Stephen L. Slocum

TL;DR: This review highlights recent observations on the molecular interactions and their functional consequences between NRF2 and the arylhydrocarbon receptor (AhR), NF-κB, p53, and Notch1 signaling pathways, which provide a multi-tiered, integrated response to chemical stresses.

TL;DR: Multiple studies now demonstrate enhanced incidence, multiplicity, and/or tumor burden in Nrf2-disrupted mice compared to wild-type in models of inflammation and colon cancer, bladder cancer, lung disease and cancer, stomach cancer, mammary cancer, skin cancer, and hepatocarcinogenesis.

TL;DR: A functional role is reported for this cross talk between the two pathways and it is shown that disruption of Nrf2 impeded liver regeneration after partial hepatectomy and was rescued by reestablishment of Notch1 signaling.

TL;DR: It appears that Notch-to-Nrf2 signaling is another important determinant in liver development and function and promotes cell-cell cytoprotective signaling responses.

TL;DR: High-fidelity DNA sequencing and a mouse model are used to reveal high-resolution mutational spectra of the liver carcinogen aflatoxin B1 in histopathologically normal liver as early as 10 wk after exposure, proposing that the 10-wk HRMS reflects a short-term mutational response to AFB1, and is an early detection metric for AFB1-induced liver cancer in this mouse model.