Colorectal cancer (CRC) continues to be one of the leading malignancies and causes of tumour-related deaths worldwide. Both impaired DNA repair mechanisms and disrupted telomere length homeostasis represent key culprits in CRC initiation, progression and prognosis. Mechanistically, altered DNA repair results in the accumulation of mutations in the genome and, ultimately, in genomic instability. DNA repair also determines the response to chemotherapeutics in CRC treatment, suggesting its utilisation in the prediction of therapy response and individual approach to patients. Telomere attrition resulting in replicative senescence, simultaneously by-passing cell cycle checkpoints, is a hallmark of malignant transformation of the cell. Telomerase is almost ubiquitous in advanced solid cancers, including CRC, and its expression is fundamental to cell immortalisation. Therefore, there is a persistent effort to develop therapeutics, which are telomerase-specific and gentle to non-malignant tissues. However, in practice, we are still at the level of clinical trials. The current state of knowledge and the route, which the research takes, gives us a positive perspective that the problem of molecular models of telomerase activation and telomere length stabilisation will finally be solved. We summarise the current literature herein, by pointing out the crosstalk between proteins involved in DNA repair and telomere length homeostasis in relation to CRC.

中文翻译：

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端粒维持与大肠癌的发病机理和治疗中的DNA修复相互作用。

大肠癌（CRC）仍然是全球范围内主要的恶性肿瘤和与肿瘤相关的死亡原因。DNA修复机制受损和端粒长度稳态失调都是CRC起始，进展和预后的关键元凶。从机制上讲，改变的DNA修复导致基因组中突变的积累，并最终导致基因组不稳定。DNA修复还决定了CRC治疗中对化学疗法的反应，表明其可用于预测治疗反应和针对患者的个体治疗方法。端粒磨损导致复制衰老，同时绕过细胞周期检查点，是细胞恶性转化的标志。端粒酶在包括CRC，它的表达对于细胞永生化至关重要。因此，一直致力于开发端粒酶特异性且对非恶性组织温和的治疗剂。但是，实际上，我们仍处于临床试验阶段。研究的现状和途径，为我们提供了一个积极的观点，即端粒酶激活和端粒长度稳定的分子模型问题将最终得到解决。我们通过指出与CRC相关的DNA修复蛋白和端粒长度稳态之间的串扰来总结本文中的当前文献。我们仍处于临床试验阶段。研究的现状和途径，为我们提供了一个积极的观点，即端粒酶激活和端粒长度稳定的分子模型问题将最终得到解决。我们通过指出与CRC相关的DNA修复蛋白和端粒长度稳态之间的串扰来总结本文中的当前文献。我们仍处于临床试验阶段。研究的现状和途径，为我们提供了一个积极的观点，即端粒酶激活和端粒长度稳定的分子模型问题将最终得到解决。我们通过指出与CRC相关的DNA修复蛋白和端粒长度稳态之间的串扰来总结本文中的当前文献。