干细胞具有修复患病或受损组织的能力，在再生医学方面拥有巨大前景。他们可显著提高医学治疗的效果，如营养不良情况下的肌肉再生、治疗烧伤患者的皮肤移植以及通过骨髓移植治疗白血病。但是，干细胞的获取所涉及伦理问题，一直是科研人员的心病。
瑞士洛桑理工大学生命科学学院院长迪埃.托诺称，通过约束一些基因的表达，体细胞能够被诱导转化为多能状态。例如，从血友病患者的毛囊中收集一些细胞，对其重编程，以具备胚胎前体的多潜能性；纠正凝血功能障碍的基因突变并对其重新管理，分化为功能齐全的细胞后代，以实现基因治愈。
增加癌变的风险？
近日，日内瓦大学生物化学系、米兰的欧洲肿瘤研究所和托诺实验室的合作研究成果发表在《细胞死亡与分化》(Cell Death and Differentiation)上，该成果表明重编程细胞的“基因不稳定性”，主要表现在细胞转化为其胚胎状态的过程中，更严重的是，观察到的基因突变类似于在肿瘤细胞中观察到的突变。
科学家总结称，重编程细胞用于再生医学研究，广泛前期研究是很有必要的。一个相同的、可靠的结论是：基因异常以一种依附于重编程过程本身的方式在成倍增加，这通常是因为致癌基因在作怪。作者认为，致癌基因有诱导基因产生不稳定性的能力。这些结果强调了开展进一步研究的必要性。
英文原文：http://www.sciencedaily.com/releases/2011/02/110221071528.htm
中文翻译：http://www.chinastemcell.org/page/zixun_xwdtlist.aspx?infoid=990
生物谷推荐英文摘要：
Cell Death & Differentiation doi:10.1038/cdd.2011.9
Genomic instability in induced stem cells
C E Pasi, A Dereli-?z, S Negrini, M Friedli, G Fragola, A Lombardo, G Van Houwe, L Naldini, S Casola, G Testa, D Trono, P G Pelicci and T D Halazonetis
The ability to reprogram adult cells into stem cells has raised hopes for novel therapies for many human diseases. Typical stem cell reprogramming protocols involve expression of a small number of genes in differentiated somatic cells with the c-Myc and Klf4 proto-oncogenes typically included in this mix. We have previously shown that expression of oncogenes leads to DNA replication stress and genomic instability, explaining the high frequency of p53 mutations in human cancers. Consequently, we wondered whether stem cell reprogramming also leads to genomic instability. To test this hypothesis, we examined stem cells induced by a variety of protocols. The first protocol, developed specifically for this study, reprogrammed primary mouse mammary cells into mammary stem cells by expressing c-Myc. Two other previously established protocols reprogrammed mouse embryo fibroblasts into induced pluripotent stem cells by expressing either three genes, Oct4, Sox2 and Klf4, or four genes, OSK plus c-Myc. Comparative genomic hybridization analysis of stem cells derived by these protocols revealed the presence of genomic deletions and amplifications, whose signature was suggestive of oncogene-induced DNA replication stress. The genomic aberrations were to a significant degree dependent on c-Myc expression and their presence could explain why p53 inactivation facilitates stem cell reprogramming.
