Malignant gliomas, including Glioblastoma multiforme (GBM) and diffuse midline glioma (DMG), formerly known as diffuse intrinsic pontine glioma (DIPG), are among the most aggressive and lethal primary brain tumours. Both present formidable challenges due to their rapid progression and poor prognosis, leaving limited options for long-term survival.
DIPG primarily affects children, often occurring in the midbrain regions, such as the brainstem, thalamus, and cerebellum. One of the defining genetic signatures of DIPG is the lysine 27 to methionine mutation in histone 3 (H3K27M), frequently accompanied by TP53 mutations. This mutation makes DIPG particularly difficult to treat, with little success in current therapeutic approaches.
In contrast, GBM is more commonly found in adults, typically in the frontal and temporal lobes of the brain. Its development is driven by a more complex array of genetic mutations. While the exact molecular drivers vary, they result in a tumour that is equally resistant to conventional therapies.
Despite differences in their typical locations and genetic underpinnings, DIPG and GBM share a tragically similar prognosis. Both tumours have a median survival rate of just 9 to 14 months. The primary challenge in treating both types lies in their high degree of heterogeneity and characteristic infiltrative growth, which allows cancer cells to spread throughout healthy brain tissue, making complete surgical removal or targeted therapies nearly impossible.
Finding effective treatments for DIPG and GBM remains an urgent area of research. The complex biology of these tumours continues to pose significant hurdles but advances in molecular and genetic research offer hope for future breakthroughs.Top of Form
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