中文摘要：

癌症干细胞，像茎的癌症房间(SLCC ) ，或开始肿瘤的房间的存在被看作肿瘤形成和复发的原因，显示学习指向 SLCC 的新奇治疗的重要性。因为二竞争假设， SLCC 的起源是争论的：SLCC 也从转变祖先房间从织物成年人干细胞或 dedifferentiated 被转变。我们的以前的研究证明 SLCC 由在癌症房间增加 genomic 不稳定性是可诱导的。在这研究，堵住 SLCC 的出现， aminoethyl isothiourea ( AET )，清除自由激进分子的混合物并且被用来保护病人免受放射性的暴露的伤害，被用作与 mitomycin C ( MMC )在联合维持 genomic 稳定性的一个代理人，损坏 DNA 的通常使用的化学疗法的药。用有 VX2 肝的癌的一个兔子肿瘤模型，我们发现 MMC 独自增加了肺转移和处于不利地位的幸存结果，但是 MMC 和 AET 的联合颠倒了这效果平延长全面幸存。而且在由 immunocompromised 老鼠的一个 VX2 异种皮移植模型， MMC 独自与 AET 在联合充实 MMC 的开始肿瘤的房间，而是管理有效地消除了肿瘤房间。而且， MMC 独自提高了 genomic 不稳定性，但是与 AET 相结合的 MMC 在主要 VX2 肿瘤织物稀释了 genomic 不稳定性的程度。一起拿，我们的数据建议 genomic 保护者 AET 能由 AET 禁止 SLCC，和这联合治疗的正式就职，细胞毒素的代理人应该为未来被看作有希望的策略临床的评估。

英文摘要：

The existence of cancer stem cells, stem-like cancer cells （SLCCs）, or tumor-initiating cells is considered as the cause of tumor formation and recurrence, indicating the importance of studying novel therapy that targets SLCCs. The origin of SLCCs is controversial because of two competing hypotheses： SLCCs are either transformed from tissue adult stem cells or dedifferentiated from transformed progenitor cells. Our previous research demonstrates that SLCCs are inducible by increasing genomic instability in cancer cells. In this study, to block the emergence of SLCCs, aminoethyl isothiourea （AET）, a compound that clears free radicals and is used to protect patients from radioactive exposure, was used as an agent that maintains genomic stability in combination with mitomycin C （MMC）, a commonly used chemotherapeutic drug that damages DNA. Using a rabbit tumor model with VX2 hepatic carcinoma, we found that MMC alone increased lung metastases and disadvantaged survival outcome, but the combination of MMC and AET reversed this effect and even prolonged overall survival. Moreover, in a VX2 xenograft model by immunocompromised mice, MMC alone enriched tumor-initiating cells, but the administration of MMC in combination with AET eliminated tumor cells effectively. Furthermore, MMC alone enhanced genomic instability, but MMC combined with AET attenuated the extent of genomic instability in primary VX2 tumor tissue. Taken together, our data suggest that the genomic protector AET can inhibit the induction of SLCCs, and this combination treatment by AET and cytotoxic agents should be considered as a promising strategy for future clinical evaluation.