Molecular and Cell Biology

Mila Grinblat

Postdoctoral Research Fellow
mila.grinblat@jcu.edu.au

Dena Francis

Lecturer, Molecular Genetics
deanne.francis@jcu.edu.au

David Whitmore

Professor, Biomedicine
david.whitmore@jcu.edu.au

Margaret Jordan

Senior Research Fellow
margaret.jordan@jcu.edu.au

Patrick Schaeffer

Associate Professor
patrick.schaeffer@jcu.edu.au

Lionel Hebbard

Associate Professor
lionel.hebbard@jcu.edu.au

Craig McFarlane

Associate Professor
craig.mcfarlane@jcu.edu.au

Alanna Sorenson

Senior Lecturer, Molecular and Cell Biology
alanna.sorenson@jcu.edu.au

Alan Baxter

Adjunct Professor
alan.baxter@jcu.edu.au

Mechanisms determining Marfan syndrome severity (Old ID 27110)

Sacha Jensen

01 Jan 2021 - 31 Dec 2023

Marfan syndrome (MFS), caused by defects in the protein fibrillin-1, has a wide spectrum of severity with symptoms affecting the heart, bones and eyes. The cause of this variation in severity is unclear. Severe, neonatal MFS and Beal's syndrome result from mutations in corresponding parts of the proteins fibrilin-1 and fibrillin-2. Using clues from these diseases, this project will use new cell engineering techniques to determine why some fibrillin mutations are more severe than others. The results are relevant not only to understanding MFS, but also to understanding how the tissues in our bodies are developed and maintained.

Improving Hepatocellular Carcinoma Immunotherapy

Craig McFarlane

31 Jul 2025 - 31 Dec 2026

Hepatocellular carcinoma (HCC) constitutes 80-90% of all liver cancers and is the third leading cause of cancer-related death globally. There are just a few therapeutic options available for HCC patients. The most promising is immunotherapy, which uses the antibodies atezolizumab, an immune check point inhibitor, and bevacizumab an angiogenic inhibitor, that direct the immune system to kill HCC tumour cells. However, immunotherapy is effective in just 30% of HCC patients and can in some instances promote tumour progression and have adverse effects. The major reason for this is that the HCC immune environment is immunosuppressed in 70% of patients, and the molecular events leading to this are poorly understood. This project will use murine HCC models and atezolizumab and bevacizumab therapeutic equivalents, single cell sequencing and advanced cell biology to decipher how HCC escapes immunotherapy, and hence determine new therapeutic targets to treat immunosuppressed HCC.