Search

Recurrent MET fusion genes represent a drug target in pediatric glioblastoma

We identified previously unidentified gene fusions involving the MET oncogene in pediatric glioblastoma

MK2 inhibition induces p53-dependent senescence in glioblastoma cells

In response to DNA damaging chemotherapy, targeting MK2 in p53-mutated cells produces a phenotype that is distinct from the p53-deficient phenotype

Simultaneous Targeting of DNA Replication and Homologous Recombination in Glioblastoma with a Polyether Ionophore

Our findings highlight the potential of salinomycin to induce DNA lesions and inhibit homologous recombination to greatly enhance the effect of radiotherapy

Challenges to curing primary brain tumours

The seven key challenges summarized in this Position Paper are intended to serve as foci for future research and investment in brain tumours

The Australian and New Zealand Children's Haematology/Oncology Group Biobanking Network

The ANZCHOG-BN was developed to improve and streamline access to high quality pediatric and adolescent/young adult cancer biospecimens for cancer research

A reference collection of patient-derived cell line and xenograft models of proneural, classical and mesenchymal glioblastoma

We present a curated panel of 12 readily-usable, cell lines representing the spectrum of molecular subtypes of IDH-wildtype glioblastoma

Use of bevacizumab as a single agent or in adjunct with traditional chemotherapy regimens in children with unresectable or progressive low-grade glioma

Bevacizumab is well tolerated and appears most effective for rapid tumor control to preserve vision and improve morbidity

International experience in the development of patient-derived xenograft models of diffuse intrinsic pontine glioma

This multi-center study provides valuable information on the success rate of establishing patient-derived pre-clinical models of diffuse intrinsic pontine glioma

Diffuse Intrinsic Pontine Glioma

This chapter summarizes recent advances in diffuse intrinsic pontine glioma and potential novel therapies

PI3K activation in neural stem cells drives tumorigenesis which can be ameliorated by targeting the cAMP response element binding protein

A novel mouse model for glioma demonstrating that the PI3K pathway is important for initiation of tumorigenesis