Given the complexity and redundancy of the PI3 K signaling network, PI3 K pathway inhibition may be most useful in combination with either chemotherapy or other targeted therapies, such as MEK inhibitors, anti-angiogenic therapy, and hormonal

therapy, in appropriately selected OC patients. Here, we discuss the relevance of the PI3 K pathway in OC and provide an 什么 up-to-date review of clinical trials of novel PI3 K inhibitors alone or in combination with cytotoxics and novel therapies in OC. In addition, the challenges of drug resistance and predictive biomarkers are addressed.
2014年,乳腺癌的治疗取得巨大进步,局部和全身复发率都显著降低了,这得益于高质量的多学科协作团队,以及多年来一些重要的改变临床实践的研究结果。Cossetti等[1]2014年在JCO上发表的一篇文章,是对英属哥伦比亚地区的人群学研究,探讨1986-1992年和2004-2008年间不同亚型乳腺癌复发风险的差异。数据显示,无论任何亚型,乳腺
黑色素瘤(melanoma)是一种恶性的黑色素细胞肿瘤。我国黑色素瘤的发病率逐年攀升,而中晚期黑色素瘤尚无有效的治疗方法,因此研发新的治疗药物显得尤为迫切。本文对当前黑色素瘤靶向药物进行了总结,重点讨论了MAPK/ERK信号通路的抑制剂(如BRAF抑制剂和MEK抑制剂)。
肺癌是全世界癌症死亡的首要原因,在我国,肺癌也是发病率和死亡率最高的恶性肿瘤。肺癌按组织病理学主要分成两大类:小细胞肺癌(small cell lung cancer,SCLC)和非小细胞肺癌(non-small cell lung cancer,NSCLC)。NSCLC主要又分成鳞状细胞癌(squamous cell carcinoma,SQCC)、腺状细胞癌(adenocarcinoma,A DC)和大细胞癌
前列腺癌是威胁中老年男性健康的常见肿瘤,成为男性癌症死因的第二位。PI3K/Akt/m

TOR信号通路能够通过维持细胞生存、抑制细胞凋亡、促进细胞周期运行及血管生成等促进前列腺癌病程发展。本文综合国内外文献,阐述PI3K/Akt/m TOR信号通路在前列腺癌发生发展中的作用以及和通路相关的药物治疗进展。
近年来,乳腺癌的发病率逐年升高,已成为威胁女性健康最常见的恶性肿瘤之一。在乳腺癌的综合治疗中,靶向治疗在乳腺癌的术后辅助治疗与晚期解救治疗中均有不可或缺的地位。近年来,随着对肿瘤发生、发展过程中分子机制的深入研究,乳腺癌的分子靶向药物被广泛应用于乳腺癌治疗,并取得了显著疗效。曲妥珠单抗是最早应用于乳腺癌靶向治疗的药物,其通过特异性地结合Her-2分子胞外段的结构域Ⅳ,可在人体内介导抗体依赖的细胞介导的细胞毒作用
Gastrointestinal stromal tumors(GISTs) are the most common 不 type of mesenchymal tumor of the gastrointestinal tract. The tumorigenesis of GISTs is driven by gain-of-function mutations in KIT or plateletderived growth factor receptor α(PDGFRA),resultingin constitutive activation of the tyrosine kinase and its downstream signaling pathways. Oncogenic

KIT or PDGFRA mutations are compelling therapeutic targets for the treatment of GISTs,and the KIT/PDGFRA inhibitor imatinib is the standard of care for patients with metastatic GISTs. However,most GIST patients develop clinical resistance to imatinib and other tyrosine kinase inhibitors. Five mechanisms of resistance have been characterized:(1) acquisition of a secondary point 并且 mutation in KIT or PDGFRA;(2) genomic amplification of KIT;(3) activation of an alternative receptor tyrosine kinase;(4) loss of KIT oncoprotein expression; and(5) wild-type GIST. Currently,sunitinib is used as a secondline treatment for patients after imatinib failure,and regorafenib has been approved for patients whose disease is progressing on both imatinib and sunitinib. Phase Ⅱ/Ⅲ trials are currently in progress to evaluate novel inhibitors and immunotherapies targeting KIT,its downstream effectors such as phosphatidylinositol 3-kinase,protein kinase B and mammalian target of rapamycin,heat shock protein 90,and histone deacetylase inhibitor.