Dr. Brad Olson

Division of Biology
Departmental Website

Cancer results from loss of control over cells in multicellular tissues. Our goal is to decipher the earliest molecular mechanisms that allowed the evolution of multicellular organisms, because these genes are likely the most important defects that lead to carcinogenesis. To do this, we use an unusual model system, the Volvocine algae (green algae), because they are biologically similar to primitive unicellular eukaryotes just before multicellularity evolved. In addition, multicellular evolution in the Volvocine algae is the most recent known example and allows us to focus on the most important genes that keep cells together in multicellular tissues and prevent cancerous growth.

The Volvocine algae also get cancer just like humans do. When the green algal homologs of the retinoblastoma tumor suppressor protein are defective, it causes the cells to hyper-proliferate and become genetically unstable, just like cells in human cancers. More importantly, in humans, the retinoblastoma tumor suppressor pathway is one of the most commonly mutated pathways in all of human tumors, so a better understanding of how this pathway works and becomes defective is essential for understanding human cancer.

Surprisingly, we have found a link between the retinoblastoma tumor suppressor pathway and the earliest events during the evolution of multicellular eukaryotes. The link between the pathway and the first steps toward multicellular organisms suggests components of the pathway may become defective very early in carcinogenesis, even before visible signs of tumors in tissues. Thus, our studies could potentially result in an early diagnosis tool. Further, a better understanding of the interplay between multicellularity and the retinoblastoma tumor suppressor pathway could lead to new therapeutic targets to treat cancer.