Treatment of Radiation‐Induced Brain Necrosis

Yang, Xiaojing; Ren, Hailong; Fei, Jie

doi:10.1155/2021/4793517

Cited by 21 publications

(13 citation statements)

References 142 publications

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“…Patients with RTLI may suffer long-term headaches, insanity, dizziness, memory loss, personality changes, and seizures ( 32 ). These symptoms may greatly affect the quality of life of patients with NPC.…”

Section: Discussionmentioning

confidence: 99%

MRI-based radiomics models for the early prediction of radiation-induced temporal lobe injury in nasopharyngeal carcinoma

et al. 2023

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ObjectiveThis study was conducted to develop and validate a radiomics-clinics combined model-based magnetic resonance imaging (MRI) radiomics and clinical features for the early prediction of radiation-induced temporal lobe injury (RTLI) in patients with nasopharyngeal carcinoma (NPC).MethodsThis retrospective study was conducted using data from 130 patients with NPC (80 patients with and 50 patients without RTLI) who received radiotherapy. Cases were assigned randomly to training (n = 91) and testing (n = 39) datasets. Data on 168 medial temporal lobe texture features were extracted from T1WI, T2WI, and T1WI-CE MRI sequences obtained at the end of radiotherapy courses. Clinics, radiomics, and radiomics–clinics combined models (based on selected radiomics signatures and clinical factors) were constructed using machine learning software. Univariate logistic regression analysis was performed to identify independent clinical factors. The area under the ROC curve (AUC) was performed to evaluate the performance of three models. A nomogram, decision curves, and calibration curves were used to assess the performance of the combined model.ResultsSix texture features and three independent clinical factors associated significantly with RTLI were used to build the combined model. The AUCs for the combined and radiomics models were 0.962 [95% confidence interval (CI), 0.9306–0.9939] and 0.904 (95% CI, 0.8431–0.9651), respectively, for the training cohort and 0.947 (95% CI, 0.8841–1.0000) and 0.891 (95% CI, 0.7903–0.9930), respectively, for the testing cohort. All of these values exceeded those for the clinics model (AUC = 0.809 and 0.713 for the training and testing cohorts, respectively). Decision curve analysis showed that the combined model had a good corrective effect.ConclusionThe radiomics–clinics combined model developed in this study showed good performance for predicting RTLI in patients with NPC.

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Section: Discussionmentioning

confidence: 99%

MRI-based radiomics models for the early prediction of radiation-induced temporal lobe injury in nasopharyngeal carcinoma

et al. 2023

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“…Currently, however, there is no evidence-based guideline yet for the diagnosis and treatment of immune-related intracranial necrosis. Clinically, radiation-induced brain necrosis is more common and there are various treatment strategies, including regular imaging follow-up (close observation for small and asymptomatic lesions), hyperbaric oxygen therapy (HBOT), medications, and surgery ( 25 ). Whether these strategies can be applied to immune-related intracranial necrosis still requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

Case report: Brain metastasis necrosis with immune checkpoint inhibitors plus chemotherapy for advanced non-small cell lung cancer

Niu

Li²,

Meng³

et al. 2022

Front. Immunol.

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The emergence of immune checkpoint inhibitors (ICIs) has reshaped the landscape of advanced lung cancer treatment. The brain is the most common metastatic site for lung cancer. Whether conventional criteria can evaluate the intracranial response of ICIs remains unclear. Here, we report a well-documented case of intracranial necrosis confirmed by post-operative pathology after only one cycle of chemo-immunotherapy without any radiation therapy, which suggests that immunotherapy elicits strong anti-tumor responses for intracranial metastasis and promotes intracranial necrosis, resulting in a temporary increase in size of the target lesions. Still, the specific mechanisms and management strategies need to be further explored.

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“…Preclinical studies on the pathogenesis of radiation‐induced cognitive impairment have provided valuable insights, but the specific molecular mechanisms involved remain unclear (Schumacher et al, 2021). Previously, radiation‐induced brain injury was thought to be due to DNA damage (Tofilon & Fike, 2000; Yang et al, 2021), but this theory has been shown to be untenable. Neurogenesis in adults has been shown to play an important role in certain types of hippocampus‐dependent cognitive function (Aimone et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

CACNA1B protects naked mole‐rat hippocampal neuron from apoptosis via altering the subcellular localization of Nrf2 after ⁶⁰Co irradiation

Yang,

Chen,

Jiang

et al. 2024

Cell Biology International

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Although radiotherapy is the most effective treatment modality for brain tumors, it always injures the central nervous system, leading to potential sequelae such as cognitive dysfunction. Radiation induces molecular, cellular, and functional changes in neuronal and glial cells. The hippocampus plays a critical role in learning and memory; therefore, concerns about radiation‐induced injury are widespread. Multiple studies have focused on this complex problem, but the results have not been fully elucidated. Naked mole rat brains were irradiated with 60Co at a dose of 10 Gy. On 7 days, 14 days, and 28 days after irradiation, hippocampi in the control groups were obtained for next‐generation sequencing. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were subsequently performed. Venn diagrams revealed 580 differentially expressed genes (DEGs) that were common at different times after irradiation. GO and KEGG analyses revealed that the 580 common DEGs were enriched in molecular transducer activity. In particular, CACNA1B mediated regulatory effects after irradiation. CACNA1B expression increased significantly after irradiation. Downregulation of CACNA1B led to a reduction in apoptosis and reactive oxygen species levels in hippocampal neurons. This was due to the interaction between CACNA1B and Nrf2, which disturbed the normal nuclear localization of Nrf2. In addition, CACNA1B downregulation led to a decrease in the cognitive functions of naked mole rats. These findings reveal the pivotal role of CACNA1B in regulating radiation‐induced brain injury and will lead to the development of a novel strategy to prevent brain injury after irradiation.

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Treatment of Radiation‐Induced Brain Necrosis

Cited by 21 publications

References 142 publications

MRI-based radiomics models for the early prediction of radiation-induced temporal lobe injury in nasopharyngeal carcinoma

MRI-based radiomics models for the early prediction of radiation-induced temporal lobe injury in nasopharyngeal carcinoma

Case report: Brain metastasis necrosis with immune checkpoint inhibitors plus chemotherapy for advanced non-small cell lung cancer

CACNA1B protects naked mole‐rat hippocampal neuron from apoptosis via altering the subcellular localization of Nrf2 after ⁶⁰Co irradiation

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Treatment of Radiation‐Induced Brain Necrosis

Cited by 21 publications

References 142 publications

MRI-based radiomics models for the early prediction of radiation-induced temporal lobe injury in nasopharyngeal carcinoma

MRI-based radiomics models for the early prediction of radiation-induced temporal lobe injury in nasopharyngeal carcinoma

Case report: Brain metastasis necrosis with immune checkpoint inhibitors plus chemotherapy for advanced non-small cell lung cancer

CACNA1B protects naked mole‐rat hippocampal neuron from apoptosis via altering the subcellular localization of Nrf2 after 60Co irradiation

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CACNA1B protects naked mole‐rat hippocampal neuron from apoptosis via altering the subcellular localization of Nrf2 after ⁶⁰Co irradiation