Variables affecting the tumor localization of131 I‐antiferritin in experimental hepatoma
Variables affecting the tumor localization of131 I‐antiferritin in experimental hepatoma
复制标题
影响实验性肝癌中 131 I-抗铁蛋白肿瘤定位的变量
DOI：
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发表时间：
1984
期刊：
影响因子：
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通讯作者：
S. Order
中科院分区：
文献类型：
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作者：
R. Rostock;K. Kopher;J. Klein;S. Order
铁蛋白是一种正常组织和肿瘤相关蛋白。在H-4-II-E大鼠肝癌模型中，在肿瘤和正常组织中研究了131 I放射性标记的抗肿瘤铁蛋白和正常IgG抗体的体内定位，剂量范围为0.67 μ g至5 mg正常和抗铁蛋白IgG，标记比（microCi 131 I/μ g IgG）为15：1、5：1和1：10。计算了rads中非穿透性辐射的总剂量，并证明抗铁蛋白在肝癌中的剂量沉积（rads）最大为正常IgG的2.9倍，而正常组织中的结合没有特异性增加。实现的最大肿瘤靶向取决于注射的IgG的量，而不取决于标记比率或程序。未标记的抗铁蛋白能抑制肿瘤结合，而未标记的正常兔IgG不能抑制，表明肿瘤结合需要特异性。正常组织不与抗铁蛋白靶向。大多数正常组织具有非特异性结合正常和抗铁蛋白IgG的能力，其与注射的IgG的量呈线性关系。结果表明，131 I-抗铁蛋白选择性靶向铁蛋白分泌肝癌超过正常组织，靶向的量取决于注射的抗铁蛋白的量。这种选择性定位的生理原因尚不清楚，但术语“生物窗”已被用来描述肿瘤铁蛋白结合的差异可用性。
Ferritin is both a normal tissue- and tumor-associated protein. The in vivo localization of 131I-radiolabeled antitumor ferritin and normal IgG antibodies in the H-4-II-E rat hepatoma model was investigated in both tumor and normal tissues over a dose range of 0.67 micrograms to 5 mg of normal and antiferritin IgG and at labeling ratios (microCi 131I per micrograms IgG) of 15:1, 5:1, and 1:10. The total dose from nonpenetrating radiation in rads was calculated and demonstrated a maximum of 2.9 times greater dose deposition (rads) of antiferritin than normal IgG in hepatoma without specific increase in binding in normal tissues. The maximum tumor targeting achieved was dependent on the amount of injected IgG and not on the labeling ratio or procedure. The binding in tumor could be inhibited by unlabeled antiferritin but not by unlabeled normal rabbit IgG and demonstrated the requirement of specificity for tumor binding. Normal tissues did not target with antiferritin. Most normal tissues have a capacity to bind normal and antiferritin IgG nonspecifically that is linear in relationship to the amount of injected IgG. The results demonstrate that 131I-antiferritin selectively targets ferritin-secreting hepatoma over normal tissues and that the amount of targeting is dependent on the amount of antiferritin injected. The physiologic reasons for such selective localization is not known, but the term "biologic window" has been used to describe the differential availability of tumor ferritin for binding.