近年来,尽管恶性肿瘤的检测和治疗手段取得了长足进步,但肿瘤转移仍然是恶性肿瘤治疗失败和患者死亡的最主要原因。系统生物学和功能基因组

近年来,尽管恶性肿瘤的检测和治疗手段取得了长足进步,但肿瘤转移仍然是恶性肿瘤治疗失败和患者死亡的最主要原因。系统生物学和功能基因组学的发展使我们从分子水平对转移本质有了深入认识,在对肿瘤遗传异质性(tumor Protein Tyrosine激酶抑制剂 heterogeneity)、转移前生境(pre-metastatic niche)、上皮间充质转化(epithelial-mesenchymal transition,EMT)、失巢凋亡抗性(anoikis resistant)、血管与淋巴管生成(angiogenesis and lymphangiogenesis)等恶性肿瘤转移相关机制形成共识的基础上,提出了加强分子靶向治疗、针对肿瘤干细胞治疗、充分利用小干扰RNA技术等临床抗肿瘤转移的治疗策略。

不能手术和已转移的原发性肝细胞癌(hepatocellular carcinoma,HCC)预后很差,放化疗难以使患者受益。近年来,分子靶向治疗对一些肿瘤已取得突破性进展,肝癌的分子靶向治疗也在临床试验中取得了令人鼓舞的结果。目前的肝癌临床研究主要针对EGFR、VEGF/VEGFR、HGF、MMP、乙肝表面抗原等靶点。本文针对肝癌的分子靶向治疗的研究进展进行了综述。
目的探讨自分泌运动因子受体(AMFR)、C-Met蛋白在舌鳞状细胞癌组织中的表达及临床意义。方法采用免疫组化SABC方法检测80例舌鳞状细胞癌组织切片中AMFR、C-Met的表达。结果与正常舌组织相比,AMFR在舌癌中高表达(76.25%),与TNM分期有相关性(P<0.05)。C-Met蛋白的阳性表达率为83.75%,与组织学分化,TNM分期,有无淋巴结转移有相关性(P<0.05)。AMFR和C-Met蛋白的表达呈正相关(P<0.05)。结论舌癌中的AMFR和C-Met蛋白高表达,对于估计舌鳞状细胞癌的生物学特性具有重要的价值,为舌鳞状细胞癌综合治疗的提供一定的理论基础。
肝细胞生长因子(HGF)是一种多肽生长因子,具有促进包括肝细胞、上皮细胞、内皮细胞、造血细胞等多种类型细胞的生长、迁移和形态发生的作用.它还参与多种细胞的增殖、迁移,对各类肿瘤的侵袭转移有着重要的诱导作用.本文通过对近年来国外有关文献的回顾,希望能够为进一步探讨HGF及其受体在卵巢癌治疗中的具体意义提供新的思路.
原癌基因c-Met是前列腺癌基因治疗研究的理想靶点,HGF/c-Met信号系统的研究历史已久。本文就HGF/c-Met信号系统在前列腺癌的研究作一综述。

目的:构建和鉴定人肝细胞生长因子受体(cM

et)的shRNA的真核表达载体。方法:人工合成针对cM et的4对shRNA序列并定向克隆到siRNA(sm all interference RNA)真核表达载体RNA i-Ready pSIREN-DNA-D sRed-Express Vector上;采用双酶切和测序法鉴定。结果:酶切及测序鉴定得到的产物与预期的目的基因一致。结论:成功构建肝细胞生长因子受体靶向shRNA的真核表达载体。
Recepteur d’origine

nantais(RON)belongs to a subfamily of receptor tyrosinekinases(RTK)with unique expression patterns and biological activities.RON isactivated by a serum-derived growth factor macrophage Tie2 信号通路 stimulating protein(MSP).The RON gene transcription is essential for embryonic development and critical inregulating certain physiological processes.Recent studies have indicated thataltered RON expression contributes significantly to cancer progression andmalignancy.In primary tumors,such as colon and breast cancers,overexpressionof RON exists

in large numbers and is often accompanied by the generation ofdifferent splicing variants.These RON variants direct a unique program thatcontrols cell transformation,growth,migration,and Barasertib细胞系 invasion,indicating that al-tered RON expression has the ability to regulate motile/invasive phenotypes.These activities were also seen in transgenic mice,in which targeted expression ofRON in lung epithelial cells resulted in numerous tumors with pathological fea-tures of human bronchioloalveolar carcinoma.Thus,abnormal RON activation isa pathogenic factor that transduces oncogenic signals leading to uncontrolledcell growth and subsequent malignant transformation.Considering these facts,RON and its variants can be considered as potential targets for therapeuticintervention.Experiments using small interfering RNA and neutralizing mono-clonal antibodies demonstrated that suppressing RON expression and activationdecreases cancer cell proliferation,increases apoptotic death,prevents tumorformation in nude mice,and reduces malignant phenotypes.

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