About Our Lab
The Burridge lab works in the field of pharmacogenomics (precision medicine) and regenerative medicine, primarily using human induced pluripotent stem cells (hiPSCs).
We aim to develop next-generation tools to study the role of the genome in drug response and complex disease traits. Using these tools we will be able to predict which patients will experience adverse drug responses, validate the causal role of particular single nucleotide polymorphisms (SNPs), probe the mechanisms of action, and discover new drugs to overcome these complications. It is our ambition to translate these techniques to the clinic, to improve personalized patient care and drug efficacy, and to eliminate off-target toxicity.
Our major effort has been focused on SNPs involved in patient-specific chemotherapy-induced cardiovascular toxicity, particularly in breast cancer and pediatric cancer patients. We ask the question: what is the genetic reason why some patients experience minimal side effects of their cancer treatments, whilst others encounter highly detrimental side effects? These side effects can include heart failure or arrhythmias, atherosclerosis, nerve damage, liver failure, or infertility. Our work has contributed to risk-based screening by functionally validating genetic changes that predispose a patient to a specific drug response.
The hiPSCs we use
Once we have discovered a genetic variant correlated to a specific drug response, we probe the underlying mechanisms of action, performing CRISPR-based genome editing and genome-wide CRISPR-knockout screens. We then perform insight-driven drug screens or screening of large drug compound libraries to discover new drugs that can minimize adverse drug responses.
In addition to this work, we have developed programs in cardiovascular regenerative medicine, repairing the heart after a heart attack or ameliorating the effects of heart failure, and studying how heritable (germline) variation influences cancer progression and oncology drug efficacy and acquisition of resistance.