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Our approach to hematopoietic progenitor cells mobilization resulted in highly effective HPC harvest in children and adolescents with high-risk cancers
Our findings highlight the potential of salinomycin to induce DNA lesions and inhibit homologous recombination to greatly enhance the effect of radiotherapy
The ANZCHOG-BN was developed to improve and streamline access to high quality pediatric and adolescent/young adult cancer biospecimens for cancer research
We discovered a previously unknown major resistance mechanism in glioma in that most EGFR domain III-targeting antibodies do not neutralize EGFRvIII
This review explores computational strategies to yield biological insight into the processes involved in the immunotherapeutic response
The WA Kids Cancer Centre has a suite of world-leading research projects to unlock new treatments for childhood cancers.
Vincristine sulphate, a microtubule inhibitor, is used extensively in veterinary oncology for treating lymphoma. Neutropenia during multiagent protocols is a common reason for treatment delay and reduced dose intensity. This study evaluated toxicities associated with treating systemically well neutropenic lymphoma patients with vincristine.
Approximately 770 children are diagnosed with cancer in Australia every year. Research has explored their experiences and developed recommendations for improving support provided to families. These have included the provision of psychology services, improved communication between healthcare professionals and parents, and increased information for families.
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.
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.