Like an image in a broken mirror, a tumor is a distorted likeness of a wound. Scientists have long seen parallels between the two, such as the formation of new blood vessels, which occurs as part of both wound healing and malignancy. Research at The Rockefeller University offers new insights about what the two processes have in common—and how they differ—at the molecular level. The findings, described in the April 20, 2017 issue of Cell, may aid in the development of new therapies for cancer. The article is titled” Epithelial-Mesenchymal Micro-niches Govern Stem Cell Lineage Choices.” At the core of both malignancy and tissue mending are stem cells, which multiply to produce new tissue to fill the breach or enlarge the tumor. To see how stem cells behave in these scenarios, a team led by scientists in Dr. Elaine Fuchs’s lab compared two distinct types found within mouse skin. One set of stem cells, at the base of the hair follicle, differentiates to form the hair shaft; while another set produces new skin cells. Under normal conditions, these two cell populations are physically distinct, producing only their respective tissue, nothing else. But when Dr. Yejing Ge, a postdoc in the Fuchs lab, looked closely at gene activity in skin tumors, she found a remarkable convergence: The follicle stem cells expressed genes normally reserved for skin stem cells, and vice versa. Around wounds, the researchers documented the same blurring between the sets of stem cells. Two of the identity-related genes stood out.
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