Rutger D. Luteijn, Ph.D., Postdoctoral Fellow University of California, Berkeley

In addition to directly promoting tumor formation by causing pro-growth mutations, DNA damage can also support tumors indirectly by causing some cells to stop growing and instead become “senescent.” These senescent cells produce factors associated with age-related diseases, including cancer, but it’s not understood exactly how DNA damage causes this activity. Therefore, Dr. Rutger Luteijn is exploring the role of an immune molecule named STING, which is involved in the DNA detection system and appears to be crucial for certain aspects of cell senescence. First, he’s determining how various STING-related pathways contribute to senescence, and then plans to test the role of these factors in tumor formation. Overall, his work aims to define the biological pathways that connect the innate immune response to senescence, and consequently, provide new understanding of this process as well as novel targets for cancer immunotherapy.

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