Identifying And Characterizing Genes That Regulate Breast Tumorigenesis And Metastasis
Funder
National Health and Medical Research Council
Summary
I am a breast cancer biologist. My research focuses on identifying the changes in normal cells that allow cancer to form, and identifying the changes in cancer cells that allows them to spread. To accomplish this, I have developed new methods using mouse models of breast cancer. My goal is to use these methods to further our understanding of the causes of breast cancer development and progression.
Regulation Of Innate Immunity And Tumour Progression By Activating Transcription Factor 3
Funder
National Health and Medical Research Council
Funding Amount
$473,469.00
Summary
Toll-like receptors (TLRs) play an essential role in innate immune responses and are involved in initiating tumourigenesis via inflammatory pathways. We have shown that the transcription factor ATF3 is a negative regulator of TLR signalling. We will study how modulation of the activity of ATF3 affects the inflammatory response and tumour progression. This will provide a molecular basis on which to design therapeutic reagents for the treatment of cancer.
Role Of MACROD2 Loss In DNA Repair, Chromosomal Instability And Development Of Colorectal Cancer: Clinical And Therapeutic Implications
Funder
National Health and Medical Research Council
Funding Amount
$772,871.00
Summary
The MACROD2 gene is deleted in one-third of human bowel cancers. We have discovered that MACROD2 deletion causes defective DNA repair and tumour chromosomal instability. Here, we will use novel laboratory models to show that MACROD2 loss actively promotes bowel cancer development. We will test the clinical implication of MACROD2 loss for predicting tumour therapy response and will investigate the potential of exploiting this deficiency for drug targeting.
Identification Of Novel ERBB2 Co-operating Tumor Suppressors Using In Vivo RNAi Screens.
Funder
National Health and Medical Research Council
Summary
Invasive breast cancer is often lethal, however, noninvasive disease has a >98% survival rate. Thus, understanding how breast cancer develops invasive ability is an important research goal. Using a new method in mice predisposed to breast cancer, we will find genes that prevent tumor invasion and determine if they are important in human cancer. By understanding how these genes restrict tumor invasion, we hope to develop therapies to improve breast cancer treatment.
Studies On The Tumour-associated PIK3CA(H1047R) Mutation Using In Vitro And In Vivo Models Of Breast And Ovarian Cancer
Funder
National Health and Medical Research Council
Funding Amount
$583,312.00
Summary
PIK3CA mutations are frequently found in breast and ovarian cancers but how they cause cancer is not clear. We will exploit a unique mouse model to investigate the functional effects of PIK3CA mutations in cells and their role in cancer development. Understanding the mechanisms by which PIK3CA mutations regulate cell function and drive tumour growth will allow the rationale design of novel anti-cancer agents that specifically target this important cancer pathway.
Tumour Induced Innate Immune Responses That Control Breast Cancer Metastases
Funder
National Health and Medical Research Council
Funding Amount
$596,164.00
Summary
The mechanisms of breast cancer spread to bone are largely unknown. We have found that cross-talk between tumour cells and the immune system exists to induce anti-tumour immune responses. By decreasing the release of proteins known to activate immune responses (type I interferons), tumour cells can hide from such responses and spread to tissues such as bone. We aim to identify the immune responses activated by type I IFN and if restoration of these pathways can block breast cancer spread to bone ....The mechanisms of breast cancer spread to bone are largely unknown. We have found that cross-talk between tumour cells and the immune system exists to induce anti-tumour immune responses. By decreasing the release of proteins known to activate immune responses (type I interferons), tumour cells can hide from such responses and spread to tissues such as bone. We aim to identify the immune responses activated by type I IFN and if restoration of these pathways can block breast cancer spread to bone.Read moreRead less
Defining The Role Of Microphthalmia-associated Transcription Factor (MITF) In Melanoma Heterogeneity By Real-time Cell Cycle Imaging
Funder
National Health and Medical Research Council
Funding Amount
$613,705.00
Summary
Metastatic melanoma is highly therapy-resistant. Modern targeted therapy is promising but suffers from rapid onset of drug resistance. Tumours consist of zones of fast growing cells next to zones of dormant cells. This tumour heterogeneity is one of the reasons for cancer drug resistance, as cells in different growth states respond differently to drugs. By understanding the causes of tumour heterogeneity we will set the basis for innovative clinical approaches against this devastating disease.
Molecular Pathways Mediating The Anti-tumour Activity Of WIF1
Funder
National Health and Medical Research Council
Funding Amount
$462,342.00
Summary
Osteosarcoma is the most common bone cancer. Treatment often entails aggressive surgery with intensive chemotherapy, although one third of those diagnosed will still die from this disease. We have found that the molecule WIF1 can suppress osteosarcoma growth. In this project we aim to identify genetic modifiers of WIF1, potential WIF1 interactors and define active domains of WIF1 for the development of more effective targeted therapeutics for osteosarcoma.
Aberrant Transcriptional Signalling In The Progression And Metastasis Of Melanoma.
Funder
National Health and Medical Research Council
Funding Amount
$353,033.00
Summary
There are currently no treatments that have any impact on decreasing mortality from metastatic melanoma. We have found 2 new variants in melanoma that may control the tumour growing and invading around the body. This study will examine the protein containing these changes with the aims of finding how they function differently, to identify their roles in the formation of melanoma, as well as to identify new targets for prevention and treatment of metastatic disease.