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同基因LSA淋巴瘤中1,3-双(2-氯乙基)-1-亚硝基脲治疗诱导的宿主抗性证据。

Evidence for host resistance in 1,3 bis(2-chloroethyl)-1-nitrosourea treatment induced in syngeneic LSA lymphoma.

作者信息

Maruyama Y, Williams A, Feola J M, Nava C

出版信息

J Cancer Res Clin Oncol. 1982;103(2):107-18. doi: 10.1007/BF00409641.

Abstract

The anticancer agent 1,3 Bis(2-chloroethyl)-1-Nitrosourea (BCNU) cures the advanced syngeneic LSA lymphoma of C57BL mice with high efficiency. The cured animals resist further tumor challenge by large numbers of viable syngeneic tumor cells. Growth assays of spleen proliferation of the intravenously inoculated tumor revealed a progressive-regressive pattern of spleen growth after LSA-tumor injection. Lymphoma colony forming units (LCFU) in the spleen initially increased then regressed. In vitro assays of serum showed a lack of cytotoxic activity in mice cured by BCNU. Added spleen, thymus, or bone-marrow cells were similarly ineffective. Spleen and bone-marrow cells from immune mice passively transferred to normal mice showed weak cytotoxic activity against the LSA tumor. BCNU-cured mouse cells were more effective in protection than those cured with Chlorozotocin (CLZ).

摘要

抗癌药物1,3-双(2-氯乙基)-1-亚硝基脲(卡莫司汀,BCNU)可高效治愈C57BL小鼠的晚期同基因LSA淋巴瘤。治愈的动物能够抵抗大量活的同基因肿瘤细胞的进一步肿瘤攻击。对静脉接种肿瘤后脾脏增殖的生长分析显示,注射LSA肿瘤后脾脏生长呈现进行性-退行性模式。脾脏中的淋巴瘤集落形成单位(LCFU)最初增加,然后减少。血清的体外分析表明,BCNU治愈的小鼠缺乏细胞毒性活性。添加的脾脏、胸腺或骨髓细胞同样无效。将免疫小鼠的脾脏和骨髓细胞被动转移到正常小鼠中,对LSA肿瘤显示出较弱的细胞毒性活性。与用氯脲霉素(CLZ)治愈的细胞相比,BCNU治愈的小鼠细胞在保护方面更有效。

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THE GROWTH OF MURINE LYMPHOMATOUS TUMOUR-CELLS AS DETERMINED BY HOST SURVIVAL-TIME.
Int J Radiat Biol Relat Stud Phys Chem Med. 1964;8:59-73. doi: 10.1080/09553006414550061.

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