Ferroptosis is a type of cell death characterized by the accumulation of intracellular iron and an increase in hazardous lipid peroxides. Ferroptosis and autophagy are closely related. Ionizing radiation is a frequently used cancer therapy to kill malignancies. We found that ionizing radiation induces both ferroptosis and autophagy and that there is a form of mutualism between the two processes. Ionizing radiation also causes lipid droplets to form in proximity to damaged mitochondria, which, through the action of mitophagy, results in the degradation of the peridroplet mitochondria by lysosomes and the consequent release of free fatty acids and a significant increase in lipid peroxidation, thus promoting ferroptosis. Ionizing radiation has a stronger, fatal effect on cells with a high level of mitophagy, and this observation suggests a novel strategy for tumor treatment.

Carbon-ion radiotherapy (CIRT) enhanced local control in patients with malignant melanoma. In several in vitro studies, carbon ions (C ions) have been also shown to decrease the metastatic potential of melanoma cells. CXC motif 10 (CXCL10) has been shown to play a crucial role in regulating tumor metastasis and it significantly increase in human embryonic kidney cells after heavy ion irradiations. This study sought to explore the regulatory effect of C ions on melanoma metastasis, emphasizing the role of CXCL10 in this process. To explore the potential regulatory effect of C ions on tumor metastasis in vivo, we developed a lung metastasis mouse model by injecting B16F10 cells into the footpad and subjected all mice to treatment with X rays and C ions. Subsequently, a series of assays, including histopathological analysis, enzyme-linked immunosorbent assay, real-time PCR, and western blotting, were conducted to assess the regulatory effects of C ions on melanoma. Our results showed that mice treated with C ions exhibited significantly less tumor vascularity, enhanced tumor necrosis, alleviated lung metastasis, and experienced longer survival than X-ray irradiated mice. Moreover, VEGF expression in B16F10 cells was significantly reduced by C-ion treatment, which could be alleviated by CXCL10 knockdown in vitro. Further investigations revealed that co-culturing with HUVECs resulted in a significant inhibition of proliferation, migration, and tube formation ability in the C-ion treated group, while the opposite effect was observed in the C-ion treated with si-CXCL10 group. In conclusion, our findings demonstrate that treatment with carbon-ion radiation can suppress angiogenesis and lung metastases in melanoma by specifically targeting CXCL10. These results suggest the potential utility of carbon ions in treating melanoma.

BACKGROUND:To explore the expression and carcinogenic mechanism of RIPK2 in human tumours, and to provide the theoretical basis for the further study of RIPK2.METHODS:We used the TCGA, CPTAC, HPA databases to analyse the expression, mutation, and prognosis of RIPK2 in human tumours. Through the Cbioportal, Ualcan, TIMER2.0, and STRING websites, We understand the genetic variation, immune infiltration and enrichment analysis of RIPK2 related genes.RESULTS:RIPK2 was highly expressed in most tumours (such as BRCA, COAD and LUSC, etc.), and the high expression of RIPK2 was correlated with tumour stage and prognosis. In addition, Amplification was the main type of RIPK2 in tumour mutation state, and the amplification rate was about 8.5%. In addition, RIPK2 was positively associated with tumour-infiltrating immune cells (such as CD8+ T, Tregs, and cancer-associated fibroblasts). According to the KEGG analysis, RIPK2 may play a role in tumour mainly through NOD-like signaling pathway and NF-kappaB signaling pathway. GO enrichment analysis showed that the RIPK2 is mainly related to I-kappaB kinase/NF-kappaB signaling, Ribonucleoprotein granule and Ubiquitin-like protein ligase binding.CONCLUSION:RIPK2 plays an important role in the occurrence, development and prognosis of malignant tumours. Our pancancer study provided a relatively comprehensive description of the carcinogenic effects of RIPK2 in different tumours, and provided useful information for further study of RIPK2.

Abstract Objective Carbon ions suppress the effect of glutathione peroxidase 4 (GPX4) on the proliferation and metastasis of lung adenocarcinoma A549 cells. Methods The clonogenic formation ability of A549 cells was calculated with different ray doses of radiation. Cell proliferation, cycle, and apoptosis of A549 cells after different ray irradiation were detected by cck8 and flow cytometry. The transwell assay was used to detect the cell migration and invasion after different rays of radiation to A549 cells. The GPX4 matrix metalloproteinase 2 and E‐cadherin expression levels were assessed by immunofluorescence and western blot. Results At the dose of 4 Gy, A549 cell viability was 22.95 ± 5.00% and 55.52 ± 3.26% when treated with carbon ions and X‐rays, respectively. The distribution of A549 cells arrested in the G2 phase by carbon ion irradiation was positively correlated with radiation dose, with a most significant increase at 4 Gy irradiation (t = 4.303, p < 0.05). The results of apoptosis after irradiation showed were no significant differences in apoptosis at 1 and 2 Gy of X‐ray compared with 0 Gy, and 4 Gy irradiation significantly induced apoptosis in A549 cells (t = 30.520, p < 0.05). The apoptotic rate of carbon ion‐irradiated cells increased in a dose‐dependent manner and was the highest at 4 Gy (t = 17.356, p < 0.05). The transwell assays showed significantly decreased migration and invasion of both ray‐irradiated cells compared with the 0 Gy control cells. The carbon ions of 2 and 4 Gy significantly inhibited A549 cell migration (t2Gy = 9.260, t4Gy = 19.052, both p < 0.05) and invasion compared with those in the control cells (t2Gy = 6.141, t4Gy = 12.700, both p < 0.05). Treatment with 2 and/or 4 Gy doses of carbon ion reduced GPX4 (t2Gy = 8.170, t4Gy = 13.811, both p < 0.05) and matrix metalloproteinase 2 (t2Gy = 207.620, t4Gy = 93.170, both p < 0.05) protein expression, but E‐cadherin expression was increased (t2Gy = 62.811, t4Gy = 102.106, both p < 0.05). Conclusion Compared with X‐ray irradiation, carbon ions have a higher relative biological effectiveness and can increase the proportion of A549 cells arrested in the G2/M stage to induce apoptosis, thereby inhibiting proliferation. At the same dose with X‐ray, carbon ions may inhibit the migration and invasion of A549 cells by regulating the expression of GPX4, matrix metalloproteinase 2, and E‐cadherin.

Background The lncRNA H19 is believed to act as an oncogene in various types of tumors and is considered to be a therapeutic target and diagnostic marker. However, the role of the lncRNA H19 in regulating the radiosensitivity of non-small cell lung cancer (NSCLC) cells is unknown. Methods The expression profiles of lncRNAs in NSCLC were explored via transcriptome sequencing. CCK-8, EdU incorporation and clonogenic survival assays were conducted to evaluate the proliferation and radiosensitivity of NSCLC cells. Flow cytometry and Western blotting were conducted to measure the level of apoptosis. The binding relationship between the lncRNA H19 and miR-130a-3p was determined by a dual-luciferase reporter assay. A binding relationship was also identified between miR-130a-3p and With-No-Lysine Kinase 3 (WNK3). Results Expression patterns of lncRNAs revealed that the lncRNA H19 was upregulated in radioresistant NSCLC (A549-R11) cells compared with A549 cells. Knockdown of the lncRNA H19 enhanced the sensitivity of NSCLC cell lines to X-ray and carbon ion irradiation. Mechanistically, the lncRNA H19 serves as a sponge of miR-130a-3p, which downregulates WNK3 expression. The lncRNA H19–miR-130a-3p–WNK3 axis modulates radiosensitivity by regulating apoptosis in NSCLC cell lines. Conclusion Knockdown of the lncRNA H19 promotes the sensitivity of NSCLC cells to X-ray and carbon ion irradiation. Hence, the lncRNA H19 might function as a potential therapeutic target that enhances the antitumor effects of radiotherapy in NSCLC.

目的 分析益气健脾方辅助奥沙利铂结合替吉奥(SOX)化疗方案对晚期胃癌患者T淋巴细胞亚群平衡及胃肠激素的影响.方法 气虚血瘀证晚期胃癌患者100例,随机分成两组,对照组(50例)奥沙利铂结合替吉奥胶囊化疗,观察组(50例)在对照组基础上加用益气健脾方;观察患者临床疗效、T淋巴细胞亚群含量、胃肠激素含量、生命质量监测量表(QLQ-C30)与卡氏(KPS)评分及不良反应情况.结果 观察组总有效率明显高于对照组(P<0.05);治疗后观察组血清CD8+含量较治疗前、对照组明显降低,CD3+含量、CD4+/CD8+比值较治疗前、对照组明显上升(P<0.05);治疗后观察组血清促胃液素(GAS)、胃蛋白酶原(PG)Ⅱ及PGⅠ含量较治疗前、对照组明显上升(P<0.05);治疗后观察组QLQ-C30评分较治疗前、对照组明显降低,KPS评分较治疗前、对照组明显上升(P<0.05).结论 益气健脾方联合化疗可显著改善患者免疫功能,提升患者生活质量与疗效,降低毒副反应.

Pelvic radiotherapy is the key treatment for pelvic malignancies, usually including pelvic primary tumour lesions and lymphatic drainage areas in the pelvic region. Therefore, the intestinal tract in the radiation field is inevitably damaged, a phenomenon clinically referred to as radiation enteritis, and diarrhoea is the most common clinical symptom of radiation enteritis. Therefore, it is necessary to study the mechanism of radiation-induced diarrhoea. It has been found that the gut microbiome plays an important role in the development of diarrhoea in response to pelvic radiotherapy, and the species and distribution of intestinal microbiota are significantly altered in patients after pelvic radiotherapy. In this study, we searched for articles indexed in the Cochrane Library, Web of Science, EMBASE and PubMed databases in English and CNKI, Wanfang data and SINOMED in Chinese from their inception dates through 13 March 2020 to collect studies on the gut microbiome in pelvic radiotherapy patients. Eventually, we included eight studies: one study report on prostatic carcinoma, five studies on gynaecological carcinoma and two papers on pelvic carcinomas. All studies were designed as self-controlled studies, except for one that compared toxicity to nontoxicity. The results from all the studies showed that the diversity of intestinal flora decreased during and after pelvic radiotherapy, and the diversity of intestinal flora decreased significantly in patients with diarrhoea after radiotherapy. Five studies observed that the community composition of the gut microbiota changed at the phylum, order or genus level before, during, and after pelvic radiotherapy at different time points. In addition, the composition of the gut microbiota before radiotherapy was different between patients with postradiotherapy diarrhoea and those without diarrhoea in five studies. However, relevant studies have not reached consistent results regarding the changes in microbiota composition. Changes in the intestinal flora induced by pelvic radiotherapy and their relationship between changes in intestinal flora and the occurrence of radiation-induced diarrhoea (RID) are discussed in this study, providing a theoretical basis for the causes of RID after pelvic radiotherapy.

[This corrects the article DOI: 10.3389/fonc.2020.601620.].

Background: To evaluate locoregional failure and its impact on survival by comparing involved field irradiation (IFI) with elective lymph node irradiation (ENI) for patients with esophageal squamous cell cancer who underwent post-operative radiotherapy. Methods and Materials: The enrolled patients were randomized allocated to IFI or ENI group. CTV of IFI was generated according to pre-operative primary tumor location and post-operative pathological characters and positive LNs regions. CTV of ENI was generated according to pre-operative tumor position to administer selective lymph node irradiation. Radiotherapy planning was delivered using either 3D-CRT or IMRT. Results: A total of 57 patients were enrolled, 28 patients in ENI group and 29 patients in IFI group. There were not statistical differences between two groups in baseline (p>0.05). The initial locoregional failure rate was 17.9 % in ENI arm and 20.7% in IFI arm respectively (p=0.085). The 1-, 3-, and 5-year Progression-free Survival (PFS) were 63.2, 43.5, and 21.8 % in ENI arm versus 78.2, 60.1, and 55.1% in IFI arm (p =0.038). The 1-, 3-, and 5-year overall survival (OS) were 78.6, 46.9, and 23.5 % in ENI arm versus 72.9, 59.7, and 54.3 % in IFI arm (p=0.06). Acute radiation pneumonitis (p=0.005) and hematological toxicities (p =0.029) also showed statistical differences between groups, ENI arm was more than IFI arm. Conclusions: The results indicated that IFI tended to improve survival and reduce toxicities for patients with operative ESCC and did not increase locoregional failure compared to ENI. It is thus suggested that IFI for ESCC PORT is worthy of clinical recommendation and further study.

Abstract Background A combination of programmed cell death protein‐1 (PD‐1)/programmed cell death ligand‐1 (PD‐L1) inhibitors and radiotherapy (RT) is increasingly being used to treat non‐small‐cell lung cancer (NSCLC). However, the safety and efficacy of this approach remains controversial. We performed a systematic review and meta‐analysis to summarize the related research. Methods We searched the China Biology Medicine, EMBASE, Cochrane Library, and PubMed databases for all the relevant studies. The Stata software, version 12.0 was used for the meta‐analysis. Results The study included 20 clinical trials that enrolled 2027 patients with NSCLC. Compared with non‐combination therapy, combination therapy using PD‐1/PD‐L1 inhibitors and RT was associated with prolonged overall survival (OS) (1‐year OS: odds ratio [OR] 1.77, 95% confidence interval [CI] 1.35–2.33, p = 0.000; 2‐year OS: OR 1.77, 95% CI 1.35–2.33, p = 0.000) and progression‐free survival (PFS) (0.5‐year PFS: OR 1.83, 95% CI 1.13–2.98, p = 0.014; 1‐year PFS: OR 2.09, 95% CI 1.29–3.38, p = 0.003; 2‐year PFS: OR 2.47, 95% CI 1.13–5.37, p = 0.023). Combination therapy also improved the objective response rate (OR 2.76, 95% CI 1.06–7.19, p = 0.038) and disease control rate (OR 1.80, 95% CI 1.21–2.68, p = 0.004). This meta‐analysis showed that compared with non‐combination therapy, combination therapy using PD‐1/PD‐L1 inhibitors and RT did not increase the serious adverse event rates (≥grade 3); however, this approach increased the rate of grade 1–2 immune‐related or radiation pneumonitis. Subgroup analyses revealed that the sequence of PD‐1/PD‐L1 inhibitors followed RT outperformed in which concurrent PD‐1/PD‐L1 inhibitor and RT followed PD‐1/PD‐L1 inhibitor. Combination of stereotactic body RT or stereotactic radiosurgery with PD‐1/PD‐L1 inhibitors may be more effective than a combination of conventional RT with PD‐1/PD‐L1 inhibitors in patients with advanced NSCLC. Conclusion Combination therapy using PD‐1/PD‐L1 inhibitors and RT may improve OS, PFS, and tumor response rates without an increase in serious adverse events in patients with advanced NSCLC. However, combination therapy was shown to increase the incidence of mild pneumonitis.

Background: Radiation is a mode of treatment for many pelvic malignancies, most of which originate in the gynecologic, gastrointestinal, and genitourinary systems. However, the healthy gut is unavoidably included in the irradiation volume, resulting in undesirable results that manifest as radiation-induced diarrhea (RID), which is the most common side effect of radiation therapy and significantly affects the patients' quality of life. This study aimed to investigate the potential mechanism of diarrhea after pelvic radiotherapy in rats based on the effect of radiation on bile acid homeostasis and sodium-dependent bile acid transporter (Asbt).Methods: In this experimental study, male Sprague-Dawley rats were divided into the following groups - pelvic irradiation, cholestyramine-concurrent radiation, and control groups. The rats in the pelvic irradiation group were irradiated in the pelvic region with 2 Gy per day for five consecutive days. The total bile acid (TBA) levels in the ileum, colon, and feces were measured using automatic biochemical analyzer, and the levels of individual bile acids were evaluated by liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS). The mRNA and protein expression of Asbt in ileum were assessed by qRT-PCR and Western blot assay. The rats in the cholestyramine-concurrent radiation group were administered with cholestyramine, a bile acid-chelating resin, and concurrent radiation for 5 days. The body weight of rats was monitored daily, and the degree of diarrhea was scored.Results: Diarrhea was observed at 2 and 3 days post-pelvic radiation. The TBA levels were significantly decreased at 4 and 5 days post-radiation in the ileum (p < .01, p < .01) and increased at 4 and 5 days post-radiation in the colon (p < .05, p < .05). The fecal excretions of TBA were significantly increased at 3, 4, and 5 days post-radiation (p < .05). The levels of individual bile acids were significantly decreased in the ileum and increased in the colon and feces, post-radiation. The mRNA and protein expression of Asbt in the ileum gradually decreased with increasing days of pelvic radiation and significantly decreased at 3 and 5 days post-radiation, respectively. Furthermore, a significant decrease in body weight was observed post-pelvic radiation, and cholestyramine administration did not reverse the weight loss. However, the incidence of RID was decreased after administration of cholestyramine.Conclusions: Bile acid malabsorption is partially responsible for RID post-pelvic radiation in rats, and the potential mechanism is related to the downregulation of the ileal Asbt.

目的:探讨益气健脾方联合SOX方案化疗对晚期胃癌患者免疫功能及临床疗效的影响.方法:选取我院2017年6月至2019年2月收治的晚期胃癌患者106例,随机分为观察组与对照组,每组53例.两组患者均进行SOX方案化疗治疗,观察组患者在此基础上,应用益气健脾方进行治疗.比较两组临床疗效、免疫功能指标及不良反应的发生情况.结果:两组治疗前CD4+、CD8+、CD4+/CD8+比率均无显著差异(P>0.05);治疗后,观察组CD4+、CD4+/CD8+比率均高于对照组(P<0.05),CD8+比率低于对照组(P<0.05).观察组治疗有效率、疾病控制率高于对照组(P<0.05).观察组各不良反应发生率均低于对照组(P<0.05).结论:益气健脾方联合SOX方案化疗治疗晚期胃癌能提高患者临床疗效及疾病控制率,改善机体免疫功能,减少不良反应发生,值得推广应用.

Objective To evaluate the efficacy and safety of carbon ion and proton therapy for hepatocellular carcinoma (HCC) by Meta-analysis. Methods PubMed, The Cochrane Library, EMBASE, Chinese Journal Full-text, Chinese Biomedical Literature and Wanfang Database were searched to collect relevant clinical studies on carbon ion and proton therapy for HCC. Two reviewers independently screened the literature and extracted data based on inclusion and exclusion criteria. Meta-analysis was carried out by Stata 12.0. Results We included 7 carbon ion and 23 proton therapy studies. According to the combined results, both carbon ion and proton therapies for HCC obtained good local control rate and low adverse reactions, and the incidence of severe adverse reactions was low. Subgroup analysis showed that carbon ion and proton therapies improved the 5-year OS of HCC patients with either favorable or poor prognosis. Conclusion Both carbon ion and proton therapies may be the effective alternative treatment options for HCC with favorable prognosis, and also show better efficacy for HCC patients with poor prognosis.

目的 评价食管癌临床指南和共识的方法学质量和报告质量.方法 计算机检索PubMed、EMbase、Web of Science、CBM、WanFang Data和CNKI数据库,同时补充检索GIN、NICE、NGC和医脉通网站,搜集食管癌相关的临床指南和共识,检索时限均从建库至2018年8月.由2位评价员按照纳入与排除标准独立筛选文献和提取资料后,采用AGREE Ⅱ和RIGHT工具对纳入指南的质量进行评价.结果 共纳入食管癌指南和共识26个.AGREE Ⅱ各领域平均得分分别为:范围和目的49.63％、参与人员25.16％、制订严谨性23.42％、清晰性49.25％、应用性16.91％和编辑独立性21.07％;RIGHT评价条目中报告率最高的条目为5(84.62％),其次为1a (80.77％)、1c (65.38％)、13a (65.38％)、4(61.54％),其余条目报告率均在50％以下.亚组分析结果显示:基于循证医学方法制订的指南和共识在AGREE Ⅱ的6个领域和RIGHT评分平均得分均高于基于专家意见或综述等制订的指南和共识;国外指南和共识在AGREE Ⅱ的3个领域(制订严谨性、清晰性、编辑独立性)和RIGHT评分平均得分均高于国内指南和共识.结论 食管癌临床指南和共识的方法学质量和报告质量均偏低,尤其是我国指南和共识更低,需进一步提高.建议指南制订者参考AGREE Ⅱ和RIGHT等标准,制订出高质量的指南并推广应用,更好地规范化食管癌的诊疗.

[目的]比较埃克替尼联合胸部放疗与单独埃克替尼治疗Ⅲ/Ⅳ期EGFR突变阳性NSCLC的临床有效性及安全性.[方法]按照纳入排除标准,选择2012年1月至2017年12月在甘肃省肿瘤医院首次采用埃克替尼联合胸部放疗或单独埃克替尼治疗的EGFR突变阳性NSCLC患者,比较两种治疗模式在胸部原发灶的近期缓解率、无进展生存时间(PFS)、总生存时间(OS)、埃克替尼耐药时间及毒副反应发生方面的差异,并分析各临床因素对患者生存的影响.[结果]共纳入76例患者,其中埃克替尼联合胸部放疗组28例,单药埃克替尼组48例.两组比较,近期疗效方面存在统计学差异(P=0.009),特别是ORR方面埃克替尼+TRT组显著优于单独埃克替尼组(P=0.002);生存情况方面,1、2年PFS和OS两组差异均无统计学意义(P＞0.05),但在中位OS(40.3个月vs25.7个月)和中位PFS(34.2个月vs19.9个月)方面,埃克替尼+TRT组均优于单独埃克替尼组;多因素分析显示,埃克替尼耐药时间及总应用时间与PFS和OS均成正相关(P=0.000),患者近期疗效与患者PFS和OS也密切相关(P=0.000).毒副反应方面,急性放射性肺炎、放射性食管炎、白细胞减少、恶心呕吐两组间存在统计学差异(P＜0.05),埃克替尼+TRT组高于单独埃克替尼组;而埃克替尼相关的皮疹、腹泻、口腔溃疡、肝功能异常、血栓形成以及贫血、血小板减少方面两组差异均无统计学意义(P＞0.05).[结论]埃克替尼联合胸部放疗与单独埃克替尼比较在治疗局部晚期或晚期EGFR突变阳性NSCLC中,能提高肺部原发灶的近期缓解率,改善无进展生存期和总生存期,且未增加TKI药物相关的毒副反应发生,是一种有效且安全的治疗模式.

AIMS:To investigate the roles of deleted in lymphocytic leukemia-2 (DLEU2) in the pathology of cervical cancer.METHODS:Differentially expressed long non-coding RNAs between cervical cancerous and para-cancerous tissues were examined in 26 clinical specimens by microarray analysis and quantitative real-time PCR. DLEU2 expression was correlated with clinical features in 108 patients with cervical cancer. The effects of DLEU2 on growth, proliferation, migration, and invasion were examined in cervical cancer cells.RESULTS:DLEU2 was correlated with lymphovascular invasion in patients with cervical cancer. DLEU2 overexpression inhibited cell proliferation, migration, and proliferation, and colony formation in cervical cancer cells.CONCLUSION:DLEU2 is involved in the pathology of cervical cancer, and it may be a target for clinical therapy.

[目的]观察影像引导后程加速超分割放疗联合奈达铂化疗治疗食管癌的有效性及安全性.[方法] 2016年1月至2017年3月60例食管癌初治患者按照随机数字表法分为后程加速超分割放疗联合奈达铂化疗(观察组)和后程加速超分割放疗联合多西他赛+顺铂化疗(对照组),各30例,放疗采用影像引导调强适形精确放疗技术,6MV-X线,4～5个共面或非共面适形照射野,前程GTV和GTVnd总剂量44Gy,2.2Gy/次,共20次,CTV总剂量36Gy,1.8Gy/次,共20次,5次/周;后程GTV和GTVnd总剂量18Gy,1.5Gy/次,共12次,CTV总剂量13.2Gy,1.1Gy/次,共12次.化疗:观察组单药奈达铂40mg/m2静脉滴注,放疗期间1次/周.对照组:多西他赛60mg/m2静脉滴注d1,顺铂25mg/m2静脉滴注d1-3,放疗第1、28天开始化疗.比较两组近期有效率、不良反应发生率、局控率和生存率.[结果]两组近期疗效评价差异无统计学意义(P＞0.05);观察组与对照组中位局部控制时间分别为(24.0±4.1)个月(95％CI:15.9～32.1)和(26.0±2.2)个月(95％CI:21.7～30.2),1-、2-、3-年局部控制率分别为80.0％、53.3％、33.3％和76.7％、63.3％、36.7％(x2=0.575,P=0.448),中位生存期分别为(27.0±3.4)个月(95％CI:20.4～33.6)和(32.0±3.0)个月(95％ CI:26.2～37.8),1-、2-、3-年生存率分别为83.3％、66.7％、40.0％和86.7％、70.0％、46.7％(x2=0.425,P=-0.515).观察组心脏、肾脏和放射性食管炎不良反应发生率均低于对照组(P=0.036、0.038、0.032),胃肠道反应及血液学不良反应无差异.[结论]影像引导后程加速超分割调强适形放疗同步奈达铂周化疗治疗食管癌有效性与后程加速超分割放疗同步多西他赛联合顺铂方案相似,安全性更优于放疗同步两药联合方案.

Objective To evaluate the safety and efficacy of carbon ion and proton therapies for pancreatic cancer (PaC). Methods The databases were electronically searched to collect the studies about the carbon ion and proton therapies for PaC from inception to June 2019. Two reviewers independently screened literature and extracted data. A Meta-analysis was performed by STATA 12.0 and MetaAnalyst Beta 3.13 software. Results A total of 8 studies involving 459 PaC patients were included. The incidence of grade 2, 3 and 5 gastrointestinal (GI) ulcer toxicities in PaC patients treated with carbon ion and proton therapies were 7%, 2% and 0; the incidence of grade 2, 3 and 4 anorexia toxicities were 6%, 3.2% and 0; the 1- and 2-year OS rates were 77% and 45%; the 2-year local control (LC), 1-year freedom from local progression (FFLP) and 1-year local recurrence(LR) rates were 81%, 88% and 15%. The incidence of grade 2, 3, 2-3 GI ulcer toxicities in carbon ion and proton therapies for PaC were 6.8%, 1.5%, 9.2% and 3.5%, 8.3%, 6.1% (P < 0.05); and the 1- and 2-year OS were 77.1%, 44.4% and 77.6%, 49.7% (P > 0.05). Conclusion Carbon ion and proton therapies for PaC are safe and effective; and the security and effectiveness of the two methods are similar.

Radiation therapy is an important component of the comprehensive treatment of esophageal cancer. However, conventional radiation resistance is one of the main reasons for treatment failure. The superiority of heavy ion radiation in physics and biology has been increasingly highlighted in radiation therapy research. The Janus Kinase 2/Signal Transducer and Activator of Transcription 3 (JAK2/STAT3) pathway plays an important role in the occurrence, development and metastasis of esophageal squamous cell carcinoma (ESCC) and is related to the development of resistance to ionizing radiation in ESCC. Therefore, the aim of the present study was to investigate the relationship between carbon ion inhibition of the proliferation and metastasis of esophageal carcinoma cells and the JAK2/STAT3 signaling pathway. The results demonstrated that carbon ion beams significantly reduced cell viability and stimulated apoptosis in human ESCC cells in a dose-dependent manner. In addition, carbon ion beams induced G2/M phase cell cycle arrest in ESCC cells and inhibited tumor metastasis in a dose-dependent manner. Additionally, poorly differentiated KYSE150 cells were more sensitive to the same carbon ion beam dose than moderately differentiated ECA109 cells. Carbon ion beam exposure regulated the relative expression of metastasis-related molecules at the transcriptional and translational levels in ESCC cells. Carbon ion beams also regulated CDH1 and MMP2 downstream of the STAT3 pathway and inhibited ESCC cell metastasis, which activated the STAT3 signaling pathway. This study confirmed the inhibition of cell proliferation and the metastatic effect of carbon ion beam therapy in ESCC cells.