为了解决这一难题，南京医科大学第一附属医院等机构的研究人员展开了深入研究。他们的研究成果发表在《Molecular Cancer》上，为非小细胞肺癌 EGFR-TKI 耐药的治疗开辟了新道路。 研究人员首先利用生物信息学分析，对来自 Gene Expression Omnibus（GEO）数据库的多个微阵列数据集进行挖掘。他们发现，烟酰胺 N - 甲基转移酶（NNMT）在 EGFR-TKI ...

进一步的实验揭示了TP63这个癌基因是ALDH3A1的“总开关”。它直接激活ALDH3A1基因，触发保护机制。当研究团队关闭TP63时，癌细胞失去了抵抗铁死亡的能力，但当重新激活ALDH3A1时，它们又恢复了保护作用。

A research team led by Prof. JIANG Yanyi from the Hefei Institutes of Physical Science of the Chinese Academy of Sciences, ...

Figure 8: Regulation of ALDH3A1 and NECTIN4 by p53. Researchers Jessica J. Miciak, Lucy Petrova, Rhythm Sajwan, Aditya Pandya, Mikayla Deckard, Andrew J. Munoz, and Fred Bunz from the Sidney ...

In this study, the researchers found that the protein ALDH3A1, known for its role in detoxifying harmful substances in the body, is overactive in SCC cells. This protein acts as an "antioxidant ...