKs," Neel said, adding researchers "still don't know why SKs resist malignant transformation but we think studying SKs will help us identify factors that prevent benign lesions from becoming malignant."