New research from the Johns Hopkins Bloomberg School of Public Health suggests that the protein keratin 17 – the presence of which is used in the lab to detect and stage various types of cancers – is not just a biomarker for the disease, but may play a critical role in tumor growth.
This new understanding of how keratin 17 works, the researchers say, could lead to the development of better ways to detect and prevent cancer, and identify new targets for therapeutic treatment. A report on the findings is published July 13 in Nature Genetics.
“Keratin 17 is a sensitive marker for various cancers and several other acute and chronic diseases affecting the skin, but we didn’t know whether it was a driver of the disease or just an innocent bystander,” says study lead author Ryan P. Hobbs, PhD, a postdoctoral fellow in the John Hopkin’s department of biochemistry and molecular biology. “We didn’t know if the keratin was actually involved in the onset and promotion of skin tumors or if it was just along for the ride. This research, focused on models for cancer affecting the skin, tells us it’s more of a driver than a passenger.”
Keratin 17 is found in healthy hair follicles, fingernails and glands, but not in healthy epidermis, the outermost layer of the skin. It emerges, however, in basal cell skin cancers and most squamous cell cancer, and its appearance in such settings precedes the actual onset of tumor growth. Other researchers have determined that the quantity of keratin 17 present in other types of tumors such as in the breast, cervix, lung and pancreas can indicate how aggressive it is and help determine a patient’s prognosis.
Dr. Hobbs and his colleagues say keratin 17 does not cause the cancer itself, but promotes an inflammatory and immune response that can allow the disease to develop more aggressively.