Liam Brunham: Associate Professor at Division of General Internal Medicine, UBC Faculty of Medicine

Associate Professor

Faculty of Medicine

Research Classification

Medical, health and life sciences

Research Interests

Lipids

Genetics

Pharmacogenomics

Cardiovascular diseases

Relevant Thesis-Based Degree Programs

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Affiliations to Research Centres, Institutes & Clusters

BC Regenerative Medicine - BCRegMed

Centre for Heart Lung Innovation

International Collaboration On Repair Discoveries

Providence Health Care Research Institute

Research Options

I am available and interested in collaborations (e.g. clusters, grants).

I am interested in and conduct interdisciplinary research.

I am interested in working with undergraduate students on research projects.

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Research Methodology

Next generation sequencing

Genome editing

Induced pluripotent stem cells

Genome wide association studies

clinical trials

Recruitment

Looking to recruit:

Master's students

Doctoral students

Postdoctoral Fellows

Desired start dates: Any time / year round

Potential research project areas:

1. SAVE BC (www.savebc.ca) is a provincial study of families with extremely premature cardiovascular disease, aimed at identifying molecular causes of this condition and reducing the burden of premature cardiovascular disease. 2. Pharmacogenomics of adverse drug reactions. We are using human stem cells to study the pharmacogenetic mechanisms of specific adverse drug reactions. This work will lead to new approaches to identify patients at risk of suffering from adverse drug reactions, and the development of safer, more effective medications. 3. Inherited dyslipidemias. We have one of the largest and most established registries in Canada of patients with Familial Hypercholesterolemia, a common cause of premature CVD which is under-recognized and under-treated. We are investigating the use of genetic testing to improve the diagnosis of patients with this condition, and understand the determinants of cardiovascular disease risk in these patients.

Other options:

I support public scholarship, e.g. through the Public Scholars Initiative, and am available to supervise students and Postdocs interested in collaborating with external partners as part of their research.

I support experiential learning experiences, such as internships and work placements, for my graduate students and Postdocs.

I am open to hosting Visiting International Research Students (non-degree, up to 12 months).

I am interested in hiring Co-op students for research placements.

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Modelling adverse drug reactions using induced pluripotent stem cell derived cardiomyocytes (iPSC-CMs) (2021)

Adverse drug reactions (ADRs) constitute the fourth leading cause of death and their incidence is steadily increasing. Cardiovascular toxicity is one of the most common and serious ADR and is the leading cause of drug discontinuation. The overarching goal of this thesis is to investigate cardiac ADRs using human pluripotent stem cell derived cardiomyocytes (hPSC-CMs). Doxorubicin is a chemotherapy drug administered to adult and pediatric patients for the treatment of hematological and solid tumors, however, it can cause doxorubicin induced cardiotoxicity (DIC). We generated induced pluripotent stem cell derived cardiomyocytes (iPSC-CMs) from patients who received doxorubicin as part of their chemotherapy regimen. iPSC-CMs from individuals who developed DIC displayed significantly greater sensitivity to doxorubicin compared to iPSC-CMs from patients who did not experience DIC. Several variants associated with DIC have been identified, with RARG –S427L having the strongest genetic evidence. iPSC-CMs together with genome editing, provide a powerful platform to establish causal relationships between genetic variants and ADRs. We used CRISPR/Cas9 to investigate the functional impact of RARG-S427L on DIC in isogenic patient derived iPSC-CMs that differed only at the RARG locus. Genetic correction of RARG-S427L decreased susceptibility to in vitro DIC, whereas introduction of RARG-S427L had the opposite effect. We also used this platform to identify novel cardioprotectants that can be used clinically to prevent DIC. Empagliflozin, a sodium-glucose co-transporter 2 inhibitor, is an FDA-approved medication for the treatment of diabetes that shows cardiovascular benefits. iPSC-CMs treated with empagliflozin exhibited reduced doxorubicin induced cell death. Finally, we showed that enriched cardiomyocyte subtype populations are necessary for accurate drug screening and disease modelling. Ibrutinib is an anticancer drug indicated for the treatment of B cell malignancies; however, it can cause atrial fibrillation. We used atrial and ventricular hPSC-CMs to study ibrutinib induced atrial fibrillation. Ibrutinib had an arrhythmogenic impact on hPSC atrial derived cardiomyocytes, while ventricular hPSC remained unaffected. Collectively, our findings demonstrate that hPSC-CMs represent a powerful platform for disease modelling and drug screening that is amenable to personalized risk prediction for the prevention of adverse drug reactions.

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