癌症中端粒维持机制：端粒酶、ALT 或缺乏端粒酶。

Telomere maintenance mechanisms in cancer: telomerase, ALT or lack thereof.

机构信息

de Duve Institute, UCLouvain, Brussels, Belgium.

出版信息

Curr Opin Genet Dev. 2020 Feb;60:1-8. doi: 10.1016/j.gde.2020.01.002. Epub 2020 Feb 27.

DOI:10.1016/j.gde.2020.01.002

Abstract

Cancer cells acquire replicative immortality by activating a telomere maintenance mechanism (TMM), either the telomerase or the Alternative Lengthening of Telomeres (ALT) mechanism. ALT is frequently activated in tumors derived from mesenchymal cells, which are more frequent in childhood cancers. Recent studies showed that, occasionally, cancer cells can arise without any TMM activation. Here, we discuss the challenge in assessing which TMM is activated in tumors. We also evaluate the prevalence of ALT mechanism in pediatric cancers and review the associated survival prognosis in different tumor types. Finally, we discuss about possible anti-TMM therapies for new emerging cancer treatments.

摘要

癌细胞通过激活端粒维持机制（TMM）获得复制永生，该机制要么是端粒酶，要么是端粒的替代延长（ALT）机制。ALT 在源自间充质细胞的肿瘤中经常被激活，而这些肿瘤在儿童癌症中更为常见。最近的研究表明，偶尔情况下，癌症细胞的出现可能不需要激活任何 TMM。在这里，我们讨论了评估肿瘤中激活了哪种 TMM 的挑战。我们还评估了 ALT 机制在儿科癌症中的流行程度，并回顾了不同肿瘤类型中相关的生存预后。最后，我们讨论了针对新出现的癌症治疗方法的可能的抗 TMM 疗法。