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Polycomb Group Genes In Murine Lymphomagenesisand Their Impact On Drug Response.
Funder
National Health and Medical Research Council
Funding Amount
$476,815.00
Summary
The success of lymphoma treatment with current drugs is limited by drug resistance. Some crucial links between genes which cause cancer and genes which alter response to cancer treatment have been identified: the cellular machinery that cancer cells use to become cancer cells in the first place, is often the same machinery that cancer cells later use to become resistant to cancer treatments. The Polycomb Group family controls expression of other critical genes: that is, they dictate which genes ....The success of lymphoma treatment with current drugs is limited by drug resistance. Some crucial links between genes which cause cancer and genes which alter response to cancer treatment have been identified: the cellular machinery that cancer cells use to become cancer cells in the first place, is often the same machinery that cancer cells later use to become resistant to cancer treatments. The Polycomb Group family controls expression of other critical genes: that is, they dictate which genes are switched on, where, and when. This determines whether a cell behaves normally or whether it may turn into a cancer cell. When Polycomb Group genes themselves are expressed at the wrong time or place, they can cause cancer. In human lymphoma, these genes have been associated with more aggressive lymphoma. This has also been shown for other cancers such as breast and prostate cancer. In some cases these genes are associated with cancers that do worse following anti-cancer treatment. So far, no research has been published looking the direct impact of the Polycomb Group genes on the success of treatment in a controlled laboratory model. We have used a powerful laboratory mouse model of lymphoma, established in the host laboratory, in which over-expression of the c-myc oncogene in developing B cells causes lymphoma. This model is easy to manipulate and this provides us with a great deal of experimental control, much more than can be achieved from working with patient samples. Two family members, Bmi-1 and Cbx7, cause lymphoma to develop aggressively and we will ask whether two other members, Ezh2 and Rybp do this as well. We will determine whether these 4 genes cause drug resistance in lymphoma, with currently used chemotherapy and also with novel anti-cancer drugs. By increasing our understanding of drug resistance in lymphoma, drugs may be utilised more effectively and new markers identified to predict which drug will be successful in treating a particular lymphoma.Read moreRead less
Bcl-2 Proteins And The Regulation Of The Megakaryocyte Lineage.
Funder
National Health and Medical Research Council
Funding Amount
$416,240.00
Summary
Platelets are tiny cells that circulate in the blood. They are essential for blood clotting. Too few platelets leads to uncontrolled bleeding. Platelets are produced in the bone marrow by cells called 'megakaryocytes'. Cancer chemotherapy often causes dangerous decreases in platelet count - this is thought to be because it kills megakaryocytes. We will pinpoint the molecules responsible for megakaryocyte life and death. This has the potential to make the side effects of chemotherapy less severe.
Functions Of ASCIZ In The Repair Of Accidental And Programmed DNA Base Damage
Funder
National Health and Medical Research Council
Funding Amount
$613,060.00
Summary
Every cell in the body encounters approximately 10,000 DNA base lesions per day. If not accurately repaired, this DNA damage may give rise to cancer. We have discovered a new protein called ASCIZ that is involved in the cellular response to base damage. We believe that ASCIZ functions by promoting the most efficient way to repair damaged DNA bases. We will investigate this hypothesis using cells that lack the ASCIZ gene, and also test if defective ASCIZ leads to increased cancer.
Mechanisms Of Uptake Of 18F-FDG In An In Vivo Model Of C-kit Induced Neoplasia
Funder
National Health and Medical Research Council
Funding Amount
$438,520.00
Summary
Recent advances in the field of tumour biology have created strong interest in development of molecularly targeted anti-tumour drugs. These targeted drugs are expected to yield higher therapeutic indices with fewer side effects than conventional cytotoxic treatments. However, due to the complicated nature of cellular processes affected by a given treatment, and the high cost of bringing new drugs to the clinic, it is important to define both mechanisms of action and in vivo functional effects of ....Recent advances in the field of tumour biology have created strong interest in development of molecularly targeted anti-tumour drugs. These targeted drugs are expected to yield higher therapeutic indices with fewer side effects than conventional cytotoxic treatments. However, due to the complicated nature of cellular processes affected by a given treatment, and the high cost of bringing new drugs to the clinic, it is important to define both mechanisms of action and in vivo functional effects of targeted therapies early in the drug development process. Gastrointestinal stromal tumour (GIST) is a prime example of a cancer for which a rationally designed drug has been successfully used. GISTs are often associated with activating mutations in c-kit, a gene encoding a cell surface protein. A new drug, Imatinib, inhibits the activity of mutated c-kit and blocks growth of many GISTs. However, over time many GISTs become resistant to Imatinib creating the need to develop additional treatments. Unfortunately, this has been hampered by lack of both a good model system for testing new drugs and robust diagnostic procedures for defining response to treatment. We have now developed a mouse model of GIST that grows and responds to treatment in a similar manner to human GIST. Furthermore, using imaging technology specifically designed for small animal studies, we can quickly monitor and evaluate changes in response during treatment. We propose to use the model system together with small animal imaging technology to define mechanisms by which GISTs respond or become resistant to Imatinib. This involves defining specific molecules within cells that change activity after Imatinib treatment as well as testing a series of gene mutations that may be involved in drug resistance. The results of the study will help to define new targets for GIST treatment as well as validate the imaging strategy that may have wide application to monitoring targeted anti-cancer therapies.Read moreRead less
Development Of Anti-tropomyosin Drugs For The Treatment Of Melanoma
Funder
National Health and Medical Research Council
Funding Amount
$578,352.00
Summary
Australia has the highest incidence of melanoma worldwide. There is a clear need to develop new strategies as melanoma is unresponsive to current treatment regimes. We have developed a compound, TR100, which targets a specific component of the cytoskeleton of melanoma tumour cells. Disruption of this cytoskeleton leads to decreased tumour cell growth and survival. Understanding the mechanism by which TR100 causes cell death is important if this novel anti-cancer compound is to be used in the cli ....Australia has the highest incidence of melanoma worldwide. There is a clear need to develop new strategies as melanoma is unresponsive to current treatment regimes. We have developed a compound, TR100, which targets a specific component of the cytoskeleton of melanoma tumour cells. Disruption of this cytoskeleton leads to decreased tumour cell growth and survival. Understanding the mechanism by which TR100 causes cell death is important if this novel anti-cancer compound is to be used in the clinic.Read moreRead less
One of the hallmarks of cancer cells is their ability to divide and multiply in an uncontrolled manner. Specific proteins that make up the skeleton of cells (cytoskeleton) play an important part in the cell division process and as such make extremely important targets for anticancer therapy. Our research is developing ways to best target cell division proteins so that we can make drug resistant cancer cells sensitive to chemotherapy.
RNA Polymerase I: A Novel Target In The Treatment Of MYC Driven Malignancies
Funder
National Health and Medical Research Council
Funding Amount
$605,963.00
Summary
Synthesis of ribosomes, the cellular protein synthetic machinery, is dysregulated during cancer leading to the hypothesis that it may be causative in the malignant process. This application will test this hypothesis using novel inhibitors or ribosome biogenesis in a mouse genetic model termed E�-MYC that faithfully that replicates human B-cell lymphoma. These studies will uncover novel mechanisms in malignant transformation and identify new therapeutics in the treatment of human cancer.
Regulated Shuttling Of Beta-catenin And IQGAP1 Between Nucleus And Plasma Membrane In Migrating Cells
Funder
National Health and Medical Research Council
Funding Amount
$511,703.00
Summary
Inherited gene mutations that cause colon cancer kill 4,700 Australians every year. About 1 in 21 Australians develop colorectal cancer by age 75. Activation of the beta-catenin protein is a critical switch in the path to colon cancer. We discovered that beta-catenin, and another protein it interacts with called IQGAP1, move between different cellular compartments. We plan to study this process in more detail, as it relates to how beta-catenin works and to understanding its role in cancer.
Regulation Of Beta-catenin Localisation And Its Role In Tumour Cell Migration
Funder
National Health and Medical Research Council
Funding Amount
$271,758.00
Summary
Colon cancer and melanoma are a major health problem and a cause of many cancer-associated deaths. Germ-line mutations in the genes encoding beta-catenin, APC and Axin increase the risk of activating beta-catenin and initiating the progression of colon cancer. A proportion of melanomas correlate with mutation of the beta-catenin gene. The beta-catenin protein is multi-functional; it can work at the outer cell membrane to help cells adhere to one another in an orderly manner, or it can move into ....Colon cancer and melanoma are a major health problem and a cause of many cancer-associated deaths. Germ-line mutations in the genes encoding beta-catenin, APC and Axin increase the risk of activating beta-catenin and initiating the progression of colon cancer. A proportion of melanomas correlate with mutation of the beta-catenin gene. The beta-catenin protein is multi-functional; it can work at the outer cell membrane to help cells adhere to one another in an orderly manner, or it can move into the nucleus where it is involved in activating genes that trigger cancer progression. We are interested in a novel aspect of beta-catenin localisation, when it is present at flexible parts of the cell membrane which are usually associated with active cell migration. In this study we aim to determine whether a fraction of membrane-bound beta-catenin contributes to cell movement or tumour cell invasion. We also will extend our study of the intracellular movement of beta-catenin, to understand how its movement out of the nucleus is regulated by different modifications of the protein, or by damage caused to DNA. This information will increase our understanding of beta-catenin regulation and function, and if successful may lead to identifying new pathways that could be targeted to alter beta-catenin action in cancer cells.Read moreRead less
Rational Design And Development Of New Anthracenedione Derivatives
Funder
National Health and Medical Research Council
Funding Amount
$471,702.00
Summary
Our laboratory has discovered a way to activate the anti-cancer drug mitoxantrone to make it bind to DNA more effectively. This involves pre-activating it with the simple molecule formaldehyde. This concept has enabled us to design new anticancer drugs that are predicted to be more effective at killing cancer cells. In this study we will synthesise these new compounds then test how effectively they bind to DNA, inhibit growth of tumour cells in culture, and inhibit growth of tumours in mice.