Speakers: Brad Olson, PhD
Brad Olson, PhD
Associate Professor, Biology
Associate Director of Bioinformatics
Kansas State University
Brad Olson is an Associate Professor of Biology and Associate Director of Bioinformatics at Kansas State University. He did his PhD at Michigan State University and post-doc at the Salk Institute for Biological Studies as a Ruth L. Kirschstein NIH Fellow where he trained in molecular cell biology as well as bioinformatics. His current research focuses on how multicellular organisms evolve, and he has numerous collaborations applying data science and machine learning to multi-omics data to determine the biological principles of large data sets.
Deep Learning About the Origin of Tumorigenesis
The evolution of multicellular organisms resulted in gene networks that control organismal development. Breakdown of these gene networks underlies tumorigenesis, so if we understand how these pathways evolved when multicellular organisms evolved, we can better diagnose and treat cancer. Surprisingly, we have found that the tumor suppressor and cell cycle transcriptional regulator Retinoblastoma is sufficient for multicellular evolution in a model for multicellular evolution (the volvocine algae). When we compare the genomes of the volvocine algae we find that they are losing genes as they gain multicellularity, suggesting that gene gain does not underly multicellular complexity, rather changes in cell cycle transcriptional regulation by RB causes multicellularity. To understand how this applies to the role of RB in human tumors we have used a machine learning based approach to develop a Generative Adversarial Neural network (GAN) and are refining to model to perform transfer learning to human data sets where RB is defective thereby causing a tumor. From this work, we have determined common a common principle that protein interaction networks play a significant role in multicellular development. Perturbations of these protein interaction networks in specific ways can cause them to collapse leading to cellular dysfunction and ultimately cancer.