Background Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin lymphoma (NHL). B-cell NHLs rely on Bruton’s tyrosine kinase (BTK) mediated B-cell receptor signaling for survival and disease progression. However, they are often resistant to BTK inhibitors or soon acquire resistance after drug exposure resulting in the drug tolerant form. The drug tolerant clones proliferate faster, have increased metabolic activity, and shift to oxidative phosphorylation; however, how this metabolic programming occurs in the drug resistant tumor is poorly understood.

中文翻译：

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多组学整合阐明了淋巴瘤中耐药性的代谢调节剂。

背景弥漫性大B细胞淋巴瘤（DLBCL）是最常见的非霍奇金淋巴瘤（NHL）。B细胞NHL依赖于布鲁顿酪氨酸激酶（BTK）介导的B细胞受体信号传导来维持生存和疾病进展。但是，它们通常对BTK抑制剂有抗药性，或者在暴露于药物后很快获得抗药性，形成药物耐受性形式。耐药性克隆增殖较快，代谢活性增强，并转变为氧化磷酸化。但是，人们对这种代谢程序如何在耐药性肿瘤中发生的了解很少。