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The Oncogenic Function Of A Histone H3K9 Demethylase And Its Contribution To The Aggressive Malignant Phenotype Of Leukaemia
Funder
National Health and Medical Research Council
Funding Amount
$762,501.00
Summary
In contrast to the significant improvements in the treatment of acute lymphocytic leukaemia, advances in acute myeloid leukaemia (AML) therapy have been limited. The difficulty in treating AML is thought to arise from a drug-resistant subpopulation of leukaemic stem cells (LSC) that are capable of reinitiating disease after chemotherapy. This project will characterise a key regulator of LSC and provide insights into an important oncogenic process that gives rise to the aggressive and often fatal ....In contrast to the significant improvements in the treatment of acute lymphocytic leukaemia, advances in acute myeloid leukaemia (AML) therapy have been limited. The difficulty in treating AML is thought to arise from a drug-resistant subpopulation of leukaemic stem cells (LSC) that are capable of reinitiating disease after chemotherapy. This project will characterise a key regulator of LSC and provide insights into an important oncogenic process that gives rise to the aggressive and often fatal AML.Read moreRead less
Chronic Lymphocytic Leukemia (CLL) is a very common blood cancer. Leukaemic tumour cells actively shut down key immune defences in patients who are very prone to severe infections. Current chemotherapies further immuno-compromise CLL patients and over a quarter will die from an infection despite having responded to cancer treatments. We propose that restoring key immune functions in CLL is key to improve resistance to infection and restore natural anti-cancer immunity.
‘Transcriptional Tumour Suppression’ By Pax5 And Ikaros In B Progenitor Acute Lymphoblastic Leukaemia
Funder
National Health and Medical Research Council
Funding Amount
$558,927.00
Summary
B-progenitor acute lymphoblastic leukaemia (B-ALL) is the most common cancer in children. The genes Pax5 and Ikaros are frequently mutated in B-ALL, but how this contributes to leukaemia development and treatment resistance remains unclear. We have recently produced new B-ALL models driven by reversible suppression of Pax5 or Ikaros activity, and propose to use these models to uncover how these genes control leukaemia differentiation and regression.
Bone Marrow Macrophages: “Resident Evil” In The Establishment And Progression Of Multiple Myeloma
Funder
National Health and Medical Research Council
Funding Amount
$570,585.00
Summary
Multiple myeloma (MM) is a cancer that develops within the bone marrow (BM). To date, which cells of the BM stroma are required for the support of MM growth remains unknown. Our preliminary data suggest BM resident macrophages, expressing CD169 and CX3CR1, are essential for MM growth. Using innovative and elegant animal models of MM, we will define the role of these macrophages in MM growth and determine if macrophage-targeted therapies can delay MM growth in the relapsed disease setting.
Mechanism Of Leukaemia Suppression By The Transcription Factor Ikaros
Funder
National Health and Medical Research Council
Funding Amount
$655,630.00
Summary
A subset of acute lymphoblastic leukaemias are characterised by mutations in the Ikaros gene. These leukaemias respond poorly to chemotherapy and require novel therapeutic approaches. We have discovered a new function of Ikaros in regulating leukaemia cell death. This project investigates how Ikaros regulates cell death and whether this is a general mechanism. Understanding Ikaros function is a step toward improved treatments for this aggressive type of leukaemia.
Studying The Novel Role For G Protein-coupled Receptor Signalling In Leukaemia Development
Funder
National Health and Medical Research Council
Funding Amount
$373,144.00
Summary
Recent research has shown the clinical importance of abnormal stem cells (LSC) in acute myeloid leukaemia (AML). LSC are resistant to therapeutics suggesting that they could be a cause of relapse. Identifying signalling pathways that drive LSC development is essential to selectively eradicate LSC that could offer substantial therapeutic benefit. This proposal aims to identify and evaluate critical signalling pathways as a potential therapeutic target for developing effective novel LSC-targeted t ....Recent research has shown the clinical importance of abnormal stem cells (LSC) in acute myeloid leukaemia (AML). LSC are resistant to therapeutics suggesting that they could be a cause of relapse. Identifying signalling pathways that drive LSC development is essential to selectively eradicate LSC that could offer substantial therapeutic benefit. This proposal aims to identify and evaluate critical signalling pathways as a potential therapeutic target for developing effective novel LSC-targeted therapy in AML.Read moreRead less
Tumour Suppressive Mechanisms Of CEBP? And PU.1 In Acute Myeloid Leukemia
Funder
National Health and Medical Research Council
Funding Amount
$497,827.00
Summary
Acute myeloid leukaemia (AML) is an aggressive leukaemia with poor overall responses to therapy. The transcription factors CEBPA and PU.1 are often lost during AML development, and therapies that can restore their normal functions hold great promise. By identifying the genes that these transcription factors regulate in normal and leukaemic white blood cells, this project aims to understand how AML develops and which genes represent rational drug targets for this disease.