Interaction of TRF2 with DNA repair proteins in Alternative Lengthening of Telomeres

10%-15%的人类癌症，包括一些最难治疗和最具侵袭性的癌症，依赖于一种称为端粒替代延长(ALT)的分子过程来持续生长。我们首次发现了一种正常作用包括抑制ALT的蛋白质。我们将研究这种蛋白质是如何工作的，它的分子伙伴是什么，以及这些分子是如何相互作用的。这一信息有望为针对ALT的癌症治疗奠定基础。

10-15% of human cancers, including some of the most difficult-to-treat and aggressive, depend for their continuing growth on a molecular process called Alternative Lengthening of Telomeres (ALT). We have identified for the first time a protein whose normal role includes repressing ALT. We will study how this protein works, what its molecular partners are, and how these molecules interact with each other. This information is expected to lay the foundations for cancer treatments that target ALT.