Colin Ross


Research Interests

Biomedical Technologies
Drug Metabolism
Gene Therapy
Gene-based therapeutics
Precision Medicine
Transgenic Model

Relevant Thesis-Based Degree Programs

Affiliations to Research Centres, Institutes & Clusters


Research Methodology

molecular biology
Clinical Research


Master's students
Doctoral students
Postdoctoral Fellows
Any time / year round


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

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Graduate Student Supervision

Doctoral Student Supervision

Dissertations completed in 2010 or later are listed below. Please note that there is a 6-12 month delay to add the latest dissertations.

An investigation of the role of pharmacogenetics in the development and prevention of anthracycline-induced cardiotoxicity (2023)

Anthracyclines (e.g., doxorubicin) are effective chemotherapeutics used to treat a broad-spectrum of childhood and adult cancers. However, the clinical utility of anthracyclines is considerably limited by anthracycline-induced cardiotoxicity (ACT). ACT remains a significant burden in the clinic, where >50% of patients receiving anthracyclines experience some degree of ACT, initially presenting as left ventricular dysfunction, and up to 16% of patients develop heart failure. Advancements in patient genetics show substantial promise as a predictive measure of ACT. The gene variants RARG-rs2229774, UGT1A6-rs17863783, and SLC28A3-rs7853758 have the strongest evidence for association with ACT in anthracycline-treated patients. First, this thesis aimed to understand the scope of genetics, focusing on the proposed roles of genes RARG, UGT1A6, and SLC28A3 in the development and prevention of ACT. Second, I investigated the roles of UGT1A6 and RARG in the development of ACT using cellular models. The research replicated the ACT susceptibility of the UGT1A6 locus using a cellular model (HEK293) of doxorubicin-induced cytotoxicity. Further, I identified that ligand-mediated activation of RARG, using all-trans retinoic acid (ATRA) and CD1530, significantly increases the cell viability of H9c2 cardiomyoblasts. Lastly, I evaluated the efficacy of ATRA in preventing the development of cardiotoxicity using a human cardiomyocyte and a mouse model of ACT. In human cardiomyocytes, ATRA enhanced cell survival during doxorubicin exposure. The protective effect of ATRA was also observed in a mouse model (B6C3F1/J) of ACT, in which ATRA treatment improved heart function of doxorubicin-treated mice. Histological analyses also indicated that ATRA treatment reduced the pathology associated with ACT. Further, in human cardiomyocytes, ATRA induces the gene expression of retinoic acid receptors (RARG, RARB), while repressing topoisomerase-II enzyme genes (TOP2A, TOP2B), which encode for the molecular targets of anthracyclines, and repressed downstream ACT response genes. This mechanism partially explains the protective effect of ATRA and why patients presenting with dysregulation of this pathway may be susceptible to ACT. Overall, the work performed in this thesis shows that gene variants that modify ACT risk belong to critical biological pathways of ACT. Further, these molecular mechanisms also provide a unique opportunity to develop safe and effective interventions to mitigate ACT.

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Assessment of biological markers to aid subtype classification in pediatric primary systemic vasculitis (2023)

Chronic primary systemic vasculitis (PSV) describes a diverse group of debilitating and potentially life-threatening diseases, characterized by inflammation of blood vessels within various organs such as the kidneys, lungs, brain, eyes, and skin. Subtypes of the small- to medium-sized vessel vasculitides are particularly challenging to classify due to many overlapping clinical symptoms. Their differentiation is important, however, as there is evidence that different subtypes benefit from different treatment approaches. The rarity of vasculitis in children has limited pediatric-specific PSV studies and the clinical approach to pediatric PSV is adapted primarily from adult studies. Not surprisingly, adult-derived classification criteria are imperfect for children and consequently, fail to classify up to two thirds of children with small- to medium-vessel PSV. The objective of this dissertation is to identify genetic markers and select, circulating biomarkers to better our understanding and clinical approach to managing the disease and to improve outcomes of children with chronic PSV. Using biological samples and clinical metadata from a worldwide cohort of children with chronic PSV, this dissertation reports (1) genetic associations specific to pediatric autoimmune vasculitis through employing a genome-wide association study; (2) a high prevalence of autoantibodies to lysosome associated membrane protein-2 in pediatric PSV that correlate to vasculitis-associated kidney dysfunction; and (3) the identification of nine patients, originally diagnosed with chronic PSV, harbouring novel and/or rare variants in adenosine deaminase 2 (ADA2) – these genetic data alongside having abrogated ADA2 enzyme activity have led to their reclassification as having a new monogenic form of vasculitis, deficiency of adenosine deaminase 2. This dissertation reports the first large-scale genotype and biomarker study of primary vasculitis focusing solely on pediatric cases. Improved classification is critical for timely therapeutic intervention, for identification of appropriately classified children for clinical trials, and for research, all of which will improve our understanding of the disease and the quality of life of children suffering from chronic PSV.

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Development of reporter mouse models to evaluate and optimize crispr/cas9 base editing therapeutics (2023)

Genetic diseases are a leading cause of death and disability worldwide with immense economic and societal burdens. However, currently fewer than 5% of genetic diseases have approved treatments, often with limited therapeutic benefit to patients. Genome editing provides a new therapeutic strategy to treat genetic diseases. In the last few years, the Clustered Regularly Interspaced Short Palindromic Repeats/CRISPR-associated protein 9 (CRISPR/Cas9) system has emerged as a promising gene editing approach due to its ease in design and flexibility to target different genetic diseases. One factor limiting its broader application is that it will introduce double-stranded deoxyribonucleic acid (DNA) breaks (DSBs). New advances in the CRISPR/Cas9 system are “base” and “prime” editing, which do not generate DSBs. Base editing has shown great potential to precisely repair the majority of pathogenic point mutations in the patient’s DNA. Prime editing, while currently less efficient, can introduce a broader range of possible edits. However, there remains a major challenge: delivery of genome editors to the affected tissues.To begin to address this challenge, two reporter gene mouse models were developed. Both models introduce a point mutation to knockout the reporter gene activity. Upon gene editing, the mutation is corrected back to the wildtype sequence, thereby restoring the reporter gene activity. The efficiency of gene editing can be visualized and measured with an in vivo whole animal imaging system, which permits repeated and long-term assessments of gene editing. To validate both mouse models, base editor mRNA and a mutation-specific single guide RNA (sgRNA) were encapsulated with lipid nanoparticles (LNPs) and intravenously administered into the reporter mice. This resulted in 83.5% restoration of wildtype reporter gene activity in the liver. One major application of these mouse models will be to evaluate and optimize gene editor delivery systems targeting various tissues. As an example, intramuscular administration of LNPs encapsulated with base editing components led to significant genome editing in the injected muscle, which could be readily visualized in the live imager. These novel reporter gene mouse models will provide critical tools for the in vivo evaluation and optimization of genome editor delivery and improved genome editor formulations.

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Investigating and identifying genetic predictors for cisplatin-induced hearing loss and anthracycline-induced cardiotoxicity (2023)

The full abstract for this thesis is available in the body of the thesis, and will be available when the embargo expires.

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Pharmacokinetics of cationic host-defense peptides and innate defense regulators in native and formulated states (2023)

The full abstract for this thesis is available in the body of the thesis, and will be available when the embargo expires.

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Therapeutic genome editing for the treatment of genetic diseases : testing the safety and effectiveness of CRISPR/Cas9 therapeutic base editing (2023)

There are currently no effective treatments for 95% of the over 7,000 known genetic diseases [1, 2]. The use of CRISPR/Cas9 has recently emerged as a powerful approach to directly repair disease-causing mutations [3-8]. The goal of this project was to optimize a novel CRISPR/Cas9 ‘base editing’ approach to treat genetic diseases by specifically repairing the disease-causing mutation in situ in the patients’ DNA. This technology uses a fusion of a partially deactivated Cas9 (nCas9) protein coupled with a nucleotide modifying enzyme to achieve 15-30% editing, and in some cases up to 75% editing in vitro [9-13]. Two-thirds of all genetic diseases are caused by point mutations [1] and base editors have now been developed that can target more than 68% of all disease-causing point mutations [8]. Despite the growing potential of base editing, limitations in the ability to quantify gene editing quickly and precisely have resulted in a lack of robust high throughput studies to compare and optimize base editors. We hypothesized that developing base editor reporter model systems would enable us to efficiently test and optimize the safety and effectiveness of base editing. To this end, we successfully developed both in vitro and in vivo reporter models and utilized these models to test the safety, delivery, and effectiveness of base editing. This series of novel model systems address a critical gap in the field of CRISPR/Cas9 gene editing. Using these, we were able to significantly increase the efficiency of base editing in vitro. We were also able to compare the safety of different base editors using a new application of my in vitro reporter model. We also demonstrated the therapeutic feasibility of our base editing approach in vitro to repair three prevalent mutations that cause a debilitating genetic disease: Lipoprotein Lipase Deficiency. Lastly, using the in vivo reporter model, we were able to demonstrate sustained correction and efficient delivery of base editors using lipid nanoparticles. Overall, these experiments have demonstrated critical steps towards the implementation of new treatment options for patients with a wide variety of genetic diseases.

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Master's Student Supervision

Theses completed in 2010 or later are listed below. Please note that there is a 6-12 month delay to add the latest theses.

Functional validation of UGT1A6 in anthracycline-induced cardiotoxicity (2022)

The pursuit of precision medicine can be achieved via pharmacogenetic testing prior to treatment onset thanks to the genomic revolution. It has allowed for large-scale genetic testing to be done relatively inexpensively resulting in specific genetic variants to be linked with a phenotype or disease of interest. While beneficial, there remains a burden of proof before translation of knowledge from bench to bedside in order to provide the best possible healthcare. In this study, novel in vitro methods were used with the goal of functionally exploring the role of UGT1A6 in relation to a patient’s risk of the adverse drug reaction (ADR) known as anthracycline-induced cardiotoxicity. More specifically, the variant in UGT1A6 known as rs17863783 has been previously shown, along with other genetic and clinical risk factors, to put a patient at increased risk for cardiotoxicity following anthracycline treatment onset. HEK293 cells were used to create stably transfected expression systems of various haplotypes of UGT1A6. These cells were validated to be expressing the correct genotype via PCR and Sanger Sequencing and subsequently treated with the anthracycline known as doxorubicin (DOX) for viability investigation. Transiently transfected HEK293 cells were also used to express UGT1A6 haplotypes of interest for an investigation of cell viability in addition to UGT1A6 enzyme activity via a 4MU general glucuronidation assay. Despite inherent limitations of in vitro analysis, we conclude that UGT1A6 1) plays a role in anthracycline-induced cardiotoxicity 2) the various haplotypes, such as rs17863783, alter functionality providing additional evidence to support prospective pharmacogenomic testing of patients along with serving as a knowledge base for future research and 3) not all model systems effectively model in vivo phenomena. This thesis will detail the methods and results obtained over the course of investigation into the role of UGT1A6 and anthracycline-induced cardiotoxicity.

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Safety of genome editing: development of a fluorescent model system to investigate reducing off-target genome edits by base editors (2022)

Gene editing is a potential treatment for genetic diseases, but current gene editingtechnologies are limited in their use and safety. CRISPR-Cas9 installs double stranded breaks inthe genome which can be hard to fix, as the homologous-driven repair mechanism it uses has lowefficiency. Newer gene editors have more specificity, such as CRISPR/Cas9-derived baseeditors, which enzymatically convert a target base to another. However, base editors are alsocapable of creating unwanted mutations, known as off-target edits, which can potentially lead totumourgenesis. The difficulty of detecting these base changes has resulted in a poorunderstanding of factors involved in off-target edits.For my study, I successfully developed a human cell fluorescent model system using amutated Green Fluorescent Protein (GFP) reporter gene with a premature stop codon. Aftersuccessful base editing to correct the mutation, the cells are analyzed using flow cytometry toquantify the editing efficiency. To simulate guide RNA (gRNA)-dependent off-target editing, Idesigned multiple mismatched sgRNAs with intentional mismatches to the target GFP sequence.These mismatched sgRNAs mimic the true GFP sgRNA matching incorrectly to sequencessimilar to GFP in the genome.I tested the model with three adenosine base editors with different deaminases: the newbase editor ABE8e, which is known for its promiscuous editing activity, an ABE8e containingthe safety mutation V106W to reduce off-target edits, and the standard ABE7.10. I hypothesizedthat using ABE8e V106W with off-target mismatched sgRNAs would have reduced genomeediting compared to ABE8e.ivUsing this model system, ABE8e was shown to correct GFP at 25.5%, ABE8e V106W at28%, and ABE7.10 at 34%. ABE8e and ABE8e V106W showed no editing difference betweenthe mismatched and matched sgRNAs, but ABE7.10 could not tolerate the mismatched sgRNAs.Sanger sequencing showed two bystander edits with ABE8e and ABE8e V106W, potentiallyreducing fluorescence of GFP. These results show the model is capable of modelling sgRNA-dependent off-target edits and was able to detect differences between versions of base editors.This mismatched model could be used to investigate off-target edits by base editors tohelp develop safe, effective gene therapies for treating genetic diseases.

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Correction of a pathogenic lipoprotein lipase deficiency mutation p207l using Crispr/Cas-mediated adenine base editors (2021)

Lipoprotein Lipase (LPL) is responsible for the clearance of triglyceride-rich lipoproteins from the blood. LPL Deficiency is an autosomal recessive genetic disease caused by mutations in the LPL gene that disrupt normal LPL enzyme function resulting in severe hypertriglyceridemia and pancreatitis. Previously, our lab developed an AAV-based gene therapy to treat LPL deficiency by delivering the LPL gene into patients demonstrating proof of concept for viral-based gene therapy. This treatment became the first gene-augmentation therapy to receive regulatory approval (Glybera®). One limitation of this approach, however, is the dysregulated expression of the delivered therapeutic transgene. Gene editing may overcome some limitations of gene augmentation gene therapies, such as dysregulated transgene expression. We hypothesize that CRISPR/Cas9 base editing delivered via lipid nanoparticles can repair the mutant LPL gene and demonstrate a proof of concept for this novel therapeutic approach. We investigated the use of CRISPR/Cas9 based editing composed of a partially deactivated Cas9 (nCas9) protein with an adenine deaminase to directly repair the common P207L mutation in the LPL gene. We generated Flp-In T-RExTM 293 cell lines stably expressing either LPLP207L and wildtype LPL as model systems to explore the gene editing repair of LPLP207L. The effectiveness of base editing was measured both by Sanger DNA sequencing and measuring the restoration of LPL enzyme activity. After optimization of this process, we observed an approximately 50% correction of the LPLP207L mutation by Sanger DNA sequencing, which corresponded with a 52% restoration of LPL enzyme activity compared to wildtype LPL, using an NG-ABE8e base editor. These results demonstrate a proof-of-concept for DNA base editing as a novel treatment strategy to directly repair the LPLP207L mutation that causes LPL deficiency.

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Genome-Wide Association Study of Cisplatin-Induced Hearing Loss in Children (2014)

Cisplatin is an effective chemotherapeutic agent used for a variety of solid organ malignancies in children and adults. However, its clinical use is limited by the high incidence of cisplatin-induced ototoxicity (CIO), which can affect up to 40-60% of children treated. To date, the genetic basis for CIO has been studied with only focused candidate-gene approaches. Here we report the findings of the first genome-wide association study (GWAS) of cisplatin-induced ototoxicity in children. We examined 738,432 genetics markers in a discovery cohort of 282 Canadian paediatric patients treated with cisplatin, followed by a replication study in an independent Canadian cohort of 82 children. In addition, clinical, therapeutic, and demographic characteristics of cases and controls were analysed to identify clinical factors that may also contribute to the susceptibility to CIO. The genome-wide analyses identified a significant association within the toll-like receptor 4 (TLR4) gene on chromosome 9. The most highly associated single nucleotide polymorphism (SNP) rs960312 conferred a highly protective effect against cisplatin-induced hearing loss (P = 1.19x10-⁸ , odds ratio = 0.22). This variant was subsequently replicated in an independent paediatric cohort (P = 0.018, odds ratio = 0.25). This variant is a tag SNP for a TLR4 promoter haplotype reported to have significantly altered transcriptional efficiency of TLR4. In both cohorts, CIO is significantly associated with younger age (P = 3.41x10-⁶), concomitant vincristine use (P = 2.03x10-¹²), and germ-cell tumour type (P = 4.50x10-⁶). After correcting for these clinical factors, TLR4 rs960312 remains highly associated (Uncorrected P = 1.16x10-⁹ ; Corrected P = 1.01x10-⁹). Several lines of evidence from in vitro and in vivo studies have implicated TLR4 in cisplatin-induced cochlear toxicity and hearing loss. Here we provide the first evidence linking TLR4 and CIO in human patients treated for cancer, leading to new insights into the mechanism underlying this pervasive and clinically limiting adverse drug reaction. The identification of additional markers that contribute to the susceptibility of CIO can be used to develop individualized patient treatments, which can potentially improve safety and treatment outcome of cisplatin.

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