Abstract
Radiation-induced glioblastomas (RIGs) are aggressive secondary neoplasms that arise following craniospinal radiation, characterized by distinct molecular including IDH-wildtype, PDGFRA amplication, and loss of CDKN2A/B. We report the case of a 24-year old male that was initially diagnosed with disseminated myxopapillary ependymoma in 2018 with a large tumor T11-L1 with nodular foci of enhancement throughout the lumbar spinal canal and in the cerebellum. He underwent surgical resection of the T11-L1 mass and subsequent craniospinal proton radiation. The patient remained stable until February 2025, when he presented with right-sided neck pain and right arm weakness. Imaging demonstrated a new expansile intramedullary tumor at C3-C5. Surgical resection of this recurrence revealed a small-cell glioblastoma, exhibiting IDH-wildtype status and PDGFRA amplification. The tumor did not have the classic loss of CDKN2A/B, but does have CDK4 amplification, affecting the cell cycle similarly. Unfortunately, the patient’s neurological status continued to decline after surgical resection due to the aggressive nature of RIGs, resulting in wheelchair dependence. Repeat imaging demonstrated progression of the C3-5 lesion as well as a new contrast-enhancing tumor in the medulla. The patient is currently undergoing medical management with bevacizumab and temozolomide in addition to palliative radiation to the cervical spinal tumor of 3500 cGy in 10 fractions. This case presentation underscores the clinical challenge presented by RIGs, particularly spinal glioblastomas, which are exceedingly rare and aggressive. Despite extensive multimodal interventions and advancements in tumor molecular testing, the prognosis remains poor. Future research into the molecular drivers of radiation-induced gliomas, specifically targeting amplified PDGFRA and CDK4 pathways, may enhance understanding and treatment of these aggressive secondary malignancies.