However, the single agent activity of these compounds in many tumor types remains modest. The mTOR axis is regulated by multiple upstream signaling pathways. Because
the genes (e.g., PIK3CA, KRAS, PTEN, and LKB1) that encode key components in these signaling pathways are frequently mutated in human cancers, a subset of cancer types may be addicted to a given mutation, leading to hyperactivation of the mTOR axis. Thus, efforts have been made to demonstrate the potential impact of genetic alterations on rapalogbased or 而且 mTOR-targeted cancer therapy. This review will primarily summarize research advances in this direction.
抗肿瘤药已成为全球医药市场中最大的产品单元,进入快速发展期。本文从肿瘤类疾病流行病学情况、全球抗肿瘤市场状况和主要跨国医药企业该类产品的发展等对抗肿瘤药市场趋势进行了综合分析,并对近年抗肿瘤药制剂技术的进展进行了简要介绍,以期为我国抗肿瘤药物的发展提供参考依据。
ALK+弥漫大B细胞淋巴瘤(anaplastic lymphoma kinase-positive diffuse large B-cell 
lymphoma,ALK+DLBCL)是弥漫大B细胞淋巴瘤的一种罕见的亚型,具有特殊的免疫母细胞或浆母细胞样的形态学特点,免疫表型独具特征,细胞遗传学异常,在儿童和成人都可发生。此病虽然罕见,但是其临床过程具有侵袭性且预后不良,因此明确认识该疾病的特点是诊断的关键。ALK+DLBCL对传统化疗方案反应性差,最近推出的小分子ALK抑制剂可能对这种疾病的患者提供了一个潜在的新的治疗选择。
目的:探讨原发系统性间变性大细胞淋巴瘤(primary 为什么 systemic anaplastic
large cell lymphoma,ALCL)患者的临床特征和预后,分析间变性淋巴瘤激酶(anaplastic lymphoma kinase,ALK)的表达及其他相关因素与预后的关系。方法:回顾性分析2002年12月-2011年9月在北京大学肿瘤医院接受诊治的45例ALCL患者的临床数据和随访资料。结果:45例原发系统性ALCL患者中,ALK表达阳性患者34例(75.6%),ALK表达阴性患者11例(24.4%)。ALK表达阳性患者和阴性患者的中位年龄分别为23.5和49.0岁,差异有统计学意义(P=0.022)。中位随访32个月,45例患者的估计5年总生存率为71.9%,其中ALK表达阳性和阴性患者的估计5年总生存率分别为71%和72%(P=0.581)。单因素和多因素分析结果均显示,仅初始疗效与预后相关(P<0.05)。结论:原发系统性ALCL患者发病年龄较轻,预后尚可。ALK表达状态并不能完全决定患者的预后。本研究提示,初始疗效是原发系统性ALCL的独立预后因素。
外周T细胞淋巴瘤(peripheral CFTR inhibitor supplier T-cell lymphoma,PTCL)是一种多样化的淋巴系统恶性增殖性疾病,起源于胸腺后成熟的T淋巴细胞或NK/T细胞,占非霍奇金淋巴瘤的5%～15%[1],呈现明显的异质性,即临床和病理特点的多样性,WHO分型中将成熟的T细胞与NK/T细胞分为22个亚型[2],其中最重要的包括外周T细胞淋巴瘤-非特异型(PTCL-NOS)、血管免疫母细胞性淋巴瘤(AITL)、间变大细胞性淋巴瘤(ALCL)及NK/T细胞淋
Objective:
To investigate PIK3CA mutation in Chinese patients with lung squamous cell carcinoma (LSCC) and explore their relationship with clinicopathological profiles. Methods: Tumor samples from 123 cases of LSCC were included in this study. PIK3CA mutations in exon 9 and 20 were screened by pyrosequencing and confirmed by clone sequencing or amplification refractory mutation system (ARMS). Denaturing performance liquid chromatography (DHPLC) was employed for evaluation of EGFR mutation in exon 19, 21 and KRAS mutation. Results: PIK3CA mutations were found in 3 (2.