NON-SMALL-CELL lung cancer (NSCLC) accounts for 75%—80% of all lung cancers. Chemotherapy is the basic treatment for the patients with NSCLCs, which are often resistant to drugs because of tumor multidrug resistance,...NON-SMALL-CELL lung cancer (NSCLC) accounts for 75%—80% of all lung cancers. Chemotherapy is the basic treatment for the patients with NSCLCs, which are often resistant to drugs because of tumor multidrug resistance, the main cause of lower cure rate. Overexpression of P-glycoprotein (Pgp), the product of multidrug resistance gene (MDR1), is the main mechamsm by which tumor produces multidrug resistance. MDR1 gene is known to induce multidrug resistance. MDR1 antisense RNA could inhibit the expression of MDR1 gene and reverse the multidrug resistance in multidrug-resistant human lung cancer. In clinical studies,展开更多
目的对^(131)I-c(RGD)_(2)在原位荷脑胶质瘤动物模型中的靶向定位作用进行研究,以探讨其应用于脑胶质瘤诊断与治疗的可能性。方法采用U87-MG人脑胶质瘤细胞接种在裸鼠右脑尾状核内,建立了原位荷脑胶质瘤动物模型;采用氯氨T法将^(131)I标...目的对^(131)I-c(RGD)_(2)在原位荷脑胶质瘤动物模型中的靶向定位作用进行研究,以探讨其应用于脑胶质瘤诊断与治疗的可能性。方法采用U87-MG人脑胶质瘤细胞接种在裸鼠右脑尾状核内,建立了原位荷脑胶质瘤动物模型;采用氯氨T法将^(131)I标记c(RGD)_(2),于原位荷脑胶质瘤裸鼠中进行生物分布研究,计算^(131)I-c(RGD)_(2)在脑胶质瘤中的摄取率及肿瘤与正常脑组织摄取率的比值(T/NT)。结果给药后3 h及6 h,肾的摄取均为所有器官中最高;给药后3 h肿瘤未累及的脑组织的摄取率为(0.16±0.10)%ID/g,胶质瘤组织的摄取率为(0.41±0.26)%ID/g,脑胶质瘤中的摄取率显著高于正常脑组织摄取率(P值为0.025);给药后6 h肿瘤未累及的脑组织的摄取率为(0.08±0.04)%ID/g,胶质瘤组织的摄取率为(0.44±0.23)%ID/g,脑胶质瘤中的摄取率亦显著高于正常脑组织摄取率(P值为0.011);给药后3 h T/NT比值为3.36±1.86,给药后6 h T/NT比值增高至5.55±1.75。结论c(RGD)_(2)具有靶向颅内胶质瘤的能力,在胶质瘤的靶向诊断与治疗中具有潜力,但其在脑胶质瘤中的摄取率相对较低,有待于进一步提高。展开更多
文摘NON-SMALL-CELL lung cancer (NSCLC) accounts for 75%—80% of all lung cancers. Chemotherapy is the basic treatment for the patients with NSCLCs, which are often resistant to drugs because of tumor multidrug resistance, the main cause of lower cure rate. Overexpression of P-glycoprotein (Pgp), the product of multidrug resistance gene (MDR1), is the main mechamsm by which tumor produces multidrug resistance. MDR1 gene is known to induce multidrug resistance. MDR1 antisense RNA could inhibit the expression of MDR1 gene and reverse the multidrug resistance in multidrug-resistant human lung cancer. In clinical studies,
文摘目的对^(131)I-c(RGD)_(2)在原位荷脑胶质瘤动物模型中的靶向定位作用进行研究,以探讨其应用于脑胶质瘤诊断与治疗的可能性。方法采用U87-MG人脑胶质瘤细胞接种在裸鼠右脑尾状核内,建立了原位荷脑胶质瘤动物模型;采用氯氨T法将^(131)I标记c(RGD)_(2),于原位荷脑胶质瘤裸鼠中进行生物分布研究,计算^(131)I-c(RGD)_(2)在脑胶质瘤中的摄取率及肿瘤与正常脑组织摄取率的比值(T/NT)。结果给药后3 h及6 h,肾的摄取均为所有器官中最高;给药后3 h肿瘤未累及的脑组织的摄取率为(0.16±0.10)%ID/g,胶质瘤组织的摄取率为(0.41±0.26)%ID/g,脑胶质瘤中的摄取率显著高于正常脑组织摄取率(P值为0.025);给药后6 h肿瘤未累及的脑组织的摄取率为(0.08±0.04)%ID/g,胶质瘤组织的摄取率为(0.44±0.23)%ID/g,脑胶质瘤中的摄取率亦显著高于正常脑组织摄取率(P值为0.011);给药后3 h T/NT比值为3.36±1.86,给药后6 h T/NT比值增高至5.55±1.75。结论c(RGD)_(2)具有靶向颅内胶质瘤的能力,在胶质瘤的靶向诊断与治疗中具有潜力,但其在脑胶质瘤中的摄取率相对较低,有待于进一步提高。
