Targeting Clonal Dynamics in Human Cancers
Just as species in an ecosystem evolve, so do human cancers. This capacity to change over time contributes to the emergence of drug resistance and even metastasis. In fact, if patients with micro-metastatic disease (cancers that spread to other sites in the body and form miniscule tumours) are not treated properly, it inevitably causes drug resistance, just as partially treated bacterial infections lead to antibiotic resistance.
As Canada Research Chair in Molecular Oncology, Dr. Samuel Aparicio is trying to gain an understanding of the processes that underlie this behaviour by examining the clones of cells in cancer. He is focusing on hard-to-treat cancers such as triple-negative breast cancer and ovarian cancer and seeking to apply his finding to other cancers such as lung and pancreatic.
Aparicio and his research team are taking two convergent approaches. In the first, they are combining genomics, and statistical and computational (article intelligence) approaches to examine clonal populations, with the aim of shedding light on the genetic factors responsible for drug resistance.
At the same time, they are also generating small molecule compounds—precursors of drugs—to explore ways of stopping cancers from evolving. To do this, they are using information about genetic factors of resistance to engineer therapies that will avoid causing tumours to evolve.
Ultimately, Aparicio hopes his research will help to identify drug-like molecules that have the potential to be developed as anti-cancer agents.