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Results: 39

Cellular Cybercriminals: DIPG Hacks into the Neural Communication Infrastructure

 My group has recently demonstrated the neuronal activity drives the growth of DIPG and other high-grade gliomas. One way that active neurons promote DIPG growth is through activity-regulated secretion of growth factors into the tumor microenvironment. We have now discovered an additional, surprising means of neuron:glioma communication – ...

Combinatorial Strategies Alongside ACVR1 Inhibition in DIPG

 We and others recently discovered a novel cancer gene, ACVR1, to be mutated in approximately 25% diffuse intrinsic pontine glioma (DIPG), most commonly in the youngest patients, and co-segregating with K27M mutations in histone H3.1 (HIST1H3B/HIST1H3C). ACVR1 encodes a receptor serine/threonine kinase mutated ...

EPIGENETIC ALTERATIONS AS THERAPEUTIC TARGETS IN PEDIATRIC BRAIN TUMORS

We and others co-discovered the presence of activating mutations in ACVR1 in 25% of human DIPGs in 2014. Subsequently, my laboratory has developed a murine DIPG model incorporating R206H ACVR1 and observed that R206H ACVR1 significantly accelerates brainstem gliomagenesis. In addition, short-term treatment with a bone morphogenetic protein pathway inhibitor (...

Using zebrafish to accelerate DIPG drug development

A critical barrier to improvements in diffuse intrinsic pontine glioma (DIPG) therapy is a lack of new drugs that have a broad therapeutic index. In DIPG, validation of new therapeutics is hampered by the long time (6 months) that most human DIPG tumors take to kill mice. This means that it ...

Repurposing mefloquine for diffuse intrinsic pontine glioma therapy

Diffuse intrinsic pontine gliomas (DIPG) are highly aggressive brain tumors found in an area of the brainstem called the pons, which controls many of the body’s most vital functions such as breathing, blood pressure, and heart rate. DIPG is the leading cause of pediatric death by brain tumor. ...