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Avantogen Limited (ACU:ASX) today announced that cancer researchers at Perth's The Kids for Child Health Research (TICHR) and Avantogen Limited

A national study is investigating diet, chemical exposure and genetic factors in a new bid to unravel the causes of childhood leukaemia.

West Australian families are being asked to play a vital role in a major new national study to unravel the causes of childhood leukaemia.

On Monday 1 September, childhood cancer researcher Jacob Byrne is lacing up his running shoes and taking the first steps of an extraordinary challenge: 30 marathons in 30 days across Perth.

Eight childhood cancer researchers have been awarded over $2 million in transformative grants from Cancer Council WA to advance their pioneering work in improving cancer treatments and outcomes for patients in Western Australia and around the world.

Associate Professor Rishi Kotecha, Co-Head of Leukaemia Translational Research at The Kids Research Institute Australia Cancer Centre and Consultant Paediatric Oncologist at Perth Children's Hospital, has been named Cancer Council WA’s 2024 Cancer Researcher of the Year.

The WA Kids Cancer Centre has a suite of world-leading research projects to unlock new treatments for childhood cancers.

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. 

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.