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Research Topic : Gene Profiling
Field of Research : Oncology And Carcinogenesis
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Oncology And Carcinogenesis (43)
Gene Expression (2)
Genetics (2)
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Protein Targeting And Signal Transduction (2)
Cell Development (Incl. Cell Division And Apoptosis) (1)
Gene Therapy (1)
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  • Researchers (8)
  • Funded Activities (43)
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  • Funded Activity

    Defining Steps In The Molecular Pathogenesis Of Lung Cancer Using Immortalized Human Bronchial Epithelial Cells

    Funder
    National Health and Medical Research Council
    Funding Amount
    $374,344.00
    Summary
    Lung cancer remains the leading cause of cancer death worldwide and is caused by abnormalities in DNA. This project aims to further our understanding of this disease by altering known cancer-related genes and studying their effect on lung cancer development. This project also aims to identify novel genes in lung cancer as well as tumour expression profiles which can predict response to chemotherapy agents. In summary, this research will identify new gene targets for therapeutic agents.
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    Funded Activity

    Identification And Characterisation Of Amplified Oncogenes In Liposarcoma

    Funder
    National Health and Medical Research Council
    Funding Amount
    $354,293.00
    Summary
    Liposarcoma is the commonest single subtype of sarcomas, a group of cancers that disproportionately affects the young. The overall mortality for liposarcomas is approximately 50%. Chemotherapy may temporarily controlling disease in under a third of patients, but is toxic and cannot achieve cure. We have identified new potential therapeutic targets, and aim to develop these in the clinic.
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    Funded Activity

    Novel Strategies In Cancer Cell Invasion In High-density 3D Matrix

    Funder
    National Health and Medical Research Council
    Funding Amount
    $60,768.00
    Summary
    The use of high-density (HD) matrix to study cell invasion sets precedence in mimicking the HD breast tissue condition that pose a real cancer risk. Cell invasion promotes the spread of cancer causing organ failures and death. The aims of this project are to determine the molecular mechanisms and to isolate new regulatory markers of cell invasion into HD matrix. Putative markers will be confirmed by investigating their expression levels in tissue arrays of 195 breast cancer samples.
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    Funded Activity

    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.
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    Funded Activity

    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).
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    Funded Activity

    Stromal Contribution To Breast Cancer Metastasis

    Funder
    National Health and Medical Research Council
    Funding Amount
    $69,784.00
    Summary
    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
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    Funded Activity

    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.
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    Funded Activity

    Uncoupled Research Fellowship

    Funder
    National Health and Medical Research Council
    Funding Amount
    $702,604.00
    Summary
    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
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    Funded Activity

    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.
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    Funded Activity

    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.
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