Targeting FLT3 Kinase Activity To Treat Haematopoietic Neoplasms
Funder
National Health and Medical Research Council
Funding Amount
$673,045.00
Summary
Most leukaemias are incurable so it is important to find new treatments. For this to occur it is essential that the mutated genes that cause leukaemia are identified. We have generated a mouse with a mutation in a gene called c-Cbl that promotes the activation a protein called FLT3 that is involved in the development of many types of leukaemias. By treating mutant mice a drug that specifically suppresses the function of FLT3 we intend to identify the most effective treatments for human leukaemia ....Most leukaemias are incurable so it is important to find new treatments. For this to occur it is essential that the mutated genes that cause leukaemia are identified. We have generated a mouse with a mutation in a gene called c-Cbl that promotes the activation a protein called FLT3 that is involved in the development of many types of leukaemias. By treating mutant mice a drug that specifically suppresses the function of FLT3 we intend to identify the most effective treatments for human leukaemias associated with activated forms of FLT3.Read moreRead less
Roles Of Cascades Of Transforming Growth Factor-beta And Matrix Metalloproteinases In The Impact Of Cancer Stem Cells On The Neoplasm Formation Of Oral Squamous Cell Carcinoma.
Funder
National Health and Medical Research Council
Funding Amount
$81,793.00
Summary
Failure of treatment of oral cancer patients is because the specific cancer cells escape from chemo-radiotherapy. These cells feature self-renew and fast growth, which are called cancer stem cells (CSC). We will test our hypothesis “the genes of TGF-?1 and MMP initiate CSCs” using our cell-mouse models to arrest cancer progression, and verify the impact of CSC on cancer formation. This study is critical to know how to arrest CSC and offer an opportunity to develop a targeted anti-cancer therapy.
Activating Transcription Factor 3 And Cancer Progression
Funder
National Health and Medical Research Council
Funding Amount
$767,794.00
Summary
We have shown that the transcription factor ATF3 suppresses bladder cancer spread. Turning off ATF3 is associated with disease progression in bladder and colorectal cancer. We will test whether levels of ATF3 can be used as a prognostic maker for disease progression, investigate the mechanisms underlying the actions of ATF3 in bladder and colorectal cancer and test whether therapeutically activating ATF3 can inhibit cancer progression.