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Introduction: Radionecrosis is a consequence of SRS (stereotactic radiosurgery) for brain metastases in 34% of cases, and if symptomatic (8%-16%), it requires therapy with corticosteroids and bevacizumab and, less frequently, surgery. Oncological indications are increasing and appropriate stereotactic adapted LINACs (linear accelerators) are becoming more widely available worldwide. Efforts are being made to treat brain radionecrosis in order to relieve symptoms and spare the use of active therapies. Case presentation: Herein, we describe a 65-year-old female patient presenting with brain radionecrosis 6 months after stereotactic radiotherapy for two brain metastatic lesions. Being symptomatic with headache and slow cognitive-motor function, the patient received corticosteroids. Because of later lung progression, the patient took cabozantinib. An impressive reduction of the two brain radionecrosis areas was seen at the brain MRI 2 months after the initiation of the angiogenic drug. Discussion: The high incidence of radionecrosis (2/2 treated lesions) can be interpreted by the combination of SRS and previous ipilimumab that is associated with increased risk of radionecrosis. The molecular mechanisms of brain radionecrosis, and its exact duration in time, are poorly understood. We hypothesize that the antiangiogenic effect of cabozantinib may have had a strong effect in reducing brain radionecrosis areas. Conclusion: In this clinical case, cabozantinib is associated with a fast and significant volume reduction of brain radionecrosis appearing after SRS and concomitant immunotherapy. This drug seems to show, like bevacizumab, clinical implications not only for its efficacy in systemic disease control but also in reducing brain radionecrosis. More research is needed to evaluate all molecular mechanisms of brain radionecrosis and their interaction with systemic therapies like third-generation TKIs.
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[This corrects the article DOI: 10.3389/fonc.2023.1136300.].
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Objectives: Dynamic susceptibility contrast perfusion weighted imaging (DSC-PWI) plays an important role in the differential diagnosis between radionecrosis and recurrence of brain metastases (BMs) after gamma knife radiosurgery (GKRS). While the perfusion condition of preliminary hyperperfusion and hypoperfusion BMs when recur has not been studied, as well the separating performance of quantitative DSC-PWI in both kinds of BMs. Methods: From February 2017 to October 2019, quantitative DSC-PWI was performed in patients with untreated BMs in this observational study. Patients were assigned to hyperperfusion and hypoperfusion group according the quantitative cerebral blood volume (qCBV). During follow-up after GKRS, patients with a diagnostic pitfall of radionecrosis and recurrence accepted second quantitative DSC-PWI. Final diagnosis was based on the histological results or follow-up results. Receiver operating curve analysis was used to explore the performance of qCBV. Results: Twenty-nine patients (mean age: 61.3 ± 9.4 years old; male/female: 13/16) were assigned to the group of hypoperfusion group, and 26 patients (mean age: 58 ± 10.4 years old; male/female: 14/12) to hyperperfusion group. The mean qCBV values between hypoperfusion and hyperperfusion groups when recurred were not significantly different (3.17 ± 0.53 ml/100 g vs. 3.27 ± 0.47 ml/100 g, p = 0.63). qCBV was feasible to separate radionecrosis and recurrence in both groups (AUC=0.94 and AUC=0.93, separately). Conclusion: Both premilitary hyperperfusion and hypoperfusion BMs would transform to a high microvascular density when recurs. qCBV is feasible to distinguish radionecrosis and recurrence among both kinds of BMs after GKRS.
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As our understanding of normal brain tissue tolerance and radiation technology have improved, central nervous system (CNS) re-irradiation has garnered more attention; whereas, in the past there had been hesitancy due to late toxicity concerns, particularly radionecrosis (RN). There is minimal prospective data evaluating repeat radiation in recurrent gliomas. In this review, the rationale for and different approaches to re-irradiation will be discussed, and the biology and clinical impact of late CNS toxicity will be reviewed.