CHARACTERISATION AND ANTIBODY-MEDIATED TARGETING OF A NOVEL SPECIFIC MARKER FOR T CELL ALL/LYMPHOBLASTIC LYMPHOMA
Funder
National Health and Medical Research Council
Funding Amount
$586,146.00
Summary
Improvements in treatment have seen some types of leukaemia (a cancer of white blood cells) being curable in up to 90% of patients with the disease; however, other types of leukaemia do not respond to these drugs and new approaches are needed. We have discovered that some leukaemia cells express a unique protein not made by any other cell type. This project will analyse how this aberrant protein is made and how this process contributes to the development of leukaemia. Also, since this protein is ....Improvements in treatment have seen some types of leukaemia (a cancer of white blood cells) being curable in up to 90% of patients with the disease; however, other types of leukaemia do not respond to these drugs and new approaches are needed. We have discovered that some leukaemia cells express a unique protein not made by any other cell type. This project will analyse how this aberrant protein is made and how this process contributes to the development of leukaemia. Also, since this protein is unique to the leukaemia cells, it offers the opportunity to develop magic bullets able to target specifically to the leukaemia cells and to kill them. This project aims to make one such drug and to conduct preliminary testing.Read moreRead less
Proteolytic And Non-proteolytic Roles For PSA And Related Kallikrein Serine Proteases In Prostate Cancer Progression
Funder
National Health and Medical Research Council
Funding Amount
$480,128.00
Summary
Prostate cancer is the most frequently occurring cancer in men in Western countries. Prostate cancer metastasis to bone and other organs is the painful end stage of this disease. The level of prostate specific antigen (PSA) in blood is often used as a marker of prostate cancer. PSA is one of 15 related enzymes in the kallikrein family of enzymes, which may be involved in breakdown of the tissue that surrounds cells in the prostate. As prostate cancer metastasis first requires spread from the pri ....Prostate cancer is the most frequently occurring cancer in men in Western countries. Prostate cancer metastasis to bone and other organs is the painful end stage of this disease. The level of prostate specific antigen (PSA) in blood is often used as a marker of prostate cancer. PSA is one of 15 related enzymes in the kallikrein family of enzymes, which may be involved in breakdown of the tissue that surrounds cells in the prostate. As prostate cancer metastasis first requires spread from the primary tumour and out of the prostate, it is possible that high production of these kallikrein enzymes by prosttae cancer cells may increase the ability of these cells to metastasise. In previous work, we have studied prostate cancer cells that we have engineered to make the kallikreins, PSA and kallikrein 4. Those cells that make PSA or kallikrein 4 are more elongated in shape and are better able to move across a porous barrier. Another important change is that these cells stop producing a protein that is usually found on the surface of these cells and is important for helping cells to stay attached to each other. When this protein is lost, these tumour cells no longer stay attached to each other and are more likely to move out of the prostate and spread into other parts of the body. The changes we observed in the cells that produce PSA and kallikrein 4 are typical of these more aggressive cancer cells. In this project, we will look at how PSA and kallikrein 4 cause the cells to undergo these changes. The majority of prostate cancer deaths arise from cancer that has spread from the primary tumour and out of the prostate capsule. This project aims to further understand the causes of prostate cancer spread and metastasis. This is a vital research priority if we are to address the mortality associated with prostate cancer metastasis and may lead to new treatment approaches for advanced metastic prostate cancer.Read moreRead less
I am a cellular immunologist with expertise in antigen processing-presentation, CTL determinant selection and immunodominance, T cell differentiation and, cancer immunotherapeutic trials and cancer vaccine development.
My research straddles biochemistry, cell biology and immunology. I am interested in the mechanisms of antigen presentation by dendritic cells, and the functions of the cystatin family of protease inhibitors.
Tumour Antigen Cross-presentation: Efficiency, Biology And Role Of Inhibitory B7 Homologue Molecules
Funder
National Health and Medical Research Council
Funding Amount
$469,500.00
Summary
It is now known that the body s immune system often attempts to attack cancers but this response is generally fairly weak. It was previously thought that one of the main reasons for this failure was that the immune system was ignorant of the presence of the cancer until too late. Our recent work over the past few years has shown that this is not the case. A process called cross-presentation seems to efficiently and continuously expose the cancer to the body s anti-cancer killer T-cells. This gra ....It is now known that the body s immune system often attempts to attack cancers but this response is generally fairly weak. It was previously thought that one of the main reasons for this failure was that the immune system was ignorant of the presence of the cancer until too late. Our recent work over the past few years has shown that this is not the case. A process called cross-presentation seems to efficiently and continuously expose the cancer to the body s anti-cancer killer T-cells. This grant will work out exactly how efficient that process is, which cells are responsible and some aspects of how it happens. We will also study whether some recently-discovered braking molecules, which slow down immune responses and which could be 'applying the brakes' to anti-cancer responses. This could lead to new approaches to therapy eg by removing these brakes during vaccination therapy.Read moreRead less
Improving Immunotherapy By Vascular Targeting And Barrier Alteration
Funder
National Health and Medical Research Council
Funding Amount
$526,878.00
Summary
Tumors grow in part because they escape destruction by the immune system. New blood vessels grow inside tumors by a process called angiogenesis, which then stops cancer-fighting cells in their tracks. We hypothesise that breaking down the blood-tumor barrier will open tumors for attack by the cancer-fighting immune system. This proposal continues our work on reversal of angiogenesis in the context of immunotherapy. We expect these findings to lead to highly effective anti-tumor therapies.