人们早就知道癌症肽组会因基因突变而改变。然而，最近，非遗传性多肽突变也与癌细胞有关。这些非基因突变发生在t30转录后，导致肽一级结构发生改变，而相应的基因保持不变。三个主要过程参与这些异常蛋白质的产生：mRNA 选择性剪接、mRNA 编辑和 mRNA 异常翻译。在这篇综述中，我们总结了这些过程背后的分子机制、异常蛋白功能的最新发现，以及由于它们在癌细胞中的特异性富集而作为新的治疗靶点的可利用性。这些非遗传异常多肽代表了独立于突变负荷水平的新型癌细胞靶标的来源，仍有待详尽探索。© 2024。作者，获得 Springer Nature Limited 的独家许可。

The cancer peptidome has long been known to be altered by genetic mutations. However, more recently, non-genetic polypeptide mutations have also been related to cancer cells. These non-genetic mutations occur post-t30ranscriptionally, leading to the modification of the peptide primary structure, while the corresponding genes remain unchanged. Three main processes participate in the production of these aberrant proteins: mRNA alternative splicing, mRNA editing, and mRNA aberrant translation. In this review, we summarize the molecular mechanisms underlying these processes and the recent findings on the functions of the aberrant proteins, as well as their exploitability as new therapeutic targets due to their specific enrichment in cancer cells. These non-genetic aberrant polypeptides represent a source of novel cancer cell targets independent from their level of mutational burden, still to be exhaustively explored.© 2024. The Author(s), under exclusive licence to Springer Nature Limited.