A standard-deviation score increase was linked to coronary disease hazard ratios (relative event rates) of 0.74 in mutation carriers versus 0.68 in noncarriers.A standard-deviation score increase was linked to coronary disease hazard ratios (relative event rates) of 0.74 in mutation carriers versus 0.68 in noncarriers.
Cohort study of 427,295 UK Biobank participants, median 13.6-year follow-upPopulations
Limit: Coronary risk reduction from actively improving cardiovascular health scores was not measured
A commentary discussed evidence that an enzyme activated during dead-cell clearance helped tissue repair as artery plaques regressed in a mouse model.A commentary discussed evidence that an enzyme activated during dead-cell clearance helped tissue repair as artery plaques regressed in a mouse model.
Lab experiments showed that Olaparib treatment lengthened copied DNA tracts, increased DNA breaks and heightened drug sensitivity in cells lacking TET2, but not DNMT3A.Lab experiments showed that Olaparib treatment lengthened copied DNA tracts, increased DNA breaks and heightened drug sensitivity in cells lacking TET2, but not DNMT3A.
Experiments in laboratory-grown cells, against cells lacking DNMT3ATET2
Limit: The proposed sequence from damaged DNA sites to breaks remains a theoretical model
For one gene involved in DNA modification, 52.8% of patients flagged as carrying a mutation had no tumour-derived mutation in that gene.For one gene involved in DNA modification, 52.8% of patients flagged as carrying a mutation had no tumour-derived mutation in that gene.
In an analysis of 889,215 people, clonal blood mutations were associated with serious bacterial infections, with a hazard ratio of 1.22.In an analysis of 889,215 people, clonal blood mutations were associated with serious bacterial infections, with a hazard ratio of 1.22.
A yearly rise of at least 7.5% in mutated gene copies’ share best predicted cancer progression among patients with unexplained low counts of certain white blood cells.A yearly rise of at least 7.5% in mutated gene copies’ share best predicted cancer progression among patients with unexplained low counts of certain white blood cells.
In mice and mouse cells, disrupting TET enzymes allowed rare pre-existing aneuploid subclones, including chromosome 17 trisomy, to dominate during rapid cellular…In mice and mouse cells, disrupting TET enzymes allowed rare pre-existing aneuploid subclones, including chromosome 17 trisomy, to dominate during rapid cellular expansion.