Transcriptional Effectors Of Oncogenic ERK Signaling In Colorectal Cancer
Funder
National Health and Medical Research Council
Funding Amount
$820,776.00
Summary
This project aims to unravel how one of the most frequently deregulated molecular pathways in colorectal cancer controls the expression of genes required for these tumours to grow and spread. We expect this work to uncover novel therapeutic targets to effectively inactivate this pathway and biomarkers to select patients most likely to benefit from existing therapies.
Genetic Programs Orchestrated By AP-1 Transcription Factors In Colorectal Cancer Progression
Funder
National Health and Medical Research Council
Funding Amount
$599,941.00
Summary
Colorectal cancer (CRC) is the third most common cancer worldwide. About half of all patients diagnosed with the disease die as a result of its spread in the body. This project will investigate the role that a specific DNA-binding protein plays in orchestrating gene expression programs required for CRCs to spread. The research will provide new insights into underlying mechanisms of CRC progression as well as identify new therapeutic targets for aggressive forms of the disease.
Mechanistic Basis Of AP-1-regulated Gene Expression During Colorectal Cancer Progression
Funder
National Health and Medical Research Council
Funding Amount
$597,802.00
Summary
The spread of colorectal cancers in the body poses a major clinical problem for which current treatment options are inadequate. This project aims to unravel how a specific DNA-binding protein regulates the expression of genes involved in the spread of these cancers. The research is expected to provide a better mechanistic understanding of how disease progression occurs and to identify novel strategies to treat aggressive tumours.
Targeting Bone Marrow Mediated Angiogenesis And Metastasis In Breast Cancer
Funder
National Health and Medical Research Council
Funding Amount
$463,006.00
Summary
Despite advances in treatment and diagnostics breast cancer (BC) remains one of the leading causes of death in women. Metastases and tumour blood vessel recruitment are linked. Work by Dr Mellick and others has shown that host bone marrow contributes endothelial progenitor cells (EPCs) to tumour vasculature. The chemokines and their receptors, which differentiate EPCs from tumour vessels, will be knocked down in the tumour cells and EPC progenitors with the aim of preventing tumour spread.
Crosstalk between breast cancer cells and the microenvironment to promote metastasis. Breast cancer spread (metastasis) to distant tissues is usually fatal. It is now clear that cross-talk between cancer cells and other normal cells is essential for metastasis and previous studies have discovered two key mechanisms: tumour cell suppression of immune defence pathways to escape immune recognition, and activation of proteases to promote invasion and blood vessel growth. Using unique models and cell ....Crosstalk between breast cancer cells and the microenvironment to promote metastasis. Breast cancer spread (metastasis) to distant tissues is usually fatal. It is now clear that cross-talk between cancer cells and other normal cells is essential for metastasis and previous studies have discovered two key mechanisms: tumour cell suppression of immune defence pathways to escape immune recognition, and activation of proteases to promote invasion and blood vessel growth. Using unique models and cellular imaging, this project aims to investigate the cell specific functions of these pathways and the therapeutic potential of altering their expression and function. This project may lead to the development of novel predictors of metastasis in patients and new targeted therapeutics to prevent breast cancer spread.Read moreRead less