IDENTIFYING AND FUNCTIONALLY CHARACTERISING RENAL CANCER DRIVER MUTATIONS

世界范围内，肾癌每年造成超过14万人死亡，其发病率在过去30年中显著增加。尽管肾癌的治疗取得了进展，但许多患者的前景仍不乐观。癌症是由DNA突变引起的。识别这些突变对于了解肾癌的病因和设计新的治疗方法至关重要。然而，对肾癌的研究主要集中在导致蛋白质变化的突变上，而没有考虑到细胞中剩余98%的DNA。在这种“非编码DNA”中已经发现了一些促进癌症突变的例子，但还没有对肾癌进行全面的分析。为了解决这一缺陷，我们将仔细检查非编码DNA编目突变和破译其功能后果。这项工作应该允许患者预后更准确地定义，并告知新的治疗目标。

Worldwide kidney cancer causes over 140,000 deaths each year and its incidence of has markedly increased over the past 30 years. Despite advances in the treatment of kidney cancer many patients still have an unfavourable outlook. Cancers are caused by DNA mutations. Identifying these mutations is crucial for understanding what drives kidney cancer and devising new treatments. Studies of kidney cancer have, however, largely focused on mutations that cause changes in the proteins, without considering the remaining 98% of the cell's DNA. Some examples of cancer promoting mutations in this "non-coding DNA" have been identified but there has not been a comprehensive analysis for kidney cancer. To address this deficiency we shall therefor scrutinise the non-coding DNA cataloguing mutations and deciphering their functional consequences. This work should allow patient prognosis to be more accriyately defined and inform new targets for therapy.