Treating KRAS-mutant lung adenocarcinoma (LUAD) remains a major challenge in cancer
treatment given the difficulties associated with directly inhibiting the KRAS oncoprotein. One�…

Abstract Approximately 20–30% of human lung adenocarcinomas (LUADs) harbor
mutations in Kelch-like ECH-associated protein 1 (KEAP1) that hyperactivate the nuclear�…

The KRAS oncoprotein, a critical driver in 33% of lung adenocarcinoma (LUAD), has
remained an elusive clinical target due to its perceived undruggable nature. The�…

Inhibitors that target the receptor tyrosine kinase (RTK)/Ras/mitogen-activated protein kinase
(MAPK) pathway have led to clinical responses in lung and other cancers, but some patients�…

Mutations in the KEAP1-NRF2 pathway are common in NSCLC, albeit with a prevalence of
KEAP1 mutations in lung adenocarcinoma and an equal representation of KEAP1 and�…

Targeting ferroptosis, a unique cell death modality triggered by unrestricted lipid
peroxidation, in cancer therapy is hindered by our incomplete understanding of ferroptosis�…

Therapeutic targeting of KRAS-mutant lung adenocarcinoma represents a major goal of
clinical oncology. KRAS itself has proved difficult to inhibit, and the effectiveness of agents�…

KRAS mutated tumours represent a large fraction of human cancers, but the vast majority
remains refractory to current clinical therapies. Thus, a deeper understanding of the�…

In KRAS-mutant lung adenocarcinoma, tumors with LKB1 loss (KL) are highly enriched for
concurrent KEAP1 mutations, which activate the KEAP1/NRF2 pathway (KLK). Here, we�…

The Kelch-like ECH-associated protein 1 (KEAP1)–nuclear factor E2-related factor 2 (NRF2)
pathway has a central role in cellular antioxidant defense. NRF2 activation due to KEAP1 or�…