BACKGROUND
Spinal dural arteriovenous fistula (SDAVF) is a rare disorder with an unknown etiology. Often, the clinical presentation and imaging findings are misleading, causing this condition to be mistaken for other entities, such as demyelinating or degenerative spinal lesions.
OBSERVATIONS
The authors report a challenging case of SDAVF in which the patient’s symptoms were initially thought to be attributable to a herniated disc based on his imaging studies at another institution. He sought the authors for a second opinion, which yielded a confirmed diagnosis of SDAVF. Due to his rapidly progressive neurological manifestations, he underwent a surgical division of the fistula using intraoperative video angiography via indocyanine green injections. His symptoms progressively improved over a 3-month period. He regained full sphincter control by 4 months, which gave him a better recovery than seen in other patients with SDAVFs, who do not generally fully regain sphincter control.
LESSONS
SDAVF is a critical spinal vascular pathology that should not be overlooked in the differential diagnosis of any patient presenting with signs of progressive myelopathy. Despite its associated vague initial clinical symptoms, SDAVF typically, but not always, demonstrates a characteristic imaging appearance on magnetic resonance (MR) imaging studies; therefore, MR angiography is still required for definitive diagnosis. Surgical treatment for SDAVF is almost always definitive and curative.
High-grade gliomas are the most common and aggressive adult primary brain tumors with a median survival of only 12–15 months. Current standard therapy consists of maximal safe surgical resection followed by DNA-damaging agents, such as irradiation and chemotherapy that can delay but not prevent inevitable recurrence. Some have interpreted glioma recurrence as evidence of glioma stem cells which persist in a relatively quiescent state after irradiation and chemotherapy, before the ultimate cell cycle re-entry and glioma recurrence. Conversely, latent cancer cells with a therapy-induced senescent phenotype have been shown to escape senescence, giving rise to more aggressive stem-like tumor cells than those present in the original tumor. Therefore, approaches are needed to either eliminate or keep these glioma initiating cells in a senescent state for a longer time to prolong survival. In our current study, we demonstrate that the radiation-induced cell cycle inhibitor P21 can provide a powerful route to induce cell death in short-term explants of PDXs derived from three molecularly diverse human gliomas. Additionally, cells not killed by P21 overexpression were maintained in a stable senescent state for longer than control cells. Collectively, these data suggest that P21 activation may provide an attractive therapeutic target to improve therapeutic outcomes.
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