MelanomaChristin Burd, E PhD, Assistant Professor in the Department of Molecular Genetics and her team have efforts underway to understand the biology of melanoma often focus on changes in-trinsic to the "seed" or tumor cell. However, recent evidence suggests that normal cells which surround tumors, i.e. "the soil", can also promote cancer progression. Secretions from such 'stromal' cells have been shown in other tumor types to enhance cancer initiation, growth and metastasis. Yet, in melanoma, very little is known about the role of stromal cells in tumor for-mation and progression.
We recently identified p16INK4a as a gene that is active in melanoma stromal cells. Although p16INK4a is not secreted, it is associated with a cellular state called se-nescence. Senescent cells no longer replicate and instead produce a wide variety of secreted factors that breakdown the surrounding tissue and cause inflammation. Early research suggests that senescent stromal cells promote melanoma development. In support of these data, we find that stromal cells only express p16INK4a in areas where tumors form and not near benign moles. Based upon these data, we believe that stromal p16INK4a expression could be used to more effectively identify melanoma at its earliest and most curable stage. Furthermore, the breadth and intensity of stromal p16INK4a expression may reflect the ability of a tumor to spread or favorably respond to treatment.
Our work will: