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Individuals with stomach cancer, the second most lethal cancer world-wide, have a poor survival rate which is largely due to our poor understanding of the mechanisms which drive this deadly malignancy. Our aims are to identify how over-activation of a specific molecule of the immune system, called STAT3, in the mitochondria of cells promotes the growth of stomach tumours, and also examine whether blocking the actions of mitochondrial STAT3 can suppress the growth of gastric cancer cells.
Integrin Beta3 As A Therapeutic Target For Breast Cancer Metastasis To Bone
Funder
National Health and Medical Research Council
Funding Amount
$431,675.00
Summary
There are limited effective treatments for advanced breast cancer. The project investigates the role of a protein called integrin beta3 in the spread of breast tumours to bone, the most common site of secondary tumour formation (metastasis) in breast cancer patients. We will determine if the presence of integrin beta3 in breast tumours identifies patients at risk of developing bone metastases and test novel drugs against integrin beta3 in mice.
Engineering MYCN Models Of High-grade Serous Ovarian Cancer (HGSC)
Funder
National Health and Medical Research Council
Funding Amount
$797,478.00
Summary
The most lethal type of ovarian cancer, high-grade serous cancer (HGSC), can be divided into four subtypes based on gene patterns. One subtype involves a set of genes/proteins that, in their specific combination, result in activation of a pathway known as MYCN. As most HGSC start in the fallopian tube, we are using fallopian tube material to make new MYCN HGSC models to observe development in the earliest stages. We hope to generate new tests and treatments for this subtype of ovarian cancer.
Genetic And Genomic Dissection Of Polycomb Repressive Complex 2 (PRC2) In Cancer
Funder
National Health and Medical Research Council
Funding Amount
$576,598.00
Summary
The evolution of normal cells to cancer involves mutations that activate cancer-causing genes and/or prevent the actions of anti-cancer genes. It has become increasingly evident that cancer development also involves changes to epigenetic regulation, or control of gene activity by chemical modification of the gene or its environment rather that changes in DNA sequence. This project aims to explore the tumour suppressor activity of an important epigenetic regulatory complex in lymphoma.
Understanding And Manipulating The Epigenetic Networks That Define Osteosarcoma
Funder
National Health and Medical Research Council
Funding Amount
$80,467.00
Summary
Osteosarcoma is the most common type of bone cancer and the fifth most common form of cancer in children. Although osteosarcoma begins in bones, the cancer often spreads to other parts of the body. Patients have a very poor chance of survival if their cancer has spread. We will use mouse and human models of osteosarcoma to improve our understanding of how the cancer is different from the normal bone forming cells. This information will help us to find new treatments to improve patient outcomes.
Expression profiling of many cancers has revealed a common signature, including upregulation of SPARC and other extracellular matrix proteins (the SPARC cluster), which correlates with poor prognosis. This signature is similar to the wound healing gene expression profile after infection by the parasite, Leishmania. Moreover, genomic regions important for differences in the wound healing response in mice have been defined that may define novel genes important for regulating SPARC cluster gene exp ....Expression profiling of many cancers has revealed a common signature, including upregulation of SPARC and other extracellular matrix proteins (the SPARC cluster), which correlates with poor prognosis. This signature is similar to the wound healing gene expression profile after infection by the parasite, Leishmania. Moreover, genomic regions important for differences in the wound healing response in mice have been defined that may define novel genes important for regulating SPARC cluster gene expression. However, these regions contain 1000s of genes , and thus to define the critical genes other approaches are neccesary. The genetically manipulable animal model, Drosophila (vinegar fly), represents a ideal system to detect SPARC interacting genes that should help define the critical genes that regulate SPARC cluster genes. These regulators that trigger SPARC cluster gene expression are likely to define novel cancer causing genes.Read moreRead less
Exploiting And Defining The Immune Regulatory Activities Of BET Bromodomain Inhibitors
Funder
National Health and Medical Research Council
Funding Amount
$923,222.00
Summary
Immune-based agents such as “checkpoint inhibitors” have the ability to re-awaken our own immune systems and activate previously dormant anti-tumor responses. We have discovered that small molecule inhibitors of gene regulatory proteins called bromodomain proteins act synergistically with checkpoint inhibitors in mouse cancer models. We will define the molecular and biological events underpinning this novel combination approach and assess the effects of the combination across different tumors.
From Functional Genomics To Precision Medicine: Identifying The Cause And Finding Optimal Therapy For Oral Squamous Cell Carcinoma
Funder
National Health and Medical Research Council
Funding Amount
$855,992.00
Summary
There is an alarming increase in mouth cancer in young patients who have never smoked. This is a debilitating and potentially fatal cancer without many treatment options. If the patient survives, the quality of life is usually very poor. Our team of medical, genetic, and mathematics experts are dedicated to finding the cause, and developing new treatments, for young non-smoking patients affected by this devastating cancer.
Understanding The Role Of PI 3-kinase Mutations In Gastrointestinal Tumourigenesis
Funder
National Health and Medical Research Council
Funding Amount
$283,880.00
Summary
Mutations in the PIK3CA gene are frequently found in bowel cancers but it remains unclear exactly how these mutations are involved in cancer development. We will exploit a unique mouse model to explore the role of PIK3CA mutations in the initiation, progression and-or metastasis of gastrointestinal cancers. This work will provide critical new insights into the biology of PIK3CA mutations and lead to the development of better models for the testing of new anti-cancer therapies.