Parker Bridge Fellows Program; Funded in partnership between Parker Institute for Cancer Immunotherapy and the V Foundation
Cancers are driven by mutations, or changes in the DNA that encode the proteins and processes that allow the cells in our body to function normally. Those mutations make proteins work differently, making cancer cells grow faster or live longer, but they also make cancer cells look different from normal cells to the immune system. This process is similar to when someone gets a viral infection, where viruses infect normal cells, and the immune system battles the infection by recognizing the infected cells by the presence of viral proteins.
There are a series of molecules, called the Human Leukocyte Antigens (HLAs), that are responsible for showing those foreign proteins to the immune system on the surface of the diseased cells. Cancer cells can also change or lose these HLAs, so that the immune system no longer sees the cancer cells as “different” from normal cells. My research is focused in understanding these HLA molecules in skin cancer, to address the question of how the cancer cells avoid getting killed by the immune system. Skin cancers are generally treated with therapies that help the immune system kill cancer cells, and my research helps us understand why these therapies may or may not work. By explaining whether HLAs are different in cancer cells, my research may improve the success of our treatment strategies in skin cancer.
