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Work by the Institute's Division of Children's Leukaemia and Cancer Research has been recognised with three research grants from the Cancer Council of WA.
Apache Energy and the Telethon Institute for Child Health Research today signed a two-year partnership
A state of the art 3D molecular imager that will help researchers monitor how brain tumours grow has been delivered to the Telethon Institute.
The Telethon Institute for Child Health Research today announced a new study investigating a vaccine to prevent infection of Human Papilloma Virus (HPV).
Our goal was to explore and compare risk factors, patterns of management and survival outcomes in Indigenous compared with non-Indigenous Australian patients using the Victorian Lung Cancer Registry.
The WA Kids Cancer Centre has a suite of world-leading research projects to unlock new treatments for childhood cancers.
Leukaemia, also spelled leukemia, is a cancer that develops in the bone marrow and results in abnormal white blood cells. It is the most common cancer in children, accounting for almost a third of all childhood & teen cancers.
Immune checkpoint blockade (ICB) evokes antitumor immunity through the reinvigoration of T cell responses. T cell differentiation status controls response, with less differentiated cells having an enhanced capacity to proliferate after ICB. Given that conventional type 1 dendritic cells (cDC1) maintain precursor exhausted T cells (TPEX), we hypothesized that expansion of cDC1s with Flt3L could enhance responses to ICB.
Osteoclasts are important regulators of bone remodeling, with an established role in maintaining skeletal homeostasis. The emergence of osteoimmunology has identified osteoclasts as key players in the immune system. In particular, osteoclasts can initiate bi-directional crosstalk mechanisms with hematopoietic stem cells and various immune cells, such as T cells, B cells and NK cells, to influence hematopoiesis and inflammatory response.
Chemotherapy often kills a large fraction of cancer cells but leaves behind a small population of drug-tolerant persister cells. These persister cells survive drug treatments through reversible, non-genetic mechanisms and cause tumour recurrence upon cessation of therapy. Here, we report a drug tolerance mechanism regulated by the germ-cell-specific H3K4 methyltransferase PRDM9.