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Abstract
The H3K27M mutation in diffuse midline gliomas increases CD99 expression, which is associated with poor prognosis.
- CD99 is notably expressed in diffuse midline gliomas, especially in those with the K27M mutation.
- Inactivation of CD99 in K27M+ glioma cells impairs tumor growth by promoting cell differentiation.
- The anti-CD99 chimeric antibody, 10D1, demonstrates antitumor efficacy by inducing apoptosis in both laboratory and animal models.
- Combining 10D1 with radiation therapy enhances its effectiveness and extends survival in xenograft models.
- These findings support the clinical development of 10D1 as a potential therapy for treating K27M+ diffuse midline gliomas.
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