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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.
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.
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.
Deciphering Mechanisms Of Disease Evolution In Melanoma
Funder
National Health and Medical Research Council
Funding Amount
$845,093.00
Summary
In many patients, cancers are ever-changing, even after they have formed. This explains why many cancers can spread beyond the point of cure by surgery and why they can become resistant to treatments. This project will use patient melanomas and laboratory modelling to understand how melanomas change as they grow and spread. The results will be used to identify the nature of evolutionary changes in cancer in order to predict and even exploit them in treatment.
Novel Role Of Innate Immune DNA Sensors In Promoting Gastric Cancer
Funder
National Health and Medical Research Council
Funding Amount
$774,025.00
Summary
Stomach cancer is the third most lethal cancer worldwide, and is strongly associated with inflammation (gastritis) caused by Helicobacter pylori bacterial infection. However it remains unknown how Helicobacter triggers gastritis and stomach cancer in people. Using a mouse model for gastritis-associated stomach cancer, our aim is to demonstrate the role of immune system proteins in the stomach which detect bacterial and host DNA to drive chronic inflammatory responses that lead to stomach cancer.
Mechanisms Of Hedgehog Signaling In Small Cell Lung Cancer
Funder
National Health and Medical Research Council
Funding Amount
$439,564.00
Summary
Some types of lung are very sensitive to chemotherapy, however they frequently relapse, at which time they become resistant to this form of treatment. This project investigates how embryonic signaling pathways, that normally function to regulate organ formation in development, are activated and promote tumor regrowth following chemotherapy for lung 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.
Cancer causes significant morbidity and mortality in Australia’s aging population. There is strong evidence that abnormal blood vessels in tumours limit drug access and drive metastases. We have identified a molecule which controls vessel remodelling in tumours. In this proposal we will study mechanisms on how the molecule itself is regulated with the aim to normalize blood vessels for improved therapy.
Bridging The GAPP Between The Laboratory And Clinic To Prevent Gastric Adenocarcinoma And Proximal Polyposis Of The Stomach (GAPPS).
Funder
National Health and Medical Research Council
Funding Amount
$724,877.00
Summary
Gastric Adenocarcinoma and Proximal Polyposis of the Stomach (GAPPS) is an inherited form of gastric cancer. Affected patients develop a large number of gastric polyps and are at risk of gastric cancer in their 30s. The only effective treatment is to surgically remove the stomach. Gastrectomy is, however, associated with significant post-operative complications. We will use laboratory and mouse models of GAPPS to identify acceptable new approaches to prevent cancer in these patients.