The Role Of Somatic Mutations In CCCTC-binding Factor (CTCF) Binding Sites In Cancer
Funder
National Health and Medical Research Council
Funding Amount
$371,114.00
Summary
The three dimensional organisation of genomic DNA has been recognised to play a crucial role in maintaining the stability and function of human cells. In cancer this organisation is often perturbed as a result of mutations to proteins that govern this process. This project will examine how mutations in the DNA may potentially alter the three dimensional organisation of cancer genomes and will identify links between these mutations with cancer development and patient prognosis.
Novel Inhibition Of Cancer Cell Growth In Gastrointestinal Cancer
Funder
National Health and Medical Research Council
Funding Amount
$47,474.00
Summary
This research project will focus on new treatment targets for gastrointestinal malignancies, focusing on the mTOR pathway which is important in driving cancer cell growth. The mTOR inhibitor drug Everolimus will be used in colon and biliary tract cancers to look for novel biomarkers of response and resistance to treatment, using cancer cell lines and correlative analysis with data obtained from patients' tumour samples and clinical assessment in current trials.
Restoration Of P53 Activity In Tumours: A New Approach Involving The P53 Coactivator ANKRD11.
Funder
National Health and Medical Research Council
Funding Amount
$465,990.00
Summary
p53 is an important protein that functions as the body�s defence mechanism against cancer. Mutation of p53 is observed in over half of all tumours. Not only do these cancer mutations abolish the ability of p53 to protect against cancer, but it also endows the tumours with an ability to spread throughout the body, or metastasize. In this research project, we will identify and develop targets that will not only prevent the spread of new tumours, but it will also re-activate the anti-cancer functio ....p53 is an important protein that functions as the body�s defence mechanism against cancer. Mutation of p53 is observed in over half of all tumours. Not only do these cancer mutations abolish the ability of p53 to protect against cancer, but it also endows the tumours with an ability to spread throughout the body, or metastasize. In this research project, we will identify and develop targets that will not only prevent the spread of new tumours, but it will also re-activate the anti-cancer function in mutant p53 leading to tumour regression.Read moreRead less
In melanoma we hypothesise there is a series of as yet unidentified gene fusions which provide oncogenic stimulatory signals that promote tumour growth and that these novel fusion products are excellent targets for the design of new therapies to treat melanoma. The aims of this study are to identify oncogenic fusions in melanoma, to assess which of these are recurrent, and to demonstrate that the resulting fusion proteins provide a selective growth and-or survival advantage to the tumour cell.
Identifying The Mechanism Of The G2 Phase UV Checkpoint And Repair Response Commonly Defective In Melanoma
Funder
National Health and Medical Research Council
Funding Amount
$569,656.00
Summary
The UV component of sunlight is the major environmental factor driving the development of melanoma. UV radiation can directly mutate genes resulting in their inability to perform normal functions which may contribute to cancer. Despite the high number of mutations directly attributable to UV radiation, the mechanisms known to repair these mutations are generally normal in melanoma. This research will investigate a repair mechanism we have identified that is commonly defective in melanomas.