National brain tumour research funding needs to increase to £30-35 million a year
Weekly pick of Neuroscience news from around the world
This study was reported on at SNO in Phoenix last week and although it is based on a small cohort (number of patients involved) it has generated much excitement because “ The oncolytic herpes virus type 1 G47 may become a preferred treatment that leads potentially to a cure of malignant glioma in the near future. ( you will need to click through to this page and then click on the first link on that page to access this update)
Some of the biggest names in US paediatric brain tumour research, in collaboration, have discovered that several types of highly aggressive and, ultimately, fatal paediatric brain tumours originate during brain development. The genetic event that triggers the disease happens in the very earliest phases of cellular development, most likely a prenatal stage, and these findings represent a significant advance in understanding these diseases. The research team leader Dr Claudia Kleinman, from the Lady Davis Institute at the Jewish General Hospital in Montreal said “The genesis of the tumours means that there are really no environmental instigators or preventive measures that parents can take. Advancing our understanding of these tumours is important because the effects are so devastating, we want to bring hope to the patients."
In other paediatric brain cancer news $150,000 funding has been pledged from the Om Foundation for investigators at Rutgers Cancer Institute of New Jersey to examine a certain type of medication that impacts gene activity in the treatment of Ependymoma , the third most common childhood brain cancer. Treatment results for Ependymoma have been unsatisfactory due to a lack of effective drugs with surgical removal and radiation therapy being the standard treatments, and chemotherapy not being shown to improve survival rates. Sadly, post-intervention recurrence is common.
Ependymomas have many potentially 'good' genes that are silenced through an epigenetic mechanism (epigenetics is the study of inherited changes in gene expression - active versus inactive genes- that do not involve changes to the underlying DNA sequence). This means that these genes are still present in the tumour but not active. Certain medications (epigenetic modifiers) can reactivate these silenced genes causing cancer cells to return to normal and increased cell killing when combined with radiotherapy.
The Om Parikh Memorial Fund for Paediatric Cancer Research was formed to honour Om Parikh, who died of oligodendroglioma last year aged 13.
In industry news, Australian Biotechnology company Kazia Therapeutics saw their share price surge following positive interim results in phase II glioblastoma trial – again note small cohort size.
Radiotherapy is essential for treating paediatric brain tumours, but the treatment comes with the risk of cognitive impairment. Researchers in the US and Canada have examined children diagnosed with medulloblastoma and treated them with two different kinds of radiotherapy—proton radiotherapy and photon radiotherapy—and found those treated with proton radiotherapy had less intellectual decline. One of the issues this raises in the US is that proton radiotherapy is more costly than photon radiotherapy and is not always covered by insurance. The researchers conclude that: “If studies continue to demonstrate that proton radiotherapy offers medical and quality of life benefits that are superior to photon radiotherapy, we will need to address barriers to access for paediatric brain tumour patients” .
Ending this week with more about Glioblastoma treatments but this time involving drug repurposing; A gene called mucosa-associated lymphoid tissue l (MALT1), is highly active in lymphoma, a type of blood cancer, and blocking MALT1 causes lymphoma cells to die. MALT1 blockers have long been in clinical use for the treatment of blood cancers. European researchers uncovered that targeting MALT1 with MALT1 blockers caused glioblastoma stem cells to undergo a rare form of cellular suicide and that this points to the possibility of further exploring MALT1 inhibitors as potential treatment of glioblastoma.
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