Fig. 3: Differential mutation frequencies associated with the NRF2 prognostic signature across eight cancer types. | npj Precision Oncology

Fig. 3: Differential mutation frequencies associated with the NRF2 prognostic signature across eight cancer types.

From: Integrative analysis of KEAP1/NFE2L2 alterations across 3600+ tumors reveals an NRF2 expression signature as a prognostic biomarker in cancer

Fig. 3

In A we show barplots representing the frequency of KEAP1 and NFE2L2 mutations in patients with worse prognosis clusters compared to those with better prognosis clusters across the eight studied cancer types: Lung Adenocarcinoma (LUAD), Lung Squamous Cell Carcinoma (LUSC), Bladder Cancer (BLCA), Cervical Squamous Cell Carcinoma (CSCC), Esophageal Adenocarcinoma (EAC), Head and Neck Squamous Cell Carcinoma (HNSCC), Hepatocellular Carcinoma (HCC), and Uterine Corpus Endometrial Carcinoma (UCEC). KEAP1 and NFE2L2 mutations were particularly enriched in LUAD, LUSC, and EAC, indicating a significant role in activating the NRF2 pathway and contributing to worse prognosis in these cancer types. In B we show the aggregated frequency of other significant genetic alterations in the worse prognosis clusters compared to better prognosis clusters in the same eight cancer types. These mutations include, but are not limited to, STK11, ROS1, IDH2, ARID5B, TAF1, ADAMTS9, AFF1, MST1R, ZNF217, CDKN2A, TP53, ARID2, AKT2, AXIN1, and TRIM31. These alterations might suggest alternative mechanisms of NRF2 activation and regulation, highlighting the complexity of NRF2 pathway dysregulation across different cancers and emphasizing the necessity for diverse therapeutic strategies.

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