Dr Sionne Lucas is a Postdoctoral Research fellow at the Menzies Institute for Medical Research at the University of Tasmania.
Sionne recently won the PACT Grant in Aid award for her work Establishing the Pulmonary Fibrosis Variation Curation Database. We recently spent some time getting to know Sionne a little better…
Tell us a bit about yourself and how you got interested in pulmonary fibrosis research.
I have always been fascinated by genetics in disease and its potential to lead to quicker diagnoses, providing answers to patients and their families, as well as lead to better management of patients and the development of new targeted treatments. My journey in pulmonary fibrosis research began as I was finishing my PhD (which focused on an eye disease) and seriously thinking about what to do next, when Prof Jo Dickinson approached me about the Genetic Research in Pulmonary Fibrosis (GRIPF) study that she was starting at the Menzies. The study recruits families with multiple case of pulmonary fibrosis, who are therefore likely to have a genetic cause for their disease and tries to identify the specific genetic cause in each family. I did a bit of reading about pulmonary fibrosis genetics and quite quickly decided it was an incredible opportunity to do the sort of research I love and be involved in a study from the very beginning. I applied and got the job, and I guess the rest is history!
How would you explain your pulmonary fibrosis research to someone unfamiliar with the field?
Pulmonary fibrosis is a condition where the lungs become scarred and stiff, making it difficult to breathe. The disease is often progressive, and many patients die within 3-5 years of diagnosis. My research focuses on identifying genetic changes that cause pulmonary fibrosis. This knowledge can help provide patients with a clear cause of their disease and for clinicians to provide targeted clinical care for that patient. Having a clear answer also allow us to more accurately predict if family members are also likely to develop pulmonary fibrosis in the future and for those that are found to be at risk, they can have regular screening to try and diagnose pulmonary fibrosis early so that they too can access the best care. Finally, by improving our knowledge of the cause of pulmonary fibrosis, this can help us develop better diagnostic tools and treatments, hopefully leading to improving the lives of those affected by this disease.
Why is this work important?
Identifying the genetic cause of pulmonary fibrosis can lead to earlier and more accurate diagnoses, personalised treatment plans, and better outcomes for patients. Additionally, understanding the underlying genetics of pulmonary fibrosis is a powerful way to understand the disease process which will help us develop more targeted treatments with fewer side effects in the future. Finally, understanding the genetics of pulmonary fibrosis can provide valuable insights into other related disease, hopefully improving more patient’s lives.
What are the best bits about working in this area?
The best part of working in this area is the potential to make a real difference in people’s lives. It’s incredibly rewarding to know that our research can provide answers to patients and their families, and potentially lead to new treatments. Additionally, the collaborative nature of this field means I get to work with brilliant scientists and clinicians from across Australia and around the world.
What are some of your biggest achievements to date?
One of my biggest achievements to date was actually winning a small seed funding grant from my institute, the Menzies Pilot Pitch Program. The project I proposed was to establish telomere length measurement methods using long-read sequencing, which could significantly improve the accuracy and accessibility of current telomere length testing methods. Telomeres are a repetitive genetic sequence that protects the ends of our chromosomes and effectively acts like the aglet or capping at the end a shoelace to stop it from unravelling. We know that at least a third of people with pulmonary fibrosis have short telomeres and the length of a person’s telomeres can help predict their prognosis and treatment response in pulmonary fibrosis, as well as predict their risk of developing other related health conditions. To be successful in this grant I had to “pitch” my idea to a broad audience in just 5 minutes. It was nerve-racking, but ultimately really fun and I was so pleased to get the funding. This work is still in progress, but I’m so excited to see the final results!
What would you like to work on in the future, if funding were not an issue?
This is an interesting question. There’s so much to do. I’d love to see the GRIPF project expanded in every way. I’d love to see a bigger team – more staff and students working in our lab on our induced pluripotent stem cell models that help us determine how genetic changes impact the cells in the lung as well as more brilliant bioinformaticians working on our sequencing data to find more pulmonary fibrosis-causing genetic changes.
What advice would you offer ECRs just starting out in the field?
My advice is to stay curious and persistent. Research can be challenging, but it’s important to keep pushing forward and seeking out new opportunities. Celebrate your successes, even the small ones. Building a strong network of mentors and collaborators is also crucial – don’t be afraid to ask for help and learn from others in the field. Most importantly, don’t lose sight of why you started doing research in the first place – remind yourself often, especially in the harder moments.
Where do you hope to see yourself in your career in the next 5 years? Are there any shifts you would like to see in in field during that time?
I would like to still be doing exciting research and making a difference. In 5 years, I would be considered a mid-career researcher, and would have established myself as a research leader, with a team of bright researchers and students working on important and interesting problems.
I think the biggest shift that I would like to see if that everyone with a family history of pulmonary fibrosis, who wants to know the genetic cause of their disease, to be able to be given a clear answer. This is not likely to happen in just 5 years but would be the ultimate goal. I would also like to see that knowledge translated into new and better treatments that could help even those without a genetic cause of pulmonary fibrosis. Ultimately, I would like to see patients living longer and healthier lives.