Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, USA.
Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, USA.
Pharmacol Ther. 2022 Sep;237:108251. doi: 10.1016/j.pharmthera.2022.108251. Epub 2022 Jul 15.
Recent advances in bulk sequencing approaches as well as genomic decoding at the single-cell level have revealed surprisingly high somatic mutational burdens in normal tissues, as well as increased our understanding of the landscape of "field cancerization", that is, molecular and immune alterations in mutagen-exposed normal-appearing tissues that recapitulated those present in tumors. Charting the somatic mutational landscapes in normal tissues can have strong implications on our understanding of how tumors arise from mutagenized epithelium. Making sense of those mutations to understand the progression along the pathologic continuum of normal epithelia, preneoplasias, up to malignant tissues will help pave way for identification of ideal targets that can guide new strategies for preventing or eliminating cancers at their earliest stages of development. In this review, we will provide a brief history of field cancerization and its implications on understanding early stages of cancer pathogenesis and deviation from the pathologically "normal" state. The review will provide an overview of how mutations accumulating in normal tissues can lead to a patchwork of mutated cell clones that compete while maintaining an overall state of functional homeostasis. The review also explores the role of clonal competition in directing the fate of normal tissues and summarizes multiple mechanisms elicited in this phenomenon and which have been linked to cancer development. Finally, we highlight the importance of understanding mutations in normal tissues, as well as clonal competition dynamics (in both the epithelium and the microenvironment) and their significance in exploring new approaches to combatting cancer.
近年来,在大规模测序方法和单细胞水平的基因组解码方面的进展,揭示了正常组织中令人惊讶的高体细胞突变负担,并且增加了我们对“局部癌变”景观的理解,即诱变暴露的正常外观组织中的分子和免疫改变,重现了肿瘤中存在的改变。绘制正常组织中的体细胞突变景观,对我们理解突变上皮细胞如何发展为肿瘤具有重要意义。理解这些突变,了解正常上皮组织、癌前病变到恶性组织的病理连续体的进展,将有助于确定理想的靶点,为在癌症发展的最早阶段预防或消除癌症提供新策略。在这篇综述中,我们将简要回顾局部癌变的历史及其对理解癌症发病机制早期阶段和偏离病理“正常”状态的意义。综述将概述正常组织中积累的突变如何导致突变细胞克隆的拼凑,这些克隆在保持整体功能平衡的状态下竞争。综述还探讨了克隆竞争在指导正常组织命运中的作用,并总结了这一现象中引发的多种机制,这些机制与癌症发展有关。最后,我们强调了理解正常组织中的突变、克隆竞争动态(在上皮组织和微环境中)及其在探索对抗癌症的新方法中的重要性。