Bevacizumab for radiation necrosis following radiotherapy of brain metastatic disease: a systematic review & meta-analysis. Khan Muhammad,Zhao Zhihong,Arooj Sumbal,Liao Guixiang BMC cancer BACKGROUND:Radiotherapy is the mainstay of brain metastasis (BM) management. Radiation necrosis (RN) is a serious complication of radiotherapy. Bevacizumab (BV), an anti-vascular endothelial growth factor monoclonal antibody, has been increasingly used for RN treatment. We systematically reviewed the medical literature for studies reporting the efficacy and safety of bevacizumab for treatment of RN in BM patients. MATERIALS AND METHODS:PubMed, Medline, EMBASE, and Cochrane library were searched with various search keywords such as "bevacizumab" OR "anti-VEGF monoclonal antibody" AND "radiation necrosis" OR "radiation-induced brain necrosis" OR "RN" OR "RBN" AND "Brain metastases" OR "BM" until 1st Aug 2020. Studies reporting the efficacy and safety of BV treatment for BM patients with RN were retrieved. Study selection and data extraction were carried out by independent investigators. Open Meta Analyst software was used as a random effects model for meta-analysis to obtain mean reduction rates. RESULTS:Two prospective, seven retrospective, and three case report studies involving 89 patients with RN treated with BV were included in this systematic review and meta-analysis. In total, 83 (93%) patients had a recorded radiographic response to BV therapy, and six (6.7%) had experienced progressive disease. Seven studies (n = 73) reported mean volume reductions on gadolinium-enhanced T1 (mean: 47.03%, +/- 24.4) and T2-weighted fluid-attenuated inversion recovery (FLAIR) MRI images (mean: 61.9%, +/- 23.3). Pooling together the T1 and T2 MRI reduction rates by random effects model revealed a mean of 48.58 (95% CI: 38.32-58.85) for T1 reduction rate and 62.017 (95% CI: 52.235-71.799) for T2W imaging studies. Eighty-five patients presented with neurological symptoms. After BV treatment, nine (10%) had stable symptoms, 39 (48%) had improved, and 34 (40%) patients had complete resolution of their symptoms. Individual patient data was available for 54 patients. Dexamethasone discontinuation or reduction in dosage was observed in 30 (97%) of 31 patients who had recorded dosage before and after BV treatment. Side effects were mild. CONCLUSIONS:Bevacizumab presents a promising treatment strategy for patients with RN and brain metastatic disease. Radiographic response and clinical improvement was observed without any serious adverse events. Further class I evidence would be required to establish a bevacizumab recommendation in this group of patients. 10.1186/s12885-021-07889-3

Treatment of Radiation-Induced Brain Necrosis. Yang Xiaojing,Ren Hanru,Fu Jie Oxidative medicine and cellular longevity Radiation-induced brain necrosis (RBN) is a serious complication of intracranial as well as skull base tumors after radiotherapy. In the past, due to the lack of effective treatment, radiation brain necrosis was considered to be progressive and irreversible. With better understanding in histopathology and neuroimaging, the occurrence and development of RBN have been gradually clarified, and new treatment methods are constantly emerging. In recent years, some scholars have tried to treat RBN with bevacizumab, nerve growth factor, and gangliosides and have achieved similar results. Some cases of brain necrosis can be repairable and reversible. We aimed to summarize the incidence, pathogenesis, and treatment of RBN. 10.1155/2021/4793517

Advances in the study of the molecular biological mechanisms of radiation-induced brain injury. American journal of cancer research Radiation therapy is one of the most commonly used treatments for head and neck cancers, but it often leads to radiation-induced brain injury. Patients with radiation-induced brain injury have a poorer quality of life, and no effective treatments are available. The pathogenesis of this condition is unknown. This review summarizes the molecular biological mechanism of radiation-induced brain injury and provides research directions for future studies. The molecular mechanisms of radiation-induced brain injury are diverse and complex. Radiation-induced chronic neuroinflammation, destruction of the blood-brain barrier, oxidative stress, neuronal damage, and physiopathological responses caused by specific exosome secretion lead to radiation-induced brain injury.