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1.
摘要 目的:研究信迪利单抗与阿帕替尼在晚期食管癌二线治疗中的应用效果。方法:根据随机数字表法将2019年1月~2022年1月本院收治的70例食管癌患者分为对照组与观察组,每组各35例,对照组给予阿帕替尼治疗,观察组给予信迪利单抗与阿帕替尼联合治疗,观察两组患者的客观缓解率(ORR)、疾病控制率(DCR),并在治疗前后利用酶联免疫吸附法检测其糖类抗原50(CA-50)、糖类抗原199(CA199)、癌胚抗原(CEA)、鳞癌抗原(SCC)水平;随后通过随访记录两组患者的预后生存期,并建立多因素Logistic模型分析影响患者达到中位OS、PFS的独立危险因素。结果:与对照组比较,观察组ORR、DCR率较高(P<0.05)。与对照组相比,治疗后观察组血清CA50、CA199、CEA、SCC水平较低(P<0.05)。与对照组比较,观察组中位OS、PFS较长(P<0.05)。多因素Logistic分析结果显示,治疗方法、CA50、CA199、CEA、SCC是影响食管癌预后生存期的独立危险因素(P<0.05)。结论:利用免疫检查点抑制剂与抗血管生成药物对晚期食管癌患者开展二线治疗,不仅能降低血清中的肿瘤标志物浓度,还能延长患者的预后生存期,治疗效果较为显著。  相似文献   
2.
目的:探讨阿帕替尼抑制肝癌细胞增殖促进凋亡的作用机制。方法:选取肝癌细胞系SNU739、HepG2,以CCK-8细胞增殖实验、平板克隆实验测定阿帕替尼对肝癌细胞增殖及克隆形成能力的影响;流式细胞术检测阿帕替尼对肝癌细胞凋亡的影响;蛋白免疫印迹法检测阿帕替尼影响肝癌细胞凋亡相关蛋白Bax、Bcl-2及Caspase3的表达情况。结果:与对照组相比,阿帕替尼可显著抑制肝癌细胞增殖(P0.05)。平板克隆实验提示与对照组相比,10μM和20μM阿帕替尼组肝癌细胞克隆数明显减少(P0.05)。流式细胞术结果提示10μM和20μM阿帕替尼处理组细胞凋亡率明显增加(P0.05)。蛋白免疫印迹法结果显示经阿帕替尼处理的肝癌细胞,促凋亡蛋白Bax及Caspase3的活性片段Cleaved-caspase3表达水平显著上调,抗凋亡蛋白Bcl-2显著下调(P0.01)。结论:阿帕替尼通过调节肝癌细胞凋亡相关蛋白从而抑制肝癌细胞增殖、促进其凋亡。  相似文献   
3.
摘要 目的:探讨伊立替康联合阿帕替尼治疗术后转移性胃癌患者临床疗效和安全性。方法:选取我院2017年5月-2018年10月期间收治的术后一线化疗失败转移性胃癌患者105例,根据随机数字表法分为研究组(53例)和对照组(52例),对照组患者给予伊立替康静脉滴注治疗,研究组在此基础上使用阿帕替尼进行联合治疗,4周为一个周期,连续治疗两个周期。比较两组患者疾病控制率、生存情况,并对治疗前后两组患者肿瘤标志物[癌胚抗原(CEA)、糖类抗原125(CA125)和糖类抗原199(CA199)]水平、基质金属蛋白酶-9(MMP-9)和血管内皮生长因子(VEGF)水平进行比较,观察治疗过程中两组患者不良反应发生情况。结果:治疗后,研究组疾病控制率、中位生存时间和中位进展时间均优于对照组(P<0.05)。治疗后,两组肿瘤标志物、MMP-9和VEGF水平均降低,且研究组低于对照组(P<0.05)。研究组不良反应发生率低于对照组(P<0.05)。结论:伊立替康联合阿帕替尼治疗术后转移性胃癌患者临床疗效确切,可延长患者生存时间,延缓疾病进展,且安全性较好,其作用机制可能与降低肿瘤标志物及MMP-9、VEGF水平有关。  相似文献   
4.
摘要 目的:观察晚期复发转移食管癌经阿帕替尼联合替吉奥治疗后的疗效及对患者T细胞亚群和血清肿瘤标志物水平的影响。方法:病例搜集时间为2015年3月至2018年3月,病例搜集范围为我院接收的晚期复发转移食管癌患者70例。采用信封抽签法将患者分为对照组和实验组,各为35例。对照组给予替吉奥治疗,实验组在对照组的基础上联合阿帕替尼治疗,两组均连续化疗2个周期。对比两组化疗2个周期后的客观缓解率、疾病控制率;对比两组化疗前、化疗2个周期后的T细胞亚群和血清肿瘤标志物水平;对比两组中位总生存期(mOS)、中位无进展生存期(mPFS)及生命质量评分,记录两组化疗期间毒副反应发生情况。结果:实验组的客观缓解率45.71%、疾病控制率68.57%高于对照组的22.86%、42.86%(P<0.05)。两组化疗2个周期后CD3+、CD4+、CD4+/ CD8+均较化疗前降低,但实验组高于对照组(P<0.05);CD8+较化疗前升高,但实验组低于对照组(P<0.05)。两组化疗2个周期后肿瘤特异性生长因子(TSGF)、癌胚抗原(CEA)、糖类抗原199(CA199)较化疗前降低,且实验组低于对照组(P<0.05)。实验组的mOS、mPFS长于对照组(P<0.05),两组化疗结束后3个月QLQ-OES24评分均升高,且实验组高于对照组(P<0.05)。两组不良反应发生率对比,差异无统计学意义(P>0.05)。结论:晚期复发转移食管癌经阿帕替尼联合替吉奥治疗后,病情得到有效控制,血清肿瘤标志物水平降低更为显著,同时还可减轻免疫抑制,延长mOS、mPFS,且不增加毒副反应,近期疗效可靠。  相似文献   
5.
摘要 目的:探讨阿帕替尼对二线化疗失败晚期胃癌患者肿瘤标志物与胃黏膜四项水平及预后的影响。方法:选取2016年12月~2020年3月医院收治的80例二线化疗失败晚期胃癌患者,随机分为研究组和对照组各40例。对照组给予常规支持对症治疗,研究组在对照组基础上给予阿帕替尼治疗。比较两组临床疗效、肿瘤标志物[癌胚抗原(CEA)、癌抗原125(CA125)、糖蛋白抗原199(CA199)]、胃黏膜四项[胃蛋白酶原Ⅰ(PG Ⅰ),胃蛋白酶原Ⅱ(PG Ⅱ),胃泌素17(G-17)、幽门螺旋抗体(Hp-Ab)]、不良反应及预后情况。结果:研究组总缓解率、疾病控制率均高于对照组,差异有统计学意义(P<0.05)。与治疗前比较,治疗后研究组血清CEA、CA125、CA199水平均降低,且研究组低于对照组(P<0.05)。与治疗前比较,治疗后研究组PG Ⅰ水平较治疗前升高,且研究组高于对照组(P<0.05);治疗后,研究组PG Ⅱ、G-17水平、Hp-Ab阳性率均较治疗后降低,且研究组低于对照组(P<0.05)。两组总不良反应发生率无差异(P>0.05)。研究组无进展生存时间(PFS)、生存时间(OS)均长于对照组、生存率高于对照组,差异有统计学意义(P<0.05)。结论:阿帕替尼对二线化疗失败晚期胃癌患者的疾病控制率较好,可有效降低血清肿瘤标志物水平,改善胃粘膜功能,延长患者生存期。  相似文献   
6.
Apatinib (YN968D1) is a small‐molecule tyrosine kinase inhibitor(TKI)which can inhibit the activity of vascular endothelial growth factor receptor‐2 (VEGFR‐2). It has been reported that apatinib has anti‐tumour effect of inhibiting proliferation and inducing apoptosis of a variety of solid tumour cells, whereas its effect on vascular smooth muscle cells (VSMC) remains unclear. This study investigated the effect of apatinib on phenotypic switching of arterial smooth muscle cells in vascular remodelling. Compared to the vehicle groups, mice that were performed carotid artery ligation injury and treated with apatinib produced a reduction in abnormal neointimal area. For in vitro experiment, apatinib administration inhibited VSMC proliferation, migration and reversed VSMC dedifferentiation with the stimulation of platelet‐derived growth factor type BB (PDGF‐BB).In terms of mechanism, with the preincubation of apatinib, the activations of PDGF receptor‐β (PDGFR‐β) and phosphoinositide‐specific phospholipase C‐γ1 (PLC‐γ1) induced by PDGF‐BB were inhibited in VSMCs. With the preincubation of apatinib, the phosphorylation of PDGFR‐β, extracellular signal‐related kinases (ERK1/2) and Jun amino‐terminal kinases (JNK) induced by PDGF‐BB were also inhibited in rat vascular smooth muscle cell line A7r5. Herein, we found that apatinib attenuates phenotypic switching of arterial smooth muscle cells induced by PDGF‐BB in vitro and vascular remodelling in vivo. Therefore, apatinib is a potential candidate to treat vascular proliferative diseases.  相似文献   
7.
目的:评估解毒颗粒联合阿帕替尼治疗中晚期肝癌患者的疗效及其不良反应。方法:对2018年12月至2019年6月收治于海军军医大学第一附属医院口服解毒颗粒联合阿帕替尼的27例肝癌患者的临床资料进行回顾性研究。无法切除或复发的中晚期肝癌患者被纳入研究,给予解毒颗粒联合阿帕替尼治疗直至疾病进展或不可耐受其毒副反应,随访观察治疗效果、生存期、炎症因子指标及不良反应。结果:治疗后完全缓解(CR)4例(14.81%),部分缓解(PR)4例(14.81%),稳定(SD)8例(29.63%),进展(PD)11名患者(40.74%),疾病控制率(DCR)为59.26%(16/27),客观缓解率(ORR)为29.63%(8/27)。中位无进展生存期(PFS)为3.630个月,中位总生存期(OS)为13.667个月。常见的不良反应是高血压59.26%(16/27)、蛋白尿59.26%(16/27)、腹泻74.07%(20/27)以及手足综合征62.96%(17/27)。治疗后炎症因子指标中C反应蛋白、白介素2水平下降,存在统计学差异(P0.05)。结论:解毒颗粒联合阿帕替尼治疗中晚期肝癌安全、有效,可降低患者炎症反应,不良反应可耐受。  相似文献   
8.
目的阐明阿帕替尼 (apatinib)和白蛋白结合型紫杉醇 (nab-Paclitaxel)诱导MDA-MB-231乳腺癌细胞凋亡的分子机制。方法本研究以MDA-MB-231乳腺癌细胞为研究对象,并以apatinib和nab-Paclitaxel处理细胞后分组:0.1 %DMSO处理为阴性对照组;10 μmol/L apatinib处理组 (APA组);经5、10、15、20 nmol/L nab-Paclitaxel 处理组 (Nab-p 5组、Nab-p 10组、Nab-p 15组和Nab-p 20组);以及10 μmol/L apatinib分别与5、10、15、20 nmol/L nab-Paclitaxel 联合处理组 (APA+Nab-p 5组、APA+Nab-p 10组、APA+Nab-p 15组和APA+Nab-p 20组)。使用乳酸脱氢酶释放测定法测定apatinib和nab-Paclitaxel对MDA-MB-231细胞诱导的细胞毒活性,结合流式细胞术分析不同处理组细胞凋亡情况,通过JC-1染色法测定不同干预方式对MDA-MB-231细胞线粒体膜电位变化 (ΔΨm)的影响,借助FAM-FLICA荧光成像检测caspase-8和caspase-9 活性,通过彗星试验评估apatinib和nab-Paclitaxel对非致瘤上皮细胞株MCF-10A细胞DNA损伤的影响。两组之间独立样本t检验或单向ANOVA进行比较,多组之间使用Tukey事后检验。结果细胞毒性检测结果显示,与阴性对照组相比,Nab-p 20组MDA-MB-231细胞杀伤率在24 h时接近90 %;与单药处理组 (Nab-p 5组和Nab-p 10组)相比,APA+Nab-p 5组和APA+Nab-p 10组联合处理24 h和48 h后,分别检测到约85 %和95 %细胞死亡,差异均具有统计学意义 (P 均 < 0.001)。流式细胞术统计结果显示,与Nab-p5组和Nab-p10组相比,APA+Nab-p 5组和APA+Nab-p 10组24 h时MDA-MB-231细胞凋亡率(31.8 %±1.48 %、33.25 %±1.77 %比76.11 %±1.14 %、89.4 %±1.07%)升高 (P 均 < 0.05)。线粒体膜电位检测结果表明,与对照组相比,在单药处理组中,仅APA组和Nab-p 10组24 h时去极化细胞 (12.35 %±1.05%比78.33%±1.11%、46.74%±1.75%)增多;在联用处理组中,APA+Nab-p 5组和APA+Nab-p 10组24 h时去极化细胞 (68.47%±1.94%比90.03%±1.79%)增多,差异均有统计学意义 (P 均 < 0.05)。FAM-FLICA荧光成像结果显示,相较于单一处理组,apatinib和nab-Paclitaxel联用处理组的caspase-8和caspase-9蛋白高度活化。结合彗星试验分析,apatinib和nab-Paclitaxel 干预对MCF-10A非致瘤上皮细胞株DNA完整性没有显著影响。结论 apatinib/nab-Paclitaxel联用通过内源性的线粒体功能扰动和外源性的caspase激活诱导三阴性乳腺癌细胞MDA-MB-231凋亡,发挥协同抗癌作用。  相似文献   
9.
BackgroundAlpha-fetoprotein-producing gastric cancer (AFPGC) poses a therapeutic challenge worldwide because of its poor prognosis. This study aimed to evaluate the efficacy and safety of antiangiogenic drug apatinib in advanced AFPGC in a real-world setting.MethodsFrom September 2015 to December 2017, twenty-one patients identified with AFPGC from the clinical trial AHEAD-G202, an open-label, prospective, multicenter, non-interventional study of apatinib for advanced metastatic gastric cancer, were enrolled to perform this analysis. Patients received oral apatinib as monotherapy or combination therapy. A treatment cycle was defined as 28 days. The primary outcome was progression-free survival (PFS) and overall survival (OS), and the secondary outcomes included safety, objective response rate (ORR), and disease control rate (DCR).ResultsTwenty patients were evaluated for the apatinib efficacy analysis. The ORR of apatinib was 10%, whereas the DCR was 70%. The median PFS was 3.5 months [95%confidence interval (CI): 2.34–4.66]. The median OS was 4.5 months (95%CI: 3.49–5.51). Median OS of AFPGC patients without carcinoembryonic antigen (CEA) elevation achieved 30.8 months. CEA elevation was considered to be a potential independent predictive factor for OS (P = 0.030) and PFS (P = 0.047) by the analysis of multivariate analysis. The most common grade 3 to 4 adverse events (AEs) were hypertension (4.8%), hand-foot syndrome (4.8%), anorexia (4.8%), and vomiting and nausea (4.8%).ConclusionApatinib showed promising efficacy and an acceptable safety profile in patients with advanced AFPGC. Antiangiogenic therapy may be a good strategy for the treatment of AFPGC as a rare sub-type of gastric cancer.Trial registrationAHEAD-G202 (NCT02668380).  相似文献   
10.
ObjectiveTo investigate the effect of apatinib when treating advanced gastric cancer (GC) as well as the mechanism of preventing infection. Methods: From January 2017 to December 2018, 100 advanced GC patients had failed to receive second-line or above treatment in XX Hospital were divided into two groups according to the experimental requirements: the experimental group and the blank group. The experimental group was treated with small molecule targeted drug apatinib, while the blank group was only treated with ordinary drugs. After 4 weeks of treatment, the diagnosis and evaluation were carried out every eight weeks. In this study, the mechanism of infection prevention and prognosis was studied through the internal treatment of GC patients with apatinib. Results: until the end of the fourth week, a significant difference can be seen in the treatment effect between the experimental group as well as the blank group. In the experimental group, the proportion of partial remission + disease stability reached about 73%, while that in the blank group was only about 33%. In addition, apatinib was better than the blank group in the control of adverse reactions like hypertension, proteinuria, myelosuppression as well as diarrhea. In addition, apatinib was better than the blank group when treating AFP positive GC. In terms of the therapeutic effect of apatinib, it is much better than that of the negative group. In addition, apatinib is also better than the blank group in drug resistance for GC patients. It is found that apatinib’s anti infection mechanism is to prevent the phosphorylation of vascular endothelial growth factor receptor-2 (VEGFR-2) as well as stop the downstream signal pathway, so as to inhibit the tumor angiogenesis, tumor growth and metastasis, so as to achieve treatment and reduce the probability of infection. Conclusion: the therapeutic effect of small molecule targeting drug apatinib on gastric cancer is better than that of other drugs, whether in therapeutic effect, drug resistance, adverse reactions or infection control. This study has important reference significance for the follow-up treatment of apatinib and cancer.  相似文献   
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