细胞增殖和存活的作用先前已被
乳腺癌细胞中促进研究过 [ 51 ]。研究药物 MK-2206 已被发现可有效治疗乳腺癌 [ 52 ]。研究表明，某些细胞系中 AKT 水平的升高与抗雌激素治疗的获得性耐药有关，抑制 AKT 会导致细胞系明显的生长抑制]。AKT 广泛参与细胞存活和癌症进展，是癌症治疗的潜在药物靶点，但找到抑制 AKT 的最佳方法一直难以实现。识别细胞生存所必需的基因和驱动肿瘤抵抗的基因是开发预防癌症进展的靶向疗法的关键信息。 p53 已被广泛研究，并因其通过启动细胞凋亡而抑制肿瘤的能力而闻名。p53 基因曾被誉为阻止癌症的潜在治疗靶点，但由于其
许多功能仍不清楚，因此面临着复杂性。它能够积极和消极地调节相同的细胞过Telegram 用户号码列表程，因此很难预测其激活的结果[ 54 ]。 此外，中位 20 个和后 20 个基因虽然不经常被研究，但可能包含治疗对治疗反应不佳的癌症的答案。例如，我们发现排在最后 20 个基因列表中的 NFAT 基因与许多实体瘤和恶性肿瘤有关 [ 55、56、57 ]。在此过程中提取的该基因和许多其他基因可用于发挥其在癌症中的作用。 通过大规模扫描 PubMed 摘要识别和提
https://lh5.googleusercontent.com/elAKSK7tgFiCgjgBHu-jmTjlv8HyM5HQoIMt6dmeVIDdg2f-jf_MpFNHIDDQuxY0s7lY0GjRbeMCnHPrRi3Vp9UqHWOaP-PdfrrBzxDR83Twk61EEzf7QpZmK03sy2ltRW7qh1P82rdrDgJWD0L2cnw
取的大多数顶级必需基因都涉及生存途径和各种恶性肿瘤这表明癌细胞的生长和存活是由基因网络维持的，这些基因的协调一致促进了癌症的进展。这清楚地表明了不仅针对必需基因的重要性，而且还针对那些可能密切相关但在助长癌症方面作用不太明显的基因的重要性。这就需要广泛挖掘数据和文献，寻找鲜为人知但在细胞过程中至关重要的基因，因为这些基因可能像罕见的 SNP 一样在复杂疾病的进展中发
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