ArticlebioRxiv : the preprint server for biology2025
HNF4α controls growth, identity and response to KRAS inhibition of invasive mucinous adenocarcinoma of the lung.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Cellular plasticity is a hallmark of cancer, enabling tumor cells to alter identity and evade therapeutic pressure. In invasive mucinous adenocarcinoma of the lung (IMA), NKX2-1 loss triggers a pulmonary to gastric switch marked by aberrant activation of HNF4α, a master regulator of gastrointestinal/hepatic differentiation. We find that HNF4α promotes IMA growth and activates a gastric pit cell-like program. SIGNIFICANCE: IMA is a genetically and epigenetically distinct LUAD subtype for which targeted therapies are lacking due to the high proportion of KRAS mutations. This study points to blockade of the HNF4α -> NRF2 axis as a potential strategy to enhance primary response to KRAS inhibition in IMA.
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