采用二乙基亚硝胺(DENA)诱发大鼠肝细胞癌的动物模型,应用新生血管抑制药物β环糊精十四硫酸酯(β CD 14S)联合肝动脉结扎的方法对其进行治疗.实验共分为5组:(1)阴性对照组;(2)β CD 14S(0.5g/kg)门静脉给药组;(3)肝动脉结扎组;(4)β ... 采用二乙基亚硝胺(DENA)诱发大鼠肝细胞癌的动物模型,应用新生血管抑制药物β环糊精十四硫酸酯(β CD 14S)联合肝动脉结扎的方法对其进行治疗.实验共分为5组:(1)阴性对照组;(2)β CD 14S(0.5g/kg)门静脉给药组;(3)肝动脉结扎组;(4)β CD 14S(0.5g/kg)肝动脉给药+肝动脉结扎组;(5)β CD 14S(0.5g/kg)门静脉给药+肝动脉结扎组.实验结果表明,β CD 14S+肝动脉结扎治疗组较单纯用药或肝动脉结扎组术后30d生存率明显提高.影象学和病理学的观察表明大鼠肝细胞癌的血供受到抑制,证实了β CD 14S对肝细胞癌诱导的新生血管有较好的抑制作用,它与血管栓塞疗法的联合应用可望为肝细胞癌的治疗提供一种更为有效的新方法.展开更多
Oncogene activation and tumor suppressor gene loss are well known as events that are responsible for the dramatic cell autonomous deregulation of growth that characterizes all malignant cells. Data accumulating more r...Oncogene activation and tumor suppressor gene loss are well known as events that are responsible for the dramatic cell autonomous deregulation of growth that characterizes all malignant cells. Data accumulating more recently indicate that these same genes are also responsible for the development of a second essential characteristic of all malignant cells, the ability to induce angiogenesis on which their progressive growth in vivo depends. Oncogene activation appears to make distinctly different contributions to the angiogenic phenotype of developing tumors. Cells in which an oncogene is activated become more an- giogenic usually because they increase their secretion of inducer of angiogenesis. Inducer enhancement seems to be essential if a normal cell is to develope into a tumor cell able to grow and metastasize in vivo.展开更多
文摘 采用二乙基亚硝胺(DENA)诱发大鼠肝细胞癌的动物模型,应用新生血管抑制药物β环糊精十四硫酸酯(β CD 14S)联合肝动脉结扎的方法对其进行治疗.实验共分为5组:(1)阴性对照组;(2)β CD 14S(0.5g/kg)门静脉给药组;(3)肝动脉结扎组;(4)β CD 14S(0.5g/kg)肝动脉给药+肝动脉结扎组;(5)β CD 14S(0.5g/kg)门静脉给药+肝动脉结扎组.实验结果表明,β CD 14S+肝动脉结扎治疗组较单纯用药或肝动脉结扎组术后30d生存率明显提高.影象学和病理学的观察表明大鼠肝细胞癌的血供受到抑制,证实了β CD 14S对肝细胞癌诱导的新生血管有较好的抑制作用,它与血管栓塞疗法的联合应用可望为肝细胞癌的治疗提供一种更为有效的新方法.
文摘Oncogene activation and tumor suppressor gene loss are well known as events that are responsible for the dramatic cell autonomous deregulation of growth that characterizes all malignant cells. Data accumulating more recently indicate that these same genes are also responsible for the development of a second essential characteristic of all malignant cells, the ability to induce angiogenesis on which their progressive growth in vivo depends. Oncogene activation appears to make distinctly different contributions to the angiogenic phenotype of developing tumors. Cells in which an oncogene is activated become more an- giogenic usually because they increase their secretion of inducer of angiogenesis. Inducer enhancement seems to be essential if a normal cell is to develope into a tumor cell able to grow and metastasize in vivo.
