个人简介

Dr Kennedy obtained his Master of Medical Science from the Queensland Institute of Medical research and his PhD from the Institute for Molecular Bioscience (IMB, University of Queensland). He has held positions as a postdoctoral fellow at the Institute for Developmental Biology (IBS, Palermo, Italy) and at IMB. Upon winning independent funding, he set up a laboratory at Griffith University where he is currently holding positions as a senior lecturer and a chief investigator.

研究领域

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investigating human disorders associated with inappropriate RNA- metabolism including ribosomal RNA processing, mRNA processing and RNA-editing. discovery and investigation of rasGRPase SH3 domain-binding protein 2 (G3BP2) and its role in the progression of breast cancer from Ductal in situ (DCIS) and Lobular carcinomas to Ductal Infiltrating (IDC) and Lobular infiltrating cancers. exploring early breast cancer biomarkers, diagnostics and therapies. discovery and investigation of Nucleolar RNA-associated protein (Nrap also called Nol6) involved in ribosomal RNA (rRNA) biogenesis.

Our group is interested in discovery of novel therapies for cancers. Our approach is to use compounds and natural products that can change the biology of cancer cells, to do this we use multi-drug resistant cancer cells from human breast, prostate and oral cancers to screen for compounds that can specifically target drug-resistant cells. We also look at the role of RNA metabolism in cancer biology. We are interested in modifying the transcriptome or ribosomal biogenesis of cancer cells with a view to either returning them to a more “normal”, non-disease state or to make them more susceptible to cancer therapeutics. Many genes are inappropriately expressed or repressed in cancer cells and, in some cases, these changes can be attributed to the chromosomal mutations and gross rearrangements that occur during cancer progression. It is important to understand these events. However, their value as cancer therapeutic targets is limited because the events are not strictly conserved between cancers derived from the same tissues. Part of our research focus is to identify genes that are required by the cancer to allow its proliferation and progression. These genes are seen as more valid therapeutic targets because they are potentially common to all cancers with a specific tissue of origin (i.e. breast cancer). As an example, over-expression of HER2 in 25 - 40% of breast cancers has been seen as a significant target because of its expression in a high percentage of cancers. However, it should be pointed out that the over-expression of HER2 is often a down-stream event of gene amplification. One focus of the group is to characterise the functional role of a family of RNA-binding proteins that have been shown to be miss-regulated during cancer progression. G3BP2 appears to be a gene that is turned on early during breast cancer progression (Ductal Cancer In Situ) and not as a result of collateral damage caused by genetic events that occur during latter stages of breast cancer progression (Invasive Ductal Carcinoma).