“We are honored to receive support from the Sontag Foundation to apply our genomics techniques and uncover the earliest events that gave rise to glioblastoma.”

About DSA-Funded Research

At the moment, we have poor baseline estimates for how many progenitor cells give rise to each tissue in the human body, the cell type of origin for various cancers and how the clonality of tissues change over the course of aging, eventually laying the groundwork for diseases like cancer. The significance of these cellular phenomena are evident in well studied conditions such as clonal hematopoiesis, where the clonal growth of hematopoietic cells gives rise to a cellular monoculture. It is estimated that 20% of all healthy humans over the age of 70 have clonal hematopoiesis, highlighting the potential size of the problem in a single organ system. These same estimates are not readily available for the brain or diseases like glioblastoma multiforme, a highly aggressive brain cancer that unfortunately recurs after therapy. To this date, we do not know the origin of the precancerous cell that transforms to cause glioblastoma, and more importantly we do not know how to eradicate it. To answer this important question, my lab is developing two sequencing technologies to study the cell type of origin in glioblastoma. By sequencing somatic mutations in single cells with spatial resolution, we will use shared mutations to infer how cells were related prior to disease. Using these data we will estimate the prevalence of precancerous clones in healthy brain tissue and define the events preceding oncogenic transformation. We anticipate that understanding glioblastoma’s natural history, will lead to the design of early detection tests and uncover new therapeutic targets.