Using MiR-200 To Find New Therapeutic Targets For Neuroblastoma
Funder
National Health and Medical Research Council
Funding Amount
$563,152.00
Summary
Neuroblastoma is one of the most common cancers in children. We have found that a genetic regulator, called microRNA, can limit the ability of neuroblastoma cells to invade surrounding tissues and metastasise. We aim use the microRNAs to find new therapeutic targets that may work in combination with existing treatments, reducing the short term toxicity and long term deleterious effects of current treatments.
This proposal investigates processes that regulate the cell cytoskeleton to control shape and the dynamics membranes, with a view to developing a generic antiviral therapy. As viruses rely upon the cell cytoskeleton to initiate an infection, we posit that enzymes that control the cytoskeleton can be targeted to block infection.
The primary aim of this grants to determine how HIV spreads through our immune system. The above knowledge will determine key Achille’s Heel moments in the HIV life cycle and thus lead to better therapeutic HIV treatments/prevention.
The migration of cancer cells (metastasis) is responsible for most cancer deaths. Central to this is dynamic organisation of the actin cytoskeleton _ an internal structure that provides cell shape and enables movement. We have identified a family of small molecules (called miR-200) that regulates this actin cytoskeleton through specifically downregulating various genes. We are investigating the nature of these genes and their role in cell motility _ an underlying pre-requisite of metastasis.
The Role Of Chemokines In Establishing HIV Latency
Funder
National Health and Medical Research Council
Funding Amount
$372,049.00
Summary
Although antiviral therapy is effective in controlling HIV, therapy must be continued life-long because the virus cannot be cleared from long lived infected CD4+ T cells that are silently or latently infected. In this proposal we will explore the mechanism of how HIV can enter these resting CD4+ T-cells and establish long lived latent infection. Understanding this process may potentially lead to new strategies to cure HIV infection.