Genome-Wide Discovery of Somatic Coding and Non-Coding Mutations in Pediatric Endemic and Sporadic Burkitt Lymphoma
This week we profile a recent publication in Blood from Bruno Grande (left) in
the laboratory of Dr. Ryan Morin (third from left) at Simon Fraser University.
Can you provide a brief overview of your lab’s current research focus?
The Morin research group leverages sequencing technologies for the identification of somatic driver mutations and the characterization of gene expression patterns in aggressive lymphomas with the goal of determining new therapeutical targets and biomarkers of treatment resistance.
What is the significance of the findings in this publication?
In addition to being the largest genomic study of paediatric Burkitt lymphoma (BL) to date, our paper sheds light on the poorly understood relationship between BL and the Epstein–Barr virus (EBV). Notably, EBV appears to induce AICDA expression, which encodes a mutator enzyme that is thought to be responsible for chromosomal rearrangements such as the oncogenic MYC translocation present in virtually all BL tumours. We also found that EBV-positive tumours lacked mutations in genes with roles in apoptosis, suggesting that this important tumour-suppressor pathway is being disrupted by EBV. In short, our data support a paradigm shift towards putting more emphasis on tumour EBV status for disease pathogenesis and associated implications for treatment.
What are the next steps for this research?
We have found compelling evidence for possible roles of EBV in BL tumour formation, but we need to confirm these using functional experiments and elucidate the mechanisms. This may in turn yield candidate targets for therapy. There is also a need to similarly investigate adult BL tumours given the limited success of current regimens in treating older patients.
This research was funded by:
This project has been primarily funded by the Foundation for Burkitt Lymphoma Research and the National Cancer Institute.