系统生物学支持的NF-κΒ和BCL2的向克服了DLBCL中微环境介导的BH3-模拟性抵抗

概括

由于蛋白质冗余,扩散性大B细胞淋巴瘤 (DLBCL) 的向治疗是复杂的. 结合分子分析和计算建模,发现了BCL2和NF-κB抑制的漏洞,克服了抵抗机制.

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