Defining The Role Of Wnt Signaling In Hepatocellular Carcinoma And The Potential Of Wnt-targeted Therapy For HCC
Funder
National Health and Medical Research Council
Funding Amount
$403,210.00
Summary
Of all cancers, liver cancer is the third biggest killer worldwide and there is currently no effective treatment options for this disease. We now know many of the common genetic changes that occur in liver tumour cells but have yet to develop targeted drug treatments. This project is aimed at determining whether reactivating a tumour cell's normal cancer suppressing functions can stop tumour growth and whether we can use this information to develop specific drugs that target liver tumour cells
A Novel Mechanism For Sustained Proliferation Of Cancer Cells
Funder
National Health and Medical Research Council
Funding Amount
$565,881.00
Summary
We have found that some tumours use a previously unknown strategy for evading the normal limits on cellular proliferation. We will analyse the molecular details of this mechanism in order to (i) understand how it works, (ii) devise a diagnostic test, and (iii) lay the foundations for developing treatments that specifically target this type of cancer.
Molecular Regulation Of Replicative Lifespan; Implications In Carcinogenesis And Haematopoiesis
Funder
National Health and Medical Research Council
Funding Amount
$420,872.00
Summary
The lifespan of normal cells in the body is limited by the number of times they can replicate. In contrast, cancer cells can replicate indefinitely – they are immortal. Our proposed investigations will determine how the mechanisms that control cell lifespan become dysfunctional as normal cells evolve into cancer cells. Understanding these mechanisms will enable the development of new anti-cancer drugs that will reverse cell immortality and halt the replication of cancer cells.
Ataxia-Telangiectasia: An Emerging Role For Inflammation In Driving Neurodegeneration And Premature Ageing
Funder
National Health and Medical Research Council
Funding Amount
$437,436.00
Summary
Ataxia-Telangiectasia (A-T) is a devastating genetic disease that arises in early childhood and causes patients to die in their twenties. To date there is no cure, and therapeutics are desperately needed. This project will use state-of-the-art brain organoids derived from stem cells of A-T patients in order to better understand this disease and evaluate novel drugs that target the molecular mechanisms that drive chronic inflammation and brain neurodegeneration in children with A-T.
Vascular Smooth Muscle Cell Senescence And The Effects Of Oestrogen
Funder
National Health and Medical Research Council
Funding Amount
$191,370.00
Summary
The incidence of cardiovascular diseases is much lower in women before menopause, and this is thought to be due to a beneficial effect of oestrogen on the cardiovascular system. However the mechanisms of the hormone’s cardiovascular-protective actions are still not clear. The proposed project will determine whether oestrogen acts by slowing the natural ageing process of cells.
Defining The Genes That Dictate The Cellular Response To Tumour Protein TP53 Activation
Funder
National Health and Medical Research Council
Funding Amount
$784,896.00
Summary
The tumour suppressor TP53 prevents the growth of abnormal cells by activating processes such as cell death and irreversible growth arrest. A cell will undergo only one of these possible responses, but it is not known why some cells die and others only stop growing. We will use innovative methods to define the genes that dictate the cellular response to TP53 activation. This research has implications for cancer, as many therapeutics aim to permanently kill cancer cells by activating TP53.
Fibroblast Senescence As A Driver Of Pulmonary Fibrosis
Funder
National Health and Medical Research Council
Funding Amount
$845,611.00
Summary
Idiopathic pulmonary fibrosis (IPF) has no cure. Currently we think that IPF develops like normal wound healing, but the normal “braking” mechanisms in the myofibroblasts (the cells that produce the connective tissue) don’t work, such that too much connective tissue is produced and oxygen transfer to the blood is stopped. We have identified a protein we think stops, the myofibroblasts from dying. Reducing the activation of this protein should return the myofibroblasts function to normal.