B 细胞恶性肿瘤包括 80 多种异质性血癌，由于复杂的致癌信号传导，对预后提出了重大挑战。新的证据强调脂质代谢紊乱在这些恶性肿瘤的发展中发挥着关键作用。磷脂、胆固醇、鞘脂和脂肪酸等脂质种类的变化在 B 细胞恶性肿瘤中广泛存在，导致细胞增殖和存活失控。磷脂在通过组成型 B 细胞受体 (BCR) 信号传导导致 B 细胞激活和恶性转化的初始信号级联中发挥着至关重要的作用。失调的胆固醇和鞘脂稳态支持脂筏的完整性，这对于传播致癌信号至关重要。鞘脂影响恶性 B 细胞干性、增殖和存活，而脂筏中的糖鞘脂则调节 BCR 激活。此外，癌细胞增强脂肪酸相关过程以满足更高的代谢需求。在肥胖个体中，脂肪细胞周围源自肥胖的脂质和脂肪因子会重新连接恶性 B 细胞中的脂质代谢，从而逃避细胞毒性治疗。 MYC 易位等遗传驱动因素也会从本质上改变恶性 B 细胞的脂质代谢。总之，内在和外在因素共同重新编程脂质代谢，促进 B 细胞恶性肿瘤的侵袭性表型。因此，针对改变的脂质代谢具有改善不同 B 细胞恶性肿瘤亚型的风险分层和临床管理的转化潜力。版权所有 © 2024。由 Elsevier Ltd 出版。

B cell malignancies, comprising over 80 heterogeneous blood cancers, pose significant prognostic challenges due to intricate oncogenic signaling. Emerging evidence emphasizes the pivotal role of disrupted lipid metabolism in the development of these malignancies. Variations in lipid species, such as phospholipids, cholesterol, sphingolipids, and fatty acids, are widespread across B cell malignancies, contributing to uncontrolled cell proliferation and survival. Phospholipids play a crucial role in initial signaling cascades leading to B cell activation and malignant transformation through constitutive B cell receptor (BCR) signaling. Dysregulated cholesterol and sphingolipid homeostasis support lipid raft integrity, crucial for propagating oncogenic signals. Sphingolipids impact malignant B cell stemness, proliferation, and survival, while glycosphingolipids in lipid rafts modulate BCR activation. Additionally, cancer cells enhance fatty acid-related processes to meet heightened metabolic demands. In obese individuals, the obesity-derived lipids and adipokines surrounding adipocytes rewire lipid metabolism in malignant B cells, evading cytotoxic therapies. Genetic drivers such as MYC translocations also intrinsically alter lipid metabolism in malignant B cells. In summary, intrinsic and extrinsic factors converge to reprogram lipid metabolism, fostering aggressive phenotypes in B cell malignancies. Therefore, targeting altered lipid metabolism has translational potential for improving risk stratification and clinical management of diverse B cell malignancy subtypes.Copyright © 2024. Published by Elsevier Ltd.