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A The Kids Research Institute Australia researcher will investigate new ways to harness the body’s own immune system to fight melanoma, thanks to Cancer Council WA funding.
A landmark study led by Dr Hetal Dholaria, The Kids Research Institute Australia researcher and Perth Children’s Hospital Oncologist, has confirmed that a “wait and watch” approach for newborns diagnosed with neuroblastoma is not only safe, but effective over the long term.
Join us as WA’s cancer research community comes together at the inaugural West Coast Cancer Meeting.
Researchers at The Kids Research Institute Australia have been awarded $4.6 million in national funding from the National Health and Medical Research Council (NHMRC) and Medical Research Future Fund (MRFF) to help support child health research.
Cancer vaccination drives the generation of anti-tumor T cell immunity and can be enhanced by the inclusion of effective immune adjuvants such as type I interferons (IFNs). Whilst type I IFNs have been shown to promote cross-priming of T cells, the role of individual subtypes remains unclear. Here we systematically compared the capacity of distinct type I IFN subtypes to enhance T cell responses to a whole-cell vaccination strategy in a pre-clinical murine model.
Despite significant advances, outcomes for children with Down syndrome (DS, trisomy 21) who develop acute lymphoblastic leukemia remain poor. Reports of large DS-ALL cohorts have shown that children with DS have inferior event-free survival and overall survival compared to children without DS.
Children with Down syndrome (DS, trisomy 21) are at a significantly higher risk of developing acute leukemia compared to the overall population. Many studies investigating the link between trisomy 21 and leukemia initiation and progression have been conducted over the last two decades.
An in-depth investigation of gene regulation and cell populations at sites of fetal blood-cell production provides clues as to why children with Down’s syndrome are predisposed to developing leukaemia.
There are few options for patients with relapse/refractory B-cell acute lymphoblastic leukemia, thus this is a major area of unmet medical need. Here, we reveal that inclusion of a poison exon in RBM39, which could be induced both by CDK9 or CDK9 independent CMGC (cyclin-dependent kinases, mitogen-activated protein kinases, glycogen synthase kinases, CDC-like kinases) kinase inhibition, is recognized by the nonsense-mediated mRNA decay pathway for degradation.
Projects to improve outcomes for leukaemia patients and reduce skin cancer rates in young Aboriginal people have received funding through Cancer Council WA.