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Improving Treatment Of Non-small Cell Lung Cancer: Suppressing Cell Division Cycle Associated Protein 3 (CDCA3)
Funder
National Health and Medical Research Council
Funding Amount
$194,446.00
Summary
Lung cancer is the leading cause of cancer-related mortality worldwide. This project will establish the worth of suppressing the molecule ‘cell division cycle associated protein 3’ (CDCA3) in lung cancer. To do so, we will adjust the levels of CDCA3 in animal lung cancer models and treat the tumours with chemotherapy and the novel drug CX-4945. We expect that reduced levels of CDCA3 combined with CX-4945 and/or chemotherapy in NSCLC patients will benefit patient outcome.
Tumours secrete factors which are contained in specific structures called exosomes, and are used to prepare other organs of the body for subsequently incoming tumour cells, thereby facilitating the often mortal spread of the cancer. This project will investigate the way exosomes alter organs before tumour cells arrive, the composition of these exosomes in lung cancer patients and if they are novel markers for diseases progression as well as therapeutic intervention.
Towards Precision Medicine For Non-small Cell Lung Cancer
Funder
National Health and Medical Research Council
Funding Amount
$463,652.00
Summary
Better outcomes are needed for lung cancer, a disease that accounts for more cancer-related deaths than any other cancer in Australia or worldwide. My goals are to 1) develop and evaluate in clinical trials targeted therapies and immunotherapies and 2) identify clinically relevant blood and tissue based biomarkers for lung cancer patients. This combination of clinical and translational research will change practice and improve outcomes by delivering precision medicine for lung cancer patients.
Identification Of Cancer Initiating Cells In Small-cell Lung Cancer
Funder
National Health and Medical Research Council
Funding Amount
$364,420.00
Summary
Lung cancer is the leading cause of cancer deaths worldwide. Recently a unique mouse model of small-cell lung cancer (SCLC) has been generated that closely mimics the human disease. We will use this model to identify the cells that give rise to SCLC upon genetic alteration. Results obtained will assist in designing more effective intervention strategies aimed at overcoming initial and acquired resistance of these tumours against cytotoxic and targeted drugs.
Microtubule Cytoskeleton In Tumourigenesis And Metastasis
Funder
National Health and Medical Research Council
Funding Amount
$612,885.00
Summary
Over one million cases of lung cancer are diagnosed each year worldwide, making this the leading cause of cancer death. Advanced non-small cell lung cancer (NSCLC) accounts for more than 80% of lung cancer cases. We have identified a protein called ?III-tubulin that is often highly expressed in aggressive and drug resistant NSCLC, and is involved in tumour formation. We will examine how ?III-tubulin is working and identify ways to target this protein to stop tumour growth.
Genetic And Epigenetic Mechanisms Determining Responses To Therapies In Non-small Cell Lung Cancer
Funder
National Health and Medical Research Council
Funding Amount
$22,677.00
Summary
Lung cancer results in more cancer related deaths than any other cancer. The aim of this study is to identify prognostic and predictive markers for patients with non-small cell lung cancer (NSCLC) treated with chemotherapy, palliative radiotherapy and also novel targeted agents. This will help to better utilise these treatments and hopefully improve outcomes in patients with NSCLC.
There is evidence that elderly cancer patients are often inappropriately treated because of their age. This is usually because of concerns that aged patients can not eliminate drugs as well as the young and, as a result, could end up being overdosed. Some drugs are removed from the body through the urine and adjusting for decreased kidney function (which often decreases with age) means that adequate doses can be calculated. However, many anti-cancer drugs are removed from the body by being broke ....There is evidence that elderly cancer patients are often inappropriately treated because of their age. This is usually because of concerns that aged patients can not eliminate drugs as well as the young and, as a result, could end up being overdosed. Some drugs are removed from the body through the urine and adjusting for decreased kidney function (which often decreases with age) means that adequate doses can be calculated. However, many anti-cancer drugs are removed from the body by being broken down (or metabolised) in the liver. The rate of this process is very difficult to estimate. Although many studies have shown that liver drug metabolism is decreased with age, it is unclear whether this is due strictly to age itself or some of the conditions which accompany ageing. We aim to study the removal of anti-cancer drugs in patients treated for cancer to see what the effects of ageing are. We will estimate the extent of liver breakdown and examine whether it is a function of age or rather of several factors which are often associated with age such as inflammation, reduced nutritional status and other medical conditions. The optimal outcome of the study will be methods for correctly adjusting the dose of anticancer drugs for maximal benefit to the elderly patient.Read moreRead less
In the past few years, an expanding number of small RNAs (ribonucleic acids) have been discovered that play a critical part in regulating multiple steps involved in the development of human tumors. One of the genes critically implicated in the development several human cancers (including breast, lung, brain, prostate and colon) is the epidermal growth factor receptor (EGFR). As a consequence, the EGFR is a key target for new biological therapies designed to reduce signaling through the EGFR path ....In the past few years, an expanding number of small RNAs (ribonucleic acids) have been discovered that play a critical part in regulating multiple steps involved in the development of human tumors. One of the genes critically implicated in the development several human cancers (including breast, lung, brain, prostate and colon) is the epidermal growth factor receptor (EGFR). As a consequence, the EGFR is a key target for new biological therapies designed to reduce signaling through the EGFR pathway resulting in reduced growth. Using a computer-based algorithm, we have recently discovered that one of these small RNAs (or microRNAs) is a master regulator of EGFR levels in human breast and lung cancer. When we add the specific microRNA to cancer cells with excess EGFRs and low levels of microRNA, we can abolish EGFR expression almost completely, associated with cell death. From our studies, it appears that the level of this microRNA in tissues relates inversely to the level of EGFR. As the major site of expression of this microRNA is in the brain, we were intrigued to demonstrate that the normally high level of the microRNA is lost in brain cancers (or gliomas) which are associated with high levels of EGFR. Thus, the loss of microRNA may enable the tumor to develop, suggesting that the microRNA may act as a tumor-suppressor . In this project, we will investigate the functional role of this microRNA in a range of human tumors, determine if it can work synergistically with other new biological therapies targeting the EGFR signaling pathway, identify some of its binding partners and determine the levels of EGFR and the microRNA prospectively in a cohort of gliomas. These studies will determine the functional role of the microRNA and form the foundation for further studies to consider strategies to deliver the microRNA for therapeutics.Read moreRead less
Role Of The LIM-only Protein LMO4 In Lung Development And Lung Cancer
Funder
National Health and Medical Research Council
Funding Amount
$490,395.00
Summary
Lung cancer is the leading cause of death in cancer patients in Australia. Although treatments have improved in the past 10 years, new therapeutic strategies are eagerly awaited. Deregulation of molecules driving development of normal tissue is often observed in cancer. Our aim is to identify key regulators of lung development and lung repair after injury. We aim to evaluate the role of these molecules in the initiation and progression of lung cancer to identify new targets for therapies.