5%,疾病控制率87.5%,中位PFS为5个月,中位颅内病灶PFS为6个月。18例患者出现治疗相关不良反应,其中3例(12.5%)出现Ⅲ~Ⅳ度血液学毒性反应。4例(16.7%)出现Ⅲ~Ⅳ度非血液学毒性反应。结论:替莫唑胺联合全脑放疗治疗肺癌脑转移疗效较满意,不良反应可耐受,治疗依从性较好,远期生存获益仍需进一步的临床研究予以验证。
目的探讨肺癌患者转移灶中棘皮动物微管相关蛋白样4-间变性淋巴瘤激酶(EML4-ALK)的阳性表达率及其与临床病理特征、血清指标的关系和使用靶向治疗后的效果。方法使用实时荧光定量PCR法(FQ-PCR)对71例肺癌转移灶中EML4-ALK融合基因进行检测,同时检测患者血清标志物癌胚抗原(CEA)、癌糖原(CA125)及血管内皮生长因子(VEGF)水平,分析EML4-ALK融合基因在转移灶中表达情况及与血清标志物水平的相关性。结果在淋巴结、脑、骨、体表软组织、肝、结肠和胸膜转移组织中检测到EML4-ALK融合基因阳性表达的组织有淋巴结、脑、骨和胸膜,总阳性表达率为7.04%。转移灶组织中EML4-ALK融合基因表达阳性率与病理类型、性别、年龄、吸烟状态、分化程度和分期因素无明显相关(P>0.05),但临床上仍以腺癌、不吸烟者人群较多见。血清CEA、CA125、VEGF水平在EML4-ALK融合基因阳性组和阴性组中差异无统计学意义(P>0.05)。接受克唑替尼治疗的肺癌患者6个月疾病控制率为66%。结论使用FQ-PCR技术检测肺癌转移灶中EML4-ALK融合基因是可行的,可以为腺癌、不吸烟这些优势人群提供靶向治疗策略。
Patients

MDV3100供应商 TWS119 with pancreatic cancer have a poor prognosis with a median survival of 4-6 mo and a 5-year survival of less than 5%. Despite therapy with gemcitabine, patient survival does not exceed 6 mo, likely due to natural resistance to gemcitabine. Therefore, it is hoped that more favorable results can be obtained by using guided immunotherapy against molecular targets. This review summarizes

the new leading targeted therapies in pancreatic cancers, focusing on passive Selleckchem MGCD0103 and specific immunotherapies. Passive immunotherapy may have a role for treatment in combination with radiochemotherapy, which otherwise destroys the immune system along with tumor cells. It includes mainly therapies targeting against kinases, including epidermal growth factor receptor, Ras/Raf/mitogenactivated protein kinase cascade, human epidermal growth factor receptor 2, insulin growth factor-1 receptor, phosphoinositide 3-kinase/Akt/m

TOR and hepatocyte growth factor receptor. Therapies against DNA repair genes, histone deacetylases, micro RNA, and pancreatic tumor tissue stromal elements(stromal extracellular matric and stromal pathways) are also discussed. Specific immunotherapies, such as vaccines(whole cell recombinant, peptide, and dendritic cell vaccines), adoptive cell therapy and immunotherapy targeting tumor stem cells, have the role of activating antitumor immune responses. In the future, treatments will likely include personalized medicine, tailored for numerous molecular therapeutic targets of multiple pathogenetic pathways.