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High Resolution Genome-wide Genomic Analysis Of DCIS To Identify Genes Involved In Disease Initiation And Progression
Funder
National Health and Medical Research Council
Funding Amount
$543,370.00
Summary
DCIS is the most common type of noninvasive breast cancer and in some women may progress to malignant disease but little in know about how it develops. We will bring to bear our experience with cutting edge technology and access to extensive clinical resources to the analysis of a large series of pure DCIS with the aim of identifying previously unknown cancer causing genes. This data will lead to the identification of novel breast cancer genes that will assist clinical management.
Identification Of Novel Low Penetrance Genes Associated With Melanoma Risk
Funder
National Health and Medical Research Council
Funding Amount
$399,830.00
Summary
Using pools of DNA samples we will conduct a genome-wide association study for melanoma predisposition genes. The most promising candidate genes will be followed up by sequencing and further geneotyping of additional SNPs in order to identify the causal variants.
Mapping And Identification Of Novel Breast Cancer Susceptibility Genes
Funder
National Health and Medical Research Council
Funding Amount
$354,419.00
Summary
Breast cancer is one of Australia?s major cancer problems, but we still do not fully understand why certain people are at higher risk of the disease than others. In recent years two genes have been shown to be abnormal in a small number of people with strong family history of breast cancer and-or ovarian cancer. This study will search for the identity of other genes of this kind. It will take advantage of a large network of researchers which has been working to recruit women with a strong family ....Breast cancer is one of Australia?s major cancer problems, but we still do not fully understand why certain people are at higher risk of the disease than others. In recent years two genes have been shown to be abnormal in a small number of people with strong family history of breast cancer and-or ovarian cancer. This study will search for the identity of other genes of this kind. It will take advantage of a large network of researchers which has been working to recruit women with a strong family history of breast cancer from around Australia over the last two years. In this short time such large numbers of women have come forward that a study of this kind will be among the largest in the world. The results of this research, in terms of location of possible new genes causing high risk of breast cancer, will be shared with other researchers in Europe and the US who are working toward the same goals. This will ensure that progress is as rapid as possible. Based on experience with the two previously discovered breast cancer genes, this research will also shed light on the types of changes that drive the malignancy of breast cancer cells. It will have implications for improved prevention, diagnosis and treatment of breast cancer.Read moreRead less
Identification Of Breast And Ovarian Tumour Suppressor Genes On Chromosome 22 By Functional Complementation
Funder
National Health and Medical Research Council
Funding Amount
$249,250.00
Summary
Cancer is fundamentally a genetic disease that arises when errors (mutations) accumulate in genes involved in regulating how and when cells grow. An important class of gene involved in this process are the tumour suppressors whose primary function is to inhibit cell growth. It is widely believed that significant improvements in the treatment and diagnosis of cancer will only be achievable once we have a detailed understanding of how these genes work. It is likely that dozens of tumour suppressor ....Cancer is fundamentally a genetic disease that arises when errors (mutations) accumulate in genes involved in regulating how and when cells grow. An important class of gene involved in this process are the tumour suppressors whose primary function is to inhibit cell growth. It is widely believed that significant improvements in the treatment and diagnosis of cancer will only be achievable once we have a detailed understanding of how these genes work. It is likely that dozens of tumour suppressor genes exist in the human genome and of these only a small proportion have been identified. The aim of this study is to identify genes on human chromosome 22 that are involved in the development of breast and ovarian cancer. Genetic evidence from many investigators, including data from our own laboratory, has indicated that multiple tumour suppressor genes are present on human chromosome 22 but as yet none have been positively identified. Part of the difficulty in identifying these genes is that cancer cells often have a lot of genetic damage and it is hard to distinguish the important changes from background genetic noise'. To circumvent this problem we are using a functional cloning approach which identifies tumour suppressor genes by their ability to inhibit the growth of cancers cells grown in culture in the laboratory. Genes that are identified in this way will be evaluated for the presence of genetic mutations in real human cancers which will give us a better idea of their true significance in tumour development. In addition to enhancing our understanding of the process tumour development this project may identify new targets for anti-cancer therapies.Read moreRead less
Primary central nervous system (CNS) tumours, arising in the brain and spinal cord, are the leading cause of cancer-related deaths in children less than 15 years of age. Medulloblastomas and other primitive neuroectodermal tumours (PNETs) are the most common form of primary childhood brain tumours, accounting for 25-30% of cases. Despite notable recent advances in our understanding of the molecular genetic basis of malignancies, the pathogenesis of CNS PNETs remains obscure. To address this prob ....Primary central nervous system (CNS) tumours, arising in the brain and spinal cord, are the leading cause of cancer-related deaths in children less than 15 years of age. Medulloblastomas and other primitive neuroectodermal tumours (PNETs) are the most common form of primary childhood brain tumours, accounting for 25-30% of cases. Despite notable recent advances in our understanding of the molecular genetic basis of malignancies, the pathogenesis of CNS PNETs remains obscure. To address this problem, we propose to apply a novel combinatorial approach for the identification of PNET tumour suppressor genes utilising both representational difference analysis (RDA) and microarray expression profiling. Data from this study will help to elucidate the molecular pathways that are compromised in the initiation and growth of PNETs. This information will have direct implications for the development of improved diagnostic and prognostic indicators necessary for the design of more effective therapeutic strategies for the treatment of PNET patients.Read moreRead less
The Molecular Function And Role Of The New Metastasis Suppressor NDRG1 In Cancer
Funder
National Health and Medical Research Council
Funding Amount
$226,425.00
Summary
With cancer now a leading cause of death in Australia, finding new ways to treat this disease is crucial. Iron is critical for cancer cell growth and metastasis, thus agents that bind iron (called iron chelators) can be used to treat cancer. These drugs up-regulate the gene NDRG1, which has been shown to prevent tumour spread. The role of NDRG1 in tumour growth and spread of cancer cells will be examined as this may lead to novel therapies against cancer (e.g. the use of novel iron chelators).
Breast cancer is a common disease that is generally incurable if detected after it has spread to other organs. There is a lack of understanding of molecular events that drive the process. Cancers contain several types of host cells that contribute to the growth of the tumour, which can be regarded as wounds that never heal. Host cells are co-opted to promote continued growth of the cancer cells. It is the aim of this project to understand how these host cells promote the spread of breast cancer
Function Of FOR Gene Products In Normal And Cancer Cells
Funder
National Health and Medical Research Council
Funding Amount
$521,310.00
Summary
Cancer cells usually exhibit the loss of control of normal cell functions. This involves the increase of proteins which promote growth and cell division and the decrease in proteins which inhibit growth and cell division. Loss of function may also occur in proteins that are normally involved in killing the cell when growth becomes uncontrolled. Many of these proteins interact with one another and in so doing establish pathways and networks of control which must be perturbed and overridden in the ....Cancer cells usually exhibit the loss of control of normal cell functions. This involves the increase of proteins which promote growth and cell division and the decrease in proteins which inhibit growth and cell division. Loss of function may also occur in proteins that are normally involved in killing the cell when growth becomes uncontrolled. Many of these proteins interact with one another and in so doing establish pathways and networks of control which must be perturbed and overridden in the cancer cell. Sometimes this is because the role of the protein is altered in the cancer cell compared to what it normally is in a normal cell. The main aim of this study is to understand the role that is played by a set of proteins that are coded by a single gene. This gene (which we refer to as the FOR gene) spans a region of the human genome which is sensitive to a particular type of mutation. This mutation takes place early in tumour development and therefore we believe that it has important role to play in determining the fate of the cell - helping to cause it to become a tumour cell. We will find out which other proteins in the cell the FOR proteins interact with. Where these proteins are known then this will help determine the pathways in the cell in which the FOR proteins participate. In another approach we will establish animal models (in mice and flies) of mutations in the FOR genes of these species. The transgenic mice will help us find out whether the mutations that we have observed in the FOR gene in various human cancers cause increased sensitivity to mutagens and in so doing aid in transforming normal cells into cancer cells. The transgenic flies will help us identify the metabolic pathways in which the FOR proteins participate. These studies will help understand the roles of the FOR proteins and their significance in cancer.Read moreRead less
I am a molecular biologist and my research is focussed on the importance of epigenetics in early development and disease, especially in cancer. My research to date has resulted in many ground-breaking discoveries relating to DNA methylation patterns, that
Convergence Of Activated C-myb And Wnt Pathways In Colon Cancer
Funder
National Health and Medical Research Council
Funding Amount
$256,320.00
Summary
c-myb is essential for the normal biology of the blood system and the colon. It is involved in regulating the balance between the production of new cells and their timely removal once they have completed their assigned tasks. Another group of factors that make up theWnt pathway also contribute to the normal biology of the colon in man and mouse. Defects that lead to too much c-myb and ineffective control of the Wnt pathway appear to work together to increase the risk and severity of colon cancer ....c-myb is essential for the normal biology of the blood system and the colon. It is involved in regulating the balance between the production of new cells and their timely removal once they have completed their assigned tasks. Another group of factors that make up theWnt pathway also contribute to the normal biology of the colon in man and mouse. Defects that lead to too much c-myb and ineffective control of the Wnt pathway appear to work together to increase the risk and severity of colon cancer. This project is designed to specifically test this observation in animals. In addition it examines in fine detail how c-myb levels increase in colon cancer and how it combines with the Wnt pathway to regulate other genes in colon cancer.Read moreRead less