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某些源自外胚层的骨外实体瘤,它们并未浸润至骨组织,但可引起血钙显著增高,提示这些肿瘤可能分泌体液因子作用于骨导致溶骨。我们从人膀胱癌、大鼠乳腺癌(Walker 256)及7.12-Dimethyl Benz[α]anthracene诱发的小鼠鳞癌的提取液中初步分离鉴定了一种溶骨因子。肿瘤提取液经ultrogel层析,发观仅有一溶骨活性峰(~(45)Ca自乳鼠顶骨培养中的释出率),相当于表观分子量15,000道尔顿。此溶骨活性峰与PGE2生成的活性峰相平行,两者均能被Indomethacin及煮沸所抑制。在膀胱癌及鳞癌中,溶骨活性峰还与刺激大鼠成骨肉瘤细胞腺苷酸环化酶的活性相平行。实验结果表明此溶骨因子不同于其它已知能引起溶骨的因子。
Some extramedullary solid tumors, which are not infiltrated into bone tissue but cause a significant increase in serum calcium, suggest that these tumors may secrete humoral factors that act on the osteolytic bone. We initially isolated and characterized an osteolytic factor from extracts of mouse squamous cell carcinomas induced by human bladder cancer, rat breast cancer (Walker 256) and 7.12-Dimethyl Benz [a] anthracene. Tumor extracts were analyzed by ultrogel and had only one active osteolytic peak (~ (45) Ca release from the top bones of neonatal rats) equivalent to an apparent molecular weight of 15,000 daltons. This osteolytic activity peak parallels the activity peak produced by PGE2, both of which can be suppressed by Indomethacin and boiling. In bladder cancer and squamous cell carcinoma, the osteolytic activity peak is also parallel to the activity of stimulating adenylate cyclase in rat osteogenic sarcoma cells. Experimental results show that this factor is different from other factors known to cause osteolytic osteolytic factor.