科学家在理解长期被视为"无法成药"的癌症基因方面取得重要突破。12费城Fox Chase癌症中心的研究人员在《分子细胞》杂志发表研究，揭示了MYC基因的控制机制。2MYC基因在约70%的癌症中处于过度活跃状态，驱动肿瘤的生长和扩散。2
研究发现，两个分子开关可以调节MYC基因的活性，导致该基因的拷贝数增加。2这一发现为开发治疗方法提供了新的思路——通过靶向这些分子开关可能比直接针对MYC基因本身更容易成为可行的药物靶点。2
Researchers have made significant progress in understanding the biology of the MYC gene, a cancer-driving gene long considered resistant to drug treatment.2 The study, published in the journal Molecular Cell by scientists at Fox Chase Cancer Center in Philadelphia, identifies two molecular switches that regulate MYC activity, potentially opening new avenues for therapeutic intervention.2
MYC is overactive in approximately 70% of cancers, where it drives tumor growth and spread.2 Unlike mutations that permanently activate genes, MYC is a normal gene whose activity becomes abnormally elevated in cancer cells.2 The research team discovered that these two molecular switches control MYC function by increasing the number of gene copies, suggesting that targeting these regulatory mechanisms may prove more feasible than directly attacking MYC itself.2 By clarifying how MYC's activity is controlled, the findings lay groundwork for developing new therapeutic approaches to address cancers driven by this previously intractable gene.12
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