癌症进展过程中细胞表型的动态变化归因于一种称为“谱系可塑性”的现象。这一过程与治疗抵抗相关，并涉及代谢状态的同时变化，从而促进适应恶性生长固有的各种应激源。某些代谢物还可以作为染色质修饰的合成库，从而将代谢状态与表观遗传调控联系起来。仍然迫切需要了解集中于谱系可塑性和代谢重编程的机制，以防止致命疾病的出现。这篇综述试图概述我们目前对癌症背景下代谢重编程和谱系可塑性之间相互作用的理解，强调癌症标志的交叉驱动因素，重点是实体瘤。版权所有 © 2024 Elsevier Inc. 保留所有权利。

Dynamic alterations in cellular phenotypes during cancer progression are attributed to a phenomenon known as 'lineage plasticity'. This process is associated with therapeutic resistance and involves concurrent shifts in metabolic states that facilitate adaptation to various stressors inherent in malignant growth. Certain metabolites also serve as synthetic reservoirs for chromatin modification, thus linking metabolic states with epigenetic regulation. There remains a critical need to understand the mechanisms that converge on lineage plasticity and metabolic reprogramming to prevent the emergence of lethal disease. This review attempts to offer an overview of our current understanding of the interplay between metabolic reprogramming and lineage plasticity in the context of cancer, highlighting the intersecting drivers of cancer hallmarks, with an emphasis on solid tumors.Copyright © 2024 Elsevier Inc. All rights reserved.