Dr Sean Burnard
Post-Doctoral Research Scientist
School of Biomedical Sciences and Pharmacy
Career Summary
Biography
Dr Sean Burnard is an Early Career Researcher within the School of Biomedical Science and Pharmacy at the University of Newcastle and is based at the Hunter Medical Research Institute. Dr Burnard is passionate about harnessing the power of bioinformatics to understand the complex biology underlying human diseases to lead to better treatments and ultimately a cure! His current research is focused on leveraging single-cell and multi-omic data to explore epigenetic changes and treatment resistance in cancer patients and has been developing an evolving interest in transposable elements and their role in disease.
Dr Burnard completed his BSc in Biochemistry at Cardiff University, UK, and PhD in Medical Genetics at the University of Newcastle, Australia, in 2021. His PhD focused on understanding the genetic predisposition and molecular phenotype of natural killer (NK) cells in Multiple Sclerosis (MS) associated with disease onset, progression, and phenotype/subtype. This involved employing and adapting machine learning approaches to re-analyse genetic wide association study (GWAS) data that identified new association signals and interaction across NK receptor loci, including SNPs that were well below conventional significance thresholds and confirmed in more recent and larger GWAS.
Following the completion of his PhD, Dr Burnard joined the Cancer Epigenetics group, led by Dr Heather Lee, as a post-doctoral research scientist. This has involved developing pipelines to process and analyse cutting-edge single-cell and multi-omic sequencing data. Projects thus far have been focused on the heterogenous response following treatment of hypomethylating agent therapy in leukemia patient and cell lines. His work has led to ongoing national collaborations and projects exploring the use of co-treatments to target pathways identified with treatment resistant. From the start of joining the Lee lab, Dr Burnard has incorporated the analysis of transposable elements, which are repetitive elements that make up almost half the human genome, to provide greater insight into their role in cancer treatment, resistance, and relapse. Dr Burnard is keen to explore collaborative opportunities to better our understanding with a broadening dream to eradicate cancers and human disease.
Qualifications
- Doctor of Philosophy, University of Newcastle
- Bachelor of Science, Cardiff University
Keywords
- Bioinformatics
- Epigenetics
- Immunogenetics
- Multi-omics
- Multiple Sclerosis
Languages
- English (Mother)
Fields of Research
| Code | Description | Percentage |
|---|---|---|
| 320406 | Immunogenetics (incl. genetic immunology) | 30 |
| 310204 | Genomics and transcriptomics | 40 |
| 310504 | Epigenetics (incl. genome methylation and epigenomics) | 30 |
Professional Experience
UON Appointment
| Title | Organisation / Department |
|---|---|
| Post-Doctoral Research Scientist | University of Newcastle School of Biomedical Sciences and Pharmacy Australia |
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (6 outputs)
| Year | Citation | Altmetrics | Link | ||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| 2023 |
Xavier A, Maltby VE, Ewing E, Campagna MP, Burnard SM, Tegner JN, et al., 'DNA Methylation Signatures of Multiple Sclerosis Occur Independently of Known Genetic Risk and Are Primarily Attributed to B Cells and Monocytes', International Journal of Molecular Sciences, 24 12576-12576 [C1]
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| 2022 |
Hunt K, Burnard SM, Roper EA, Bond DR, Dun MD, Verrills NM, et al., 'scTEM-seq: Single-cell analysis of transposable element methylation to link global epigenetic heterogeneity with transcriptional programs', SCIENTIFIC REPORTS, 12 (2022) [C1]
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| 2022 |
Burnard SM, Lea RA, Benton M, Eccles D, Kennedy DW, Lechner-Scott J, Scott RJ, 'Capturing SNP Association across the NK Receptor and HLA Gene Regions in Multiple Sclerosis by Targeted Penalised Regression Models', Genes, 13 (2022) [C1] Conventional genome-wide association studies (GWASs) of complex traits, such as Multiple Sclerosis (MS), are reliant on per-SNP p-values and are therefore heavily burdened by mult... [more] Conventional genome-wide association studies (GWASs) of complex traits, such as Multiple Sclerosis (MS), are reliant on per-SNP p-values and are therefore heavily burdened by multiple testing correction. Thus, in order to detect more subtle alterations, ever increasing sample sizes are required, while ignoring potentially valuable information that is readily available in existing datasets. To overcome this, we used penalised regression incorporating elastic net with a stability selection method by iterative subsampling to detect the potential interaction of loci with MS risk. Through re-analysis of the ANZgene dataset (1617 cases and 1988 controls) and an IMSGC dataset as a replication cohort (1313 cases and 1458 controls), we identified new association signals for MS predisposition, including SNPs above and below conventional significance thresholds while targeting two natural killer receptor loci and the well-established HLA loci. For example, rs2844482 (98.1% iterations), otherwise ignored by conventional statistics (p = 0.673) in the same dataset, was independently strongly associated with MS in another GWAS that required more than 40 times the number of cases (~45 K). Further comparison of our hits to those present in a large-scale meta-analysis, confirmed that the majority of SNPs identified by the elastic net model reached conventional statistical GWAS thresholds (p < 5 × 10-8 ) in this much larger dataset. Moreover, we found that gene variants involved in oxidative stress, in addition to innate immunity, were associated with MS. Overall, this study highlights the benefit of using more advanced statistical methods to (re-)analyse subtle genetic variation among loci that have a biological basis for their contribution to disease risk.
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| 2020 |
Maltby VE, Lea RA, Burnard S, Xavier A, Van Cao T, White N, et al., 'Epigenetic differences at the
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| 2018 |
Rhead B, Brorson IS, Berge T, Adams C, Quach H, Moen SM, et al., 'Increased DNA methylation of
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| 2017 |
Burnard S, Lechner-Scott J, Scott RJ, 'EBV and MS: Major cause, minor contribution or red-herring?', Multiple Sclerosis and Related Disorders, 16 24-30 (2017) [C1] Multiple Sclerosis (MS) is a chronic neurological disease with genetic and environmental risk factors. Epstein Barr-Virus (EBV) has been closely associated with MS but with a sign... [more] Multiple Sclerosis (MS) is a chronic neurological disease with genetic and environmental risk factors. Epstein Barr-Virus (EBV) has been closely associated with MS but with a significant amount of conflicting evidence. Some of the evidence for EBV involvement in MS includes: almost 100% of MS patients showing past EBV infection, an association with Infectious Mononucleosis (acute EBV infection), higher titres of EBV antibodies associated with an increased risk of MS development, and an overall altered immune response to EBV found in peripheral blood and the CNS of MS patients. However, evidence for EBV presence in the CSF and T cell responses to EBV in MS have been particularly conflicting. Several hypotheses have been proposed for direct and indirect EBV involvement in MS such as 1) Molecular Mimicry 2) Mistaken Self 3) Bystander Damage and 4) Autoreactive B cells infected with EBV. More recently, an association between EBV and human endogenous retrovirus in MS has been shown, which may provide an alternative pathogenetic target for MS treatment. However, if EBV is not the major contributor to MS and is instead one of several viral or infectious agents able to elicit a similar altered immune response, MS development may be the result of a failure of viral clearance in general. This review aims to evaluate the evidence for the currently discussed theories of EBV involvement in MS pathogenesis.
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| Show 3 more journal articles | |||||||||||
Conference (1 outputs)
| Year | Citation | Altmetrics | Link | ||
|---|---|---|---|---|---|
| 2018 |
Groen K, Burnard S, Maltby V, Scott R, Tajouri L, Lechner-Scott J, 'Plasma-borne exctracellular vesicles in multiple sclerosis where did they come from?', MULTIPLE SCLEROSIS JOURNAL, GERMANY, Berlin (2018)
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Preprint (4 outputs)
| Year | Citation | Altmetrics | Link | |||||
|---|---|---|---|---|---|---|---|---|
| 2024 |
Bond DR, Burnard SM, Uddipto K, Hunt KV, Harvey BM, Reinhardt LS, et al., 'Upregulated cholesterol biosynthesis facilitates the survival of methylation-retaining AML cells following decitabine treatment (2024)
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| 2023 |
Humphries S, Burnard S, Keely S, Bond D, Lee H, 'Hypoxia alters the effects of hypomethylating agents in acute myeloid leukaemia cells (2023)
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| 2022 |
Hunt K, Burnard S, Bond D, Lee H, 'Protocol for targeted analysis of transposable element methylation levels and transcriptome in single cells using scTEM-seq (2022)
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| Show 1 more preprint | ||||||||
Grants and Funding
Summary
| Number of grants | 1 |
|---|---|
| Total funding | $6,500 |
Click on a grant title below to expand the full details for that specific grant.
20231 grants / $6,500
The Mike and Karin Calford Travel Fellowship$6,500
Funding body: Hunter Medical Research Institute
| Funding body | Hunter Medical Research Institute |
|---|---|
| Project Team | Doctor Sean Burnard |
| Scheme | Research Grant |
| Role | Lead |
| Funding Start | 2023 |
| Funding Finish | 2023 |
| GNo | G2300270 |
| Type Of Funding | Scheme excluded from IGS |
| Category | EXCL |
| UON | Y |
Research Supervision
Number of supervisions
Current Supervision
| Commenced | Level of Study | Research Title | Program | Supervisor Type |
|---|---|---|---|---|
| 2023 | PhD | Clinical Implications of Treatment-Induced Epigenetic Heterogeneity in Acute Myeloid Leukaemia | PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle | Co-Supervisor |
Dr Sean Burnard
Position
Post-Doctoral Research Scientist
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
Contact Details
| sean.burnard@newcastle.edu.au |
Office
| Room | L3W |
|---|---|
| Building | Hunter Medical Research Institute |
| Location | Hunter Medical Research Institute (HMRI) , |
Connect with me
