Structural Biology of Inflammation and Cancer
Wong group
Auto-inflammatory disorders, cancers, and telomere biology disorders are a group of diseases caused by inherited mutations that result in mis-regulated inflammation and cell proliferation. The Structural Biology of Inflammation and Cancer group investigates how these mutations contribute to disease progression with the aim of developing new therapeutics.
Research group
Overview
The Structural Biology of Inflammation and Cancer Research Group investigates the molecular mechanisms underlying autoinflammatory disorders, cancer and telomere-associated diseases, which collectively affect millions of people in Australia and worldwide.
Our research focuses on how inherited and somatic mutations disrupt inflammatory signalling, genome stability and cell proliferation to drive disease initiation and progression. We use structural biology, biochemistry and biophysical approaches to define the organisation, regulation and function of protein complexes involved in innate immunity, cancer and cellular ageing.
NLRP1 Inflammasome Dysregulation in Autoinflammatory and Skin Disease
The research group investigates NOD-like receptor (NLR) inflammasomes, innate immune sensors that detect infection, cellular stress and environmental damage and initiate inflammatory signalling.
Our research examines how these sensors function, how disease-associated mutations cause inappropriate inflammasome activation, and how potential drug candidates suppress their activity. We are particularly interested in NLRP1, whose dysregulation is linked to autoinflammatory skin disorders characterised by chronic inflammation, abnormal skin development and, in some cases, increased susceptibility to skin tumours.
By defining the molecular and structural mechanisms that regulate inflammasome activity, we aim to support the development of new treatments for inflammatory and skin diseases.
Telomere Dysfunction and Familial Melanoma Development
The research group investigates how inherited mutations that disrupt telomere integrity contribute to the development of genetically defined forms of familial melanoma.
Telomeres are protective structures located at the ends of chromosomes. Inherited mutations can alter the structure and function of shelterin, a protein complex that protects telomeric DNA. This disruption can lead to abnormal telomere elongation, genome instability and uncontrolled cell proliferation, creating conditions that promote melanoma initiation and progression.
By defining the molecular mechanisms that link telomere dysfunction to melanoma development, our research aims to identify biomarkers for early diagnosis and reveal new opportunities for targeted prevention and therapeutic intervention in individuals with inherited melanoma susceptibility.
Research Focus
- Defining the roles of NLR inflammasomes in inflammatory signalling and autoinflammatory disease
- Identifying drug candidates that inhibit NLR inflammasome activity
- Determining how the shelterin complex protects telomeric DNA at the ends of chromosomes
- Understanding how mutations in the telomere-protective shelterin complex contribute to familial melanoma
Diseases we research
Areas of focus
- Understanding the role of NLR inflammasomes in inflammatory signalling and auto-immune diseases
- Identifying drug candidates that inhibit NLR inflammasome activity
- Understanding how the shelterin complex protects the telomeric-DNA at the ends of chromosomes.
- Evaluating how disruptions to the DNA-protecting shelterin complex could lead to genomic instability and disease such as cancer and pre-mature aging
Research Group Head | Dr Wilson Wong
Auto-inflammatory disorders, cancers and telomere biology disorders are caused by inherited mutations and affect millions of Australians and nationalities worldwide. I investigate how mis-regulated inflammation and cell proliferation drives these disorders with the aim of developing treatments for patients.
Student opportunities
Collaborators
Publication highlights