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Vascular damage is followed by vascular endothelial growth factor (VEGF) expression at high levels, which is an important mechanism for cerebral radiation necrosis (CRN) development. Antiangiogenic agents (Bevacizumab) alleviates brain edema symptoms caused by CRN through inhibiting VEGF and acting on vascular tissue around the brain necrosis area. Many studies have confirmed that Bevacizumab effectively relieves symptoms caused by brain necrosis, improves patients' performance status and brain necrosis imaging. Considering that the efficacy of antiangiogenic therapy is mainly related to the duration of drug action, low-dose antiangiogenic agents can achieve favorable efficacy. Prevention is the best treatment. The occurrence of CRN is associated with tumor-related factors and treatment-related factors. By controlling these factors, CRN can be effectively prevented. .
Subject(s)
Humans , Angiogenesis Inhibitors/pharmacology , Bevacizumab/therapeutic use , Brain/metabolism , Consensus , Lung Neoplasms/drug therapy , Necrosis/etiology , Radiation Injuries/etiology , Vascular Endothelial Growth Factor A/metabolismABSTRACT
Objective To evaluate the efficacy and safety of stereotactic body radiation therapy (SBRT) using Cyberknife in the treatment of patients with recurrent cholangiocellular carcinoma (RCC) after surgery.Methods Clinical data of 26 patients with recurrent RCC after surgery undergoing Cyberknife SBRT from 2010 to 2015 were retrospectively analyzed.The median recurrence time was 10 months (range 2.0-63.0 months) and the median tumor diameter was 2.8 cm (range 1.2-4.8 cm).The median prescription dose/fraction was 45 Gy/5f (range 40-50 Gy/3-8 f).The tumor progression was evaluated based on enhanced CT or MRI.Overall survival (OS),progression-free survival (PFS) and local control rate (LC) were analyzed by Kaplan-Meier method.Toxicity was assessed using the common terminology criteria for adverse events version 4.0.Results For the entire cohort,the median OS and PFS were 13.5 months and 6.5 months at a median follow-up of 29.3 months (range 2.1-62.0 months).The 1-and 2-year OS and PFS rates were 52％ and 21％ as well as 28％ and 15％,respectively.Among them,4 patients (4/26,15％) were recurrent in situ after SBRT.Three patients experienced grade Ⅲ adverse reactions including 1 case of gastrointestinal reaction,1 case of liver dysfunction and 1 case of biliary tract infection.Only 1 patient suffered from ≥ grade Ⅳ gastrointestinal bleeding during the advanced stage.Conclusions SBRT using Cyberknife is a safe and effective treatment for patients with recurrent RCC after surgery.The adverse reactions can be tolerated by patients.
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Objective To evaluate the efficacy and safety of CyberKnife stereotactic body radiation therapy (SBRT) in the treatment of hepatic hilar cancer.Methods A retrospective study was performed on the clinical data of 36 patients with hepatic hilar cancer who were admitted to our hospital and treated with CyberKnife SBRT from 2009 to 2015.In the 36 patients,37 lesions were found with tumor diameters ranging from 1.5 to 5.5 mm (median diameter 3 cm).The Synchrony respiratory tracking system was used for 21 lesions in 20 patients,while the XSight spinal tracking system was used for 16 lesions in 16 patients.Local progression was evaluated based on contrast-enhanced computed tomography and/or magnetic resonance imaging.The Kaplan-Meier method was used to calculate local control (LC) and overall survival (OS) rates,and the log-rank test was used for survival comparison and univariate prognostic analysis.Results The median follow-up time was 12.7 months.The 1-and 2-year postoperative LC rates were 90％ and 76％,respectively.The 1-year OS and progression-free survival (PFS) rates were 63％ and 39％,respectively.The median OS and PFS times were 15.2 and 10 months,respectively.The incidence of grade 3 adverse reactions was 11％.Conclusions The CyberKnife SBRT is a safe and effective way to treat hepatic hilar cancer.
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Objective To evaluated the role of postoperative radiotherapy (PR) after surgery in patients with uterine sarcoma,and analyzed the prognostic factors.Methods A total of 182 patients with uterine sarcoma were included between June 1994 and October 2014.Radiotherapy dose were 30-50 Gy/10-25 fractions/5 fractions/week.The LRFFS and OS were calculated with Kaplan-Meier method,and difference was analyzed with log-rank method.Cox regression analyses were used to determine prognosticators.Results There were 114 patients which survived more than 5-years in this whole group,including PR 24 cases and no PR 90 cases.The 5-year LRRFS and OS were 62.1％ and 56.2％,respectively.The 5-year LRRFS were 78.0％ and 55.3％ on PR and no PR (P=0.013);with OS 64.1％ and 51.7％ on PR and no PR (P=0.070).A multivariate analysis showed that pathological types,histological grade and clinical stage were associated with LRRFS and OS (P=0.032,0.008,0.000 and 0.046,0.000,0.000).PR was significant influencing factor for OS (P=0.013).Conclusions Uterine sarcoma patients treated with PR after surgery had an improved LRRFS compared to those treated with surgery,especially those with leiomyosarcoma.The role of PR personalized radiation for uterine sarcoma still needs to be further discussed.
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Objective To investigate the impacts of pyruvate kinase M2 isoform (PKM2) silencing on the radiosensitivity of lung adenocarcinoma cell line (A549 cells) and the radiation synergy of xenografts, and to explore their mechanisms. Methods Plasmid pshRNA?PKM2 for interference with PKM2 expression was transfected into A549 cells, and empty vector?transfected cells and untransfected cells were set as con?trols. The silencing efficiency of pshRNA?PKM2 and the expression level of microtubule?associated protein 1 light chain 3(LC3) were measured by Western blot assay. The radiosensitizing effects in A549 cells and xen?ografts after PKM2 silencing were determined by colony?forming assay and xenografts growth curves. Autoph?agy formation in A549 cells and xenografts was analyzed by transmission electron microscopy, and the ex?pression level of PKM2 in xenografts was measured by immunohistochemistry. Comparison between groups was made by Student′s t?test, and the body weights of nude mice and xenograft volumes were subjected to a?nalysis of variance for continuous variables. Results Stable A549 cell lines transfected with pshRNA?PKM2 were successfully produced. Transfection with pshRNA?PKM2 significantly down?regulated PKM2 expression in A549 cells and xenografts (P= 0?? 001;P= 0?? 000). The sensitizer enhancement ratios for A549 cells and xenografts were 1?? 47 and 2?? 00, respectively. Interference with PKM2 expression enhanced radiation?in duced autophagy formation and significantly increased the ratio of LC 3 ? II / I ( P= 0.000 1 ) . Conclusions Silencing of PKM2 expression may enhance the radiosensitivity of A549 cells and xenografts by regulation of autophagy, which holds promise for becoming an effective radiosensitizing target for non?small cell lung canc?er, but still needs to be confirmed by further studies.
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Objective:To investigate the effects and underlying mechanisms of XRCC3 on esophageal squamous-cell carcinoma (ESCC) radiotherapy response. Methods:Expression levels of XRCC3 were detected by reverse transcription PCR, Western blot, and immunohistochemistry. We knocked down XRCC3 with lentiviral infection in ESCC cells. Cell apoptosis was examined by flow cytom-etry. DNA damage and telomere dysfunction-induced foci were determined by immunofluorescence. Results:The expression levels of XRCC3 in ESCC cells and tissues were higher than those in normal esophageal epithelial cells and corresponding adjacent noncancer-ous esophageal tissues. Knockdown of XRCC3 in ESCC cells substantially increased the therapeutic efficacy of radiation. We demon-strated that the radiation resistance of XRCC3 was attributed to the XRCC3-maintaining telomere stability, which reduced ESCC cell death through radiation-induced apoptosis. Conclusion: Our data suggested that XRCC3 protects ESCC cells from ionizing radia-tion-induced DNA damage and death by enhancing telomere stability. Thus, XRCC3 can be used as a promising therapeutic target for ESCCs.
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Objective: Small-cell esophageal cancer (SCEC) is a rare malignant tumor. Radiotherapy and chemotherapy have been considered as standard treatments for limited-stage SCEC (LS-SCEC). This study aimed to analyze the comprehensive treatment and prognosis of extensive-stage SCEC (ES-SCEC). Methods: We retrospectively analyzed the clinical data of 35 Patients with ES-SCEC from the Cancer Hospital of Tianjin Medical University between January 1989 and April 2012. Results:A total of 33 patients (94.3%) participated in follow-up visits. The overall survival of the patients ranged between 0.6 and 42.4 months with a median of 9.5 months. All of the patients suffered from extensive metastasis. Among these patients, 33 manifested metastasis at diagnosis and 2 showed metastasis after surgery. One-and two-year survival rates were 27.2%(9/33) and 9.0%(3/33), respectively. Univariate and mul-tivariate analysis results revealed that the number of chemotherapy cycles (≥4) is a risk factor of OS (P=0.02) and the only indepen-dent risk factor (P=0.049). Conclusions:ES-SCEC is a malignant tumor with poor prognosis. Radiotherapy could not improve patient survival. Chemotherapy combined other therapeutic procedures could be considered as an effective treatment.