Michael Karin

Jan 1, 2025 | nature.com | Michael Karin

AbstractHepatocellular carcinoma (HCC) originates from differentiated hepatocytes undergoing compensatory proliferation in livers damaged by viruses or metabolic-dysfunction-associated steatohepatitis (MASH)1. While increasing HCC risk2, MASH triggers p53-dependent hepatocyte senescence3, which we found to parallel hypernutrition-induced DNA breaks. How this tumour-suppressive response is bypassed to license oncogenic mutagenesis and enable HCC evolution was previously unclear.

Nov 5, 2024 | sciencedirect.com | Yongfeng Lai |Weimin Wang |Peng Zhang |Michael Karin

Section snippetsFructose promotes tumor growth in APCmin/+ mouse modelTo investigate the role of fructose in CRC immune microenvironment, we employed both spontaneous adenoma and orthotopic tumor models.

Sep 12, 2023 | cell.com | Michael Karin

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