Cancer arises through a combination of common DNA mutations which are associated with very poor survival in certain cancers. However, the cause of these mutations was always believed to be external factors (eg. UV light, toxins), Our exciting preliminary results show internal molecules, called circular RNAs, can drive these mutations and this project will investigate how this occurs and study whether targeting these molecules can reduce the incidence of cancers.
Targeting The Oncoprotein MDMX As A Novel Treatment For Triple Negative Breast Cancer
Funder
National Health and Medical Research Council
Funding Amount
$561,672.00
Summary
Breast cancer (BrCa) is a leading cause of cancer death in women worldwide. BrCas unable to respond to current therapies have the worst outcomes. We propose a novel strategy to treat these cancers, based on our new findings. Our two protein targets are: (1) MDMX, that we found drives BrCa with its partner, (2) mutant p53, which causes cancer spread. We plan to directly target these drivers of aggressive BrCas, using new drugs that individually show great promise in trials in a number of cance
Deciphering The Role Of DNA Methylation In The Regulation Of Alternative Splicing
Funder
National Health and Medical Research Council
Funding Amount
$865,494.00
Summary
When a gene is turned on, the messenger RNA must be correctly processed to generate functional proteins. This ‘splicing’ process is essential for normal cellular activity, and is disrupted in many human diseases. We have discovered that an epigenetic modification, DNA methylation (mC), may control splicing. This project will investigate how mC influences splicing and use new epigenome-editing tools to control it, in order to ultimately understand and treat diseases involving aberrant splicing.
Investigating The Role Of Aberrant Splicing (intron Retention) In Acute Myeloid Leukaemia
Funder
National Health and Medical Research Council
Funding Amount
$1,135,745.00
Summary
In 2013, we made a breakthrough discovery that certain parts of genes, previously considered “Junk DNA”, are actually carrying signals to control the amount of proteins produced in cells. Our preliminary work now suggests these signals controlling protein levels can be faulty in cancers. Here, we wish to determine whether these faulty signals could cause a deadly blood cancer called acute myeloid leukaemia (AML). We aim to decipher previously unknown causes of AML that will spur novel therapies.