FBP1 controls liver cancer evolution from senescent MASH hepatocytes.

Hepatocellular carcinoma (HCC) originates from differentiated hepatocytes undergoing compensatory proliferation in livers damaged by viruses or metabolic-dysfunction-associated steatohepatitis (MASH). While increasing HCC risk, MASH triggers p53-dependent hepatocyte senescence, 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.

Considerations for Social Networks and Health Data Sharing: An Overview.

The use of network analysis as a tool has increased exponentially as more clinical researchers see the benefits of network data for modeling of infectious disease transmission or translational activities in a variety of areas, including patient-caregiving teams, provider networks, patient-support networks, and adoption of health behaviors or treatments, to name a few. Yet, relational data such as network data carry a higher risk of deductive disclosure. Cases of reidentification have occurred and this is expected to become more common as computational ability increases.

Mitochondrial metabolism and epigenetic crosstalk drive the SASP.

Senescent cells drive tissue dysfunction through the senescence-associated secretory phenotype (SASP). We uncovered a central role for mitochondria in the epigenetic regulation of the SASP, where mitochondrial-derived metabolites, specifically citrate and acetyl-CoA, fuel histone acetylation at SASP gene loci, promoting their expression. We identified the mitochondrial citrate carrier (SLC25A1) and ATP-citrate lyase (ACLY) as critical for this process.