Gregor Reid

Prospective Graduate Students / Postdocs

This faculty member is currently not actively recruiting graduate students or Postdoctoral Fellows, but might consider co-supervision together with another faculty member.

Associate Professor

Research Classification

Research Interests

paediatric cancer
cancer immunology
animal models of cancer

Relevant Thesis-Based Degree Programs

Affiliations to Research Centres, Institutes & Clusters

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.

Research Methodology

mouse modelling of cancer
in vivo bioluminescent imaging
patient-derived xenografts

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.

The identification of immune responses required for durable control of childhood acute lymphoblastic leukemia (2019)

Remarkable clinical successes have been achieved with targeted immunotherapies directed at a surface antigen of leukemia blasts in patients with relapse or chemotherapy-refractory B-ALL. This single antigen-targeted approach, however, is highly prone to tumor immune escape. Development of resistance to therapy, commonly caused by the emergence of target-negative escape variants, remains a major drawback of CD19-directed therapies for B-ALL. The efficacy of strategies that direct T cell-mediated cytotoxicity towards leukemic cells bearing non-immunogenic antigens is limited, with a lack of evidence that these interventions establish immunological memory. In this study, I use the Eμ-ret mouse model to better understand the limitations of current single antigen-targeted immunotherapies and to identify immune responses required for the achievement and, more importantly, maintenance of remission in childhood B-ALL. My results uncovered the ability of target-directed therapy to elicit epitope spreading, enabling the generation of a secondary immune response against additional non-targeted leukemia-associated antigens that contributes to sustaining durable remission. Importantly, these results also suggest that such diversification of protective immune response is limited in an immunological setting where immune tolerance towards leukemia-associated antigens is established early in the course of leukemia progression. Furthermore, I have shown the ability of TLR agonist-mediated immune modulation to target leukemia cells in bone marrow, and induce durable immune control of primary B-ALL cells. Finally, I have demonstrated that NKT cells as a population is capable of influencing disease progression in the Eμ-ret mouse by playing a role in immunoediting.Overall, these findings support that the generation of immune response with a broad specificity for range of leukemia-associated antigens contributes to the maintenance of remission. Furthermore, my results suggest that overcoming immune tolerance established against leukemia-associated antigens may be critical for maximizing the therapeutic benefits of immunotherapies for childhood B-ALL. Collectively, the therapeutic impact of innate immune modulation presented here in the context of B-ALL may contribute to the eradication of MRD, and thus reduce the risk of relaspse in MRD-positive patients.

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The influence of the immune system on acute lymphoblastic leukemia progression (2017)

The immune system has been proposed to have an impact on the etiology of B-cell ALL; however, a mechanistic explanation of this influence remains elusive. Epidemiological studies have uncovered a paradox, such that surrogates of infection exposure have consistently been associated with reduced ALL risk, while documented infections have a more variable influence, with both positive and negative risk associations being uncovered. Despite these contradictory findings, timing of infection exposure has been identified as a critical variable. A mechanistic explanation for the variable influences of infection or the importance of timing remain poorly defined. In this study, I use the Eµ-RET and E2A-PBX1 mouse models to assess how the basal and stimulated immune system is capable of influencing disease progression. My results indicate that in the absence of infection, resting IFN-γ is capable of influencing disease progression in the Eμ-RET mouse. By modulating SOCS-1 expression levels, IFN-γ restricted the IL-7-driven proliferation of leukemia-initiating cells (LICs) and caused a significant delay in disease progression. Furthermore, TLR ligand-mediated immune modulation inhibited disease progression by inducing the depletion of LICs through a mechanism that involved the direct activity of type-1 and type-2 interferon. Importantly, the relevance of this mechanism in humans was validated through the use of both human immune-effector and leukemia cells. Finally, I demonstrate that quantitative and qualitative differences in neonatal immune responses, in particular the increased capacity for IL-17A production by γδ T-cells, confer significant infection-induced protection from ALL progression in neonatal mice.Mechanistically these findings represent several firsts in the investigation of how the immune system influences B-cell ALL progression. They identify both type-1 and type-2 IFN and IL-17A as important inhibitory factors, and demonstrate the significant impact of immune modulation during the pre-leukemic phase on subsequent disease risk and progression. Furthermore, the results presented here provide a mechanistic explanation for the importance of timing in the association between infection exposure and ALL risk. Collectively, my results indicate that in addition to the educational influence suggested by the “delayed infection” hypothesis, early-life infection exposure may also have an active inhibitory impact on the progression of B-cell ALL.

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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.

Application of Saccharomyces cerevisiae to improve pediatric acute lymphoblastic leukemia outcomes (2018)

Pediatric acute lymphoblastic leukemia (ALL) is the most commonly diagnosed childhood cancer in Canada and continues to need improvements in the care patients receive. Saccharomyces cerevisiae (S. cerevisiae) is a generally nonpathogenic organism that has the potential to affect both stages of leukemia (preleukemia and leukemia) and improve ALL outcomes by acting as a drug delivery vehicle for L-ASNase and/or influence leukemogenesis by inducing early-life, antileukemic immune activity. Mild infectious exposures during infancy and childhood has consistently been shown to influence leukemogenesis. In mice, early-life infections can deplete preleukemic cells and prevent preleukemia developing into leukemia. If preleukemia develops into ALL, children undergo chemotherapy that includes the enzyme L-asparaginase (L-ASNase). ALL cells characteristically stop expressing the enzyme asparagine synthetase (AS) and rely on extracellular sources for L-ASN. L-ASNase depletes extracellular L-ASN, selectively starving ALL cells of L-ASN, and consequently inducing their apoptosis. To evaluate the efficacy of S. cerevisiae to improve L-ASNase therapy, it was first engineered to constitutively express cell-wall associated L-ASNase-II (AEY – asparaginase expressing yeast). The cell-wall association may improve ALL therapy by shielding L-ASNase from immune detection and consequently reducing the cost, toxicity, and immunogenicity of L-ASNase therapy. In vitro, AEY co-cultured with ALL cell lines can deplete L-ASN levels leading to apoptosis and inhibited cell growth in the asparagine synthetase (AS)-negative cell line RS4;11, but not the AS-positive cell lines BV173 and 697. The AEY biomass required to yield a therapeutic L-ASNase dose exceeds the current ethical limitations for further study in vivo. To determine if S. cerevisiae can activate early-life, antileukemic immune activity, S. cerevisiae was injected intraperitoneally into day-6-old Eμ-RET mice and the effect on preleukemic burden was assessed. S. cerevisiae is unable to activate the IL-17A and Natural Killer (NK) cell-dependent immune response that has been shown to deplete preleukemic cells. Additionally, both in vitro and in vivo stimulation of NK cells with IL-17A does not directly lead to their activation. Further investigation into the mechanism leading to the activation of antileukemic NK cells may uncover new immunotherapeutic approaches for ALL.

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Membership Status

Member of G+PS
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BC Children's Hospital

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