The transcription factor NRF2 is known as the master regulator of the oxidative stress response. Tumor entities presenting oncogenic activation of NRF2, such as lung adenocarcinoma, are associated with drug resistance, and accumulating evidence demonstrates its involvement in immune evasion. In other cancer types, the KEAP1/NRF2 pathway is not commonly mutated, but NRF2 is activated by other means such as radiation, oncogenic activity, cytokines, or other pro‐oxidant triggers characteristic of the tumor niche. The obvious effect of stress‐activated NRF2 is the protection from oxidative or electrophilic damage and the adaptation of the tumor metabolism to changing conditions. However, data from melanoma also reveal a role of NRF2 in modulating differentiation and suppressing anti‐tumor immunity. This review summarizes the function of NRF2 in this tumor entity and discusses the implications for current tumor therapies.

中文翻译：

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NRF2依赖性应激防御在肿瘤抗氧化控制和免疫逃避中

转录因子 NRF2 被称为氧化应激反应的主要调节因子。呈现 NRF2 致癌激活的肿瘤实体，例如肺腺癌，与耐药性有关，并且越来越多的证据表明其参与免疫逃避。在其他癌症类型中，KEAP1/NRF2 通路通常不会发生突变，但 NRF2 会通过其他方式被激活，例如辐射、致癌活性、细胞因子或其他具有肿瘤生态位特征的促氧化触发器。应激激活的 NRF2 的明显作用是保护免受氧化或亲电损伤，并使肿瘤代谢适应不断变化的条件。然而，黑色素瘤的数据也揭示了 NRF2 在调节分化和抑制抗肿瘤免疫中的作用。